Cardiac disease patho exam 2

Coronary artery disease

coronary artery supplies the myocardium with blood

 disruption of blood flow to the heart = damage to the myocardium

 ischemia=deficient blood supply to tissues

 Continued ischemia = lead to death (infarct)

 Can be temporary or prolonged leading to a Myocardial infarction (irreversible)

CAD Etiology

Atherosclerosis: luminal narrowing leads to an inability of the disease vessel to

supply the myocardium with adequate blood

-most common cause

 Coronary artery blockage from blood clot

 Coronary artery vasospasm

CAD Pathogenesis

This leads to an imbalance between oxygen demand and supply

 When oxygen demand exceeds what the diseased artery can supply, localized ischemia

results; Commonly seen during exertion

Angina Pectoris

Chest pain* from reduction in blood flow to cardiac muscles despite increased oxygen demand

 Stable angina: chronic chest pain , patient has felt before

 Unstable angina: chest pain that patient has felt for first time

What causes the pain????

 Transient ischemia causes reversible changes at the cellular level, depressing myocardial function

 if Untreated = necrosis (infarct)

 Oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism

 Lactic acid accumulates= reduced cellular pH (acidosis)

 Lactic acid and adenosine (breakdown of ATP) diffuses into extracellular space and causes pain

Angina Pectoris Clinical Manifestation

Asymptomatic

 Bouts of oppressive chest pain that may radiate into neck or arms; caused by myocardial ischemia

 Can radiate to jaw, back, epigastric area

 Women: episodic dyspnea, dizziness, pain of jaw, epigastric region

 Pain is accompanied by nausea, vomiting, fainting; Cool extremities

Treatment goals of unstable angina

Oxygen therapy

 Aspirin- decreases platelet aggregation to decrease clot formation

 Coronary angioplasty

 Morphine for pain

Myocardial Infaction

More severe and prolonged myocardial ischemia with irreversible damage

 Results in an infarct

 involves muscles of left ventricle and septum

MI Etiology/lab findings

Etiology

 complete obstruction of Coronary artery

 Atherosclerotic plaque thrombus or hemorrhage

 Increase demand of myocardial muscle

 Severe hypertension, hypertrophy, aortic valve stenosis

Laboratory Findings

 Heart cells die / contents spill into blood stream

 Blood analysis of cardiac enzymes and proteins

CPK-MB cardiac enzyme

 Rise within 4 hours after MI, peak between 18 – 24 hours, and decline

over 3 to 4 days

 larger the infarct, longer it takes for the elevated level to return to normal

TROPONIN-more sensitive and not detectable in healthy blood

slight damage results in rise within a few hours, peaks 24 hours and

remains elevated for up to 2 weeks

MI Diagnostic tests/complications

Diagnostic tests

 ECG

 STEMI indicates infarction is completely through the heart wall-indicates

extensive myocardial damage

 NSTEMI indicates it is subendocardial and not through the wall. Indicates less damage; more favorable prognosis

Complications of MI

 Premature ventricular contractions

could increase the risk of developing irregular heart rhythms (arrhythmias)

 Ventricles beat independently without waiting for SA or AV nodes

 No P or T wave and characterized by wide bizarre QRS wave

 faulty signaling = heart beats greater than 100 bpm (tachycardia),

less than 60 bpm (bradycardia) or irregularly.

 Types of arrythmias

 Atrial fibrillation: extremely fast and irregular beats from the upper chambers of the heart

most common and rapidly fatal is ventricular fibrillation

 Disordered electrical activity causes the ventricles to quiver, or fibrillate, instead of contracting (or beating) normally.

 This prohibits the heart from pumping blood, causing collapse and cardiac arrest

 Asystole: complete cessation of cardiac contractions

 Heart failure due to badly damaged ventricles

 Blood accumulates in chambers and hydrostatic pressure builds within and results in pulmonary edema

 Intracardial thrombi: mural thrombus forms on ventricular wall from stagnant blood; bits of clot embolize into systemic circulation causing infarct in brain, kidneys

 Embolus: foreign material traveling in blood

 Blood clot, amniotic fluid, fat, for example

Embolism: sudden blockage of a vessel from an Embolus

 Cardiac rupture: blood leaks into pericardial sac from perforation in necrotic muscle, prevents

ventricular filling (cardiac tamponade)

 Cardiac tamponade is a serious medical condition in which blood or fluids fill the space between the sac that encases the heart and the heart muscle.

 Clotted blood around heart compressing heart, preventing ventricular filling

 Ventricular aneurysm: late complication; outward bulging of healing infarct during ventricular systole; reduces left ventricular function and cardiac output; rather than being ejected, blood

fills aneurysm sac

 Weakened area can rupture

Asystole/intracardial thrombi/embolus/embolism/cardiac rupture/cardiac tamponade/ventricular aneurysm

 Asystole: complete cessation of cardiac contractions

 Intracardial thrombi: mural thrombus forms on ventricular wall from stagnant blood; bits of clot embolize into systemic circulation causing infarct in brain, kidneys

 Embolus: foreign material traveling in blood

 Blood clot, amniotic fluid, fat, for example

Embolism: sudden blockage of a vessel from an Embolus

 Cardiac rupture: blood leaks into pericardial sac from perforation in necrotic muscle, prevents

 Cardiac tamponade is a serious medical condition in which blood or fluids fill the space between the sac that encases the heart and the heart muscle.

Ventricular aneurysm: late complication; outward bulging of healing infarct during ventricular systole; reduces left ventricular function and cardiac output; rather than being ejected, blood

Endocarditis

infection of the cardiac endothelium

 Most commonly affects the heart valves

 Mainly caused by bacteria

Endocarditis Pathogenesis

Microorganisms enter into blood stream from site of localized infection (example: S.

aureus enters through skin from iv drug use)

 Those with underlying heart valve defects are at more risk

 Bacteremia develops and allows microbes to travel to heart; they adhere to

endocardium and attract WBCs and platelets

 This results in fibrin deposits and form tiny masses that contains microbes within a fibrin meshwork called vegetations

 These form most commonly on heart valves

 They can fragment and embolize into blood-called septic emboli

Clinical Manifestation

nonspecific-fever, chills, weight loss

 Heart murmur

 Abnormal sounds heard on auscultation (stethoscope)

 Caused by abnormal flow of blood through the heart valves or vessels

 Contingent upon where emboli travel, which can cause ischemia or infarction to target organ

Myocarditis/pericarditis

MYOCARDITIS: Inflammation of heart muscle

 Viruses common cause --hepatitis B & C , COVID

 Signs and symptoms of myocarditis include chest pain, fatigue, heart failure and

abnormal heart rhythms.

PERICARDITIS: inflammation of the epicardium and pericardium from viral infections or commonly occurs after MI

Pathogenesis

 The capillaries that supply the pericardial membranes become permeable allowing plasma, plasma proteins and fibrinogen to enter into pericardial cavity

 Creates a fibrin rich exudative edema

 Results in scar tissue formation and adhesions between the 2 pericardial membranes

 Restricts optimal filling of the ventricles and decreases cardiac output

 Heard on auscultation as friction rub-a scratching sound

Heart Failure

Weakened ventricular muscle is unable to sufficiently pump blood into the arterial

circulation to meet the needs of the tissue

 4 major changes that lead to development of HF

 Increased fluid volume or volume overload

 Impaired ventricular filling

 Degeneration of ventricular muscle

 Decreased ventricular contraction function

Heart Failure Etiology

Etiology

 Ischemic heart disease –most common

 Results in scarred fibrotic heart muscle with diminished contractile strength

 Chronic hypertension results in hypertensive heart disease

 Leading cause of LVF

 Chronic pulmonary disease- leading cause of RVF

 Cor pulmonale is condition of RVF caused by pulmonary disease

 Cardiomyopathy

hypertrophic cardiomyopathy OR Dilated cardiomyopathy

Dilated/hypertrophic Cardiomyopathy

DILATED CARDIOMYOPATHY: enlargement of heart and dilatation of chambers; impaired ventricular action leads to chronic heart failure

HYPERTROPHIC CARDIOMYOPATHY: hereditary, transmitted as dominant trait, muscle fibers in disarray with marked hypertrophy of heart muscle

 Hypertrophy reduces size of ventricles and do not readily dilate in diastole

 Septal muscles more hypertrophied than rest of myocardium → impedes flow into aorta

 leaflet is drawn open by fast moving blood being ejected during systole

 conduction irregularities results in arrhythmias –(ventricular fibrillation)

 cause of death

 genetic predisposition

2 CLINICAL PRESENTATIONS OF HEART FAILURE: LEFT SIDED versus RIGHT SIDED

Right Sided Heart failure: results in a build-up of blood flowing into the right side of the heart. Usually begins at right ventricle (RVF)

RVF backward effects: weak right ventricle causes backup of hydrostatic pressure into the right atrium, superior vena cava and jugular veins, then into inferior vena cava, causing venous congestion in gastrointestinal, peritoneal, hepatic and splenic veins

 This build-up results in edema of the ankles, distention of the neck veins, and

enlargement of the spleen because of congestion in the veins that cannot empty

properly into the heart.

 Symptoms and signs: jugular neck vein, distension, peripheral swelling ( ankles,

sacral, fingers) , anorexia, indigestion, ascites, hepatomegaly

Left-sided failure – leads to a build-up of fluid in the lungs or pulmonary edema, which causes shortness of breath. Most common to begin with failure of the Left Ventricle (LVH)

 LVH (BACKWARD EFFECTS)

 Weak left ventricle causes a backup of hydrostatic pressure in the left atrium,

pulmonary veins, and pulmonary capillaries

 Hydrostatic pressure increases in the lungs and fluid builds up in the

interstitium(increase stiffness) and in alveoli (pulmonary edema)

 Non inflammatory fluid-Transudates: Low protein

 Acute pulmonary edema

 Manifestation of acute heart failure from temporary

disproportion in output of blood from ventricles

 Temporary reduction in output from left ventricle “right heart”

pumps blood into lungs faster than “left heart” can deliver

blood to peripheral tissues

Signs & Symptoms: cough with pink frothy sputum (pulmonary edema), orthopnea (dyspnea

when lying flat)from fluid distributed through the lung fields, which is relieved by sitting up to

distribute fluid to move lung bases

 LVH FORWARD EFFECTS: Weak left ventricle forward pumping of blood into aortal, peripheral,

and cerebral arteries

 Kidneys sense low circulation caused by weak pumping action of heart and release

renin, which triggers angiotensin II and aldosterone

 Blood volume increases, peripheral vasoconstricti0n  blood pressure increases

 Low circulation is sensed by baroreceptors, which trigger SNS

 SNS causes increased HR and peripheral arterial vasoconstriction

These compensatory mechanisms worsen LVF by requiring a failing ventricle to pump

out a greater volume of blood against increase resistance

Symptoms and signs

cool, pale extremities, decrease peripheral pulses, confusion, disorientation and

nocturia

VALVULAR DISEASES

Mitral valve prolapse or mitral valve regurgitation: mitral valve leaflets prolapse into L atrium during systole allowing regurgitation of blood flow into Left atrium

 Severe forms can lead to pulmonary edema

 Results in heart murmur

 etiology

 Genetic or Congenital

 Papillary muscle dysfunction from a MI: infarcted papillary muscle unable to

control mitral valve leaflet resulting in mitral valve prolapse and mitral

insufficiency

 Aortic stenosis: narrowed valve opening, which reduces blood flow from L ventricle

 Pulmonic stenosis: narrowed pulmonic valve does not allow sufficient blood flow into the

pulmonary artery resulting in back up of blood into R ventricle and right ventricular hypertrophy