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Arrhythmias
Mechanically inefficient
CO decreases
Atrial flutter
rapid, regular atrial rhythm ~ 300 beats/min
Atrial fibrillation
rapid, irregular atrial rhythm AV node filters out alot decreased CO
Each year heart disease accounts for about 1/3 of deaths in the US, most of which are associated with coronary artery atherosclerosis. If cerebrovascular disease, vascular complications of diabetes, & other vascular diseases are included, the figure is over 40%. After age 40 the lifetime risk for developing symptomatic coronary artery disease is 50% in men & 40% in women.
Heart Block
Atrial signal is delayed & cannot cross into the ventricle Common cause is anatomic abnormalities Can also be caused by digitalis 1st degree
delay of signal but no missed ventricular beats
2nd degree
delay long enough to cause missed ventricular beats
3rd degree
total block of atrial signal decreased CO
Ventricular tachycardia
spontaneous, regular beating at > 120 beats/min decreased CO
Ventricular fibrillation
extremely rapid & irregular negligible CO
Most common cause is cardiac muscle damage usually due to CAD Less commonly due to valve defects Heart tries to compensate for either of these by increasing HR & force of contraction & through cardiac muscle hypertrophy
In L ventricular failure, low CO causes systemic hypoperfusion & pulmonary venous congestion In R ventricular failure, low CO causes systemic venous congestion The most common cause of R heart failure is L heart failure The low CO of L heart failure reduces renal blood flow which stimulates the renin-angiotensin-aldosterone system
R & L ventricles can fail independently but usually fail together 2 components to uncompensated failure
forward failure
low ventricular output
backward failure
venous congestion
L Heart Failure
L ventricle dilates Forward component
decreased blood flow to organs
Backward component
blood backs up into L atrium & lungs pulmonary edema
dyspnea
R Heart Failure
R ventricle dilates Forward component
decreased blood flow to lungs
Backward component
systemic venous congestion congestion of liver, spleen edema in feet & legs ascites
Etiology
L heart failure
damaged cardiac muscle HTN valve disease cardiomyopathy
R heart failure
L heart failure pulmonary HTN lung disease valve disease congenital heart disease involving L to R shunt
Epidemiology
Begins in the crib Risk factors
age high LDL low HDL HTN smoking fatty diet sedentary lifestyle diabetes familial history
Average patient
overweight diet high in saturated fat big belly little exercise high cholesterol has diabetes or HTN
Complete obstruction
usually an unstable plaque
Angina Pectoris
Distinctive sensation caused by myocardial ischemia Described as
smothering pressing aching heaviness jaw shoulder arms upper abdomen
Stable angina
rises & falls smoothly over a few minutes rest & medication helps usually precipitated by exertion or emotion
Unstable angina
caused by platelets aggregating on a plaque may herald an impending MI new onset, intensification, nocturnal, prolonged need intervention
May radiate to
Unremitting angina
does not fluctuate no relief due to MI
Myocardial Infarction
MI Area of necrosis caused by ischemia Most common cause of death in industrialized nations Most initiated by plaque disruption & accompanying thrombosis Size of infarct determined by vessel involved Age of infarct determined by gross & microscopic findings
coagulative necrosis early development of granulation tissue mature scar
Nearly of all infarcts involve anterior descending About 1/3 involve the R coronary artery The rest involve the circumflex artery
In 3-6 hours, can enlarge to involve the full thickness of the ventricular wall
transmural infarct
Anatomic complications
Infarct papillary muscles Release of substances from necrotic muscle that attracts platelets & WBCs to form mural thrombus
Causes
Inflammation & infection Syphilitic aortitis Myxomatous degeneration of the mitral valve Ruptured mitral valve chordae tendineae Massive L ventricular dilation
May embolize
Infective Endocarditis
Almost always caused by bacterial infection L-sided valves most commonly affected Vegetations containing microbes May embolize Greatest hazard is erosion & perforation of the valve Usually affects previously disease valves Staphylococcus more dangerous than Streptococcus or Enterococcus
Myocarditis
Usually due to virus
coxsackie A or B
Cardiomyopathies
Primary
Intrinsic disease of cardiac muscle Cause usually unknown
Secondary
Associated with
ischemic heart disease HTN infections valvular disease congenital abnormalities
Dilated Cardiomyopathy
Hypertrophy, dilation, & low ejection fraction Cause usually unknown Heart is flabby & weak All chambers dilated
Hypertrophic Cardiomyopathy
About the cases are genetic Sudden death in children & young adults during or immediately after exertion Myocardium is stiff Diastolic filling incomplete
Restrictive Cardiomyopathy
Stiff, noncompliant ventricle which fills incompletely during diastole Systole not forceful Usual outcome is CHF
Cause usually unknown Defects develop in 1st 10 weeks Malrotation defects Expansion defects Septal defects
Pericardial Disease
Pericarditis
usually viral infection atypical chest pain friction rub
Pericardial effusion
may occur in noninflammatory conditions hemopericardium