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)

Conditions affecting the Cardiac Nervous System . Obstruction or restriction B. Conditions affecting the Cardiac Valves C. Inflammation C. Dilation or distention 3 COMPONENTS: A. Conditions affecting the Heart Muscles B.CARDIAC DISORDERS CARDIAC PATHOPHYSIOLOGY: A.

CONDITIONS AFFECTING THE HEART MUSCLES A. -It is an isufficient blood supply to the myocardium secondary to blocked or narrowed coronary artery that leads to: Myocardial Infarction Angina Pectoris . 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. Ischemic heart disease or coronary heart disease (CAD) -And the most common type of coronary artery disease is the CORONARY ATHEROSCLEROTIC HEART DISEASE (CAHD).k.a.

in older persons and in the affluent CAUSES: A.a. Spasm: sudden constriction of coronary artery (nicotine. clot formation and rupture of the blood vessels B. plaque can cause bleeding. 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. Thrombus: when the plaque builds up on the arterial wall (THROMBOSIS) • blood flow becomes slow and a clot may form in the plaque C. Atherosclerosis a.EPIDEMIOLOGY: Most common cause of death (CAHD) The incidence is higher in men than in women. cocaine and cold air) .k.

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

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 .

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

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. 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) . 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.


ANGINA DECUBITUS -nocturnal angina . focal spasm of epicardial coronary artery (30-40 y/o) 4.ELEVATED) . recurrent prolonged attacks of severe angina caused by episodic. UNSTABLE ANGINA -angina at rest -accelarating angina characterized by chronic stable angina who develops angina that is more frequent. 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. prolonged or precipitated by less exertion than previously -3 episodes/ day 3.Form of angina pectoris. severe.TYPES OF ANGINA PECTORIS 1. PRINZMETAL’S ANGINA PECTORIS (ST SEGMENT. 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.

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 . or a sudden progression of atherosclerotic changes.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.

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 .

proximal bundle of His and the SA node (abnormalities in impulse conduction leading arrythmias) Lateral 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.MANIFESTATIONS Anterior 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. Occlusion of the left circumflex coronary artery -same as anterior wall MI .

        Pain (most frequent complaint). 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 . sudden.



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

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

Decrease ventricular emptying c. Leads to cardiac failure .-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.

Diminishes or absent point of maximal impulse 2.Accumulation of fluid (1 L) in the pericardial sac (gradual.A. ACUTE PERICARDITIS . Paradoxical pulse 5. swallowing.A predominant clinical manifestation (PERICARDIAL FRICTION RUB) with severe chest pain (left shoulder which radiates to the neck and down to the left arm) . Narrowed pulse pressure 6. or breathing deeply . Diminished heart sound 3. the patient notice little pain) SYMPTOMS OF CARDIAC TAMPONADE: 1.Intensified when: lying supine. Tachycardia 4. Distended neck veins . coughing.

B. fatigue. exhibits a symptoms of congestive heart failure (inability of the heart to pump blood) . 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.

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. Production of toxin c. Autoimmune reaction . virus (north america) b. Invasion of the myocardial tissue by an organism (most common: bacteria and protozoan (worldwide).

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

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 .ALCOHOLIC CARDIOMYOPATHY -when a person consumes a large quantities of alcohol for more than 5 years (ethanol.

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

scarring and proliferates the leaflet -HALLMARK: (+) plateletfibrin-bacteria mass ENDOCARDITIS Most severe: if the mass breaks free. enters the bloodstream and become an emboli . resulting in vegetative growth.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.

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


" "Hippocratic fingers.DIGITAL CLUBBING -also known as "Drumstick 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 .

joint and skin -Usually caused by STREPTOCOCCAL INFECTION Symptoms include (but are not limited to): sudden onset of sore throat pain on swallowing fever. nausea and vomiting may also occur. especially in children . usually 101–104°F headache red throat/tonsils abdominal pain. brain.RHEUMATIC HEART DISEASE Rheumatic fever: is an inflammtory disease that affects the heart.

OTHER SYMPTOMS: fever painful. tender. valvular stenosis. painless nodules under the skin RHEUMATIC HEART DISEASE: -endocarditis. myocarditis and pericarditis -damaged in the heart valves . red swollen joints pain in one joint that migrates to another one heart palpitations chest pain shortness of breath skin rashes fatigue small.

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

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

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

(R) sided-heart failure .Stiffening of the Mitral Valve 1. Increase (L) atrial pressure 2. (L) atrial hypertrophy 3. Pulmonary congestion 5. Decrease cardiac output 1. Decrease ventricular filling 2. Increase pulmonary pressure 4. (L) ventricular hypertrophy 3.


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 a form of mitral insufficiency seen most often in thin. . young women and it is often asymptomatic.


Pulmonary congestion 5. Left atrial pressure 2. (R) sided heart failure . Increase pulmonary pressure 4. Left ventricular hypertrophy 2. Decrease cardiac output 1. Left atrial hypertrophy 3.BACKFLOW OF BLOOD TO LEFT ATRIUM 1.


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

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

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

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


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

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 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 decompensation. cardiac insufficiency. 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 .

First group: conditions that result in direct damage to the heart (MI. Myocarditis. the effectiveness of the contraction diminishes. myocardial fibrosis. Ventricular aneurysm) B. resulting to HEART FAILURE Examples: mitral or aortic regurgitation.ETIOLOGY: 3 groups: A. 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. 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 .

constrictive cardiomyopathies. or pulmonary hypertension C. pericarditis . systemic hypertension. 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.Examples: aortic and pulmonary stenosis.

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

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

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


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 .