11. Cardiovasc.disorders

Cardiac Anatomy & Physiology:
• anatomy: located in mediastinum (fig. 10 - 1 & ppt. 1), protected by sternum
- pericardium: heart is enclosed in pericardial cavity, bounded by parietal
pericardium and visceral pericardium (= epicardium) (figs. 10 -2, 10 - 3 & ppts. 2 & 3);
pericardium is anchored to diaphragm
- myocardium: cardiac muscle constitutes middle layer; fibrous skeleton
(annuli fibrosi) encloses valves (fig. 10 - 4 & ppt. 4); provides anchorage for muscle
(fig. 10 - 5 & ppt. 5)
- endocardium: thin internal lining of epithelium, continuous with
endothelium of blood vessels (fig. 10 - 3 & ppt. 3)
- chambers: two atria (reception chambers) and two ventricles (pumping
chambers); left side pumps to systemic circuit & right side pumps to pulmonary
circuit) (fig. 10 - 6 & ppts. 6 & 7)
- valves: atrioventricular valves (tricuspid - right; mitral - left) separate
atria from ventricles and semilunar valves (pulmonary - right; aortic - left) separate
ventricles from arteries (figs. 10 - 4, 10 - 8 & ppt. 4)
- valves facilitate one-way flow (fig. 10 - 7) through the heart -- from
atrium to ventricle and from ventricle to artery; atrioventricular valve function is
aided by attachment to papillary muscles via chordae tendineae (fig. 10 - 9)
• cardiac cycle (ppt. 8): = one heartbeat; two main periods -- systole
(contraction) & diastole (relaxation) -- usually in reference to ventricular activity
- diastole accomplishes filling of both atrium and ventricle; end-diastolic
volume = amount of blood in heart at end of diastole
- systole accomplishes pumping of blood into the arteries; end-systolic
volume = amount of blood in heart at end of systole
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- stroke volume = amount pumped/cycle (EDV - ESV = SV); may be
elevated by increased venous return (preload), or by factors that stimulate
contractility (positive inotropic effect), e.g. sympathetic NS, epinephrine, digitalis; SV
may be depressed by factors opposing ventricular emptying (afterload), or factors
that decrease contractility (negative inotropic effect), e.g. hypoxia, toxins
- heart rate: accelerated (positive chronotropic effect) by various stimuli, e.g.
increased sympathetic signal, epinephrine; slowed (negative chronotropic effect) by
increased parasympathetic signal (fig. 10 - 12 & ppt. 9)
- cardiac output is the volume of blood pumped by left ventricle per
minute, and is governed by heart rate (beats per minute) and SV; CO = SV x HR
• electrical activity of heart (fig. 10 - 10 & ppt. 10): SA node = pacemaker in
right atrial myocardium governs the heart rate -- sinus rhythm
- atrial myocardium conducts the signal throughout both atria; AV node is
needed to pass the signal across the annuli fibrosi to the ventricles; this involves a
delay of signal (~.12 - .2 sec.); thus, atria contract before ventricles contract
- AV bundle & Purkinje fibers relay signal from AV node throughout
ventricular myocardium
- irritated regions of myocardium (ectopic foci) may override pacemaker
causing departure from sinus rhythm & altered heart function
• ECG or EKG (electrocardiograph): recording of heart's electrical activity
features P wave (depolarization of atria), QRS complex (ventricular depolarization),
& T wave (ventricular repolarization) (fig. 10 - 11 & ppt. 11)
- PR interval = time from beginning of P wave to beginning of R spike = AV
node delay; extended PR intervals are known as 'heart blocks' and signify impairment of
AV node, AV bundle or Purkinje system
- ST segment = time from end of QRS complex to beginning of T wave;
depressed or elevated ST segments indicate myocardial ischemia or infarction
- many other findings from EKG are valuable in diagnosing various heart
problems (see text pp. 250 - 251 & ppt. 12)
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- p. 3 -
• coronary circulation (fig. 10 - 14 & ppt. 13): left coronary a. produces anterior
interventricular (left anterior descending) branch and circumflex branch
- right coronary a. supplies a posterior interventricular (posterior descending)
Heart Failure: inability to maintain adequate cardiac output
• acute heart failure: rapid onset (few seconds to a few days), lethal to about
1/3 of sufferers
• chronic heart failure: gradual accumulation of impairments
(mostly due to ischemic heart disease - see below); sufferers are vulnerable to sudden acute
failure due to therapeutic failure or excessive demand, e.g. snow shoveling
Ischemic Heart Disease (IHD):
• coronary artery disease (CAD): consequence of atherosclerosis, usually in
aorta and its branches, including coronaries; also called atherosclerotic heart disease
- plaques or emboli may obstruct coronary circulation causing ischemia,
angina pectoris (fig. 10 - 20 & ppt.14), infarction, and weakening of the heart perhaps to
point of failure
- ischemia: impaired blood flow
- chronic ischemia often develops slowly enough to permit adaptive
changes, e.g., development of collateral circulation
- acute ischemia is sudden and often leads to acute myocardial infarction
(MI) (fig. 10 - 19)
- ischemia most often develops in left coronary and its branches, frequently
involving multiple plaques (may necessitate multiple bypasses)
• acute myocardial infarction: plaque rupture & bleeding into lesion produces
thrombosis and severe ischemia resulting in necrosis of downstream myocardium
- symptoms vary from almost no pain to intense angina accompanied by
dyspnea, diaphoresis, and extreme anxiety
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- signs - derived from ECG and from monitoring of levels of various blood
components: creatine kinase, lactic dehydrogenase (enzymes released from damaged
muscle), & troponin (contractile protein released from damaged heart muscle)
- treatments involve coronary bypass surgery (using great saphenous veins,
sections of mammary arteries, internal thoracic arteries, or artificial Teflon vessels)
- angioplasty (distending narrowed vessel with balloon catheter, followed
by insertion of a stent)
- administration of tissue plasminogen activator (t-PA), a 'clot buster' may
be used but its effects may be delayed, compared to benefits of angioplasty
- sequelae of acute MI may include arrhythmias (including dangerous
ventricular fibrillation), thrombosis, cardiogenic shock (due to heart failure), ventricular
aneurysm (fig. 10 - 21 & ppt. 15) and danger of rupture (causes abrupt hemopericardium
that leads to rapid heart failure) (fig. 10 - 22 & ppt. 16)
Congestive Heart Failure (= chronic heart failure - CHF):
• left-sided failure: usually the first to occur (compromised cardiac output,
e.g., fig. 10 - 24 & ppt. 17), followed by right-sided failure
- characterized by lung conditions, e.g., edema, congestion (poor venous
drainage) or by failing dependent organs, e.g. kidney failure, cerebral ischemia
• right-sided failure is characterized by congestion of liver (hepatomegaly), spleen
(splenomegaly), and kidney (impaired clearing of fluids, nitrogenous waste)
- cor pulmonale produces right-sided failure independently of left-sided failure,
due to pulmonary hypertension from various lung conditions (emphysema,
embolisms, pulmonary fibrosis: see table 10 - 5)
• etiology: may stem from weakened myocardium, pumping restrictions, or
increased afterload
- i) myocardial weakness most often due to ischemia from coronary
atherosclerosis (fig. 9 - 20 & ppt. 18)) or coronary thrombosis
- other contributing conditions: myocarditis (see below) or cardiomyopathy
(fig. 10 - 37 & ppts. 19 & 20), which may produce dilated (thin, distended
myocardium), hypertrophic (thickened myocardium that may restrict ventricular
lumen), restrictive (stiffening of myocardium) conditions, or a combination of these
Bio 307/607 lec 11
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- ii) restrictions to pumping (table 10 - 4) arise from valvular disorders, from
obstructions (e.g., tumor, - fig. 10 - 25 & ppt. 21)
- congenital heart defects (figs. 10 - 38, 10 - 39, 10 - 41, table 10 -8 &
ppts.22 to 24) include ventricular septal defects, tetralogy of Fallot, aortic coarctation &
patent ductus arteriosus (PDA)
- disturbances of electrical rhythm (dysrhythmias, e.g., heart blocks,
fibrillation), and pericarditis (see below) with associated tamponade, are other factors
that may restrict pumping (fig. 10 - 22 & ppt. 16)
- iii) increased afterload includes any conditions increasing heart's
workload, most often systemic conditions provoking left-sided failure as a prelude to
both-sided failure; systemic hypertension is most likely cause
- summary of etiologic factors for CHF (fig. 10 - 26 & ppt. 25)
- pathogenesis of CHF (figs. 10 - 27, 10 - 30 & ppt. 26): pulmonary
hypertension and associated consequences follow left-sided failure, as well as
weakness & fatigue (due to reduced cardiac output); cardiomegaly (fig. 10 - 31 & ppt.
27) is a compensatory response of both sides, and hepatomegaly and splenomegaly
follow right-sided failure
- compensations in CHF (fig. 10 - 32 & ppt. 28): cardiomegaly, renal
adjustments (renin-angiotensin system), & nervous system adjustments (sympathetic
outflow causes positive chronotropic and positive inotropic effects, as well as
peripheral vasoconstriction)
Inflammatory Conditions:
• pericarditis: pericardial inflammation characterized by fluid accumulation in
pericardial cavity (pericardial effusion); accumulated exudate = hydropericardium;
accumulated blood = hemopericardium; such conditions impair ventricular filling due
to external pressure on atria (cardiac tamponade) (fig. 10 - 22 & ppt. 29)
- acute pericarditis: effusions ranging from serous (watery) to fibrinous
(coagulative); rheumatic heart disease, myocardial infarction, and viral infections
(fig. 10 - 15) are causes; extensive adhesions severely compromise cardiac output
- chronic pericarditis: prolonged inflammation may cause 'hardening of the
pericardium' (fibrosis & calcification)
- commonly associated with tuberculosis pericarditis
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• myocarditis: ranges from mild condition to one that involves serious
weakening of myocardium; viral infection is commonest cause
• endocarditis: infective endocarditis (bacterial, fungal) exhibits typical lesion
called a vegetation (fig. 10 - 16)
- vegetation is a thrombus, containing infective agents (which may be
inaccessible to immune defenses)
- vegetations are most often associated with valves & may compromise
valve function
Valvular Disease (table 10 - 1):
• stenosis: failure to open effectively, often causing heart murmur
- commonly associated with rheumatic heart disease, infective endocarditis,
congenital malformation, or calcification of cusps
- aortic stenosis compromises left ventricular output, causes left ventricular
hypertrophy, & may lead to left-sided failure
• insufficiency: failure to close properly, results in regurgitation; often
uneventful for many years & may be undiagnosed
Rheumatic Heart Disease (RHD) (fig. 10 - 18 & ppt. 30):
• rheumatic fever: more generalized inflammatory condition that includes
RHD, but also numerous other tissues (joints, skin, vessels, serosa, & lungs)
- usually post-streptococcal in origin resulting in valve disorders (most
common) and may lead to congestive heart failure; cross-reacting antibodies cause
lesions in uninfected tissues including myocardium
- most effective treatment is aimed at minimizing streptococcal infection via
antibiotics, such as penicillin
Treatment Strategies (fig. 10 - 35 & ppt. 31):
- minimize thrombosis - antiplatelet drugs, blood thinners
- treatment of heart rate - positive or negative chronotropes
- treatment of contractility - positive or negative inotropes
- lower blood volume - diuretics
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- alleviate arrhythmias - antiarrhythmics
- reduce vascular resistance - vasodilators
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