heart Flashcards
cardiac pump problems
-Failure of the pump –MC problem
-contracts weakly and chambers cant empty properly— (systolic dysfunction)
-cant relax enough to allow ventricular filling – (diastolic dysfunction)
-Obstruction to flow- calcific aortic valve stenosis or cause increased ventricular chamber pressures (systemic hypertension) can overwork myocardium (has to pump against obstruction)
-Regurgitant flow
-Shunted flow - Defects (congenital or acquired) that divert blood, leading to pressure and volume overloads
-Disorders of cardiac conduction
-Rupture of the heart or major vessel - Loss of circulatory continuity
CHF
-Heart cant pump blood adequately to meet demands of tissues
-Causes: Fluid overload, abrupt valvular dysfunction, MI
-Initially, compensatory to maintain organ perfusion:
-!!!!Frank-Starling mechanism: Increased filling volumes dilate the heart, enhancing contractility and stroke volume
-Activation of neurohumoral systems: aid heart function and/or regulate filling volumes and pressures
-Release of norepinephrine: elevates HR, augments myocardial contractility and increases vascular resistance
-Activation of RAAS: water and salt retention, increases vascular tone
-Release of ANP: counterbalances the RAAS by diuresis and vascular smooth muscle relaxation
-Myocardial adaptations
-Ventricular remodeling
CHF causes
-decrease in EF - blood ejected from ventricle during systole- WNL- 45% to 65%
-Reduction in EF:
-ischemic injury
-inadequate adaptation to pressure or volume overload due to HTN or valvular disease
-ventricular dilation
-left ventricular hypertrophy, myocardial fibrosis, constrictive pericarditis, or amyloid deposition
cardiac hypertrophy: patho and progression to HF
-increase in mechanical work of ventricle due to pressure overload, volume overload, or trophic signals (activation of β-adrenergic receptors) causes increase in !myocyte size (hypertrophy)!
-Pressure-overload hypertrophy (HTN or aortic stenosis): results in concentric wall thickness increase
-Volume-overload hypertrophy (valvular regurgitation): ventricular dilation
-Hypertrophied heart vulnerable to ischemia:
-Larger myocytes need more blood
-Larger heart has increased metabolism needs because of increased mass, heart rate, contractility – increase oxygen consumption
flow chart
LEFT sided HF: Causes
-Most often caused by:
-ischemic heart disease
-HTN
-Aortic and mitral valvular diseases
-Primary myocardial diseases
-Clinical and morphologic effects of left-sided CHF: consequence of passive congestion (blood backing up in the pulmonary circulation), stasis of blood in left-sided chambers, and inadequate perfusion of downstream tissues leading to organ dysfunction
-Systolic failure - insufficient EF (pump failure)
-Diastolic failure - LV abnormally stiff; HTN MCC
left sided HF
-Enlarged heart, tachycardia
-volume overload (S3)
-increased myocardial stiffness (S4)
-lung micro will show “heart failure cells”
-dyspnea- blood tinged sputum
-tachy- heart has to work harder
-Moderate CHF: reduced EF leads to decreased renal perfusion -> activating RAAS -> leading to salt and water retention -> prerenal azotemia (excess nitrogen compounds in blood) -> may lead to renal failure
-Very severe- cerebral hypoperfusion can lead to hypoxic encephalopathy: irritability, loss of attention span, and restlessness; can progress to stupor and coma
right sided heart failure causes
-MCC by left-sided HF
-isolated right-sided heart failure- lung diseases (cor pulmonale)
-Pulmonary congestion minimal; engorgement of systemic and portal venous systems pronounced
right sided HF
-changes in liver, spleen, and gi:
-hepatomegaly- caused by passive congestion; Grossly: congested red-brown pericentral zones, with relatively normal-colored tan periportal regions, produce characteristic “nutmeg liver”
-congestive splenomegaly
-effusions in pleural, pericardial, or peritoneal spaces (ascites)
-Hallmark - foot/ankle (pedal) and pretibial edema
-Renal congestion more marked with right-sided heart failure = more fluid retention and peripheral edema, azotemia
-Hypoxia of CNS can also produce deficits of mental function
-FATIGUE
-“Dependent” edema
-JVD
-ASCITES, PLEURAL EFFUSION
-Cyanosis
-Increased peripheral venous pressure (CVP)
CHF labs
-Usually both right and left sided HF
-Serum BNP
-Echocardiography- measure EF, wall motion, valvular function, and possible mural thrombosis
-Tx - underlying cause (valvular defect or inadequate cardiac perfusion)
-salt restriction, diuretics, inotropes (increase myocardial contractility), adrenergic blockers or ACE inhibitors (reduce afterload)
CHD, L to R
-Left-to-right shunts (all have “D”s in their names) increase pulmonary blood flow but NOT initially associated with cyanosis; may develop pulmonary HTN
-Atrial Septal Defect - Usually asymptomatic until adulthood; increase only right ventricular and pulmonary outflow volumes
-Ventricular septal defect - MC; only 30% are isolated; often with TETRALOGY of FALLOT
-50% close spontaneously
-large - early right ventricular hypertrophy and pulmonary hypertension
-Patent Ductus Arteriosus -
-harsh “machinery-like” murmur
congenital HD R to L shunts
-hypoxemia and cyanosis- pulmonary circulation is bypassed and poorly oxygenated venous blood shunts directly into systemic arterial supply
-Right-to-left shunts: (all have “T”s in their names)
-tetralogy of Fallot (TOF)!!!
boot shaped heart
-tetralogy of fallot
ischemic heart disease
-90% of IHD patients have ATHEROSCLEROSIS
-Angina Pectoris: Stable, Unstable
-MI
-Chronic IHD- > CHF
-Sudden Cardiac Death (SCD)
-“Acute” Coronary Syndromes:
-UNSTABLE ANGINA
-Acute myocardial infarction
-SCD (Sudden Cardiac Death)
coronary artery patho in ischemic heart disease
dont need severe stenosis for an MI
angina pectoris
-Chest pain
-Paroxysmal (sudden)
-Recurrent
-15 sec - 15 min.
-Reduced perfusion, but NO infarction!
-THREE TYPES
-STABLE: relieved by rest or nitro
-PRINZMETAL: SPASM is main feature, responds to nitro
-UNSTABLE (crescendo, PRE-infarction, Q-wave angina): pattern of increasingly frequent, prolonged (>20 min), or severe angina, usually occurring at rest -> associated with plaque disruption and superimposed partial thrombosis
MI
-Transmural (full thickness) vs. Subendocardial (inner 1/3)
-Most are TRANSMURAL, and MOST are caused by coronary artery occlusion
-In the 10% of transmural MIs NOT associated with atherosclerosis:
-Vasospasm
-Emboli
-UNexplained
lab enzymes
-EKG
-CK-MB
-Troponin
-C-reactive protein predicts risk of AMI in angina patients
-coagulation necrosis
CHARACTERIZED BY THE LOSS OF THE NUCLEUS
-TEST QUESTION
-A WEEK LATER AFTER MI -> AND YOU LOOK AT TISSUE -> GRANULATION TISSUE- A BUNCH OF MACROPHAGES, COLLAGEN, & NEW VESSELS
-TEST QUESTION
-if CK-MB is low it doesnt rule out MI -> must do troponins
complications of MI
-Wall motion abnormalities
-Arrhythmias (usually within first 24 hours)!!!!- MC
-Rupture (4-5 days) – cardiac tamponade
-Pericarditis
-Dressler syndrome (autoimmune pericarditis 2 weeks – 2 months post MI)
-RV infarction
-Infarct extension
-Mural thrombus
-Ventricular aneurysm
-Papillary muscle dysfunction (regurgitation)
-CHF
hypertensive heart disease
usually causes ventricular hypertrophy, CHF may develop, myocardial dysfunction, or sudden death
mitral annular calcification
-Degenerative calcific deposits in the mitral valve usually develop in the fibrous annulus
-Irregular, stony hard, occasionally ulcerated nodules at base of the leaflets
-Usually does not affect valvular function; however, rarely can lead to:
-* Regurgitation by interfering with physiologic contraction of the valve ring
-* Stenosis by impairing opening of the mitral leaflets
-* Arrhythmias and occasionally sudden death by penetration of calcium deposits deep enough to impinge on AV conduction system
-Increases with age, more common in women and individuals with mitral valve prolapse
mitral valve prolapse (MVP) aka myxomatoid degeneration of the mitral valve
-One or both mitral valve leaflets are “floppy” and protrude into left atrium during systole
-2% to 3% of adults in US, more common in women; mostly incidental finding, but may lead to serious complications in small minority
-parachute valve
-Cause not really known
-Uncommonly, associated with heritable disorders of connective tissue including Marfan syndrome
-!!Ballooning (hooding) of mitral leaflets; affected leaflets often enlarged, redundant, thick, and rubbery; associated tendinous cords may be elongated, thinned, or even ruptured, and the annulus may be dilated
MVP: clinical features
-Usually asymptomatic
-Mid-systolic “click” (caused by abrupt tension on redundant valve leaflets and chordae tendineae as valve tries to close)
-May or may not be associated regurgitant murmur
-Diagnosis confirmed by echocardiography
-Minority of patients - occasional chest pain, dyspnea
-3% may develop Infective endocarditis, mitral insufficiency, arrythmias, stroke or other systemic infarct (from embolism of leaflet thrombi), sudden death
rheumatic heart disease- just know ab pain carditis and joint pain
-Acute rheumatic carditis in active RF may progress to chronic rheumatic heart disease (RHD)
-RHD (chronic)- deforming fibrotic valvular disease, esp. of the mitral valve
-Migratory polyarthritis (large joints)
-Pancarditis (myocarditis, pericarditis, or endocarditis) -> all three layers
-Subcutaneous nodules (typically on extensor surfaces of extremities)
-Erythema marginatum, irregular circinate skin rash
-Sydenham chorea, a neurologic disorder with involuntary rapid movements
-Aschoff bodies (with plump activated macrophages called Anitschkow cells (aka “caterpillar cells”)