NSBO22- Complete Lecture and Tutorial Information

Topics covered: Acute contexts: Peri-operative nursing Abdominal Aortic Aneurysm repair Nursing care of patients with cardiovascular health concerns o Coronary artery disease risk o Factors including hypertension o Acute coronary syndrome Percutaneous Cardiac Intervention (PCI) Balloon Angioplasty and Stent Insertion Nursing care of patients undergoing cardiac surgery o Including paediatric cardiac surgery Adult with hypertension Adult with Acute Coronary Syndrome Nursing care of patients with respiratory health concerns o Lower respiratory tract problems: pneumonia and bronchitis o Obstructive respiratory problems: COPD o Obstructive respiratory problems: asthma across the lifespan o Obstructive respiratory problems: paediatric respiratory focus- cystic fibrosis Child with asthma Adult with COPD Adolescent with Cystic Fibrosis Shock states o Revisit Hypovolaemic & Cardiogenic shock o Septic shock o Anaphylactic o Neurogenic shock The post-operative adult with hypovolaemic shock Nursing Care of patients with respiratory health concerns o Acute respiratory failure o Non-invasive ventilation o Arterial blood gasses Nursing care of patients with vascular health concerns

SOME DEFINITIONS and ELABORATIONS *Chronic illness- an illness of long duration, with slow progression or unpredictable course.

*Primary health care- health care encompassing a broad spectrum of activities to encourage health and wellbeing. First point of consultation for education, immunisation etc. *Secondary health care- Health care services provided by medical specialists and other professionals who generally do not have first contact with patients. It includes acute care; a necessary treatment for a short period of time for a brief but serious illness. Eg. Acute services for diagnosis and treatment. Eg. Treatment for stroke or radiological procedures *Tertiary health care- Specialized consultative health care, usually for inpatients and on referral from a primary or secondary health professional. Eg. Neonatal care, critical and emergency trauma care, neuroscience and chronic illness services. *Self efficacy- an individuals belief in their capacity to successfully learn and perform a specific behaviour. *incidence rate- number of new cases of a disease in a certain time period *Prevalence- number of new and old cases of a disease in a certain time period. Peri-operative nursing: Surgical settingsElective surgery- carefully planned event for the correction of a non-acute problem Emergency surgery- Requires immediate intervention because of life threatening consequences Urgent- requires prompt intervention; is potentially life threatening if treatment is delayed >24 48 hours. Diagnostic: requires intervention to determine origin/cause (eg. Laparoscopy) Palliative: is performed to relieve symptoms of a disease process but is not curative Cosmetic: intervention is primarily for alteration of personal appearance

Day-of-surgery admission- admission to the hospital on the day of the surgery Day surgery- endoscopes etc. usually take 2 hours or less and require a less than 3-4 hour stay, do not require overnight.

Suffix -ectomy -lysis -orrhaphy -oscopy -ostomy

Meaning Excision of removal of Destruction of Repair or suture of Looking into Creation of opening into

Example Appendectomy Electrolysis Herniorrhaphy Endoscopy Colostomy

-otomy -plasty

Cutting into or incision of Repair or reconstruction of

Tracheotomy Mammoplasty

Risk factors for surgeryAge- higher morbidity and mortality due to decreasing physiological status Cigarette smoking Alcohol Nutritional status malnourished and obese Pre-existing disease Current regular medications

Perioperative phase: This preoperative phase is initiated by the patients decision to have surgery and ends with the transfer of the patient onto the theatre trolley. Patient assessment: Admitting a patient to the surgical ward in a warm, welcoming manner Communication should be initiated with politeness Acknowledge individual responses to impending surgery Ensure privacy and confidentiality of data Ask patient for explanation, in own words, of why having surgery and what they are expecting. Physiological assessment: use an assessment framework systems approach or head to toe assessment hospital documentation. Focus on: Key areasHealth history Identify acute or chronic problems Respiratory Cardiovascular Integumentary and musculoskeletal Nutritional status and elimination Allergies (food, medications, tapes and latex) Herbs/vitamins/health supplements- ginseng, St Johns wort, ginko Previous anaesthetics/family history of problems with GA

Systems approach: Respiratory-

Note the presence of infection o History of dyspnoea, cough, asthma and COPD What to bring to the Anaesthetists attention Note history of smoking-link to post of comp ?medications- bronchodilators Auscultate breath sounds Determine baseline respiratory rate and pattern

CardiovascularNote the presence of angina, hypertension, arrhythmias, congestive heart failure, history of recent myocardial infarction, congenital, rheumatic or valvular heart disease. Pacemakers- diathermy avoided as can create alternative electrical current route that may impair fx Cardiac medications Assess baseline pulses- apical, radial and pedal for rate, rhythm and regularity Assess peripheral perfusion, capillary refill- baseline especially pre orthopaedic surgery Take blood pressure Assess for oedema- note location and severity

NeurologicalCognitive function, hearing and vision Cognitive fx especially among older patients Stress of surgery, dehydration, fasting, hypothermia, medications may impact on older patients more than younger patients Post-operative delirium History of stroke, TIAs spinal cord injury or disease of the nervous system such as CP, MG, Parkinsons Disease and MS

Urinary system History of renal or urinary problems/conditions Renal alterations can impact on fluid and electrolyte balance, coagulation, risk for infection and wound healing, medication metabolism and excretion Renal function tests such as serum creatinine and urea

Hepatic & Endocrine Problems with liver may impact on detoxification of anaesthetics and surgical medications, glucose control, clotting and response to medications may be altered. History of jaundice, hepatitis, alcohol abuse Endocrine Diabetic patients at risk for hypoglycaemia, hyperglycaemia, ketosis, cardiovascular alterations, impaired wound healing and infection risk. Preoperative BLS, ?usual dose of insulin or altered dose Thyroid dysfunction- altered metabolic fx and thyroid medications

Integumentary and musculoskeletal systems Assess mucous membranes for dryness and intactness Determine skin status- bruising breaks, dryness Note any limitations in range of motion Identify any medications that may affect coagulation Nail beds need to be visible therefor nail polish removed

Nutritional status Weigh patient Determine recent weight loss or gain through diet history Assess food and fluid intake patterns Identify medications that may affect imbalance o Diuretics o Laxatives o Antacids Assess presence of dentures and bridges/crowns, loose teeth

Baseline observations Blood pressure Heart rate Temperature Respirations SaO2 Urinalysis Weight

Psychosocial assessment Gather information about how the patient perceives their surgery Consider Situational changes Concerns with the unknown Concerns with body image Past experiences Knowledge

Diagnostic assessment & Screening Blood tests o FBC, Hb, WBC o Type & cross match Prothrombin time & INR o Electrolytes o Blood glucose o Urea and Creatinine, liver function tests

o Arterial Blood gases o Urinalysis Chest X-ray Electrocardiogram o Usually in men >40yrs, women >50yrs and significant cardiac history Pulmonary function tests

Other preoperative considerations Informed consent o Responsibility of the medical staff Consists of clear explanation of nature and intended purpose of procedure including risks and side effects Written consent o Signed by patient and doctor o Should be obtained prior to premedication Nil by mouth status During administration of anaesthetic there is potential to inhale contents of full stomach into lungs gastric juices have low pH Most elective patients will fast from food and fluids prior to surgery (usually 6-8 hrs) Recent research clear fluids up to 2 hours pre-op o Fasting for children standard 6 hrs. evidence shows that clear fluids up to 2 hours pre-op makes no difference Pre-medication o As per chart and doctors order Local hospital policy Skin preparation o Skin cannot be sterilised but effort is made to ensure it is as clean as possible o Determined by hospital policy Clipping or shaving of hair near the surgical site o shaving has potential infection problems with small cuts and abrasions of the skin o shower with aseptic wash reduction of complications deep vein thrombosis & pulmonary embolism use of compression stockings prior to surgery may be contraindicated o see JBI best practice on TED stockings possible marking of site- confirmed with surgical notes, patient x-rays education regarding leg exercises & deep breathing techniques

Deep breathing: helps prevent postoperative pneumonia and atelectasis. The patient should inhale and exhale as much air as possible. You are to explain the procedure and its purpose to the patient. 1.) Inhale slowly through the nose, distending the abdomen and exhaling slowly through pursed lips. 2.) Deep breathe as often as possible, preferably 5 to 10 times every hour during the postoperative, immobilized period.

Post-op venous thromboembolism Risk factorsCancer or treatment Heart or respiratory failure Acute medical illness Age over 60 CVL Travel >3hrs approx. 4 weeks prior, immobility Irritable bowel disease Obesity History Pregnancy or puerperium Recent MI or stroke Severe infection Contraceptive pill use Varicose veins

Need to assess the patient for risk and all patients unless contraindicated should be offered thigh length stockings & correct sizing and fitting. Hip surgery patients should be on low molecular weight heparin as well. Encourage mobility as soon as possible post-surgery. Nursing role to assist with transfer and accompany patient. - ensure all medical notes, X-rays and scans accompany patient to theatre complete pre-operative checklist. Intraoperative phase- commences when the patient is transferred onto the theatre trolley and ends when the patient is admitted into the recovery room. Roles in theatre: - Anaesthetic nurse - scrub nurse - Scout nurse NURSING PROBLEMS AND INTERVENTIONS Abdominal Aortic aneurism repairThe most common vascular problems that affect the aorta are aortic aneurysms and aortic dissection. Aneurysms are outpouchings or dilations of the arterial wall and are common problems involving the aorta, with most being found in the abdominal aorta. The larger the

aneurysm, the greater the risk of rupture and the dilated aortic wall becomes lined with thrombi that can embolise, leading to acute ischaemic symptoms to distal branches. Surgical therapyThe technique involves: 1. Incising the diseased segment of the aorta 2. Removing intraluminal thrombus or plaque 3. Inserting a synthetic graft which is sutured to the normal aorta proximal and distal to the aneurysm 4. Suturing the native aortic wall around the graft to that it will act as a protective cover All aneurysm resections require cross-clamping of the aorta proximal and distal to the aneurysm and can be completed in 30 -45 minutes, after which time the clamps are removed and blood flow to the lower extremities is restored. ComplicationsPerigraft leaks Aortic dissection Bleeding Graft dislocation and embolization Renal artery occlusion do to graft migration Graft thrombis Incisional site haematoma Incisional infection

ConstipationInterventionsHigh fibre diet Fluid intake Increase physical activity/mobilisation as soon as possible Proper positioning when defecating- sitting with knees flexed slightly higher than hips Work on contracting abdominal muscles on those with abdo muscle weakness

Urinary retention- This can be related to bladder pain, supine positioning, fear, analgesics and anaesthetic agents, surgical procedures. InterventionsAssess for bladder pain & distension Assess urine output and fluid balance Notify if no urine output within 6 hours post op

Normal position for voiding where possible Relieve pain Provide privacy

Emetogenic profiling- Determining the risk factors for Post-operative nausea and vomiting in the patient Risk factorsSurgical o Emergency o Inadequate pre-op fasting o Type: abdo, gynae, orthopaedic, laparoscopic, ENT o Duration >3hrs o Possibility of swallowing blood: tonsillectomy, rhinoplasty Anaesthetic o Opioid premed o General o Inhalation o Neostigmine use (drug- increases neve messages to gut) Patient characteristics o Women (2-3 times more likely) o Children (2x) o Obesity- accumulation of fat soluble anaesthetic agents o Medical history of gynae surgery, indigestion o Previous PONV o Non-smoker o Anxiety o Medications: eg. Digoxin o Metabolic disorders Post-operatively o Lack of pain control o Movement o Use of ng tube, oral airway o Prolonged fasting o Premature intake of food and fluids o Low BP o Dehydration o Environmental (hearing someone else vomit)

**Apfel risk scoring system: tick off appropriate matches to grade likelihood of PONV- take required action. Nursing interventionsAssess for and eliminate precipitating/causative factors

Pain, movement, prolonged fasting, premature intake post op, low BP, dehydration, sights sounds smell taste of vomiting, mouth care If on ng drainage ensure patency to reduce build up of gastric secretions Assess bowel sounds to consider re-introduction of oral intake Assess meds o Any that may cause nausea. Eg. Opioids? Medication therapy to treat nausea (collaborative)

Anti-emetics5Ht3 agonist - Zofran: ondanzetron o Blocks the serotonin at the vagal nerve terminators and in the chemoreceptor trigger zone o Acts peripherally and centrally

Cardiovascular disease- a class of diseases affecting the heart and blood vessels. It includes: Coronary artery disease Hypertension Angina and MI Heart failure Cardiac arrhythmias Inflammatory and valvular heart disease Peripheral vascular disorders

Risk parametersNon-ModifiableModifiableSmoking status o Lifestyle advice: quit Hypertension o Lifestyle advice: Limit salt to <6g/day Elevated serum lipids o Lifestyle advice: Limit foods containing saturated and trans fats High BMI o Lifestyle advice: limit energy intake to maintain a healthy weight. Ideal weight should be BMI >25kg/m2 and waist circumference <94cm in men, <80cm in women Poor nutrition Family history of premature CVD Increasing age Social history: ethnicity, socioeconomic status and mental health

Lifestyle advice: Consume a varied diet, rich in vegetables, fruits, wholegrains etc. Low physical activity o Lifestyle advice: at least 30 minutes moderate intensity physical activity on most or preferably every day of the week. Alcohol intake o Lifestyle advice: limit alcohol intake to <2standard drinks per day.

Related conditionsDiabetes Chronic kidney disease Familial hypercholestrolaemia Evidence of atrial fibrillation

Goals for serum lipoproteins (lipids) LDL (bad lipids) at <1.8mmol/L HDL (good lipids) at >1.0 mmol/L Triglyceride (TG) at <2.0mmol/L Non- High-density lipoprotein cholesterol (NHDL) at <2.5mmol/L

*Primary hypertension- is an elevated BP without identified cause (accounts for 90 95% of cases) Contributing factorsIncreases SNS activity Overproduction of Na retaining hormones and vasoconstrictors Increased sodium intake Greater than ideal body weight Diabetes mellitus Excessive alcohol consumption

*Secondary hypertension- accounts for 5 10% of cases Causes includeCoarctation or congenital narrowing of the aorta Renal disease (such as renal artery stenosis and parenchymal disease) Endocrine disorders (Cushings syndrome and hyperaldosteronism) Neurological disorders (brain tumours, head injury) Sleep apnoea Medications: o SN stimulants inc. cocaine o MAO taken with tyramine containing foods o Oestrogen replacement therapy o Oral contraceptive pill o NSAIDs

Liver cirrhosis Pregnancy induced hypertension

Pathophysiology of hypertension- for a rise in arterial pressure there has to be an increase in CO or SVR. CO= the total blood flow through the systemic or pulmonary circulation per minute SVR (systemic vascular resistances)= the force opposing the movement of blood within the blood vessels. The radius of the small arteries and arterioles is the principal factor determining vascular resistance and a small change in the radius can produce a major change in the SVR. Most with primary hypertension have normal CO but elevated SVR which indicates that it is contraction of the smooth muscle in the blood vessels causing this increase in BP. In a healthy person there are regulation measures for blood pressure (see below), when hypertension develops, one or more of the BP-regulating mechanisms are defective. Sympathetic nervous system regulationIn response to changes in BP baroreceptors in the carotid artery and aortic arch signals are transmitted to the vasomotor centre in the brain stem and noradrenaline is released. This binds to receptors on the heart. Alpha 1- causes vasoconstriction and increased contractility Alpha 2- causes vasoconstriction and inhibits noradrenaline release

Renal system regulationContributes to BP through the control of sodium excretion. The renin-angiotensin-aldosterone system increases or decreases BP in response to changes. RAASLow BP kidney releases Renin Renin converts angiotensinogen to angiotensin I ACE converts angiotensin I into angiotensin II angiotensin II stimulates the adrenal cortex to secrete aldosterone aldosterone stimulates the kidneys to retain sodium and water in increase BP. angiotensin II causes vasoconstriction it also causes tissue growth and remodelling of vessel walls- changes which are associated with primary hypertension and long term effects.

Classification of hypertensionNormal: >120/ >80. recheck in 2 years (or earlier if patient at cardiovascular risk) High-normal: 120-139/80-89. recheck in 1 year (or earlier) Grade 1: Mild hypertension. 140-159/90-99. confirm within 2 months Grade 2: Moderate hypertension. 160-179/100-109. reassess or refer within 1 month

Grade 3: Severe hypertension. 180/110. reassess or refer within 1-7days Isolated systolic hypertension: >140/<90 Isolated systolic hypertension with widened pulse pressure: >160/<70

InterventionsMedication: o Calcium channel blockers: Block the movement of extracellular calcium into the cells, causing vasodilation and decreased heart rate, contractility and SVR. o Low-dose thiazide diuretic: Inhibit NaCl reabsorption in the distal convoluted tubule; increase the excretion of Na and Cl Manage associated conditions Lifestyle modification Monitor BP

*Acute Coronary Syndromes (ACS)- This includes a broad spectrum of clinical presentations, spanning ST elevation MI through to an accelerated pattern of angina without evidence of myonecrosis. Clinical presentations- these result from myocardial ischaemia Unstable angina Acute MI ST segment elevation MI (STEMI) Non-ST segment elevation acute coronary syndromes (non-STEMI)

Pathophysiology of CADCoronary artery disease is included in the general category of atherosclerosis. Atherosclerosis is characterised by a focal deposit of cholesterol and lipids, primarily within the intimal wall of the artery. It can affect any blood vessels, though it has a preference for coronary blood vessels. As these lipids begin to deposit in the blood vessels they cause damage which causes a local inflammatory response which attracts platelets etc. and results in a thickening of the arterial wall. This build-up of plaque causes a narrowing of the arterial lumen and blocking of blood supply. *Angina- a condition where there demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart with oxygen and myocardial ischaemia occurs however there is no muscle damage. Angina PectorisPain or discomfort due to oxygen deficiency to the myocardium. It is divided into 3 major categories:

Stable angina: predictable episodes of chest pain (following exercise etc) it is the result of fixed obstructive coronary artery lesion. Vasospastic angina: also known as variant or Prinzmetals angina. It is caused by a coronary artery spasm and occurs in clusters- common during sleep, rest, walking. Unstable angina: also known as pre-infarction angina, acute coronary insufficiency and crescendo angina. It is unpredictable and represents and emergency. It may be reported as a worsening of symptoms with more severe and prolonged chest pain.

Assessment of chest painAll chest pain should be treated as if cardiac in origin- until proven otherwise. Rapid focused assessment of chest painP- Precipitating & palliative factors Q- Quality R- Region & radiation S- Severity, associated symptoms T- time Usually heavy, dull, retrosternal in nature and often accompanied with dyspnoea, nausea and diaphoresis. Consider patient history and risk factors to support the clinical picture. Perform and ECG and review urgently. Electrocardiogram (ECG)An ECG is a recording of the electrical activity of the heart as it undergoes depolarisation and repolarization to initiate the heartbeat. Other diagnosis for chest painNon-ischaemic cardiac o Eg. Pericarditis Gastric origin o Eg. Peptic ulcer, hiatus hernia Respiratory/thoracic o Eg. Pneumothorax, pulmonary embolis Musculoskeletal o Eg. Fractured rib, chest wall pain

How to distinguishAssessment using-

Administration of antacids, anginine (if not contraindicated) Patient history/presentation story Physical assessment ECG Biochemical markers

Health professionals role: education to reduce delaysProvide patients with written materials such as NHFA CHD will you recognize your heart attack fact sheet Encourage patients to refer to the heart attack facts website Educate key concepts of: o Warning signs of heart attack o Potential for these to differ in the future o How and when to use nitrate medicine (if appropriate) Importance for quick calling of 000 Importance of early treatment to reduce heart muscle damage To act quickly even if unsure Include patients immediate family

InterventionsAssess patient- are symptoms consistent with ACS Assess vital signs Perform 12 lead ECG within 5min o Determine underlying rhythm and ischaemic/infarct changes Administer nitroglycerine o PRN order, unless contraindicated, ambulance may have administered IV cannulation for emergency drug therapy Apply oxygen if O2sat <93% (B&E states pt. should be given 10L/min via rebreather mask) Organise blood tests o Troponin, FBC, electrolytes, blood glucose, lipids (within 24hrs) Assist to obtain chest X-ray as ordered if required. Medical staff to review pt. within 10 min of present Determine if pt meets criteria for reperfusion therapy: Yes or No: If NO: Assess/monitor the patient for: o Chest pain o ECG o Cardiac biomarkers o Pain relief If YES: assess symptom time of onset and proceed with appropriate treatment pathway o PCI vs Fibrinolysis therapy Sit patient comfortably: semi-fowlers Assess pain using PQRST Provide positive reassurance, ensure medical staff are alerted

Reassess

Ongoing monitoringVital signs Level of consciousness ECG rhythm, changes Pain and medication Monitor for complications: o Cardiac arrhythmias o Acute MI o Cardiac arrest

Pharmacological management of CHDAntiplatelet (aspirin) Anticoagulation (warfarin) ACEI/ARA Beta-blockers Statins (lipid lowering) Nitrates (Gtn) Insulin/oral hypoglycaemics

Non-pharmacological managementRest Reassurance Education- lifestyle advice Regular monitoring- consider cardiac rehabilitation Assess for depression, level of social support.

Cardiac markersTypically used to diagnose and MI: CK-MB: levels rise 3-12 hours after an MI, peak in 24hrs and return to normal within 2-3 days. Troponin: Highly specific markers with a greater sensitivity. Peaks more slowly than CK, but initial results are still available within hours of a myocardial event. Levels rise 3-12 hours after the onset of MI, peak at 24-48hrs and return to baseline over 5-14 days. Myoglobin: released into circulation within a few hours after an MI, however lacks cardiac specificity and is rapidly excreted in urine so blood levels return to normal range within 24hrs post MI.

Acute Myocardial Infarction (AMI)Occurs when coronary blood flow is interrupted for an extended period of time, causing myocite (heart muscle cells) necrosis, resulting in myocardial infarction (MI).

The extent of damage to the myocardium correlates to the length of time and surface area of the ischaemia. The ischemia begins in the subendocardium and if it persists, takes approximately 4-6hrs for entire thickness necrosis to occur (STEMI). ST-segment elevation MI (STEMI)STEMI is an acronym meaning ST segment elevation myocardial infarction. This is the more severe type as the coronary artery is completely blocked off by the blood clot and as a result virtually all the heart muscle being supplied by the affected artery starts to die. It produces the characteristic ECG change of elevation in the ST segment of the ECG. This indicates that a relatively large amount of heart muscle damage is occurring. (Full thickness of the heart muscle) Non-STEMIIn a non-STEMI MI, the blood clot only partly occludes the artery, and as a result only a portion of the heart muscle being supplied by the affected artery dies (partial thickness of the heart muscle wall). In contrast to the STEMI, this type does not produce characteristic elevation in the ST segment portion of the ECG. Percutaneous Cardiac Intervention (PCI) treatment for MIPCI is recommended as the first line of treatment for patients with confirmed MI (definitive ECG changes and/or positive cardiac markers). The goal is to open the affected artery within 90 minutes of arrival to the ED. The patient will have cardiac catheterisation to locate the blockage(s), assess the severity, determine the presence of collateral circulation and evaluate left ventricular function. With visualisation treatment can be selected. Benefits: Provides an alternative to surgical intervention Performed with local anaesthesia Patient is ambulatory within 24hrs Shorter hospital stay

Balloon angioplastyDuring this procedure a catheter equipped with an inflatable balloon tip is inserted into the appropriate coronary artery. When the blockage is located, the catheter is passed through it, the balloon is inflated and the atherosclerotic plaque is compressed, resulting in vessel dilation. Intracoronary stents are often inserted in conjunction with balloon angioplasty. A stent is an expandable mesh-like structure designed to maintain vessel patency by compressing the arterial wall and resisting vasoconstriction. Stents are carefully placed over the angioplasty site to hold the vessel open.

Because stents are thrombogenic (foreign body is likely to create clots), the patient is also treated with oral antiplatelet agents such as aspirin or clopidogrel. ComplicationsThrombis/embolis Abrupt closure and vascular injury Coronary spasm Possibility of arrhythmias during and after Artery damage Haemorrhage Infection

Fibrinolysis treatment for MITreatment with fibrinolytic therapy is aimed at stopping the infarction process by dissolving the thrombus in the coronary artery to reperfuse the myocardium. Should be given ASAP (ideally within 1hr, or within first 6hrs of symptoms)

Heart failureHeart failure is an abnormal clinical condition that involves impaired cardiac pumping. it may be caused by any interference with the normal mechanisms regulating cardiac output. CO depends on: preload; afterload; myocardial contractility; heart rate and the metabolic state of the individual. *Left-sided heart failure- the most common form of initial heart failure, it results from LV dysfunction which causes blood to back up through the left atrium and into the pulmonary veins. *Right-sided heart failure -causes a backup of blood flow into the right atrium and into venous circulation. The primary cause of right heart failure is left heart failure. It can also be caused by cor pulmonale which is right ventricular dilation and hypertrophy caused by pulmonary pathology (eg. COPD). Systolic HFThe most common cause of HF, results from an inability of the heart to pump blood. When the left ventricle loses its ability to generate enough pressure to eject blood forwards through the high-pressure aorta. The hallmark is a decrease in the LV ejection fraction (EF: the fraction of total ventricular filling volume that is ejected during each ventricular contraction)

Diastolic HFThis is heart failure with preserved systolic function. It is an impaired ability of the ventricles to relax and fill during diastole. This is can be show a preserved LV EF and systolic function, but with impaired LV filling.

PathophysiologyCAD and hypertension are major contributors to HF. As the heart begins to fail CO drops and initiates several compensatory mechanisms from the body: Sympathetic nervous response- increased release of adrenaline and noradrenaline increased HR, contractility and peripheral vascular constriction. Initially this helps compensate, but over time they are detrimental as they increase the myocardial demand for oxygen and increase the workload of a failing heart. Neurohormal responseLow CO results in lower kidney perfusion and resulting in the activation of the RAAS sodium and water retention increased Blood volume decreased CO Low CO results in decrease in cerebral perfusion pressure. Posterior pituitary secretes ADH to increase water reabsorption increased blood volume decreased CO DilationAn enlargement in the chambers of the heart following constant elevated pressure in the heart chambers. The muscle fibres of the heart stretch in response to the volume of blood in the heart at the end of diastole. Initially this results in increased CO, however eventually the elastic elements of the muscle fibres are overstretched and can no longer contract effectively, resulting in decreased CO. HypertrophyIn chronic HF this is an increase in the muscle mass and cardiac wall thickness in response to overwork and strain. It generally follows persistent dilation and leads to an increase in CO and tissue perfusion. However the hypertrophic heart muscle has poor contractility, higher oxygen demand and poor coronary artery circulation. Clinical signs of HFRight-sided heart failure Signs RV heaves Murmurs Peripheral oedema Weight gain Increased HR Oedema of dependent body parts (sacrum, anterior tibias, pedal oedema) Ascites Anasarca (massive generalised body oedema) Jugular venous distension Hepatomegaly Right-sided pleural effusion Symptoms Left-sided heart failure LV heaves Cheyne-stokes respirations Pulsus alternans (alternating pulses: strong, weak) Increased HR PMI displaced inferiorly and posteriorly (LV hypertrophy) Reduced PaO2, slightly increased PaCO2 (poor O2 exchange) Crackles (pulmonary oedema) S3 and S4 heart sounds

Fatigue Dependent oedema Right upper quadrant pain Anorexia and GI bloating Nausea

Fatigue Dyspnoea (shallow resps up to 32-40 breaths/min) Orthopnoea (shortness of breath in recumbent positions) Dry, hacking cough Pulmonary oedema Nocturia Paroxysmal nocturnal dyspnoea

DiagnosisOften difficult since neither patient signs nor symptoms are highly specific and may mimic many other medical conditions. Clinical presentation Chest X-ray Echocardiogram ECG Laboratory data o Cardiac enzymes (HF can result from MI) o BNP (hormones produced by the heart muscle that promote venous and arterial vasodilation)

ClassificationClass I- No limitation of physical activity. Ordinary physical activity does not cause fatigue, dyspnoea, palpitations or anginal pain. Class II- Slight limitation of physical activity. No symptoms at rest. Ordinary physical activity results in fatigue, dyspnoea, palpitations or anginal pain. Class III- Marked limitation of physical activity. Usually comfortable at rest. Ordinary physical activity causes fatigue, dyspnoea, palpitations or anginal pain. Class IV- Inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or angina may be present even at rest. If any physical activity is undertaken, discomfort is increased.

General cardiac knowledgeCO = HR x SV SV requires 3 factors: o Preload- The distending force that stretches the ventricular muscle immediately before electrical excitation and contraction o Myocardial contractility- Myocardial muscle undergoes fibre shortening to contract and force the blood out o Afterload- The resistance the LV has to overcome to maintain CO.

Acute decompensated HF-

Typically manifests as pulmonary oedema. In most cases of ADHF there is an increase in the pulmonary venous pressure caused by decreased efficiency of the LV. Ventilator support Positive inotropes o Dobutamine- Beta1 agonist- rise BP, increase CO o Dopamine- renal/mesenteric dilation o Noradrenaline- peripheral vasoconstriction, increase BP, CO

AssessmentSubjective Past health history o CAD (including recent MI), hypertension, cardiomyopathy, valvular or congenital heart disease, diabetes mellitus, thyroid or lung disease, rapid or irregular heart rate. Medications o Us of and compliance with any cardiac medications; use of diuretics, oestrogens, corticosteroids, phenylbutazone, NSAIDs, over the counter drugs. Health perception o Fatigue, depression Nutritional/metabolic o Usual sodium intake, nausea, vomiting, anorexia, stomach bloating; weight gain Elimination o Nocturia, decreased daytime urinary output, constipation Activity/exercise o Dyspnoea, orthopnoea, cough, palpitations, dizziness, fainting Sleep/resto Using a number of pillows for sleeping, paroxysmal nocturnal dyspnoea Cognitive/perceptual o Chest pain or heaviness, RUQ pain, abdominal discomfort, behaviour changes.

Objective Integumentary o Cool, diaphoretic skin, cyanosis or pallor, peripheral oedema Respiratory o Tachypnoea, crackles, rhonchi, wheezes; frothy, blood tinged sputum Cardiovascular o Tachycardia, S3S4 murmurs; pulsus alternans, PMI (point of maximal impulse) displaced inferiorly and posteriorly, jugular vein distension Gastrointestinal o Abdominal distension, hepatosplenomegaly, ascites Neurological o Behavioural changes, restlessness, confusion, decreased attention or memory

Priority interventions

Decreasing intravascular volume o Diuretics o Ultrafiltration o Fluid and sodium restrictions Decreasing venous return o High fowlers position (legs horizontal or dangling) o Gtn (vasodilator) Decreasing afterload o Vasodilators (sodium nitroprusside) Improving gas exchange o Oxygen mask o IV morphine o Non-invasive ventilator support (BiPAP, CPAP) Improving cardiac function o haemodynamic monitoring o more drugs Reducing anxiety o Sedative medications (benzodiazepines, morphine) o Nurse support

Less priority (still important) interventionsPhysical activity and rehabilitation o Techniques to conserve energy Education o Disease process teaching o Fluid/diet restrictions o Common S&S o Decompensated HF o Minimising side effects o Lifestyle modification o Influenza vaccine o Medication compliance

Alternative management therapiesCheck for/treat iron deficiency Consider fish oils as second line treatment Direct sinus node inhibition Use of devices: o Biventricular pacemakers Biventricular PPM- cardiac resyncronisation therapy o Implantable cardiac defibrillators

Management goalsTreat underlying cause

Alleviate the symptoms & improve QOL Decrease disease progression, prolong survival Improve activity tolerance Reduce hospital readmission o Reduce workload of heart o Increase force of myocardial contractility o Reduce venous congestion o Improve oxygenation and maintain respiratory status o Decrease sodium and water retention o Assess and treat iron deficiency

Pharmacological interventionsACE inhibitor o Dilates peripheral blood vessels o Reduces BP o Angiotensin II receptor antagonists are an alternative Diuretics o Reduce venous return (eg. Furosemide) Beta-adrenergic blockers o Decrease HR, conductivity, contractility and O2 demand o Selective and non-selective beta blockers Fish oil Cardiac glycoside o Principally used AF and HF o Increase force of contraction o Slows heart rate Vasodilator therapy o Arteriolar- reduce afterload, augment CO o Venous- reduce preload, lower ventricular filling pressure, reduce pulmonary congestion (eg. Nitrates- nitroglycerin) Iron supplements

Mechanical interventionsIntra-aortic balloon pumps o Used to improve coronary artery perfusion and decrease left ventricular afterload L ventricular assist devices o A mechanical pump used to support heart function and blood flow in people with weakened hearts

Intra-aortic balloon pumpThis device provides temporary circulatory assistance to the compromised heart by reducing afterload (via reduction in systolic pressure) and augmentating the aortic diastolic pressure.

It consists of a sausage-shaped balloon, a pump that inflates and deflates the balloon, control devices for synchronising the balloon inflation to the cardiac cycle, and fail-safe devices. The balloon is inserted percutaneously or surgically, under strict aseptic technique, into the femoral artery, advanced towards the heart and positioned in the descending thoracic aorta just below the left subclavian artery. Following placement, the positioning is confirmed by Xray. A pneumatic device cyclically fills the balloon with helium at the start of diastole (immediately after aortic valve closure) and deflates it just before systole. In the patient with a regular rhythm, the ECG is the primary trigger used to initiate deflation on the R wave and inflation on the T wave. During systole the balloon is deflated- facilitates ejection of the blood into the periphery In early diastole the balloon begins to inflate In late diastole the balloon is totally inflated- this augments aortic pressure and increases the coronary perfusion pressure. ComplicationsSite infection from invasive lines Pneumonia associated with immobilisation Arterial trauma- caused by insertion or displacement of balloon Thromboembolism caused by trauma, balloon obstruction of blood flow distal to catheter Haematological complications caused by platelet aggregation along the balloon Haemorrhage from insertion site Balloon leak or rupture

Cardiac surgeryReasonsCongenital abnormalities o Ventricular septal defect, tetralogy of fallot, patent ductus arteriosus) Conduction abnormalities Cardiac transplantation Valvular disease Coronary artery bypass grafting Repair of ventricular aneurysm

Coronary artery bypass graft (CABG)Consists of the construction of new conduits between the aorta or other major arteries and the myocardium distal to the obstructed coronary artery(ies).

Purpose- to alleviate angina symptoms and improve survival. Need suitable vessels for grafting ContraindicationsSevere aortic sclerosis LVF; renal, pulmonary or carotid disease

The procedure involves one or more grafts using the internal mammary artery, saphenous vein, radial artery, gastroepiploic artery and/or inferior epigastric artery. Internal mammary artery- most common artery used for bypass grafts. It is left attached to its origin (the subclavian artery) and dissected from the chest wall, it is then anastomosed (connected with sutures) to the coronary artery distal to the stenosis. (patency 98% at 5yrs) Saphenous vein- is also used for bypass grafts. It is removed from one or both legs and sections are anastomosed proximally to the ascending aorta and to a coronary artery distal to the blockage. (patency 71% at 10yrs) Radial artery- a thick, muscular artery that is prone to spasm when mechanically stimulated. Need to assess collateral circulation. (patency 89% at 4 yrs) Assessment- as above Intra-operative careCardiopulmonary bypassProvides a still, bloodless field for surgery Goal: provide body tissue with sufficient oxygen to meet metabolic requirements and remove by-products.

How: Causes heart arrest (cardioplegia solution) Post-operative periodComplicationsCardiovascular o Post-operative bleeding o Cardiac tamponade o Myocardial depression o Perioperative AMI o Arrhythmias Respiratory o CPB changes- increase in capillary permeability o Atelectasis o Pneumothorax o Pulmonary emboli

Renal o Lowered GFR and renal blood flow due to CPB GIT o Abdominal distension o GI bleeding o Electrolyte disturbances Neuropsychological o CNS deficits from cerebral ischaemia, infarction or emboli Associated with prolonged CPB time, perioperative hypotension or carotid artery disease Post-surgery delirium o Mild confusion, insomnia, hallucinations & agitation. Late post-operative complications o Wound infection

Priority interventionsAirway, breathing, Circulation Adequate oxygen while patient is intubated o Suctioning Assist in breathing After intubation: o Turning, coughing, deep breathing Pain control? o Positioning (fowlers) Monitor pulmonary function Watch for arrhythmias Assess for cardiac function o Monitor for BP, CO etc Fluid deficiency following surgery o IV fluids? o Assess urine output o Fluid resus? o Patient in supine position, with legs elevated. Fluid retention o Back to pre-op weight by discharge Re-warming Post-op bleeding o Monitor for shock o Inspect wound sites and dressings for blood Monitor for neurological function o Return to consciousness o Strength in extremities o Neurological assessment (motor and sensory)

BEGIN PAEDIATRICS

Paediatric cardiac careClinical assessment of cardiac functionHistory, especially mothers health history, pregnancy and birth history Birth weight & prematurity Family history Feeding patterns, weight gain, development Older children: ?exercise tolerance, activities, resp problems, oedema, palpitations, neurologic-fainting, headaches Recent infections or toxic exposure may precede heart diseases such as cardiomyopathy, rheumatic fever Physical examination

Inspection: Chest deformities o Check symmetry of chest wall and note bulging, an enlarged heart sometimes distorts the chest configuration Nutritional state o Failure to thrive or poor weight gain is associated with heart disease Colour o Cyanosis is a common feature of CHD, and pallor is associated with poor perfusion Unusual pulsations o Visible pulsations of the neck veins are seen in some patients Respiratory excursion o This refers to the ease or difficulty of respiration (eg. Tachypnoea, dyspnoea, expiratory grunt) Clubbing of fingers o This is associated with cyanosis

Palpation and percussion: Capillary refill 1-2secs (remember cool temp prolongs) Palpate to determine apical pulse o Usually lateral to Mid-clavicular line and 4th intercostal space in children under 7yrs o At the left mid-clavicular line and 5th intercostal space in children over 7yrs o Gives an idea as to the size of the heart as it is lower and more lateral with enlargement Abdomen o Hepatomegaly or splenomegaly may be evident Peripheral pulses o Rate, regularity, and amplitude may reveal discrepancies Percussion- not done

Auscultation: Heart rate and rhythm o Listen for tachycardia and bradycardia, or irregular rhythms o Listen for quality, intensity, rate and rhythm o S1 and S2 should be clear and distinct with a rate equal to radial pulse, regular and even o Aortic area- (2nd RICS close to sternum) the S2 should be greater than S1 o Pulmonic Area- (2nd LICS close to sternum) splitting of S2 heard best (normally widens on inspiration) o Erb point- (2nd and 3rd LICS close to sternum) innocent murmurs frequently heard from this site. o Tricuspid area- (5th R&LICS close to sternum) S1 louder sound than receding S2 o Mitral or Apical Area- (5th ICS left MCL in children, in infants 3-4th ICS and lateral to LMCL) S1 heard loudest, splitting of S1 may be audible

S3 and S4 heart soundsS3- a result of vibrations produced during ventricular filling and is normally heard in some children and young adults but considered abnormal in older adults S4- recoil vibrations between atria and ventricles following atrial contraction at end of diastole- rarely heard as a normal heart sound, further investigation needed. Innocent murmursUsually occur with or after S1 Usually low pitched, musical or groaning quality Grade 3 or less in intensity and dont increase over time Usually loudest in pulmonic area with no transmission to other areas of the heart Audible in supine position but absent in the sitting position Not associated with other physical signs of cardiac disease

Variations of heart ratePulsus paradoxus- intensity or force of pulse decreases with inspiration o Marked seen in significant airway obstruction Pulsus bigeminus- coupled rhythm, beat felt in pairs because of premature beat Sinus arrhythmia- rate increases with inspiration, decreases with expiration

Foetal anatomyOxygenated blood from mother comes through Umbilical vein goes into the right atrium but straight through foramen ovale into the left atrium into left ventricle oxygenated blood pumped up primarily through to the carotid (supply the brain) Deoxygenated blood gets returned through the superior vena cava into the right atrium into the right ventricle pumped through the ductus arteriosus (to bypass the lungs, no need to

oxygenate) which joins up with the aorta distal to the branches for carotid arteries joins with rest of the blood to return to the mother for re-oxygenation via the umbilical artery. Foramen ovaleAn opening between the right and left atria which allows the blood to flow into the aorta and decreases PAP. Adaptations to extrauterine lifeNegative pressures generated 60 90mmH20 o Fill lungs with air- fluid expelled and absorbed into lymphatic system With the first few breaths PaO2 or arterial oxygen tension increases from 2-3.5kPa to the newborn level of 9-13kPa and the relative hyperoxia results in closure of the ductus arteriosus. o Functionally closed by 10-15hrs, anatomically closed 4-7 days Fall in pulmonary vascular resistance and increase in pulmonary blood flow o Decreases pressure in rt side of heart, blood no longer shunts across Foramen ovale.

Classification of congenital heart diseaseAcyanotic defects- Includes blood flow patterns of: Increased pulmonary blood flow; Atrial septal defect Ventricular septal defect Patent ductus arteriosus Atrioventricular canal

Obstruction to blood flow from ventricles Coarctation of aorta Aortic stenosis Pulmonic stenosis

Cyanotic defects- includes blood flow patterns of: Decreased pulmonary blood flow; Tetralogy of fallot Tricuspid atresia

Mixed blood flow Transposition of great arteries Total anomalous pulmonary venous return Truncus arteriosus Hypoplastic left heart syndrome

Patent ductus arteriosusFailure of the fetal ductus arteriosus (artery connecting the aorta and pulmonary artery) to close within the first weeks of life. The continued patency of this vessel allows blood to flow from the higher-pressure aorta to the lower-pressure pulmonary artery, which causes a left to right shunt. DiganosisClinical findings: -most children with PDA do not have heart related symptoms. If the ductus is large in size, symptoms of congestive heart failure may develop. Congestive heart failure can develop at any time but more commonly presents during the firsts 2 3 months of life. The symptoms include: Rapid breathing Poor feeding Slow growth Cold, clammy sweating Characteristic machinery-like murmur Widened pulse pressure Bounding pulse

Medical tests Electrocardiogram Oxygen saturation Chest x-ray Diagnosis confirmed by echocardiogram

Top 10 cardiac abnormalities (brief overview, unsure if need to know about them)Atrial septal defect- abnormal opening between the atria, allowing blood from the higherpressure left atrium to flow into the lower-pressure right atrium. Ventricular septal defect- abnormal opening between the right and left ventricles. Coarctation of the aorta- localized narrowing near the insertion of the ductus arteriosus, which results in increased pressure proximal to the defect (head an upper extremities) and decreased pressure distal to the obstruction (body and lower extremities) Aortic stenosis- narrowing or stricture of the aortic valve, causing resistance to blood flow in the left ventricle, decreased cardiac output, left ventricular hypertrophy, and pulmonary vascular congestion. Pulmonic stenosis- narrowing at the entrance to the pulmonary artery. Resistance to blood flow causes right ventricular hypertrophy and decreased pulmonary blood flow. Tetralogy of Fallot- The classic form includes four defects: 1. Ventricular septal defect, 2. Pulmonic stenosis, 3. Overriding aorta, and 4. Right ventricular hypertrophy.

Tricuspid atresia- The tricuspid valve fails to develop; consequently there is no communication from the right atrium to the right ventricle. Transposition of the Great Arteries (or great vessels)- the pulmonary artery leaves the left ventricle, and the aorta exits from the right ventricle, with no communication between the systemic and pulmonary circulations. Total anomalous pulmonary venous connection- Rare defect characterized by failure of the pulmonary veins to join the left atrium. Instead, the pulmonary veins are abnormally connected to the systemic venous circuit via the right atrium or various veins draining toward the right atrium, such as the superior vena cava. Hypoplastic left heart syndrome- underdevelopment of the left side of the heart, resulting in a hypoplastic (underdeveloped) left ventricle and aortic atresia. Most blood from the left atrium flows across the patent foramen ovale to the right atrium, to the right ventricle, and out the pulmonary artery. Congestive heart failure in childrenCHF is the inability of the heart to pump an adequate amount of blood to the systemic circulation at normal filling pressures to meet the bodys metabolic demands. In children, CHF most frequently occurs secondary to structural abnormalities (eg. Septal defects) that result in increased blood volume and pressure within the heart. Clinical manifestationsTypically fall into three main groups: Impaired myocardial function, manifests as: Tachycardia Sweating Decreased urinary output Fatigue Weakness Restlessness Anorexia Pale, cool extremities Weak peripheral pulses Decreased blood pressure Gallop rhythm Cardiomegaly

Pulmonary congestion, manifests as: Tachypnoea Dyspnoea Retractions (infants) Flaring nares

Exercise intolerance Orthopnoea Cough, hoarseness Cyanosis Wheezing Grunting

Systemic venous congestion, manifests as: TreatmentThe goals of treatment are to: Improve cardiac function: Use of digoxin (drug) to improve contractility ACE inhibitors to reduce vasoconstriction and decrease afterload Weight gain Hepatomegaly Peripheral oedema (especially periorbital) Ascites Neck vein distention (children)

Remove accumulated fluid and sodium: Diuretics (eg. Lasix, spironolactone) to eliminate excess water and salt

Decrease cardiac demands: Minimise metabolic needs by: o Limiting physical activity o Maintaining body temperature o Treating any infections o Reducing the effort of breathing (semi-fowlers) o Using medication to sedate an irritable child

Improve tissue oxygenation All the preceding measures serve to increase tissue oxygenation Supplemental cool humidified oxygen may be administered to increase the amount of available oxygen during inspiration.

ACE inhibitors- These drugs inhibit the normal function of the renin-angiotensin system in the kidney. Angiotensin II is one of the bodys most potent vasoconstrictors. The ACE inhibitors block the conversion of angiotensin I to angiotensin II so that, instead of vasoconstriction, vasodilation occurs. Vasodilation results in decreased pulmonary and systemic vascular resistance, decreased BP and decreased afterload.

Drugs- Catopril and Lisinopril Beta blockers- These drugs block the alpha and beta adrenergic receptors which causes decreased heart rate, decreased BP and vasodilation Side effects: dizziness, headache and hypotension Digoxin- Helps the make the heart beat stronger with a more regular rhythm. ConsiderationsAlways take apical pulse for one minute before administering o Do not gibe if HR below 90-110bpm (infants), below 70 (young children) Give at regular intervals, usually every 12 hours Administer carefully o Slowly direction it to the side and back of the mouth Do not mix with foods or other fluids If the child has teeth, give water after administration of the drug If dose is missed, do not give make-up dose If child vomits, do not give second dose Frequent vomiting, poor feeding or slow heart rate can be signs of toxicity. Contact the physician Keep digoxin in a safe place, preferably in a locked cabinet

Nutritional needs of infants with CHFMetabolic rate greater due to poor cardiac fx and increases HR and RR Caloric requirements greater than healthy infants Ability to take inc calories made difficult by their fatigue Feeding = exercise = lack of energy and cardiac reserve 3hrly feeding optimal to allow rest between and limit volume amount (large amounts not tolerated) 150mls/kg/day or 120kcal/kg/day for newborns Nasogastric feeding may be required Increased calories by adding polycose, MCT oil, fortifying breastmilk Breastfeeding possible and recommended for infants

Promote fluid lossDiuretics Strict fluid balance chart recording and monitoring Potassium losing diuretics o Serum potassium levels checked frequently o Diet high in potassium (eg. Bananas, oranges)

Cardiovascular demand in the neonatal periodCO in proportion to body weight is high o O2 consumption high

Period of large growth RR= 22 35/min o Limited by small number of large alveoli Normal adaptation of CVS that occurs after birth is delayed in sick newborns o Hypoxaemia, hypercapnoea, hypothermia, sepsis, low gestational age & haematological abnormalities

Circulating blood volume: Neonates o 85-90mls/kg Infants o 75-80mls/kg Children o 70-75mls/kg Adults o 65- 70mls/kg

Paediatric shockShock in the infant occurs with alteration in supply or demand of oxygen, water, and/or glucose. There is generally an: Inadequate substrate uptake o This may be caused by primary pulmonary disease, intrapulmonary or intracardiac shunting, diarrhoea, starvation etc. Inadequate substrate delivery o This may be caused by poor cardiac performance, disturbed vascular tone, inadequate circulating volume (absolute and relative) Inadequate substrate utilisation

Physiological response to shockSNS responseBut CO is already high. Therefore reliance is on tachycardia Emphasis is on alpha adrenergic receptors

Renal responseRAAS activation ADH Cortisol (stress)

Early (compensated or reversible) shock-

Vital organ function is maintained by intrinsic compensatory mechanisms; blood flow is usually normal or increased but generally uneven or maldistributed in the microcirculation. In early shock the SNS is stimulated in response to decreased CO, resulting in: Pre-capillary sphincters close Blood is shunted to vital organs Increased HR and strength of contraction Increased RR, bronchodilation Increased PVR BP is normal but with narrowed pulse pressure

Assessment via: Heart rate o Unexplained tachycardia Perfusion to brain o Level of consciousness o o Apprehensiveness o Irritability Skin o Pallor o Capillary refill o Skin temp Kidneys o Urinary output BP o Normal BP o Narrowing pulse pressure

Late (decompensated) shockCompensatory mechanisms begin to fail and the efficiency of the cardiovascular system gradually diminishes until perfusion in the microcirculation becomes marginal despite compensatory adjustments. Classic signs present Adrenaline and noradrenaline release- maximum constriction o Constriction results in ischaemia to tissues o Impaired cell metabolism and release of waste products that affect vascular tone, heart contractility CO output falls and hypotension Liver and spleen release stored RBC and plasma Blood stagnates in capillary beds due to constriction o Coagulation Anaerobic metabolism

o Lactic acid metabolic acidosis Reduction in O2 carrying capacity o Microthrombi form as deoxygenated RBC clump together Disseminated Intravascular coagulation (DIC) Irreversible shock o Cardiac dysrhythmias Irreversible damage to vital organs death

Assessment via: Heart rate o Non-specific BP o Still maintained Skin o Cool, pale extremities o Degreased skin turgor o Poor capillary filling Level of consciousness o Confusion and somnolence Respiratory rate o Tachypnoea Kidney o Decreased urine output

RememberInitial signs may be subtle in infant/child Progression from compensated to decompensated shock occurs suddenly and rapidly By the time BP drops 25% of circulating blood volume is lost and cardiac arrest is imminent

Causes of shockHypovolaemic Haemorrhage Diarrhoea Vomiting Burns Peritonitis

Distributive Septicaemia Anaphylaxis Vasodilating drugs Spinal cord injury

Cardiogenic Arrhythmias Cardiomyopathy Heart failure Valvular disease Myocardial contusion Myocardial infarction

Obstructive Tension pneumothorax Haemopneumothorax Flail chest Cardiac tamponade Pulmonary embolism Hypertension

Dissociative Profound anaemia Carbon monoxide poisoning Methaemoglobinaemia

Paediatric cardiac arrest90% of infants have a non-cardiac, usually pre-respiratory cause for arrest o Acidosis 10% of infants have a cardiac cause of arrest o Without acidosis Management requires a systematic, coordinated approach o PALS

END PAEDIATRICS Care of the respiratory patientRespiratory defence mechanismsParticle filtration in nostrils Sneezing Mucociliary escalator o Mucous production to trap microorganisms o Cilia waft mucous (sputum) towards epiglottis o Most sputum swallowed & microbes destroyed by pH in stomach Coughing o Sputum expectorated o Sputum in oropharynx swallowed

Risk factors for chronic respiratory diseaseTobacco smoke (second hand also) Other indoor air pollutants (eg. Smoke from solid fuels) Outdoor air pollutants (eg traffic related air pollution) Allergens (eg. Mites, animals, plants, fungi) Occupational agents (eg asbestos, coal)

Respiratory assessmentNote signs of: Cough Sputum and nasal secretions Dyspnoea Pain Sleep/rest disturbances Environmental factors

Perform: Inspection, palpation, percussion, auscultation Vital signs- T, P, RR, BP o Respiratory pattern o Accessory muscle use SpO2 Arterial blood gas Pulsus parodoxus Chest X-ray CT MRI Pulmonary angiogram Ventilation/perfusion scan Pulmonary function test

Acute bronchitis: inflammation/infection of the bronchi in the lower respiratory tract. Damage to epithelial cell lining Viruses or bacteria replicate and destroy cells Peaks 2-3 days then epithelial cells replaced Extensive damage > sloughing > favourable environment for bacterial infection ** most caused by viruses (rhinovirus, influenza)

Clinical signs and symptoms: Persistent cough Clear, mucoid sputum Headache

Malaise SOB on exertion Mildly raised T, P, RR Occasionally crackles or wheeze Clear chest X-ray Bacterial- chest pain from cough

Management: Rest Fluids Cough suppressants Bronchodilators (if wheeze) If bacterial- antibiotics

Pneumonia- an acute inflammation of lung parenchyma caused by infection Causative agents: o Bacteria o Viruses o Fungi o Protozoa (uncommon) o Parasites (uncommon) Classification o Community acquired o Hospital acquired (nosocomial)

PathophysiologyPneumonia can be caused by a number of agents. These organisms can reach the lung by three methods: Aspiration- from the nasopharynx or oropharynx. Many of the organisms that cause pneumonia are normal inhabitants of the pharynx in healthy adults. Inhalation- of microbes present in the air. Eg. Mycoplasma pneumonia and fungal pneumonias Haematogenous spread- from a primary infection elsewhere in the body. Eg. Staphylococcus aureus.

The most common cause of bacterial pneumonia is pneumococcal pneumonia which has four characteristic stages: 1. Congestion- after the pneumococcus organisms reach the alveoli via droplets or saliva, there is an outpouring of fluid into the alveoli. The organisms multiply in the serous fluid and the infection is spread. The pneumococci damage the host by their overwhelming growth and interference with lung function.

2. Red hepatisation- There is massive dilation of the capillaries and the alveoli are filled with organisms, neutrophils, red blood cells and fibrin. *notes: oedematous fluid and pneumococci- red appearance of lung tissue. 3. Grey hepatisation- Blood flow decreases and leucocytes and fibrin consolidate in the affected part of the lung. ** notes: fibrin development over pleural surface, phagocytosis. 4. Resolution- Complete resolution and healing occur if there are no complications

*This pathophysiology is similar to other types of pneumonia. InterventionsAppropriate antibiotic therapy Increased fluid intake (at least 3L per day) Limited activity and rest Antipyretics Analgesics Oxygen therapy (if indicated) Position to minimise respiratory efforts (fowlers, over-bed table for patient to lean on) Remove secretions o Encourage coughing Sitting position with head slightly flexed, shoulders relaxed and knees flexed. Inhale deeply several times, exhale slowly and cough at the end of exhalation o Suctioning to clear airway

Severity assessmentPORT (pneumonia Outcomes Research Team) Severity index CURB-65 o C- Confusion o U- BUN >7mmol/L o R- RR 30 or higher o B- BP systolic <90mmHg or diastolic <60mmHg o 65- patient >65yrs 1 point for each. Score >3 results in higher hospitalisation and mortality. Consider ICU.

ComplicationsPreventionAtelectasis Pleurisy Pleural effusion Delayed resolution Acute respiratory failure

Cease smoking Pneumococcal influenza vaccine for patients: o With chronic illness (ie. COPD) o Recovering from severe illness o 65yrs or older o Resident of long term care facility Adequate nutrition, exercise and rest Hospitalized patient: o Monitor and intervene for at risk patients- altered level of consciousness, dysphagia, postoperative, immobilised, mechanically ventilated.

COPDA lung disease which is characterized by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible It is usually considered to be a combination of both chronic bronchitis and emphysema. Airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking. PathophysiologyNoxious particles and gases cause: inflammation of central airways o Inflammatory cells (lymphocytes, macrophages, neutrophils) o Inflammatory mediators Peripheral airway remodelling Parenchymal destruction o Imbalance between proteinase and antiproteinase Pulmonary vascular changes o Thick vessels o Inflammatory cells infiltrate o Collagen deposition o Destruction of capillary bed Results in: o Mucus hypersecretion o Cilia dysfunction o Airflow limitation o Hyperinflation of lungs o Gas exchange abnormalities o Pulmonary hypertension o Cor pulmonale

Oxygen use for COPD-

Oxygen therapy is frequently used in the treatment of COPD. Long term O2 therapy improves survival, exercise capacity, cognitive performance and sleep in hypoxemic patients. It should be: o Titrated to achieve SpO2 90% o Given through appropriate delivery device to achieve this o Start with low concentrations and titrate up o Consider humidification if tenacious sputum

COPD guidelinesC: confirm diagnosis and assess severity O: optimise function P: Prevent deterioration D: Develop support network X: Manage eXacerbations

Pulmonary rehabilitationPatient assessment: o Medical history o Smoking and nutritional status o Spirometry o Exercise capacity (eg. 6min walk test) o Quality of life (eg. Chronic respiratory disease questionnaire) o Breathlessness (eg. Modified Borg scale) o Patient goals Design exercise program: o Lower limb endurance o Upper limb endurance o Lower limb strength o Upper limb strength o Flexibility, strength, balance Determine appropriate exercise: o Intensity o Duration o Frequency Patient education: o Medications o Breathing techniques/managing breathlessness o Exercise o Nutrition o Coping with chronic lung disease Management of depression, anxiety, panic attacks Program evaluation o Patient outcomes o Patient feedback

Communication with GP o Pre and post program patient assessment Maintenance o If possible supervised session 1/week or regular assessment every 6 months o Encourage home exercise program

Complications of COPDAcute exacerbations o Excess sputum, coughing, dyspnoea etc Acute respiratory failure o Patients who ignore exacerbations or discontinue bronchodilator treatment are at risk for acute respiratory failure. Peptic ulcer o The incidence of peptic ulcer disease is increased in people with COPD. The reason for this occurrence is partly explained by hypersecretion of gastric acid resulting from increased arterial carbon dioxide and decreased arterial oxygen tension. This occurs only in patients who chronically retain carbon dioxide. o Ulcers are more common in the duodenum rather than the stomach and do not present with pain. Depression/anxiety o Patients with COPD experience many losses as the disease progresses over time. They can feel helpless with low self-esteem and be unable to vent their emotions for fear of compromising their breathing. o Anxiety can complicate respiratory compromise and may precipitate dyspnoea and hyperventilation. Cor Pulmonale o This is hypertrophy of the right side of the heart, with or without heart failure and resulting from pulmonary hypertension. o In COPD, pulmonary hypertension is caused primarily by constriction of the pulmonary vessels in response to alveolar hypoxia. o Cor pulmonale is a late manifestation of chronic pulmonary heart disease. o When pulmonary hypertension develops, the pressure on the right side of the heart must increase to push blood into the lungs- eventually the right side hypertrophies and right-sided heart failure develops.

AsthmaFacts and figuresAustralias asthma prevalence is high by international standards. It has declined in kids over the past decade but has remained stable in adults More boys than girls have asthma, but after about age 15 its more common in woman than in men Asthma is more common in Indigenous Australians, particularly adults, than in other Australians In 201, 416 people died from asthma, with the risk highest in the elderly

Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. Causing widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. Inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning. The inflammation also exacerbates existing bronchial hyperresponsiveness. Attacks may last for a few minutes to several hours, patient may be asymptomatic between attacks with normal or near-normal pulmonary function.

PathophysiologyThe primary pathophysiological process in asthma is persistent but variable inflammation of the airways. This results in: Smooth muscle hypertrophy and hyperplasia Inflammatory cell infiltration Oedema Goblet cell and mucous gland hyperplasia Mucous hypersecretion Protein deposition including collagen Epithelial desquamation

These inflammatory changes lead to airway obstruction or narrowing and can cause permanent changes in the airways. Long term changes include: Increased smooth muscle Increase in bronchial blood vessels Thickening of collagen layers Loss of normal dispensability of the airway.

Asthma triggersAllergy Viral respiratory infections Gastro-oesophageal reflux Cold air exposure Exercise House dust mites, pollens or moulds Animal fur Work-related triggers (eg. Wood dust, chemicals, metal salts) Irritating substances breathed in the air, such as cigarette smoke Some food additives Certain medications (eg. Aspirin, some blood pressure drugs)

Diagnosing asthma in childrenIn the majority of children, the diagnosis of asthma is based on a history of recurrent or persistent wheeze in the absence of any other apparent cause In young children, the diagnosis of asthma can be confirmed by a clinical response to an inhaled bronchodilator. In children aged 7yrs and over, use spirometry to confirm the diagnosis of asthma. In young children, care is needed to exclude non-asthma causes of wheeze. When cough is the predominant symptom of suspected asthma, careful assessment is needed to avoid making an incorrect diagnosis of asthma, or instigating inappropriate management. Exercise-induced dyspnoea is not always due to asthma, even in children with a confirmed diagnosis of asthma. Other causes of wheeze in young childrenTransient infant wheezing o Onset in infancy o No associated atopy o Associated with maternal smoking Cystic fibrosis o Recurrent wheeze and failure to thrive Inhaled foreign body o Sudden onset o Milk aspiration-cough during feeds, especially liquids o Associated with developmental delay Structural abnormality o Onset at birth Cardiac failure o Associated with congenital heart disease

Diagnosis of asthma in adultsHistory The presence of one or more of the following characteristic symptoms is suggestive of asthma: o Wheeze o Chest tightness o Shortness of breath o Cough Asthma is especially likely if any of the following applies: o Symptoms are recurrent or seasonal o Symptoms are worse at night or in the early morning

Symptoms are obviously triggered by exercise, irritants, allergies or viral infections o Symptoms are rapidly relieved by a short-acting bronchodilator However symptoms of asthma vary widely from person to person. The absence of typical symptoms does not exclude the diagnosis of asthma. In some aboriginal and Torres Strait Islander communities, asthma is commonly known as short wind. Health professionals should be aware of this term so as to avoid potential misdiagnosis or confusion with other causes of exertional dyspnoea.

Physical assessmentWheeze is suggestive, but not diagnostic of asthma The absence of physical signs does not exclude a diagnosis of asthma Crackles on chest auscultation indicate an alternate or concurrent diagnosis History or signs of allergic rhinitis Chest x-ray not routinely done but can show hyperinflation & will confirm or rule out other problems if uncertain presentation.

Key elements of Asthma managementPharmacological management: Bronchodilator (reliever) medication Anti-inflammatory (preventer) medication Long-acting beta2 agonist (symptom controller) medication usually prescribed in combination with an inhaled corticosteroid (ICS) preventer. Combination medications consist of and ICS and a symptom controller in a single inhaler device.

Education to improve asthma control: Allergen avoidance/control Use of a written asthma action plan Smoking cessation, diet and exercise (including specific management of exercise-induced asthma if required)

Incorrect inhaler techniqueIncorrect technique is common among older patients with asthma & COPD, maintenance of correct technique wanes over time. Reasons may include: Co-morbidities Inadequate coordination of inspiration and inhaler Inability to achieve a high enough inspiratory flow rate Inability to achieve a firm seal around mouthpiece Lowe educational level associated with ^incorrect technique Technique can be improved by education and mount by HP ^likelihood of correct technique

Can you show me how to us your inhaler?

Cystic fibrosis- The most common lethal genetic disease among Caucasian children, adolescents and young adults. Diagnosis is usually made within 10days of birth using Guthrie test and confirmed using sweat test. 1 in every 2000 births produces a child with CF It is transmitted as an autosomal recessive trait 1 in 25 people in Australia are symptomless carriers of the CF gene If both parents are carriers: o 25% chance of having a child with CF o 50% chance that the child will be a carrier

It is characterised by altered function of the exocrine glands involving primarily the lungs, pancreas and sweat glands. Abnormally thick, abundant secretions from mucus glands can lead to a chronic, diffuse, obstructive pulmonary disorder in almost all patients. It is not curable at present but life expectancy has increased with advances in treatment & medication. Severe chronic lung diseaseMucous clogs bronchi and bronchioles Increases susceptibility to infection and obstruction Infection caused by staph aureus and pseudomonas Fibrosis of lung tissue with can lead to pneumothorax and impaired gas exchange

Gastrointestinal changesThick mucous blocks pancreatic ducts Cysts formed in pancreas- replaced by fibrous tissue These prevent the secretion of pancreatic enzymes o Trypsinogen, lipase & amylase do not reach the intestine to digest ingested nutrients- malabsorption of fats and proteins, and fat soluble vitamins. o Fats remain undigested o Steatorrhoea (the presence of excess fat in the faeces) and azotorrhea (excessive discharge of nitrogenous substances in the faeces or urine) Impairment of digestion and absorption of nutrients

Clinical manifestationsMeconium Ileus (bowel obstruction in babies first movement, due to it being even thicker and stickier than normalAbdominal distention Vomiting Failure to pass stools Rapid development of dehydration

GI manifestationsLarge, bulky, loose, frothy, extremely foul-smelling stools Voracious appetite (early in disease) Loss of appetite (later in disease) Weight loss Marked tissue wasting Failure to grow Distended abdomen Thin extremities Sallow skin Evidence of deficiency of fat-soluble vitamins A,D,E and K Anaemia

Pulmonary ManifestationsInitial signs o Wheezy respirations o Dry, non-productive cough Eventuallyo Increased dyspnoea o Paroxysmal cough o Evidence of obstructive emphysema and patchy areas of atelectasis Progressive involvemento Overinflated, barrel-shaped chest o Cyanosis o Clubbing of fingers and toes o Repeated episodes of bronchitis and bronchopneumonia

Nursing interventionsManaging GI problems and nutrition Maintain optimal nutrition Replace pancreatic enzymes o Cotazyme, pancrease o 1-5 caps with meal-enteric coated High protein, limited fat diet. Or may tolerate normal diet if taking enzymes Require up to 150% of Recommended Daily Intake to meet growth needs Vitamin and possible iron supplementation Added dietary salt whenever sweating is excessive Enteral feeding for prolonged malnutrition o Supplemental night gastrostomy feeding Management of constipation and rectal prolapse Cystic fibrosis related diabetes GOR (Gastroesophageal reflux?)

Managing pulmonary problems Prevention and control of respiratory infections o Treated with appropriate antibiotics o Guided by sputum cultures Maintenance of airway patency o Bronchodilators o Chest physio x2/day + flutter o Mucous clearance devices & PEP masks

Monitor for signs of chest infection Fever Tachypnoea Chest pain Also anorexia, weight loss, decreased physical activity o May require admission to the hospital for CHEST TUNE UP o PICC lines and portacaths o Oxygen used cautiously because of chronic carbon dioxide retention

Phychosocial supportParents Siblings Infant/child/adolescent with CF Self-esteem and body image Peer relationships Puberty (late development of secondary sex characteristics) Easing transition to adult settings Fertility

Paediatric end-of-life care- Life expectancy is improved but many young people with CF may need end of life care. What needs to be considered when involving children with life-threatening and life-limiting illnesses in medical decisions: The child, the parents and the parent-child relationship With regard to the child: o The childs age or stage of development, experiences over the course of the illness, view of the illness and options for care and treatment, participation in the context of mutual pretense and the childs actions to protect his or her parents With regard to the parent: o The parents legal and moral responsibility for their child, their positions regarding their childs care and treatment, place in this decision-making process and regarding what their child should/can be told

With regard to the parent/child relationship: o Children are not autonomous beings, Parents and their child have their usual decision-making routines and are likely to have different information about the illness and treatment options, Children are prone to defer to authority figures, the likelihood of the childs dissent from parents sanctioned decisions and the role of social and cultural factors in care and treatment for all ill people-adults and children.

Shock- when the cardiovascular system fails to perfuse tissues and there is inadequate oxygen delivery to meet cellular demands. It is a life threatening condition with a variety of possible causes. Cardiogenic shock- A result of systolic dysfunction of the myocardium resulting in a compromised CO. It is the inability to maintain perfusion when there is adequate circulating volume. *Systolic dysfunction: means that the heart ineffectively pumps blood forwards and is characterised by poor contractility of the myocardium. Precipitating causes: MI, cardiomyopathies, severe systemic or pulmonary hypertension, blunt cardiac injury May also be caused by diastolic dysfunction or both *diastolic dysfunction: is an impaired ability of the right or left ventricle to fill during diastole results in decreased SV. Clinical presentationTachycardia Hypotension Narrowed pulse pressure Tachypnoeic Crackles on auscultation Cyanosis, pallor, cool and clammy skin, delayed cap refill time

Decreased renal perfusion results in Na and water retention decreased urine output Anxiety and delirium in response to decreased cerebral perfusion Collaborative managementAirway and breathing o Oxygen/NIPPV/Mechanical ventilation Increase O2 supply Decrease O2 consumption Manage underlying cause o AMI- reperfusion o Arrhythmias- anti-arrhythmic drugs o Cardiac tamponade- Pericardiocentesis Re-establish coronary artery blood flow (thrombolytics, angioplasty)

Haemodynamic support- improve tissue oxygenation o Manage/reduce preload o Improve contractility o Afterload control Drug therapy: o Dilate coronary arteries o Improve contractility (inotropes) o Reduce preload (nitrates, morphine, diuretics, ACE inhibitors) o Reduce afterload (ACE inhibitors) o Correct arrhythmias Adjunctive therapy o Intra-aortic balloon pumping (see previous)

Hypovolaemic shock- occurs with a loss of intravascular volume (inadequate to fill vascular space and maintain perfusion) *Absolute hypovolaemia- where fluid is lost via haemorrhage, GI losses, fistula drainage, diuresis, diabetes insipidis *Relative hypovolaemia- where fluid moves out of the vascular space into the extravascular space. Eg. Ascites. Reduction in intravascular volume results in decreased venous return to the heart, therefore a decreased preload, SV and CO result. This decreased CO leads to decreased tissue perfusion and impaired cellular metabolism. Stages of shockInitial- signs very subtle, the body is compensating Compensatory- signs still subtle as compensatory mechanisms continue. Though blood begins to be shunted to vital organs leaving peripheral tissues inadequately perfused. Progressive- signs are obvious, hypotension usually apparent. Compensatory mechanisms are failing. Cellular metabolism in anaerobic build-up of wastes, cellular damage. Refractory- profound hypotension and hypoxaemia. Leads to failure of liver, kidneys and lungs rapid accumulation of waste products. Recovery unlikely as organs fail.

Nursing assessment (for both cardiogenic and hypovolaemic)ABC RR, HR, BP Skin colour and temp Decreased peripheral perfusion (cool, clammy, pale) capillary refill Level of consciousness (decreased cerebral perfusion = anxious, confusion, agitation or unresponsive) Peripheral pulses

Urine output (<0.5mls/kg/hr)

Collaborative management (mostly for hypovolaemic)Airway and oxygenation (possible intubation) Volume expansion needed (not cardiogenic) Establish IV access for fluid resus Crystalloids initially and then colloids Large volume fluid resus. can have risks o Hypothermia o Coagulation o No clotting factors in stored blood (use 1-2U of FFP per 5U of RBCs) Control bleeding- pressure to external wounds NGT IDC Ongoing monitoring of vital signs

*Colloids- type of IV fluid with larger molecules to allow the fluid to stay in the intravascular space for longer *Crystaloids- type of IV fluid with smaller molecules, moves out of intravascular space quicker, maintain fluid balance (eg. Normal Saline) Paediatric/child considerationsCirculating blood volume, higher per kg of body wt than an adult but the actual volume is small so small amounts of blood loss are critical: o Neonates- 85-90mls/kg o Infants- 75 80mls/kg o Children- 70 75mls/kg o Adults- 65- 70mls/kg Initial increase in HR Blood pressure is maintained until shock is severe- LATE SIGN Once a childs BP has fallen Cardiac Arrest is imminent BP = 80 + childs age in years x 2

Hypovolaemic shock due to dehydrationClinical signsSunken eyes Decreased tearing Dry mucous membranes Poor skin turgor Cool extremities Decreased capillary refill time Decreased alertness/lethargy/irritability

Urine output: Should be approx. 1ml/kg/hr <2yrs- UO 5% 1 wet nappy in 8hrs 10% 1 wet nappy in 12hrs Severe- 1 wet nappy in 24hrs

>2yrs- UO - 5% voids once in 12hrs 10% voids once in 18 24 hrs Severe- no urine output in 24hrs

Maldistribution shockSeptic shockA systemic inflammatory response to a documented or suspected infection, which may be bacterial, viral, fungal or parasitic. Septic shock is the presence of sepsis with hypotension, despite fluid resuscitation, along with the presence of tissue perfusion abnormalities and organ dysfunction. Other terms: Infection Bacteraemia Systemic inflammatory response syndrome (SIRS) Sepsis Severe sepsis Septic shock Multiple organ dysfunction

PathophysiologyWith the invading microorganisms there is an activation of biochemical pathways and a release of multiple cytokines from leucocytes through various mechanisms. These mediators stimulate the release of other inflammatory mediators and the combined effects result in: Damage to the endothelium Coagulation Stimulation of the SNS system o Vasodilation o Hypermetabolic state o Myocardial depression Increased capillary permeability Neutrophil and platelet aggregation and adhesion to the endothelium

This tissue injury and damage to the endothelium lead to coagulation and massive thrombin formation and fibrin clots. While the increase in cardiac output combined with the increased capillary permeability leads to third-spacing fluid loss and therefore relative hypovolaemia. This leads to: Maldistribution of circulating blood volume Decreased cellular O2 supply Increased O2 demand Ineffective tissue perfusion Impaired cellular metabolism

Clinical manifestationsDecreased systemic vascular resistance and increased CO Hypotension Tachypnoea Alterations in blood count Loss of temperature control (high temp) Tachycardia Hyperventilation- respiratory acidosis Hypoxaemia Respiratory failure ARDS Pulmonary hypertension Crackles Decreased urine output Warm and flushed skin (early), cool and mottled (late) Alteration in mental status- agitated. Eventual coma GI bleeding, paralytic ileus

InterventionsOxygen/mechanical ventilation o Decrease O2 consumption o Increase O2 supply Fluid volume replacement o Crystalloid/colloid o Initial aggressive volume resuscitation Haemodynamic support o Vasopressors (target MAP 65mmHg)- noradrenalin o Inotropes- dobutamine Antibiotic therapy o 2 drug combination- cover all likely organisms, empirical broad spectrum o Start immediately o Blood cultures Identification and removal of focus of infection Other supportive strategies

Anaphylactic shockAn acute and life-threatening hyper-sensitivity (allergic) reaction to a sensitising substance (eg. Drug, vaccine, food or insect venom). Anaphylaxis is an immunomicroglobulin E (IgE) mediated hypersensitivity reaction to an allergen. The allergic response is via a host mastcell reaction mediated by IgE and an antibody produced in response to the allergen that is attached to mast cells. PathophysiologyThe physiological response is related to release of many vasoactive mediators this leads to: Increased capillary permeability o Third spacing of fluid- relative hypovolaemia Bronchoconstriction Excessive mucous secretion Coronary vasoconstriction > myocardial depression Inflammation Cutaneous reactions itching, pain Constriction smooth muscle of intestinal wall, bladder, uterus

Clinical presentationSudden onset of symptoms including: Swelling of the lips and tongue Wheezing, rhinitis and stridor Skin changes o Flushing o Pruritus o Urticarial (hives/rash) Hypotension Chest pain Third spacing of fluid Anxiety o Feeling of impending doom Confusion Reduced level of consciousness Metallic taste in mouth Cramping Abdominal pain Nausea, vomiting, diarrhoea

InterventionsPrevention o Identification of at risk, cautious assessment of response to drugs, blood etc. Identify and remove offending cause

Facilitate ventilation/maintain patent airway o Intubation/mechanical ventilation o positioning Drug therapy: o Adrenaline- subcut, IV, nebulised o Bronchodilators- nebulised, IV o Antihistamines o Corticosteroids (if hypotension persists) Fluid resuscitation o With colloids o Through a large bore cannulae Promote comfort and emotional support o Medications to relieve itching Monitor for complications

Neurogenic shockA form of distributive shock cause by loss of vasomotor (sympathetic) tone, which is generally thought to occur due to inhibition of neural output. The primary cause is spinal cord injuries above T6, secondary to the disruption of the sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance with associated vascular dilation and pooling of blood in the blood vessels. **Sympathetic tone- the constant firing under normal conditions of the sympathetic (and the parasympathetic conversely) nervous system to maintain normal conditions- increase heart rate, promote vasoconstriction etc. PathophysiologyWith this disruption of the sympathetic nervous system (SNS) comes a loss of sympathetic tone. This results in an unopposed (because SNS tone isnt working) parasympathetic response, resulting in: Venous and arterial vasodilation Decreased venous return Decreased stroke volume Decreased cardiac output o Pooling of blood in the blood vessels

This decrease in cardiac output results in: Decreased cellular O2 supply Ineffective tissue perfusion Impaired cellular metabolism

Clinical manifestationsUnpredictable temperature

Pulmonary dysfunction (relative to level of injury) Lowered skin perfusion Cool or warm, dry skin Flaccid paralysis (below the level of the lesion) Loss of reflex activity Loss of bowel and bladder function

InterventionsThe specific treatment of neurogenic shock is dependent on the cause. If the cause is spinal cord injury: Promotion of spinal stability o Cervical stabilisation with collar o Patient supine, with legs positioned in alignment with the torso. Manage cardiovascular instability o Monitor for arrhythmias- Atropine for symptomatic bradycardia o Cardiac pacing if unresponsive to atropine Careful administration of fluids o Maintain the MAP >80-85mmHg. Drug therapy: o Dopamine for hypotension and bradycardia o Administration of phenylephrine or noradrenaline to increase SVR o Vasopressors- BP and organ perfusion Monitor for hypothermia o Warming measures DVT and pulmonary embolism prophylaxis Respiratory monitoring- especially in higher than T11 spinal injuries

Assessment of end organ perfusion: Laboratory tests: o Creatinine, bilirubin o Lactate o WBC count, platelets o Urine specific gravity Urine output o Indicates renal function o Less than 0.5ml/kg/hr Neurological function o LOC, confusion etc. Indicates low cerebral perfusion Peripheral/central cyanosis o Pallor, mottled skin o Capillary refill Indicates inadequate tissue perfusion

Central Venous Pressure monitoring (CVP)Central venous pressure is a measurement of right ventricular preload. It can be measured with a Pulmonary artery (PA) catheter using one of the proximal lumens, or with a Central Venous catheter (CVC) placed in the internal jugular or subclavian vein. This CVP is measured as a mean pressure at the end of expiration. An elevated CVP may indicate right ventricular failure or volume overload. A low CVP may be the result of intravascular hypovolaemia (can also be low due to peripheral dilation from sepsis). These devices can also the Cardiac output to determine the amount of blood circulating the body each minute. This monitoring can be used to guide fluid resuscitation Central Venous Pressure should be- between 2- 8mmHg Cardiac Output should be- 4- 8 L/min at rest, depending on size, age and gender Nursing care of patients with respiratory concernsCompensatory mechanismsThe body maintains acid-base balance (arterial pH between 7.35-7.45) by compensatory mechanisms called buffers: Phosphate system Protein system Carbonic acid-bicarbonate buffer system

Carbonic acid/bicarbonate systemLow pH (too many H+ ions) = H+ combines with HCO3 (bicarbonate) to become H2CO3 (carbonic acid) carbonic acid breaks down to H2O and CO2 (carbon dioxide) lungs can blow off excess carbon dioxide This formula works both ways to restore levels from alkalosis. Arterial Blood Gas (ABG) normal valuespH = 7.35 7.45 PaO2 = 80 100mmHg paCO2 = 35 45mmHg HCO3 = 22-28mmol/L SaO2 = 95 100%

Pa = partial pressure Sa = arterial saturation

Respiratory acidosis = pH of <7.35 and PaCO2 of >45mmHg Respiratory alkalosis = pH of >7.45 and PaCO2 of <35mmHg Metabolic acidosis = pH of <7.35 and HCO3 of <22mmol/L Metabolic alkalosis = pH of >7.45 and HCO3 of >26mmol/L General rules of ABG analysis1. Check the value of each number for acid base status o Does it represent acidity or alkalinity o Mark with an arrow if the value is increased or decreased o Remember the normal value 2. Check the pH o If >7.45 alkalaemia o If <7.25- acidaemia o If 7.35-7.45 normal 3. Find the value that matches the acid/base status of the pH o If paCO2 matches, the problem is respiratory o If HCO3 matches, the problem is metabolic 4. Determine compensation o If both PaCO2 and HCO3 deviate from normal, where is the origin of the problem? HCO3 greater change from normal metabolic problem PaCO2 greater change from normal respiratory problem 5. Look at the PaO2 and SaO2 o Consider in relation to FiO2 (fraction of inspired Oxygen?)

Acute respiratory failureRespiratory failure occurs when the respiratory system fails to achieve one or both of its essential gas exchange functions: oxygenation ore elimination of carbon dioxide. When the lungs cant take in enough O2 or cant eliminate CO2 fast enough to keep up with production. Failure is present when: PaO2 is < or = 60mmHg PaCO2 is > or = 60mmHg

Other criteria pH of <7.35 SaO2 of <90%

Causes of ARF-

Lower airways Alveolar capillary membrane gas exchange unit Pulmonary circulation Chest wall Pleura Upper airways Respiratory centre Spinal cord Neuromuscular junction

Types of failureType I- Failure of oxygenation- hypoxaemic Type II- Failure of ventilation- hypoxaemic/hypercapnoeic o Inbalance between load on the lungs and the ability of bellows to compensate

Mechanisms of failureAlveolar hypoventilation Occurs when the amount of oxygen being brought into the alveoli is insufficient to meet the metabolic needs of the body. Inadequate ventilation o Inability to move gas out of alveoli

Inadequate alveolar ventilation leads to: CO2 retention Low O2

Ventilation/perfusion (V/Q) mismatch Occurs when ventilation and blood flow are mismatched in various regions of the lung in excess of what is normal V/Q ratio should be: Alveolar ventilation = 4L/min Cardiac Output = 5L/min o Average ratio of ventilation to blood flow is 4:5 or about 0.8 o ^ this is the V/Q ratio

V/Q mismatch can occur whenBlood passes through alveoli that are underventilated Alveoli are ventilated but blood flow impaired

Shunt (extreme form of V/Q mismatch) Occurs when blood reaches the arterial system without participating in gas exchange. The mixing of unoxygenated (shunted) blood and oxygenated blood lowers the average level of oxygen present in the blood. Intrapulmonary shunting occurs when blood passes through a portion of a lung that is not ventilated. This may be the result of: Alveolar collapse (secondary to atelectasis) Alveolar flooding with pus, blood, or fluid

V/Q ratio for shunted areas = 0:5L (zero L of oxygenation: perfusion maintained at 5L)j Diffusion impairment Diffusion limitation occurs when gas exchange across the alveolar-capillary membrane is compromised by a process that thickens or destroys the membrane. When this is impaired there is an increased diffusion pathway which prevents the ability to achieve equilibrium between alveolar O2 and pulmonary capillary blood.

Compensation mechanisms for hypoxaemiaIncrease in alveolar ventilation proportional to the degree of arterial desaturation o tachypnoea Pulmonary arteriolar vasoconstriction o Attempt to limit blood flow to unoxygenated alveoli SNS response o Catecholmines released into the blood stream Released in times of physical or emotional stress (norepinephrine and epinephrine etc) They act on the alpha and beta receptors Have effects such as increasing resp rate, heart rate blood pressure; vasoconstriction

Problems and interventionsIneffective airway clearance Assess patients ability to cough o determine need for suction Positioning to promote effective breathing o fowlers Humidify O2 if over 2L/min Perform chest physiotherapy

Turn every 2hours to prevent stasis of secretions Unsure adequate fluid intake of 2-3L/day to liquefy secretions Administer prescribed routine and as needed bronchodilators

Ineffective breathing patternMonitor for altered breathing rate Provide comfort measures (eg. Analgesics) to reduce anxiety and promote patient cooperation Anticipate the need for possible application of NIPPV or intubation

AnxietyPerform intervention in a clam, assured manner to lessen anxiety Reassure the patient of the competence of caregivers Teach and demonstrate relaxation techniques o Pursed-lip breathing o Progressive relaxation o Guided imagery

Impaired gas exchangeMonitor for clinical manifestation of hypoxaemia and hypercapnia Administer O2 as ordered Place the patient on continuous pulse oximetry

Risk of imbalanced fluid volume Assess for manifestations of fluid volume excess, such as abnormal breath sounds (crackles), dyspnoea, weight gain, peripheral or sacral oedema etc Monitor intake and output Restrict fluid intake and administer diuretics as ordered

Imbalanced nutrition Provide high-protein, high kilojoule, enteral or parenteral nutrition as ordered. Provide 6 small meals per day if able to eat orally Maintain the ordered O2 delivery device during meals

Non-Invasive positive pressure ventilation (NIPPV, NPPV, NIV)The provision of assisted ventilation without the use of and endotracheal tube. Rationale- inspiratory assistance (assisting excess work of breathing) while avoiding adverse consequences of ETT intubation. BenefitsRecruits collapsed alveoli (to maintain gas exchange through the whole respiratory cycle)

Increases tidal volume Increases functional residual capacity and improves lung compliance Increases intra-alveolar forces against pulmonary oedema Increases cardiac output o Decreasing LV preload in heart failure o Decreasing LV afterload by reducing systolic wall stress

ModelsContinuous Positive Airway Pressure (CPAP) Biphasic (bilevel) Positive Airways Pressure (BiPAP)

AdvantagesPreservation of airway defence mechanism Early ventilatory support Intermittent ventilation Patient can eat, drink and communicate Ease of application and removal Patient can cooperate with physiotherapy Improved patient comfort Reduced sedation requirements Avoidance of complications of intubation Ventilation outside hospital setting possible

Disadvantages Mask is uncomfortable/claustrophobic Time consuming for medical and nursing staff Airway is not protected No direct access to bronchial tree for suction

Nursing assistance with management and comfortChose a mask that fits correctly Proper placement and positioning of the mask Hydrocolloid dressing to skin on bridge of nose and forehead Abdomen distension possible- assess at regular intervals Risk of aspiration if the patient vomits in the mask o Assess for emesis risk, antiemetics if required

START PAEDS Paediatric clinical presentation acute respiratory failureCardinal signsRestlessness Tachypnoea

Tachycardia Diaphoresis Flaring nares Chest wall retractions Expiratory grunt Wheezing or prolonged expiration

Children haveEND PAEDS Chest traumaChest injuries are diverse and include much life-threatening trauma which accounts for a great number of all trauma related deaths. A high percentage of road accidents result in chest trauma. Penetrating traumaAn injury caused by foreign objects set in motion that penetrate the body o Eg. Gun shot or stab wound Thin and compliant chest wall Poorly developed intercostal and accessory muscles The diaphragm is most important High intrathoracic pressures

Blunt traumaOccurs when the body is struck by a blunt object (such as a steering wheel). The external injury may appear minor but the impact may cause severe, life-threatening internal injuries. (No opening in the skin or communication to the outside environment) Definitive diagnosis is difficult as the extent of the injuries are less obvious than with penetrating injury- though may be more life-threatening Direct impact causes the greatest injury o Acceleration/deceleration injuries o Road trauma accidents

Pathophysiology of chest injuriesInjuries are divided and described by effects they have on respiratory and cardiovascular systems. Injuries to the chest wall, diaphragm and lungso Disrupt respiratory work, causing inadequate ventilation Alveolar hypoventilation, V/Q mismatch, shunt, diffusion impairment Injuries to the heart o Compromise circulatory system- decrease CO Injuries to the thoracic vascular system

o Pneumothorax-

Cause blood loss and lead to decreased circulating volume and decreased CO

Is air in the pleural space (The pleural cavity in which the lungs sit). There is an associated complete or partial collapse of a lung due to the accumulation of air in the pleural space. This condition should be suspected after any blunt trauma to the chest. (Also from penetrating injury Open pneumothorax- occurs when air enters the pleural space through and opening in the chest wall (stab or gunshot wound) Closed pneumothorax- has no associated external wound. Some causes include; Injury to the lungs from broken ribs Injury to the lungs from mechanical ventilation

HaemothoraxIs an accumulation of blood in the intrapleural space. It is frequently found in associated with open pneumothorax and is then call a haemopneumothorax. What does this mean for the patientIf the pneumothorax is small, mild tachycardia and dyspnoea may be the only manifestations. If the pneumothorax is large, respiratory distress may be present, including shallow, rapid respirations, dyspnoea and air hunger. Assessment signsDyspnoea Decreased movement of involved chest wall Diminished or absent breath sounds on the affected side Hyperresonance to percussion Dullness to percussion (hemothorax) Shock

ManagementDepends on the presence/degree of compromise. If patient is stable and the amount of air and fluid accumulated in the intrapleural space is minimal, no treatment may be needed as the pneumothorax resolves spontaneously. If the amount of air or fluid is minimal, the pleural space can also be aspirated with a large-bore needle. Emergency Pneumothorax o Chest tube insertion with chest drainage system Haemothorax o Chest tube insertion with chest drainage system

o o

Autotransfusion of collected blood Treatment of hypovolaemia as necessary

Chest tubes and pleural drainage- The purpose is to remove air and fluid from the pleural space and to restore normal intrapleural pressure so that the lungs can re-expand. Chest tubes- can be inserted in the emergency department at the patients bedside or in the operating room. After the tubes are in place in the pleural space, they are connected to drainage tubing and a closed or underwater pleural drainage system and the clamp is removed. Pleural drainage- most systems have three basic compartments, each with its own separate function. First compartment- the collection chamber, receives fluid and air from the chest cavity. The fluid stays in this cavity while the air vents to the second compartment. Second compartment- contains water, which acts as a one-way valve. The incoming air enters from the collection chamber and bubbles up through the water. The air then enters the suction chamber. Third compartment, the suction control chamber applies controlled suction to the chest drainage system. (WHO THE FUCK CARES, I AM NOT WRITING ANY MORE ON THIS)

Rib fracturesRib fractures are the most common type of injury resulting from trauma. If a fractured rib is splintered or displaced, it may damage the pleura and lungs. Clinical manifestationsPain (esp on inspiration) at the site of injury Splinting of the affected area with shallow breaths to try to decrease the pain Atelectasis may develop because of decreased ventilation

ManagementMain goal is to decrease pain so the patient can breath adequately

Flail segmentFlail chest results from multiple rib fractures, causing instability of the chest wall. Two or more ribs fractured in two or more places Flail segment created- the ribs no longer have a bony attachment to rib cage Paradoxical movement of the chest wall (that section move in on inspiration and out on expiration)

ManagementInitial therapy o Adequate ventilation

o Humidified oxygen o Careful administration of resuscitation fluids Definitive therapy o Re-expand the lung o Ensure adequate oxygenation Positive end-expiratory pressure (PEEP) used with mechanical ventilation to improve oxygenation will maintain positive pressure in the lungs throughout the respiratory cycle. The lung parenchyma and fractured ribs will heal with time

Cardiac tamponadeResults from blunt or penetrating injury. It is where blood rapidly collects in the pericardial sac and compresses my myocardium because the pericardium does not stretch. This prevents the heart from pumping effectively. Clinical manifestationsMuffled, distant heart sounds Hypotension Neck vein distension Increased central venous pressure

ManagementThis is a medical emergency: o Pericardiocentesis with surgical repair as appropriate.

Other thoracic injuriesAirway obstruction Transbronchial trauma Myocardial contusion Aortic dissection Oesophageal rupture Diaphragm injury

Peripheral arterial disease (PAD)The progressive narrowing and degeneration of arteries in the neck, abdomen and extremities. Onset > 60yrs or in the patient with diabetes. Risk factors <50: patients with o Diabetes, plus 1 of; o Smoking

o Dyslipidaemia o Hypertension o Hyperhonocysteinemia Ages 50 69 in patients with a history of; o Smoking o Diabetes Aged >70, patients with; o Leg symptoms with exertion o Ischaemic rest pain o Abnormal lower extremity pulse exam o Atherosclerotic coronary, carotid, or renal artery disease

Signs and symptoms Intermittent claudication o Ischaemic muscle ache or pain that is precipitated by a consistent level of exercise, resolves within 10 minutes or less with rest and is reproducible. Paraesthesia- numbness or tingling occurring in the toes or feet Reduced peripheral pulses Physical appearance of the limb; o Skin becomes thin, shiny and taut, and there is a loss of hair on the lower legs o When the leg is elevated: there is pallor or blanching of the foot o When the leg is lowered: there is redness of the foot

ComplicationsProlonged ischaemia leads to atrophy (wasting away) of the skin and underlying muscles Delayed healing, wound infection and tissue necrosis Arterial ulcers- most commonly over bony prominences on the toes, feet and lower leg Gangrene amputation

DiagnosisHealth history and physical examination o Palpation of peripheral pulses Segmental blood pressures Doppler ultrasound o Sound frequencies bounce off the blood cells at a rate that corresponds with the velocity of the blood flow through the vessel Ankle-brachial index (ABI) o Using a hand held Doppler ultrasound o Calculated by dividing the ankle systolic BP by the highest brachial systolic BP o An ABI between 0 0.89 indicates PAD of various stages Angiography o Used to further delineate the location and extent of the disease process

Management-

Education; o Reduction of risk factors Anti-platelet drugs o Aspirin, ticlopidine, clopidogrel, oxpentifylline Exercise Diet Proper foot care Surgery o Percutaneous transluminal angioplasty (with or without stent) o Peripheral arterial bypass surgery o Amputation

Problems commonly found in patients with PADIneffective peripheral tissue perfusion o Interventions include Encourage the patient to participate in a structured waling program Teach the patient to avoid tight girdles, garters and socks, and avoid crossing legs Impaired skin integrity related to decreased peripheral susceptibility to infection o Interventions include; Avoid trauma to lower extremities Check temperature of bath water with fingers rather than toes Proper care and daily inspection of feet Wear roomy, soft footwear, obtain callus and toenail care by a healthcare professional Apply a mild lotion daily to the lower extremities Acute pain related to ischaemia secondary to reduced peripheral circulation o Interventions include; Rest when pain occurs Activity intolerance related to an imbalance between oxygen supply and demand o Develop a structured exercise program that includes warm-up exercises o Inform the patient to walk to the point of pain, rest until the pain subsides and then resume walking

Venous Thrombo-embolismThe most common disorder of the veins is venous thrombosis, the formation of a thrombus in association with inflammation of the vein. It is classified as either superficial thrombophlebitis or deep vein thrombosis. This includes Deep-vein thrombosis and pulmonary embolism: Deep vein thrombosisIs a disorder involving a thrombus in a deep vein, most commonly the iliac, popliteal and femoral veins. There are three important factors in the aetiology of venous thrombosis:

1. Venous stasis: venous stasis occurs when the valves are dysfunctional or the muscles in the extremities are inactive. 2. Endothelial damage: damage to the endothelial surface of the vein may be caused by trauma or external pressure and occurs any time a venepuncture is performed. 3. Hypercoagulability of blood: this occurs in many haematological disorders, particularly polycythaemia, severe anaemias etc. Only 3.5% of clients who develop DVT will have symptoms, these can be: Palpable, firm, subcutaneous cord-like vein Area surrounding the vein may be tender to the touch Area may be reddened and warm A mild systemic temperature elevation and leucocytosis may be present Oedema of the affected extremity may or may not occur

Surgical risk stratificationRecommendations-surgical High risk Hip or knee arthroplasty Major trauma Hip fracture surgery Other surgery with prior VTE and/or active cancer

Prophylaxis 5-10 days in most cases 28 35 days for hip arthroplasty and hip fracture surgery

Pharmacological prophylaxisEndoxaparin daily (40mg or 20mg) Low dose unfractionated heparin (5000U BD or TDS)

Non-pharmacological methodsEarly mobilisation o Routine part of postoperative care o As sole prophylaxis in low-risk patients only Graduated compression stockings o Should be used with caution in patients with arterial insufficiency (eg. PAD) Intermittent pneumatic compression Venous foot pump

*Generally less effective than pharmacological prophylaxis Pulmonary embolism-

If the thrombis breaks away if can lodge in the small blood vessels of the lungs, known as pulmonary embolism (Can also be caused by air or fat).This can manifest as: Dyspnoea Diaphoresis Anxiety Cough/haemoptysis Cyanosis Tachycardia Wheeze/crackles Severe hypotension Cardiac arrest Signs of RV failure +/- dull substernal chest discomfort

DiagnosisPulmonary arteriography Lung perfusion scans ECG changes: RBBB: RAD: SV arrhythmias

ManagementAnalgesia Oxygen therapy o Intubation may be necessary IV access for heparin and fluids Patient will be initially Heparinized (IV heparin infusion) Thrombolytic therapy Pulmonary embolectomy Consider source o Treat possible DVT

Activated Partial Thromboplastin Time- Used to monitor the results of anticoagulation therapy with heparin. The goal of heparin therapy is to maintain the aPTT in therapeutic range. With a prolonged aPTT there is a longer clotting time therefore thrombus or embolus is less likely to occur. Peripheral vascular assessmentPalpate pulses o +/- Doppler Colour of nail beds and skin Sensation Movement Warmth Oedema Venous pattern Ulcer/insufficiency

o Arterial vs. venous Oral history o Pain o Claudication o Comorbidities

Lifespan considerationsPregnant women Lowered systemic vascular resistance Increased peripheral vasodilation Hypotension (supine) Pelvic veins + IVC compression

Older adults Calcified arterial walls Reduced elasticity and vasomotor tone Increased systemic vascular resistance Reduced lymphatic tissue