HYPOVOLEMIC SHOCK Hypovolemia (also hypovolaemic shock) is a state of decreased blood volume; more specifically, decrease in volume of blood

plasma. It is thus the intravascular component of volume contraction (or loss of blood volume due to things such as hemorrhaging or dehydration), but, as it also is the most essential one, hypovolemia and volume contraction are sometimes used synonymously. Hypovolemia is characterized by salt (sodium) depletion and thus differs from dehydration, which is defined as excessive loss of body water. Causes Common causes of hypovolemia are dehydration, bleeding, vomiting, severe burns and drug vasodilators typically used to treat hypertensive individuals. It is also common during surgery due to the use of anesthetics, nil-by-mouth, and in-operation bleeding. A ruptured ovarian cyst associated with PCOS (polycystic ovarian syndrome) may cause severe internal bleeding, causing hypovolemic shock. Diagnosis Clinical symptoms may not be present until 1020% of total whole-blood volume is lost. Stages of hypovolemic shock Most sources state that there are 4 stages of hypovolemic shock, however a number of other systems exist with as many as 6 stages. The 4 stages are sometimes known as the "Tennis" staging of hypovolemic shock, as the 4 stages of % volume of blood loss mimic the scores in a game of tennis: 15, 15-30, 30-40, 40. It is basically the same as used in classifying bleeding by blood loss. Stage 1 Stage 3 Up to 15% blood volume loss (750 mL)[9] 3040% blood volume loss (15002000 mL) Compensated by constriction of vascular bed [9] Blood pressure maintained Systolic BP falls to 100mmHg or less Normal respiratory rate Classic signs of hypovolemic shock Pallor of the skin Marked tachycardia >120 bpm Normal mental status to slight anxiety Marked tachypnea >30 bpm Normal capillary refill Alteration in mental status (confusion, Normal urine output anxiety, agitation) Sweating with cool, pale skin Delayed capillary refill Urine output of approximately 20 milliliters/hour Stage 2 Stage 4 1530% blood volume loss (7501500 mL) Loss greater than 40% (>2000 mL) Cardiac output cannot be maintained by Extreme tachycardia (>140[12]) with weak arterial constriction pulse Tachycardia >100bpm Pronounced tachypnea Increased respiratory rate Significantly decreased systolic blood Blood pressure maintained pressure of 70 mmHg or less Increased diastolic pressure Decreased level of consciousness, lethargy, Narrow pulse pressure coma Sweating from sympathetic stimulation Skin is sweaty, cool, and extremely pale Mildly anxious/Restless (moribund) Delayed capillary refill Absent capillary refill Urine output of 20-30 milliliters/hour Negligible urine output Treatment Minor hypovolemia from a known cause that has been completely controlled (such as a blood donation from a healthy patient who is not anemic) may be countered with initial rest for up to half

an hour. Oral fluids that include moderate sugars and electrolytes are needed to replenish depleted sodium ions. Furthermore the advice for the donor is to eat good solid meals with proteins for the next few days. Typically, this would involve a fluid volume of less than one liter, although this is highly dependent on body weight. Larger people can tolerate slightly more blood loss than smaller people. More serious hypovolemia should be assessed by a physician. For a patient presenting with hypovolemic shock in hospital the following investigations would be carried out: Blood tests: Glucose, Cross-match Central Venous Line/Blood Pressure Arterial Line/Arterial Blood Gases Urine output measurements (via urinary catheter) SpO2 Oxygen saturations The following interventions would be carried out: IV access Oxygen as required Surgical repair at sites of hemorrhage Inotrope therapy (Dopamine, Noradrenaline) Fresh frozen plasma/whole blood Nursing Interventions: Hypovolemic Shock 1. Check for patent airway and adequate circulation. 2. Begin an I.V. infusion with normal saline solution or lactated Ringers solution delivered through a large bore. 3. Help insert a central venous line and pulmonary artery catheter for hemodynamic monitoring. 4. Insert an indwelling urinary catheter. 5. Draw an arterial blood sample to measure ABG levels. 6. Obtain and record the patients blood pressure, pulse and respiratory rates, and peripheral pulse rates. 7. Monitor the patients CVP, right arterial pressure, pulmonary artery pressure, and cardiac output at least hourly as ordered. 8. Measure the patients urine output hourly. 9. Monitor the patients ABG and electrolyte levels frequently as ordered. 10.Watch for signs of impending coagulopathy such as petechiae, bruising, bleeding or oozing from guns or venipuncture site. 11.Explain all procedures and their purposes to ease the patients anxiety. 12.Discuss the risk associated with blood transfusions to the patient and his family. CARDIOGENIC SHOCK Cardiogenic shock is based upon an inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively. Since this is a type of shock there is insufficient perfusion of tissue (i.e. the heart) to meet the required demands for oxygen and nutrients. Cardiogenic shock is a largely irreversible condition and as such is more often fatal than not. The condition involves increasingly more pervasive cell death from oxygen starvation (hypoxia) and nutrient starvation (e.g. hypoglycemia). Because of this it may lead to cardiac arrest (or circulatory arrest) which is an acute cessation of cardiac pump function. Etiology Cardiogenic shock is caused by the failure of the heart to pump effectively. It can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes include arrhythmia, cardiomyopathy, cardiac valve problems, ventricular outflow obstruction (i.e. aortic

valve stenosis, aortic dissection, systolic anterior motion (SAM) in hypertrophic cardiomyopathy) or ventriculoseptal defects. Exams and Tests An examination will show: Low blood pressure (usually less than 90 systolic) Blood pressure drop of more than 10 points when you stand up after lying down (orthostatic hypotension) Weak (thready) pulse To diagnose cardiogenic shock, a catheter (tube) may be placed in the lung artery (right heart catheterization). Tests may show that blood is backing up into the lungs and the heart is not pumping properly. Tests include: Cardiac catheterization Chest x-ray Coronary angiography Echocardiogram Electrocardiogram Other studies may be done to find out why the heart is not working properly. Lab tests include: Arterial blood gas Blood chemistry (chem-7, chem-20, electrolytes) Cardiac enzymes (troponin, CKMB) Complete blood count (CBC) Treatment Cardiogenic shock is a medical emergency. You will need to stay in the hospital, usually in the Intensive Care Unit. The goal of treatment is to find and treat the cause of shock to save your life. You may need medicines to increase blood pressure and improve heart function, including: Dobutamine Dopamine Epinephrine Norepinephrine Nursing Interventions: Cardiogenic Shock 1. Administer oxygen by face mask or artificial airway to ensure adequate oxygenation of tissues. 2. Adjust the oxygen flow rate to higher or lower level, as blood gas measurements indicate. 3. Administer an osmotic diuretic, such as mannitol, if ordered to increase renal blood flow and urine output. 4. Never flex the patients ballooned leg at the hip because this may displace or fracture catheter. 5. To ease emotional stress, allow frequent rest periods as possible. 6. Allow family members to visit and comfort the patient as much as possible. 7. Monitor and record blood pressure, pulse, respiratory rate, and peripheral pulse every 1 to 5 minutes until the patient stabilizes. 8. Record hemodynamic pressure readings every 15 minutes. 9. Monitor ABG values, complete blood count, and electrolyte levels. 10.During therapy assess skin color and temperature and note any changes. Cold and clammy skin may be a sign of continuing peripheral vascular constriction, indicating progressive shock.

SEPTIC SHOCK Sepsis is a systemic inflammatory response to infection. If the systemic inflammatory response is not caused by an infection (i.e. pancreatitis, ischemia or trauma), it is referred to as SIRS, or systemic inflammatory response syndrome. Two or more of the following are present in sepsis (and SIRS): Temperature > 38 OR <36 degrees Celsius Heart rate > 90 bpm Respiratory rate > 20 breaths/minute OR PaCO2 < 32 mm Hg White blood cell count > 12,000/mm3 OR < 4,000/mm3 OR > 10% immature (band) forms If a patient has accompanying organ dysfunction, hypoperfusion or hypotension, (s)he is in severe sepsis. Severe sepsis may be manifested as altered mental status, hypotension, lactic acidosis and/or oliguria. If the hypotension does not respond to adequate fluid resuscitation, the patient is in septic shock. It is sometimes initially difficult to distinguish severe sepsis from septic shock. Septic shock carries a mortality rate of 40 - 60%. Etiology Gram-negative organisms account for most adult cases of septic shock. In the hospitalized patient, the most common gram-negative organisms are E. Coli, Klebsiella, Enterobacter and Pseudomonas aeruginosa. Gram-positive organisms are becoming increasingly associated with sepsis due to the use of intravenous catheters and invasive devices. The most common gram-positive organisms seen are the Staphylococcus and Streptococcus species as well as Pneumococcus and Enterococcus faecalis. Viruses, protozoa, parasites, fungi (i.e. Candida albicans) and anaerobic organisms (i.e. Clostridium, Bacteroides fragilis) are also known to be associated with sepsis. The most common sites of origin are: Urinary tract (i.e. upper) Gastrointestinal tract (i.e. peritonitis) Respiratory tract (i.e. pneumonia) Skin and wounds (i.e. cellulitis) Predisposing Factors Predisposing factors for developing sepsis and septic shock include: Extremes of age (very old and very young) Granulocytopenia (reduced number of neutrophils, eosinophils and basophils) Prior antibiotic therapy Severe burn injury, recent trauma, recent surgery and/or invasive procedures Functional asplenia (no spleen) Immunosuppression Malnutrition and total parenteral nutrition Alcohol and drugs of abuse Prolonged ICU stay, especially endotracheal intubation > 48 hours and ventilator-associated pneumonia Symptoms Septic shock is usually preceded by bacteremia, which is marked by fever, malaise, chills, and nausea. The first sign of shock is often confusion and decreased consciousness. In this beginning stage, the extremities are usually warm. Later, they become cool, pale, and bluish. Fever may give way to lower than normal temperatures later on in sepsis. Other symptoms include: rapid heartbeat shallow, rapid breathing decreased urination. reddish patches in the skin

Septic shock may progress to cause "adult respiratory distress syndrome," in which fluid collects in the lungs, and breathing becomes very shallow and labored. This condition may lead to ventilatory collapse, in which the patient can no longer breathe adequately without assistance. Diagnosis Diagnosis of septic shock is made by measuring blood pressure, heart rate, and respiration rate, as well as by a consideration of possible sources of infection. Blood pressure may be monitored with a catheter device inserted into the pulmonary artery supplying the lungs (Swan-Ganz catheter). Blood cultures are done to determine the type of bacteria responsible. The levels of oxygen, carbon dioxide, and acidity in the blood are also monitored to assess changes in respiratory function. Treatment Septic shock is treated initially with a combination of antibiotics and fluid replacement. The antibiotic is chosen based on the bacteria present, although two or more types of antibiotics may be used initially until the organism is identified. Intravenous fluids, either blood or protein solutions, replace the fluid lost by leakage. Coagulation and hemorrhage may be treated with transfusions of plasma or platelets. Dopamine may be given to increase blood pressure further if necessary. Respiratory distress is treated with mechanical ventilation and supplemental oxygen, either using a nosepiece or a tube into the trachea through the throat. Identification and treatment of the primary infection site is important to prevent ongoing proliferation of bacteria. Nursing Interventions: 1. Monitor neurologic status, including mental status and level of consciousness. 2. Monitor cardiovascular status, including arterial blood pressure; rate, rhythm, and quality of pulses; central venous pressure; pulmonary artery pressure; and cardiac output. 3. Monitor color and character of skin. 4. Monitor results of arterial blood gases, blood counts, clotting times, and platelet counts. 5. Monitor respiratory status, including respiratory rate, rhythm, and breath sounds. 6. Monitor body temperature every 2 hours. 7. Monitor urinary output hourly, reporting any output of less than 30 mL per hour. 8. Explain procedures and provide comfort measures (oral care, skin care, turning, positioning). Neurogenic Shock Neurogenic shock, sometimes called vasogenic shock, results from the disruption of autonomic nervous system control over vasoconstriction. Under normal conditions, the autonomic nervous system keeps the muscles of the veins and arteries partially contracted. Neurogenic shock occurs after an injury to the spinal cord. Sympathetic outflow is disrupted resulting in unopposed vagal tone. The major clinical signs are hypotension and bradycardia. CLINICAL FEATURES Patients are generally hypotensive with warm, dry skin. The loss of sympathetic tone may impair the ability to redirect blood flow from the periphery to the core circulation leading to excessive heat loss and hypothermia. Bradycardia is a characteristic finding of neurogenic shock; however, it is not universally present. These symptoms can be expected to last from one to three weeks. The anatomic level of the injury to the spinal cord impacts the likelihood and severity of neurogenic shock. Injuries above the T1 level have the capability of disrupting the spinal cord tracts that control the entire sympathetic system. Injuries occurring in the levels from T1 to L3 may only partially interrupt the sympathetic outflow. The higher the level of injury the more likely it is for the patient to exhibit severe symptoms. DIAGNOSIS AND DIFFERENTIAL The diagnosis of neurogenic shock should be one of exclusion. Neurogenic shock must be differentiated from other types of shock, particularly hypovolemic. When dealing with a trauma patient, one must always assume that any hypotension is a result of ongoing blood loss. A patient

suffering from neurogenic shock may also have concomitant injuries which may contribute to hemodynamic instability. Clinical clues such as hypotension, bradycardia, neurologic dysfunction, and warm, dry skin may lead the clinician to suspect neurogenic shock; however, only after other injuries have been identified and treated can the diagnosis of neurogenic shock safely be made. Treatment Fluid is always the initial treatment of shock, especially since concomitant hemorrhagic shock must be excluded following trauma. Most institutions will additionally utilize pressor agents to achieve hemodynamic stability. Dopamine (Intropin) is often used either alone or in combination with other inotropic agents. Vasopressin (antidiuretic hormone Certain vasopressors (ephedrine, norepinephrine). Phenylephrine may be used as a first line treatment, or secondarily in patients who do not respond adequately to dopamine. Atropine (speeds up heart rate and cardiac output) Nursing Management It is important to elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock when a patient receives spinal or epidural anesthesia. Elevation of the head helps prevent the spread of the anesthetic agent up the spinal cord. In suspected spinal cord injury, neurogenic shock may be prevented by carefully immobilizing the patient to prevent further damage to the spinal cord. Nursing interventions are directed toward supporting cardiovascular and neurologic function until the usually transient episode of neurogenic shock resolves. Applying anti-embolism stockings and elevating the foot of the bed may minimize pooling of blood in the legs. Pooled blood increases the risk of thrombus formation. Therefore, the nurse must check the patient daily for any lower extremity pain, redness, tenderness, and warmth. If the patient complains of pain and objective assessment of the calf is suspicious, the patient should be evaluated for deep vein thrombosis. Administrationof heparin or low-molecular-weight heparin (Lovenox) as prescribed, application of anti-embolism stockings, or use of pneumatic compression of the legs may prevent thrombus formation. Passive range of motion of the immobile extremities helps promote circulation. A patient who has experienced a spinal cord injury may not report pain caused by internal injuries. Therefore, in the immediate post injury period, the nurse must monitor the patient closely for signs of internal bleeding that could lead to hypovolemic shock. HYPOADRENAL SHOCK Shock secondary to adrenal insufficiency occurs quite infrequently and usually with the context of a concomitant critical illness. As a result, the diagnosis of adrenal insufficiency as a cause of the shock state is rarely suspected until late in the disease process. Unfortunately, if the diagnosis is missed, the patient will likely succumb to refractory shock. In North America, adrenal insufficiency most commonly arises as a consequence of the chronic therapeutc administration of high-dose exogenous corticosteroids with resultant suppression of the hypothalamic-pituitary-adrenal axis. If adrenal insufficiency is slow in onset, there may be adequate cortisol production to maintain homeostasis in the unstressed state. By contrast, once the patient is severely stressed, typically following major infection, operation, or trauma, adrenocortical function may be insufficient to support the necessary physiological response and the clinical picture of shock due to adrenal insufficiency will become manifest. In a small proportion of patients, adrenal insufficiency is abrupt in onset and occurs directly as a result of the acute underlying illness. For example, overwhelming sepsis may cause adrenal insufficiency because of adrenal infarction secondary to hypotension or adrenal hemorrhage caused by coagulopathy. Emergency treatment of hypoadrenal shock requires immediate treatment with high-dose hydrocortisone (100mg IVTT q8h) with a rapid taper to an appropriate maintenance dose. To avoid interfering with the cosyntropin stimulation test and measurement of basal cortisol levels, dexamethasone rather than hydrocortisone may be administered during the time the test is administered. ANAPHYLACTIC SHOCK

Anaphylaxis is a severe, whole-body allergic reaction to a chemical that has become an allergen. After being exposed to a substance such as bee sting venom, the person's immune system becomes sensitized to it. On a later exposure to that allergen, an allergic reaction may occur. This reaction happens quickly after the exposure, is severe, and involves the whole body. Anaphylaxis can occur in response to any allergen. Common causes include: Drug allergies Food allergies Insect bites/stings Pollens and other inhaled allergens rarely cause anaphylaxis. Some people have an anaphylactic reaction with no known cause. Anaphylaxis is life-threatening and can occur at any time. Risks include a history of any type of allergic reaction. Signs and symptoms of anaphylaxis. Anaphylaxis typically presents with many different symptoms over minutes or hours with an average onset of 5 to 30 minutes if exposure is intravenous and 2 hours for foods. The most common areas affected include: skin (8090%), respiratory (70%), gastrointestinal (3045%), heart and vasculature (1045%), and central nervous system (1015%)[3] with usually two or more being involved. Diagnosis Anaphylaxis is diagnosed based on clinical criteria. When any one of the following three occurs within minutes/hours of exposure to an allergen there is a high likelihood of anaphylaxis: Involvement of the skin or mucosal tissue plus either respiratory difficulty or a low blood pressure Two or more of the following symptoms:a. Involvement of the skin or mucosa b. Respiratory difficulties c. Low blood pressure d. Gastrointestinal symptoms Nursing Interventions: Anaphylaxis 1. Provide supplemental oxygen and observe. If hypoxia continues, prepare to help insert an artificial airway. 2. Insert an I.V. line for giving emergency drugs and volume expanders. 3. Continually reassure the patient and explain all tests and treatments to reduce fear and anxiety. 4. If the patient undergoes skin or scratch testing. Keep emergency resuscitation equipment nearby during and after the test. 5. Continuously assess the patients response to treatment. 6. Monitor vital signs and cardiopulmonary and neurologic function. 7. Observe for complications associated with anaphylaxis, such as vascular collapse and acute respiratory insufficiency or obstruction. 8. Closely observe a patient with known allergies for anaphylaxis when giving a drug with high anaphylactic potential. CONGESTIVE HEART FAILURE Heart failure (HF) often called congestive heart failure (CHF) is generally defined as the inability of the heart to supply sufficient blood flow to meet the needs of the body. Heart failure can cause a number of symptoms including shortness of breath, leg swelling, and exercise intolerance. The condition is diagnosed with echocardiography and blood tests. Treatment commonly consists of lifestyle measures (such as smoking cessation, light exercise including breathing protocols,

decreased salt intake and other dietary changes) and medications. Sometimes it is treated with implanted devices (pacemakers or ventricular assist devices) and occasionally a heart transplant. Common causes of heart failure include myocardial infarction and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy. The term "heart failure" is sometimes incorrectly used to describe other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest, which can cause heart failure but are not equivalent to heart failure. Classification There are many different ways to categorize heart failure, including: the side of the heart involved (left heart failure versus right heart failure). Left heart failure compromises aortic flow to the body and brain. Right heart failure compromises pulmonic flow to the lungs. Mixed presentations are common, especially when the cardiac septum is involved. whether the abnormality is due to insufficient contraction (systolic dysfunction), or due to insufficient relaxation of the heart (diastolic dysfunction), or to both. whether the problem is primarily increased venous back pressure (preload), or failure to supply adequate arterial perfusion (afterload). whether the abnormality is due to low cardiac output with high systemic vascular resistance or high cardiac output with low vascular resistance (low-output heart failure vs. high-output heart failure). the degree of functional impairment conferred by the abnormality (as reflected in the New York Heart Association Functional Classification the degree of coexisting illness: i.e. heart failure/systemic hypertension, heart failure/pulmonary hypertension, heart failure/diabetes, heart failure/renal failure, etc. Functional classification generally relies on the New York Heart Association functional classification. The classes (I-IV) are: Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities. Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion. Class III: marked limitation of any activity; the patient is comfortable only at rest. Class IV: any physical activity brings on discomfort and symptoms occur at rest. This score documents severity of symptoms, and can be used to assess response to treatment. While its use is widespread, the NYHA score is not very reproducible and doesn't reliably predict the walking distance or exercise tolerance on formal testing. In its 2001 guidelines the American College of Cardiology/American Heart Association working group introduced four stages of heart failure: Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder. Stage B: a structural heart disorder but no symptoms at any stage. Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment. Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care. The ACC staging system is useful in that Stage A encompasses "pre-heart failure" a stage where intervention with treatment can presumably prevent progression to overt symptoms. ACC Stage A does not have a corresponding NYHA class. ACC Stage B would correspond to NYHA Class I. ACC Stage C corresponds to NYHA Class II and III, while ACC Stage D overlaps with NYHA Class IV. Signs Left-sided failure Common respiratory signs are tachypnea (increased rate of breathing) and increased work of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe hypoxemia, is a late sign of extremely severe pulmonary edema.

Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow, or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g., mitral regurgitation) of the heart failure. Right-sided failure Physical examination can reveal pitting peripheral edema, ascites, and hepatomegaly. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by eliciting hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength. Biventricular failure Dullness of the lung fields to finger percussion and reduced breath sounds at the bases of the lung may suggest the development of a pleural effusion (fluid collection in between the lung and the chest wall). Though it can occur in isolated left- or right-sided heart failure, it is more common in biventricular failure because pleural veins drain both into the systemic and pulmonary venous system. When unilateral, effusions are often right sided. Symptoms Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation. However, heart failure is not exclusively backward failure (in the part of the circulation which drains to the ventricle). There are several other exceptions to a simple left-right division of heart failure symptoms. Left sided forward failure overlaps with right sided backward failure. Additionally, the most common cause of right-sided heart failure is left-sided heart failure. The result is that patients commonly present with both sets of signs and symptoms. Left-sided failure Backward failure of the left ventricle causes congestion of the pulmonary vasculature, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea (shortness of breath) on exertion (dyspne d'effort) and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, occurs. It is often measured in the number of pillows required to lie comfortably, and in severe cases, the patient may resort to sleeping while sitting up. Another symptom of heart failure is paroxysmal nocturnal dyspnea a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigueability and exercise intolerance are also common complaints related to respiratory compromise. "Cardiac asthma" or wheezing may occur. Compromise of left ventricular forward function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest. Right-sided failure Backward failure of the right ventricle leads to congestion of systemic capillaries. This generates excess fluid accumulation in the body. This causes swelling under the skin (termed peripheral edema or anasarca) and usually affects the dependent parts of the body first (causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down). Nocturia (frequent nighttime urination) may occur when fluid from the legs is returned to the bloodstream while lying down at night. In progressively severe cases, ascites (fluid accumulation in the abdominal cavity causing swelling) and hepatomegaly (enlargement of the liver) may develop. Significant liver congestion may result in impaired liver function, and jaundice and even coagulopathy (problems of decreased blood clotting) may occur. Diagnosis Imaging - Echocardiography & Chest X-rays Electrophysiology

An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Monitoring -- fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts) Framingham criteria By the Framingham criteria, diagnosis of congestive heart failure (heart failure with impaired pumping capability) requires the simultaneous presence of at least 2 of the following major criteria or 1 major criterion in conjunction with 2 of the following minor criteria: Major criteria: Cardiomegaly on chest radiography S3 gallop (a third heart sound) Acute pulmonary edema Paroxysmal nocturnal dyspnea Crackles on lung auscultation Central venous pressure of more than 16 cm H2O at the right atrium Jugular vein distension Positive abdominojugular test Weight loss of more than 4.5 kg in 5 days in response to treatment (sometimes classified as a minor criterium) Minor criteria: Tachycardia of more than 120 beats per minute Nocturnal cough Dyspnea on ordinary exertion Pleural effusion Decrease in vital capacity by one third from maximum recorded Hepatomegaly Bilateral ankle edema Minor criteria are acceptable only if they cannot be attributed to another medical condition such as pulmonary hypertension, chronic lung disease, cirrhosis, ascites, or the nephrotic syndrome. The Framingham Heart Study criteria are 100% sensitive and 78% specific for identifying persons with definite congestive heart failure. Management Treatment focuses on improving the symptoms and preventing the progression of the disease. Reversible causes of the heart failure also need to be addressed: (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). Treatments include lifestyle and pharmacological modalities. Nursing Interventions: Heart Failure 1. Place the patient inn Fowlers position and give supplemental oxygen, as ordered. 2. Organize all activities to provide maximum rest periods. 3. To prevent deep vein thrombosis due to vascular congestion, assist the patient with rangeof-motion exercises. 4. Weigh the patient daily to help detect fluid retention and observe for peripheral edema. 5. Assess the patients vital signs for increased respiratory and heart rates and for narrowing pulse pressure and mental status.

6. Frequently monitor blood urea nitrogen and serum creatinine, potassium, sodium, chloride, and magnesium levels. 7. Watch for calf pain and tenderness. 8. Advise the patient to avoid foods high in sodium content. 9. Stress the need for regular medical check up and periodic blood tests to monitor drug levels. 10.Stress the importance of taking medications exactly as prescribed. 11.Tell the patient to notify the doctor if his pulse rate is usually irregular or less than 60 beats/min.