CARDIOVASCULAR DISORDERS

SIGNS AND SYMPTOMS:

1. Chest Pain: maybe cardiac or non-cardiac Cardiac: it is accompanied by: a. Nausea b. Vomiting c. Diaphoresis d. Dyspnea e. Fatigue f. Pallor g. Syncope 2. Palpitation: irregular heartbeat It maybe bump, pounding, jumping, flopping, fluttering or raising sensation of the heart (normal: less than 6 minutes; abnormal: last for hours with SOB, pain, severe lightheadedness) It is accompanied by: a. Lightheadedness b. Syncope

3. Dyspnea: breathelessness or SOB due to: a. Cardiac origin: Maybe felt with exertion also called dyspnea with exertion Maybe caused by impaired left ventricular function Leads to: PULMONARY CONGESTION and SOB If severe: dyspnea occurs at rest Severe dyspnea includes: a. Paroxysmal Nocturnal Dyspnea (PND) b. Orthopnea: breathelessness that is relievd by sitting upright (effective ventilation and perfusion of the lungs

b. Pulmonary in Origin Dyspnea relieved by specific breathing pattern (pursed lip breathing) Relieved by specific body position
4. Cardiac Syncope (Fainting) mild lightheadedness Due to: Arrythmias (syncope without warning of lightheadedness, dyspnea or nausea) Orthostatic hypotension Poor ventricular function Coronary artery disease (CAD) Vertebral artery insufficiency

Non-cardiac origin: Anxiety Emotional stress Medication 5. Fatigue Cardiac Origin: it is provoked by minimal exertion It is accompanied by: a. Dyspnea b. Chest pain c. Palpitation d. Headache 6. Cough Left Ventricular CHF: cough is often hacking with frothy bloodtinged secretion

7. Cyanosis 8. Edema: Congestive Heart Failure 9. Claudication or Leg Pain: TYPES a. Vascular Claudication: skin discoloration, trophic skin changes, cool skin b. Intermittent Claudication: normal skin appearance at rest, exercising to the point of claudication (marked pallor in the skin)

CARDIAC DISORDERS
CARDIAC PATHOPHYSIOLOGY: A. Obstruction or restriction B. Inflammation C. Dilation or distention

3 COMPONENTS:
A. Conditions affecting the Heart Muscles B. Conditions affecting the Cardiac Valves C. Conditions affecting the Cardiac Nervous System

CONDITIONS AFFECTING THE HEART MUSCLES

A. Coronary artery disease (Coronary heart disease or Ischemic Heart Disease -Designation for many different conditions that involve obstructed blood flow through the coronary arteries -A.k.a. Ischemic heart disease or coronary heart disease (CAD) -And the most common type of coronary artery disease is the CORONARY ATHEROSCLEROTIC HEART DISEASE (CAHD); -It is an isufficient blood supply to the myocardium secondary to blocked or narrowed coronary artery that leads to: Myocardial Infarction Angina Pectoris

EPIDEMIOLOGY:
Most common cause of death (CAHD) The incidence is higher in men than in women, in older persons and in the affluent CAUSES: A. Atherosclerosis a.k.a. Arteriosclerosis: it is a disease problem involving the hardening of the arteries Begins in childhood where the arteries begin to fill with fatty substances or lipid which then calcify or hardens to become PLAQUES Gradually lines the arterial walls then progressively narrowing the arteries When fully developed, plaque can cause bleeding, clot formation and rupture of the blood vessels B. Thrombus: when the plaque builds up on the arterial wall (THROMBOSIS) blood flow becomes slow and a clot may form in the plaque C. Spasm: sudden constriction of coronary artery (nicotine, cocaine and cold air)

RISK FACTORS
NON MODIFIABLE 1. Age 2. Gender 3. Race 4. Family history MAJOR RISK FACTORS 1. Hyperlipoproteinemia (serum lipid level) 2. Habitual diet (high cholesterol, fat, refined carbohydrates, sodium) 3. Hypertension 4. Obesity 5. Glucose intolerance 6. Cigarette smoking 7. High level of fibrinogen (binds together platelet cells to form blood clot) 8. Large amount of C-reactive protein: a specialized protein for tissue repair 9. The presence of troponin T (regulatory protein that help to heart muscle contract MINOR RISK FACTORS 1. Personality type 2. Sedentary lifestyle 3. Psychologic stress

MODIFIABLE

PATHOPHYSIOLOGY OF CAHD The exact cause is unknown Coronary Atherosclerosis

involves a localized accumulation of lipid and fibrous tissue within the coronary artery

Arterial narrowing and occlusion

As the disease progresses, it is accompanied by vascular changes (it affects the functional ability of the artery to dilate) Results in the variable reduction of blood flow to the myocardium

Imbalance between oxygen demand and oxygen supply (myocardium) MYOCARDIAL ISCHEMIA (produce the clinical manifestation of CAHD) 1. angina pectoris 2. acute mayocardial infarction 3. sudden cardiac death

NORMAL PERSON: MYOCARDIAL OXYGEN

SUPPLY

DEMAND

SUPPLY DECREASED DEMAND UNCHANGED

Myocardial oxygen

POSSIBLE CAUSES:
-coronary artery osbtruction -hypoxia -inadequate perfusion -inadequate hemoglobin

SUPPLY UNCHANGED

DEMAND INCREASED

Myocardial oxygen

POSSIBLE CAUSES: -increase heart rate

-increase contractile state of the myocardium -increased afterload -left ventricular size

ANGINA PECTORIS
-It

is characterized by paroxysmal substernal pain, radiating down the inner aspect of the left arm -Patient describes it as: a. Heaviness or tightness of the chest b. It maybe interpreted as indigestion c. Pain is usually diffuse and rarely can be pinpointed at a specific site d. Patient maybe gripping the sternum e. It is associated with exertion and relieve by rest CAUSE: temporary inadequacy of the blood supply of heart muscles (an increase in myocardial oxygen demand with inadequate myocardial oxygen supply)

TYPES OF ANGINA PECTORIS

1. STABLE ANGINA -Angina caused by exertion or emotion and relieve by rest -Common in 50-60 y/o (men) and 65-75 y/o (female) -Characterized by squeezing, central, substernal discomfort usually with cresendo and decresendo lasting for 1-5 minutes and can radiate to left shoulder, and to both arms usually on the ulnar surface of FA and hands (ST SEGMENT DISPLACED)
2. UNSTABLE ANGINA -angina at rest -accelarating angina characterized by chronic stable angina who develops angina that is more frequent, severe, prolonged or precipitated by less exertion than previously -3 episodes/ day 3. PRINZMETALS ANGINA PECTORIS (ST SEGMENT- ELEVATED) - Form of angina pectoris, recurrent prolonged attacks of severe angina caused by episodic, focal spasm of epicardial coronary artery (30-40 y/o) 4. ANGINA DECUBITUS -nocturnal angina

MYOCARDIAL INFARCTION
-It

is caused by a sudden block (CORONARY OCCLUSION) of one of the branches of the coronary artery which leads to necrosis or death of of the portion of the myocardium with subsequent healing by scar formation or fibrosis -Causes maybe: Coronary thrombosis, or a sudden progression of atherosclerotic changes, or prolonged constriction of the coronary arteries -A prolonged ischemia (lasting more than 35 to 45 minutes) produces irreversible cellular damage and necrosis of myocardial muscle MYOCARDIAL INFARCTION

Myocardial Ischemia

Increased myocardial oxygen demand Decrease coronary perfusion Increase afterload Decrease diastolic filling Increase HR
Peripheral vasoconstriction

Decrease Myocardial oxygen supply Increase Cellular hypoxia Altered cell membrane integrity Decrease myocardial integrity Decrease cardiac output Decrease arterial pressure

Increase myocardial contractility Sympathetic response

Stimulation of baroreceptors

MANIFESTATIONS
Anterior wall myocardial infarction: a. There is an occlusion of the anterior descending branch of the left main coronary artery (supplies the left ventricle) -Substantial loss of left ventricular muscle mass and can result to severe hemodynamic disturbances Inferior wall myocardial infarction: a. There is an occlusion of right coronary artery and it supplies the AV node and SA node -ischemia of the AV node, proximal bundle of His and the SA node (abnormalities in impulse conduction leading arrythmias) Lateral wall myocardial infarction: a. Occlusion of the left circumflex coronary artery -same as anterior wall MI

Pain (most frequent complaint); sudden, severe, crushing pain in the substernal region which radiates into the left and sometimes the right arm and up the sides of the neck Simulates indigestion or a gallbladder attack with abdominal pain and vomiting Restlessness and fear Shortness of breathe and cyanosis Wheezes and crackles upon auscultation Rapid and barely perceptible pulse Hypotension Soft systolic murmurs

HEART DISEASES
Classification: a. Congenital heart disease b,. Acquired heart disease

A. PERICARDITIS

Result from bacterial, viral or fungal infection or it occurs due to complication of a systemic disease (RA, SLE, uremia, scleroderma, MI or trauma)

-Inflammatory process of the pericardium -Characterized by accumulation of fluid in the pericardial sac CARDIAC TAMPONADE (COMPRESSION OF THE HEART) Effects: a. Decrease venous return b. Decrease ventricular emptying c. Leads to cardiac failure

A. ACUTE PERICARDITIS - A predominant clinical manifestation (PERICARDIAL FRICTION RUB) with severe chest pain (left shoulder which radiates to the neck and down to the left arm) - Intensified when: lying supine, coughing, swallowing, or breathing deeply - Accumulation of fluid (1 L) in the pericardial sac (gradual, the patient notice little pain)

SYMPTOMS OF CARDIAC TAMPONADE: 1. Diminishes or absent point of maximal impulse 2. Diminished heart sound 3. Tachycardia 4. Paradoxical pulse 5. Narrowed pulse pressure 6. Distended neck veins

B. CHRONIC PERICARDITIS -results from fibrosis of the pericardial sac secondary to trauma or neoplastic disease -pericardium becomes tighten around the heart and decreases its efficiency as a pump -dyspnea, fatigue, exhibits a symptoms of congestive heart failure (inability of the heart to pump blood)

MYOCARDITIS
-It

is an inflammatory diseaseof the myocardium -Maybe primary or secondary (drug hypersensitivity or toxicity and infection) INFECTION CAN RESULT IN ONE OF 3 WAYS: a. Invasion of the myocardial tissue by an organism (most common: bacteria and protozoan (worldwide); virus (north america) b. Production of toxin c. Autoimmune reaction

SYMPTOMS: ACUTE PHASE OF INFECTION: a. Flulike symptoms b. Fever c. Lymphadenopathy d. Pharyngitis e. Myalgia f. GIT complaints g. Hepatitis h. Encephalitis i. Nephritis j. Orchitis The most common cardiac symptom: PERICARDIAL PAIN Heart failure, pericardial effusion, syncope and ischemia Preliminary laboratory findings are non-specific; elevated ESR, leukocytosis, X-ray may show normal heart size

ALCOHOLIC CARDIOMYOPATHY
-when

a person consumes a large quantities of alcohol for more than 5 years (ethanol; direct toxic effect on cardiac tissues) Gradual fatigue dyspnea on exertion Pulmonary crackles Cardiac murmurs Increase BP Conduction defects Dysrythmias X-ray heart is flabby Left ventricular hypertrophy

INFECTIVE ENDOCARDITIS
-It is the infection of the endocardium and mostly the heart valves secondary to streptococcal infection (subacute) or staphylococcus infection TYPES a. Acute- occurs rapidly often on a normal valve and if untreated may cause death b. Sub-acute- occurs in an already damaged valve

PATHOPHYSIOLOGY
Previously damaged heart valve Allows a turbulent blood flow and bacteria settling on the stenotic side of the valve The organism bombard the valves, resulting in vegetative growth, scarring and proliferates the leaflet -HALLMARK: (+) plateletfibrin-bacteria mass

ENDOCARDITIS

Most severe: if the mass breaks free, enters the bloodstream and become an emboli

MANIFESTATIONS
1. Often gradual 2. Malaise and general achiness 3. Low grade fever 4. arthralgia, arthritis, low back pain, myalgias, tenosynovitis, anorexia, weight loss, chest pain and occasional hemoptysis 4. Reveals splenomegaly, clubbing of fingers, the presence of OSLERS NODES (small-raised, tender, bluish areas on fingers and toes), petechiae (small capillary hemorrhages conjunctiva, mouth and extremities) 5. Murmurs over the cardiac valves

DIGITAL CLUBBING -also known as "Drumstick fingers," "Hippocratic fingers," and "Watch-glass nails

Fluctuation and softening of the nail bed (increased ballotability) Loss of the normal <165 angle (Lovibond angle) between the nailbed and the fold (cuticula) Increased convexity of the nail fold Thickening of the whole distal (end part of the) finger (resembling a drumstick) Shiny aspect and striation of the nail and skin

RHEUMATIC HEART DISEASE

Rheumatic fever: is an inflammtory disease that affects the heart, brain, joint and skin -Usually caused by
STREPTOCOCCAL INFECTION

Symptoms include (but are not limited to): sudden onset of sore throat pain on swallowing fever, usually 101104F headache red throat/tonsils abdominal pain, nausea and vomiting may also occur, especially in children

OTHER SYMPTOMS: fever painful, tender, red swollen joints pain in one joint that migrates to another one heart palpitations chest pain shortness of breath skin rashes fatigue small, painless nodules under the skin

RHEUMATIC HEART DISEASE: -endocarditis, valvular stenosis, myocarditis and pericarditis -damaged in the heart valves

VALVULAR HEART DISEASE

TYPES A. MITRAL VALVE STENOSIS The most common and the primary cause is rheumatic fever - Thickening of the valve by calcification and fibrous tissue formation - Valve leaflets become stiff, narrows, and immobile - The chorda tendineae shortens, thick, and mitral orifice decreases in size

LEADS TO: a. Hypertrophy of the left atrium b. Elevated left atrial pressure c. Pulmonary hypertension and congestion (higher pulmonary pressure) d. Impede the function of the right ventricle resulting to rightsided heart failure e. Insufficient blood receive by the left ventricle- decrease Cardiac output f. Left ventricular atrophy

SYMPTOMS: a. Dyspnea on exertion b. Paroxysmal nocturnal dyspnea c. Orthopnea d. Dry cough e. Dysphagia f. Brochitis or bronchial irritation g. Pressure exerted on the laryngeal nerve causes hoarsness h. Excessive fatigue and weakness (decrease CO) i. Peripheral and facial cyanosis j. Hemoptysis (later) (rupture of bronchial veins) k. Right sided heart failure l. Distended jugular veins m. Pitting edema and hepatomegaly

Stiffening of the Mitral Valve

1. Decrease ventricular filling 2. Decrease cardiac output 1. Increase (L) atrial pressure 2. (L) atrial hypertrophy

3. (L) ventricular hypertrophy

3. Increase pulmonary pressure

4. Pulmonary congestion 5. (R) sided-heart failure

MITRAL REGURGITATION

MITRAL REGURGITATION It is due to papillary muscle dysfunction allows the leaflet to flop in the direction of the left atrium during systole causing blood to backflow MITRAL VALVE PROLAPSE- is a form of mitral insufficiency seen most often in thin, young women and it is often asymptomatic.

BACKFLOW OF BLOOD TO LEFT ATRIUM

1. Left ventricular hypertrophy 2. Decrease cardiac output

1. Left atrial pressure

2. Left atrial hypertrophy 3. Increase pulmonary pressure 4. Pulmonary congestion 5. (R) sided heart failure

AORTIC STENOSIS

congenital malformation (the most common etiologic factor)

LEADS TO: a. Obstruction of left ventricular outflow b. Left ventricular hypertrophy c. As the disease progresses, CO decreases d. Left atrium cannot empty adequately e. Pulmonary congestion f. Left ventricle (elevated myocardial oxygen need) (compression of the coronary arteries) decrease supply g. Give rise to Myocardial ischemia and angina (severe) h. Eventually right sided heart failure

Three characteristic symptoms: a. Exertional dyspnea b. Angina pectoris c. Extertional syncope Late stage: a. fatigue b. Weakness c. Orthopnea d. Paroxysmal nocturnal dyspnea e. Pulmonary edema f. Symptoms of right-sided heart failure (hepatomegaly, atrial fibrillations, systemic venous distention)

Stiffening of the aortic valve

1. (L) ventricular hypertrophy 2. Decrease cardiac output 2. Compression of coronary arteries 3. Increase pulmonary pressure 4. Pulmonary congestion 5. (R) sided-heart failure
1. Increase (L) atrial pressure

2. (L) atrial hypertrophy

AORTIC REGURGITATION
-there is a backflow of blood to the left ventricle due to incompetent aortic valve
SYMPTOMS: a. Tachycardia (exertion) b. Premature ventricular beats c. Exertional dyspnea d. Angina pectoris (rest or exertion) e. Hepatomegaly, ankle edema and ascites (end-stage disease) f. Aortic diastolic murmurs g. Widened pulse pressure h. ST segment depression and T wave inversion (left ventricular hypertrophy)

BACKFLOW OF BLOOD TO THE LEFT VENTRICLE

1. Increase (L) atrial pressure

1. (L) ventricular hypertrophy 2. (L) sided heart failure

2. (L) atrial hypertrophy

3. Increase pulmonary pressure 4. Pulmonary congestion 5. (R) sided-heart failure

TRICUSPID STENOSIS
Narrowing of the tricuspid orifice secondary to thickening of the tricuspid valve with fused and shortened chordae tendinae Signs and Symptoms: - Show symptoms of Right sided heart failure Hepatomegaly Jugular vein distention Cardiac cirrhosis Jaundice

Decrease venous return Decrease cardiac output Fatigue, weight loss and hypotension

TRICUSPID STENOSIS

TRICUSPID REGURGITATION

-backflow of blood to the right atrium secondary to dilation of the right ventricle that may cause dilation of the ventricular ring and displacement of the papillary muscles (-) right ventricular output

PULMONARY STENOSIS
-narrowing of the pulmonary valve causing less blood to flow towards the pulmonary circulation Hypertrophy of the right ventricle and right atrium
SYMPTOMS Harsh systolic murmurs Fatigue and dyspnea on exertion Have symptoms of right sided heart failure (hepatomegaly, ascites and edema)

PULMONARY REGURGITATION
-the pulmonic valve leaflets become incompetent and fails to close which results in the back flow of blood to the right ventricle during systole right atrium and right ventricle hypertrophies Px exhibits symptoms of right sided heart failure

CONGESTIVE HEART FAILURE

-Or heart failure, cardiac insufficiency, cardiac decompensation, and cardiac incompetence -IT IS A STATE IN WHICH THE HEART NO LONGER IS ABLE TO PUMP ADEQUATE SUPPLY OF BLOOD TO MEET THE DEMANDS OF THE BODY

ACUTE CONGESTIVE HEART CHRONIC CONGESTIVE FAILURE: HEART FAILURE: -Develops quickly without warning and often -Develops gradually and the patient is seen initially with milder symptoms -The heart is capable to compensate for the decrease performance, thus lessening the symptoms

CLINICAL PICTURE: Syncope Shock Cardiac arrest Sudden death

CAUSE: by myocardium failing to function adequately or decrease effectiveness of the heart after myocardial infarction

ETIOLOGY: 3 groups: A. First group: conditions that result in direct damage to the heart (MI, Myocarditis, myocardial fibrosis, Ventricular aneurysm) B. Second Group: conditions that result in ventricular overload Preload: is the ventricular blood volume at end-diastole or the maximum blood volume for the beat of the heart STARLING LAW: once the preload is reached a given limit, the effectiveness of the contraction diminishes, resulting to HEART FAILURE Examples: mitral or aortic regurgitation, atrial or ventricular septal defect or rapid infusion of IV solutions Afterload: force that the ventricle must develop to eject blood into the circulatory system

Examples: aortic and pulmonary stenosis, systemic hypertension, or pulmonary hypertension C. Third Group: conditions that can lead to heart failure are does resulting in the constriction of the ventricles that limits ventricular filling (decrease SV) Example: Cardiac tamponade, constrictive cardiomyopathies, pericarditis

PATHOPHYSIOLOGY

CARDIAC COMPENSATORY MECHANISMS (ability of the weakened heart to meet the metabolic demands of the body Tachycardia- increasing the HR, CO increases; as HR increases diastole is shortened up to the point where an inadequate filling of the ventricles occurs (decrease CO) Ventricular dilation- increase the VR leads to excessive stretching of the cardiac fibers (ventricular dilation), this allows for a more forceful contraction, increases the SV and CO Hypertrophy of the myocardium- increase in the diameter of the cardiac fibers (thickening of the walls); Increase in muscle mass, increases the effectiveness of the heart to contract, increases the CO (problem: increase in muscle mass limits coronary artery supply leading to hypoxia and decrease effectiveness)

HOMEOSTATIC COMPENSATORY MECHANISM Vascular system- if circulating blood decreases, SNS releases epinephrine and norepinephrine (generalized vasoconstriction) Kidneys- when CO decreases, the glomerular filtration is reduced (retention of water and sodium), Aldosterone release is stimulated (results in further reabsorption of sodium and water); ADH release is stimulated (further increase water reabsorption), the end-result is fluid overload and edema Liver- venous volume increases, results to liver congestion (decrease ability to metabolizes the aldosterone and ADH)

CLASSIFICATION OF HEART FAILURE 1. Backward heart failure: result from the damming up of blood in the vessels proximal to the heart 2. Forward heart failure: it is the result of the inability of the heart to maintain cardiac output 3. High output heart failure: when the CO remains normal or above normal but the metabolic needs of the body are not met 4. Low output Heart failure: when cardiac output falls below normal

RIGHT-SIDED HEART FAILURE

Peripheral edema or dependent edema (pitting and non-tender) progresses into bi pedal edema Liver congestion and tenderness on the right upper quadrant of the abdomen Ascites (10L) Displacement of the diaphragm resulting to respiratory distress Distended neck veins Increase systemic venous pressure (sitting position)

LEFT-SIDED HEART FAILURE

Pulmonary congestion leading to pulmonary edema and pleural effusion Dyspnea Orthopnea Alternating apnea and hyperpnea (Cheynestoke respiration) Coughing and hemoptysis Crackles upon auscultation

CARDIAC PAIN IS NOT A TYPICAL SYMPTOM OF HEART FAILURE