Chapter 10 - Heart Pathology Flashcards
Congestive Heart Failure
Multisystem derangement occurring when the heart is unable to eject the blood delivered to it by the venous system, “forward failure”
Caused by: Left - systemic hypertension, mitral/aortic valvular disease, ischemic heart disease, primary cardiomyopathies
Right - 2 to L heart failure, pulmonary hypertension
Stages of Congestive Heart Failure
1 - compensated failure: increased catecholamines (improve contractility), hypertrophy of myocytes and chamber dilation
2 - uncompensated failure: clinical signs of venous congestion appear (pulmonary edema, peripheral edema, congestion of abdominal viscera), cyanosis & acidosis due to decreased tissue perfusion
Clinical signs of Left heart failure
pulmonary edema pleural effusions dyspnea dyspnea lying down "orthopnea" fatigue, tachycardia
Clinical signs of Right heart failure
systemic venous congestion soft tissue edema distended neck veins enlarged liver inc. deep vein thromboses/pulmonary emboli
Hypertensive heart disease
left ventricular hypertrophy in an indiv w/ history of hypertension
*Concentric ventricular thickening rather than eccentric
Clinical features: CO normal = asymptomatic
L heart failure appears with ischemia (angina pectoris)
Cor Pulmonale
R ventricular hypertrophy secondary to pulmonary arterial hypertension (lung disease, esp w/ scarring, multiple small pulmonary emboli)
Both reduce vascular bed, inc pulmonary arterial pressure
Congenital heart disease
atrial septal defects, ventricular septal defects, patent (persistent) ductus arteriosus, tetralogy of Fallot, transposition of the great arteries, coarctation of aorta
Shunts
small hole or passage which allows movement of fluids from one part of the body to another
Left to right shunt
pressure higher in left heart than in right heart, no cyanosis initially, late cyanosis when shunt reverses due to pulmonary hypertension
Atrial septal defect
*Most common congenital cardiac malformation first diagnosed in adults, no symptoms in childhood, pulmonary hypertension may reverse shunt and produce cyanosis
Ventricular Septal Defect (VSD)
Most common congenital heart disease (CHD) diagnosed at birth (most are small and close spontaneously)
Patent Ductus Arteriosus
Ductus arteriosus normally closes shortly after birth, Patent ductus arteriosus usually identified early on the corrected w/ medication or surgery, eventually shunt reverses due to pulmonary hypertension and cyanosis develops
Right to left shunt
pressure higher in right heart than in left heart
**Cyanosis initially since blood is shunted away from lungs (reduced oxygenation)
Tetralogy of Fallot
Blood is diverted from pulmonary circulation to systemic thus reducing oxygenation, cyanosis at or near birth
Tetralogy of Fallot
1 - Pulmonary Artery Stenosis
2 - Overriding aorta
3 - Ventriculoseptal defect
4 - Right ventricular hypertrophy
May also have a patent ductus which helps oxygenate the blood
Transposition of the Great Arteries
Second leading cause of congenital cyanosis
abnormal truncal septation, aorta arises from R ventricle and the pulmonary artery arises from L ventricle
*Cyanosis is the main clinical sign
Coarcation of Aorta
Abnormal narrowing of the aortic lumen (blood pressure higher in arms than legs)
Cerebral hemorrhages common due to inc intracranial arterial pressure
Weak pulses in the lower extremities with signs and symptoms of intermittent claudication (ischemic leg pain)
Ischemic Heart Disease
imbalance between myocardial supply (perfusion) and cardia demand for oxygenated blood
most common cause: atherosclerotic narrowing of coronary arteries
4 forms or manifestations of ischemic heart disease
1) angina pectoris (ischemic chest pain)
2) myocardial infarction (MI)
3) sudden cardiac death (SCD)
4) chronic ischemic heart disease w/ heart failure
“Acute Coronary Syndrome”
an umbrella term for 3 acute conditions resulting from coronary artery disease
1 - unstable angina pectoris
2 - acute myocardial infarction
3 - sudden cardiac death
**All 3 result from acute changes in the morphology of coronary atherosclerotic plaques
Etiology of Coronary Artery Disease
Hypertension, Diabetes (type I and II), Smoking, High levels of LDL, Low levels of HDL, Poorly understood hereditary factors
Coronary Artery plaque
critical stenosis
> 75% luminal reduction of 1+ coronary arteries,
compensatory vasodilation is insufficient to compensate
Acute Plaque Changes
abrupt changes in plaque followed by thrombosis (fissuring, hemorrhage into plaque, overt plaque rupture w/ embolization of atheromatous debris)
may occur w/ plaques less than 75% occlusive and in prev asymptomatic individuals
Coronary Artery Thrombosis
1 - plaque rupture exposes thrombogenic lipids and subendothelial collagen initiating thrombosis
2 - if vessel completely occluded, infarction occurs
If vessel incompletely occluded, unstable angina or lethal ventricular arrhythmia results
Angina Pectoris
Intermittent chest discomfort or pain caused by transient, reversible myocardial ischemia
Stable Angina Pectoris
Associated with fixed atherosclerotic narrowing of 1+ coronary arteries
Discomfort in chest described as deep, poorly localized pressure, squeezing or burning sensation
Produces by physical activity, emotional excitement, or physiological stress
Pain relieved by rest and/or nitroglycerin or calcium channel blockers
Prinzmetal Angina Pectoris
Anginal pain occurring at rest or awakening patient from sleep
Usually associated with coronary artery spasm often adjacent to a site of atherosclerotic plaque
Mechanism underlying spasm poorly misunderstood
Unstable Angina Pectoris
Increased frequency of angina episodes
Precipitated by progressively less exertion
Described as intense pain
More intense - last longer than “stable anginga” (>20 min)
Induced by acute plaque change w/ a superimposed partial thrombosis or vasospasm or both
Myocardial Infarction
development of an area of myocardial necrosis caused by localized ischemia
Risk factors are same as atherosclerosis
Myocardial necrosis begins w/ 20-30 min reaching full size within 3-6 hours
Begins in subendocardium extending toward epicardium
Thrombolytic agents may limit size of infarct during this time frame
Clinical complications of Acute MI
sudden death, cardia arrhythmias, left heart failure, cardiogenic shock, myocardial rupture w/ hemopericardium and cardia tamponade, thromboembolism
Anatomic Complications of MI
Infarcted papillary muscle and mitral valve insufficiency
External rupture of the infarct w/ cardia tamponade
Mural thrombus giving rise to systemic arterial emboli
Ventricular aneurysms
Sudden Cardiac Death
Most common cause: ischemic heart disease (coronary artery atherosclerosis) (acute “cor pulmonale” due to massive pulmonary artery thromboembolism
Valvular Heart Disease
Mitral valve stenosis
Regurgitation
Calcific Aortic Stenosis
age related degeneration, most common cause of isolated aortic stenosis in USA, L ventricular hypertrophy and dec aortic outflow lead to myocardial ischemia, death within 3-4 years unless treated
Mitral Valve Prolapse
results in mitral regurgitation, common cardiac disorder, prone to infective endocarditis/ arrhythmias/ emboli from L atrium
*most cases are sporadic; may be seen with Marfan syndrome
Rheumatic Fever
acute, immunologically-mediated, multisystem inflammatory disease usually following group A streptococcal pharyngitis after an interval of a few weeks
Pharyngitis severity not related to risk of developing RF
Pathogenesis: Hypersensitivity reaction induced by group A streptococci, antibodies developed against “M” proteins of group A strep cross-react w/ similar epitopes in heart, joints, skin, and other, comprised of **“Anitschkow cells”
Acute RF - rarely causes heart failure due to myocarditis and valvular injury
Chronic RF - irreversible valvular deformity (Mitral valve 95%, Mitral+Aortic 25%)
Infective Endocarditis
Infection of cardiac valves or mural surfaces of endocardium
Gradual onset or explosive onset depending upon the virulence of the organism (Low - low-grade fever, malaise, weight loss) (High - high ever, shaking chills, overt septicemia)
Acute Infective Endocarditis
Organisms of high virulence Staph aureus
Often involves normal valves
Intravenous drug use
Often tricuspid and pulmonic valves rather than left heart valves
Subacute Infective Endocarditis
Organisms of low virulence
50-60% of cases of endocarditis occurring on damaged valves are caused by Strep viridans
Pre-existing cardiac abnormalities, especially valvular disease (small ventriculoseptal defects, chronic rheumatic valvular disease, calcific aortic stenosis, mitral valve prolapse
Noninfective Endocarditis
Systemic Lupus Erythematosus: Endocarditis Usually mitral valve “Libman-Sacks disease”
Dilated Cardiomyopathy
4 chamber dilation and hypertrophy
Idiopathic
Fundamental defect is ineffective contraction: ejection fraction < than 25%. Normal = 55-70%
Some association w/ alcoholism and prior viral myocarditis
Occur at any age, more often in men, 20-30% due to inherited genetic disorders
Hypertrophic Cardiomyopathy
“Idiopathic hypertrophic subaortic stenosis”
Heavy, muscular, hypercontracting heart
Genetic basis of 50% of cases; AD
One of most common causes of sudden unexpected death in young athletes
Myocarditis
Inflammatory process of the myocardium resulting in injury to cardiac myocytes
Causes: viral, bacterial, parasitic, fungal, immune-mediated myocardial injury
Pericarditis
Inflammatory process involving the pericardium as a result of a systemic disease or a primary pericardium disorder
Morphologically classified in 5 types: fibrinous, serous, purulent, hemorrhagic, caseous
Fibrinous Pericarditis “Bread & Butter” pericarditis
most frequent type
pericardium opaque and granular
associated w/ acute myocardial infarction, SLE, chest irradiation and trauma
May develop a loud pericardial friction rub
Can compromise cardiac output due to fluid accumulation in pericardial sac
Histology shows the deposition of fibrin and leukocytic exudate
Bacterial (purulent) Pericarditis
Occurs by direct infection during trauma, thoracic surgery, or catheter drainage, by spread from an intrathoracic, myocardial, or subdiaphragmatic focus, and by hematogenous dissemination
Frequent causes are staph, Haemophilus, and M. tuberculosis
Hemorrhagic pericarditis
Involves blood mixed w/ a fibrinous or suppurative effusion
Most commonly caused by tuberculosis or direct neoplastic invasion
Can occur in sever bacterial infections or in patients w/ a bleeding diathesis
Pericardial effusions
Fluid accumulation in the pericardial space
Nature of fluid varies with the cause of the effusion
-Serous: congestive heart failure, hypoalbuminemia
-Serosanguineous (watery, blood tinged): blunt chest trauma, malignancy
-Chylous (milky) mediastinal lymphatic obstruction, usually by mediastinal neoplasm
Clinical features: Cardiac tamponade (heart unable to expand during diastole due to fluid in sac)
Hemopericardium
Ruptured infarction
Penetrating cardiac trauma
Cardiac tamponade results
Atrial Fibrillation
a disease of the heart characterized by irregular and often faster heartbeat
Predisposes the patient to thromboemboli from the left heart resulting in ischemic strokes
Most patients on long-term anticoagulation are being treated for this reason
Clinical Features:
may be asymptomatic, dizziness, light-headness, syncope, tachycardia, stroke,
Treatment: Warfarin and Factor X/ Thrombin antagonists
