10 Heart Disorders

10 Heart Disorders
Ventricular Hypertrophy
Pathogenesis of left and right ventricular hypertrophy
1. Sustained pressure increases wall stress.
a. Causes duplication of sarcomeres
i. Duplication in parallel thickens muscle.
ii. Duplication in series lengthens muscle.
b. Sarcomeres are the contractile element of muscle.
2. Contraction against an increased resistance (afterload
a. Produces concentric thickening of the ventricular wall
!ew sarcomeres duplicate in parallel to the long a"es of the cells.
b. Causes of concentric left ventricular hypertrophy (#$%&
i. 'ssential hypertension (most common
ii. (ortic stenosis
b. Causes of concentric right ventricular hypertrophy ()$%
i. Pulmonary hypertension
ii. Pulmonary artery stenosis
*. $olume overload (increased preload
c. Causes dilation and hypertrophy (eccentric hypertrophy of ventricular wall
i. +rank,Starling mechanism causes increased force of contraction.
ii. Sarcomeres duplicate in series and cell length and width are increased.
d. Causes of eccentric hypertrophy of left ventricle
i. -itral valve or aortic valve regurgitation
ii. #eft,to,right shunting of blood (e.g.& ventricular septal defect
Causes more blood to return to the left side of the heart
e. Causes of eccentric hypertrophy of right ventricle
.ricuspid valve or pulmonary valve regurgitation
Ventricular Hypertrophy
i. 'ssential hypertension (most common
ii. (ortic stenosis
c. 'ssential hypertension (most common
i. (ortic stenosis
Conse/uences of ventricular hypertrophy
1. #eft, or right,sided heart failure
2. (ngina (primarily #$%
*. S0 heart sound
a. Correlates with atrial contraction in late diastole
b. Caused by blood entering a noncompliant ventricle
Congestive Heart Failure (CHF)
.he heart fails when it is unable to e1ect blood delivered to it by the venous system
'pidemiology
1. -ost common hospital admission diagnosis in elderly patients
2. .ypes of C%+
a. #eft,sided heart failure (most common type
b. )ight,sided heart failure
c. 2iventricular heart failure (left, and right,sided heart failure
d. %igh,output heart failure
#eft,sided heart failure (#%+
Systolic dysfunction is characteri3ed by a low e1ection fraction ('+ (4056.
.he '+ e/uals the stroke volume divided by the left ventricular end,diastolic
volume. .he normal value ranges from 776 to 856. Diastolic dysfunction is
characteri3ed by normal to high '+ (stiff ventricle and an S0 gallop due to
increased resistance to filling in late diastole. .here is an increase in left atrial
pressure. .he '+ is normal.
page 195
page 191
-itral regurgitation is a problem in closing the mitral valve. .he mitral valve
normally closes in systole. 2lood entering the left atrium during systole
produces a pansystolic murmur that increases in intensity on e"piration. .he
murmur is best heard at the ape".
1. +orward failure
a. #eft side of the heart cannot e1ect blood into the aorta
b. :ncrease in left ventricular end,diastolic volume and pressure
c. 2ackup of blood into the lungs causing pulmonary edema
2. Pathogenesis
a. Decreased ventricular contraction (systolic dysfunction; causes<
i. :schemia (most common cause
ii. -yocardial fibrosis& myocarditis& cardiomyopathy
b. !oncompliant ventricle (diastolic dysfunction
i. )estricted filling of the ventricle
ii. Causes
Concentric #$% (most common cause
:nfiltration of muscle with amyloid& iron& or glycogen
c. :ncreased workload
Due to increased afterload (resistance or preload (volume
22 =ross and microscopic findings
a. #ungs are congested and e"ude a frothy pink transudate (edema.
b. (lveolar macrophages contain hemosiderin (>heart failure> cells.
22 Clinical findings
a. Dyspnea
i. Difficulty breathing
ii. Patient cannot take a full inspiration
b. Pulmonary edema
i. 2ibasilar inspiratory crackles
ii. Chest radiograph shows congestion in upper lobes and alveolar infiltrates
c. #eft,sided S* heart sound
i. ?ccurs in early diastole
:ntensity of the heart sound increases with e"piration.
ii. Caused by blood entering a volume,overloaded left ventricle
iii. +irst cardiac finding in #%+
d. -itral valve regurgitation
Caused by stretching of the valve ring
b. Paro"ysmal nocturnal dyspnea
i. Choking sensation at night due to increased venous return to the failed
left side of the heart
ii. 2lood backs up into the lungs& producing pulmonary edema
iii. )elieved by standing or placing pillows under the head (pillow orthopnea
.hese maneuvers increase the effect of gravity on reducing
venous return to the heart.
)ight,sided heart failure ()%+
.ricuspid regurgitation is a problem in closing the tricuspid valve. .he
tricuspid valve normally closes in systole. 2lood entering the right atrium
during systole produces a pansystolic murmur that increases in intensity on
inspiration. .he murmur is best heard along the left parasternal border.
1. 2ackward failure
a. )ight side of the heart cannot pump blood from the venous system to the lungs.
b. 2lood accumulates in the venous system.
2. Pathogenesis
a. Decreased contraction (e.g.& right ventricular infarction
b. !oncompliant right ventricle (e.g.& )$%
c. :ncreased afterload (left,sided heart failure most common cause
d. :ncreased preload (e.g.& tricuspid valve regurgitation
*. Clinical findings
a. Prominence of 1ugular veins
Due to increased venous hydrostatic pressure
b. )ight,sided S* heart sound due to volume overload in the ventricle
:ncreases in intensity with inspiration
c. .ricuspid valve regurgitation
Caused by stretching of the valve ring
d. Painful hepatomegaly
Passive liver congestion due to backup of venous blood into the central
veins
e. Dependent pitting edema and ascites
Due to an increase in venous hydrostatic pressure
%igh,output heart failure
1. Definition
o +orm of heart failure in which cardiac output is increased compared with values
for the normal resting state
2. Pathogenesis
a. :ncrease in stroke volume
'"ample,hyperthyroidism
b. Decrease in blood viscosity
'"ample,severe anemia
c. $asodilation of peripheral resistance arterioles
'"amples,thiamine deficiency& early phase of endoto"ic shock
d. (rteriovenous fistula
22 (rteriovenous communications bypass the microcirculation
222 :ncreases venous return to the heart
2222 Causes
.rauma from knife wound (most common cause
Surgical shunt for hemodialysis
Ischemic Heart Disease
:mbalance between myocardial ?2 demand and supply from the coronary arteries
Coronary artery blood flow
1. Provides o"ygen to cardiac muscle
a. Coronary vessels fill in diastole.
b. .achycardia (@185bpm decreases filling time& leading to ischemia.
2. #eft anterior descending (#(D coronary artery
a. Distribution
i. (nterior portion of the left ventricle
ii. (nterior two thirds of the interventricular septum
b. (ccounts for 056 to 756 of coronary artery thromboses
*. )ight coronary artery ()C(
a. Distribution
i. Posteroinferior part of the left ventricle
ii. Posterior one third of the interventricular septum
iii. )ight ventricle
iv. Posteromedial papillary muscle in left ventricle
v. 2oth atrioventricular and sinoatrial nodes
b. (ccounts for *56 to 056 of coronary artery thromboses
0. #eft circumfle" coronary artery
a. Supplies the lateral wall of the left ventricle
b. (ccounts for 176 to 256 of coronary artery thromboses
'pidemiology
1. -a1or cause of death in the Anited States
a. :schemic heart disease is more common in men.
b. Peaks in men after age B5 and in women after age 95
2. .ypes of ischemic heart disease
a. (ngina pectoris (most common type
b. Chronic ischemic heart disease
c. Sudden cardiac death
d. -yocardial infarction
*. )isk factors
a. (ge
-en 07 years old and up& women 77 years old and up
b. +amily history of premature coronary artery disease or stroke
c. #ipid abnormalities
22 #ow,density lipoprotein above 1B5 mgCd#
222 %igh,density lipoprotein below *7 mgCd#
b. Smoking tobacco& hypertension& diabetes mellitus
(ngina pectoris
page 19*
page 190
1. Stable angina (most common variant
a. Causes
i. (therosclerotic coronary artery disease (most common
ii. (ortic stenosis with concentric #$%
iii. %ypertrophic cardiomyopathy
b. Pathogenesis
Subendocardial ischemia due to decreased coronary artery blood flow
b. Clinical findings
i. '"ercise,induced substernal chest pain lasting *5 seconds to *5 minutes
ii. )elieved by resting or nitroglycerin
iii. Stress test shows S.,segment depression.
2. Prin3metalDs angina
b. Pathogenesis
i. :ntermittent coronary artery vasospasm at rest
ii. $asoconstriction due to platelet thrombo"ane (2 or decrease in
endothelin
c. Clinical findings
i. Stress test shows S.,segment elevation (transmural ischemia.
ii. )esponds to nitroglycerin and calcium,channel blocker (vasodilator
*. Anstable angina
d. Pathogenesis
i. Severe& fi"ed& multivessel atherosclerotic disease
ii. Disrupted pla/ues with or without platelet nonocclusive thrombi
e. Clinical findings
i. +re/uent bouts of chest pain at rest or with minimal e"ertion
ii. -ay progress to acute myocardial infarction (-:
0. )evasculari3ation procedures
f. Percutaneous transluminal coronary angioplasty (P.C( and stenting
i. 2alloon angioplasty dilates and ruptures the atheromatous pla/ue
Problem with restenosis
ii. :ntracoronary stents
Decrease the rate of restenosis
iii. -ost common early complication is a locali3ed dissection with thrombosis
g. Coronary artery bypass graft (C(2=
i. Ased for multivessel coronary artery atherosclerosis
ii. :nternal mammary artery graft
2est graft patency after 15 years
iii. Saphenous veins
>(rteriali3ation> of the vessels& fibrosis& and occlusion common
after 15 years
Chronic ischemic heart disease
1. Progressive C%+ resulting from long,term ischemic damage to myocardial tissue
2. )eplacement of myocardial tissue with noncontractile scar tissue
a. 2iventricular C%+
b. (ngina pectoris
c. -ay develop dilated cardiomyopathy
Sudden cardiac death
1. Ane"pected death within 1 hour after onset of symptoms
2. Diagnosis of e"clusion after other causes are ruled out
*. Pathogenesis
a. Severe atherosclerotic coronary artery disease
b. Disrupted fibrous pla/ues
c. (bsence of occlusive vessel thrombus (@856 of cases
0. Cause of death is ventricular fibrillation.
-yocardial infarction
page 19E
1. Pathogenesis
a. Se/uence<
i. Sudden disruption of an atheromatous pla/ue
ii. '"posed subendothelial collagen or thrombogenic necrotic material
iii. Platelet adhesion and eventual formation of a platelet thrombus
b. )ole of thrombo"ane (2
i. Contributes to formation of the platelet thrombus
ii. Causes vasospasm of the artery
2. #ess common causes of acute -:
a. $asculitis (e.g.& polyarteritis nodosa& Fawasaki disease
b. Cocaine use
c. 'mboli3ation of pla/ue material
d. .hrombosis syndromes (e.g.& antithrombin ::: deficiency& polycythemia
*. .ypes of myocardial infarction
a. .ransmural infarction (G,wave infarction
i. :nvolves the full thickness of the myocardium
ii. !ew G waves develop in an electrocardiogram ('C=.
b. Subendocardial infarction (non,G wave infarction
i. :nvolves the inner third of the myocardium
ii. G waves are absent.
0. )eperfusion
a. -ay follow thrombolytic therapy (e.g.& tissue plasminogen activator
b. 'arly reperfusion salvages some in1ured but not necrotic myocytes.
:mproves short, and long,term function and survival
b. )eperfusion histologically alters irreversibly damaged cells.
i. Produces contraction band necrosis
ii. %ypercontraction of myofibrils in dying cells due to the influ" of Ca
2H
and
7. =ross and microscopic findings of acute -:
b. During 5 to 20 hours
i. !o gross changes until 20 hours after -:
ii. Coagulation necrosis without neutrophil infiltrate within 12 to 20 hours
c. During 1 to * days
i. Pallor of infarcted myocardium
ii. -yocyte nuclei and striations disappear.
iii. !eutrophils lyse dead myocardial cells.
d. During 0 to 9 days
i. )ed granulation tissue surrounds area of infarction.
ii. -acrophages begin removal of necrotic debris.
e. During 9 to 15 days
i. !ecrotic area is bright yellow
ii. =ranulation tissue and collagen formation are well developed.
f. During 2 months
:nfarcted tissue replaced by white& patchy& noncontractile scar tissue.
a. Sudden onset of severe retrosternal pain
i. #asts more than *5 to 07 minutes
ii. !ot relieved by nitroglycerin
iii. )adiates down the left arm into the shoulders or into the 1aw or
epigastrium
iv. (ssociated with sweating (diaphoresis& an"iety& and hypotension
g. >Silent> acute -:s
i. -ay occur in the elderly and in individuals with diabetes mellitus
ii. Due to high pain threshold or problems with nervous system
B. Complications
h. (rrhythmias
i. $entricular premature contractions (most common
ii. -ost common cause of death is ventricular fibrillation.
+re/uently associated with cardiogenic shock
i. Congestive heart failure
Asually occurs within the first 20 hours
b. )upture
i. -ost commonly occurs between days * and 9 (range 1,15 days
ii. (nterior wall rupture
Causes cardiac tamponade
(ssociated with thrombosis of the #(D coronary artery
iii. Posteromedial papillary muscle rupture or dysfunction
(ssociated with )C( thrombosis
(cute onset of mitral valve regurgitation and #%+
iv. :nterventricular septum rupture
(ssociated with #(D coronary artery thrombosis
Produces a left,to,right shunt causing )%+
1. -ural thrombus
i. -ost often associated with #(D coronary artery thrombosis
ii. Danger of emboli3ation
k. +ibrinous pericarditis with or without effusion
i. Days 1 to 9 of transmural acute -:
Substernal chest pain relieved by leaning forward
Precordial friction rub is present.
Due to increased vessel permeability in the pericardium
ii. (utoimmune pericarditis
Develops B to 8 weeks after an -:
(utoantibodies are directed against pericardial antigens.
+ever and precordial friction rub
l. $entricular aneurysm
i. Clinically recogni3ed within 0 to 8 weeks
ii. Precordial bulge during systole
2lood enters the aneurysm causing anterior chest wall
movement.
iii. Complications
C%+ due to lack of contractile tissue
Danger of emboli3ation of clot material
)upture is uncommon.
m. )ight ventricular acute -:
i. (ssociated with )C( thrombosis
ii. Clinical findings
%ypotension& )%+& and preserved left ventricle function
9. #aboratory diagnosis of acute -:
n. Creatine kinase isoen3yme -2 (CF,-2
i. CF,-2 appears within 0 to 8 hours; peaks at 20 hours; disappears within
1.7 to * days.
ii. )einfarction
)eappearance of CF,-2 after * days
o. Cardiac troponins : (c.n: and . (c.n.
i. !ormally regulate calcium,mediated contraction
ii. c.n: and c.n. appear within * to B hours; peak at 20 hours; disappear
within 9 to 15 days.
iii. .roponins are the gold standard for diagnosis of acute -:.
-ore specific for myocardial tissue than CF,-2 and last longer
p. #actate dehydrogenase (#D%1,2 >flip>
i. !ormally& #D%2 is higher than #D%1.
:n acute -:& #D%1 in cardiac muscle is released causing the >flip.>
ii. #D%1,2
(ppears within 15 hours; peaks at 2 to * days; disappears within
9 days
8. Correlation of 'C= changes with microscopic changes
/. :nverted . waves
Correlate with areas of ischemia at the periphery of the infarct
c. 'levated S. segment
Correlate with in1ured myocardial cells surrounding the area of necrosis
d. !ew G waves
Correlate with the area of coagulation necrosis
Congenital Heart Disease
+etal circulation
1. Chorionic villus in the placenta
a. +etus,derived
b. Primary site for gas e"change in the fetus
c. Chorionic villus vessels become the umbilical vein.
2. Ambilical vein
o $essel with the highest amount of o"ygen (?2 in the fetal circulation
2. :nferior vena cava blood drains into the right atrium.
o -ost blood is directly shunted into the left atrium through the foramen ovale.
3. Superior vena cava blood
o -ost blood is directed from the right atrium into the right ventricle.
4. Pulmonary artery blood
a. -ost blood is shunted through a patent ductus arteriosus into the aorta.
Fept open by prostaglandin '2& a vasodilator
b. +etal pulmonary arteries
22 %ypertrophied from chronic vasoconstriction due to decreased P?2
222 Prevents blood from entering the pulmonary capillaries and left atrium
2. Descending aorta
a. 2lood flows toward the placenta via two umbilical arteries.
b. .hese vessels have the lowest ?2 concentration.
*. Changes at birth
a. Ductus arteriosus closes (becomes ligamentum arteriosum
b. =as e"change occurs in the lungs.
c. +oramen ovale closes.
+etal circulation
1. Chorionic villus in the placenta
a. +etus,derived
b. Primary site for gas e"change in the fetus
c. Chorionic villus vessels become the umbilical vein.
2. Ambilical vein
o $essel with the highest amount of o"ygen (?2 in the fetal circulation
2. :nferior vena cava blood drains into the right atrium.
o -ost blood is directly shunted into the left atrium through the foramen ovale.
3. Superior vena cava blood
o -ost blood is directed from the right atrium into the right ventricle.
4. Pulmonary artery blood
a. -ost blood is shunted through a patent ductus arteriosus into the aorta.
Fept open by prostaglandin '2& a vasodilator
b. +etal pulmonary arteries
22 %ypertrophied from chronic vasoconstriction due to decreased P?2
222 Prevents blood from entering the pulmonary capillaries and left atrium
2. Descending aorta
a. 2lood flows toward the placenta via two umbilical arteries.
b. .hese vessels have the lowest ?2 concentration.
*. Changes at birth
a. Ductus arteriosus closes (becomes ligamentum arteriosum
b. =as e"change occurs in the lungs.
c. +oramen ovale closes.
Congenital heart disease
page 182
page 182
page 18*
1. ?2 saturation (Sa?2 in shunts
a. #eft,sided to right,sided heart shunts
:ncreased Sa?2 from 976 to 856 in affected chambers and vessels
b. )ight,sided to left,sided heart shunts
Decreased Sa?2 from E76 to 856 in affected chambers and vessels
2. #eft,sided to right,sided heart shunts
a. $olume overload occurs in the right side of the heart; complications<
22 Pulmonary hypertension
222 )$% due to pulmonary hypertension
2222 #$% due to e"cess blood originating from the right side of the heart
2v2 )eversal of the shunt
?ccurs when pressure in right ventricle overrides left ventricular
pressure
Cyanosis ('isenmenger syndrome develops.
b. $SD
22 Defect in the membranous interventricular septum
222 (ssociated with cri du chat syndrome& trisomy 1*& and trisomy 18
2222 :ncreased Sa?2 in right ventricle and pulmonary artery
2v2 -ost spontaneously close
c. (trial septal defect ((SD
22 Patent foramen ovale (most common type
222 (ssociated with fetal alcohol syndrome
2222 :ncreased Sa?2 in right atrium& right ventricle and pulmonary artery
2v2 Congenital heart disease in children with Down syndrome
:ncomplete septum between the ventricles and the atria
(bnormal tricuspid valve
d. Patent ductus arteriosus (PD(
22 Ductus arteriosus remains open.
222 (ssociated with congenital rubella
2222 :ncreased Sa?2 in pulmonary artery
2v2 )eversal of the shunt due to pulmonary hypertension
Ano"ygenated blood enters the aorta below the subclavian artery
Produces a pink upper body and cyanotic lower body
v2 -achinery murmur is heard during systole and diastole.
2. )ight,sided to left,sided heart shunts
a. Cyanotic congenital heart disease
b. Complications
22 Secondary polycythemia
'rythropoietin response due to decreased Sa?2
222 :nfective endocarditis of damaged valves
:ncreased incidence of septic emboli3ation and metastatic
abscesses
c. .etralogy of +allot
22 -ost common cyanotic congenital heart disease
222 Defects
$SD
:nfundibular or valvular pulmonary stenosis
)$%
?verriding aorta (least important
2222 -inimal pulmonary stenosis
#eads to o"ygenation of blood in the lungs
#ess right,to,left shunting through the $SD
(bsence of cyanosis (Sa?2 @ 856
2v2 Severe pulmonic stenosis
#ess o"ygenation of blood in the lungs
:ncreased right,to,left shunting through the $SD
Cyanosis (Sa?2 4 856
v2 Decreased Sa?2 in the left ventricle and aorta
v22 Cardioprotective shunts increase o"ygenation
(SD steps up Sa?2 in the right atrium.
PD( shunts blood from the aorta to the pulmonary artery.
v222 .et spells
?ccur when hypo"emia is severe
S/uatting increases systemic vascular resistance causing
temporary reversal of the shunt.
Ano"ygenated blood is forced into the pulmonary artery for
o"ygenation.
d. Complete transposition of the great vessels
22 Defects
(orta arises from the right ventricle.
Pulmonary artery arises from the left ventricle.
#eft and right atria are normal
222 Cardioprotective shunts
(SD steps up Sa?2 in the right atrium
:ncreases Sa?2 in the right ventricle for delivery to tissue
via the aorta
$SD shunts blood into the left ventricle for o"ygenation in the
lungs via the pulmonary artery.
PD( shunts blood into the pulmonary artery for o"ygenation in
the lungs.
e. ?ther types of cyanotic congenital heart disease
22 .otal anomalous pulmonary venous return
Pulmonary vein empties o"ygenated blood into the right atrium.
222 .runcus arteriosus
(orta and pulmonary artery share a common trunk and intermi"
blood.
2222 .ricuspid atresia
Asually have an (SD with a right,to,left shunt
*. Coarctation of the aorta
a. :nfantile (preductal coarctation
22 Constriction of aorta between the subclavian artery and ductus arteriosus
222 (ssociated with .urnerDs syndrome
b. (dult coarctation
22 Develops during adult life
222 Constriction of the aorta distal to the ligamentum arteriosum
2lood flow into the pro"imally located branch vessels is
increased.
2lood flow below the constriction is decreased.
Produces a systolic murmur
(dditional defect is a bicuspid aortic valve (756 of cases
2222 Clinical findings pro"imal to the constriction
:ncreased upper e"tremity blood pressure
Dilation of aorta and aortic valve ring (regurgitation
:ncreased risk for developing an aortic dissection
:ncreased cerebral blood flow (increased risk for berry
aneurysms
2v2 Clinical findings distal to the constriction
Decreased blood pressure in the lower e"tremity
#eg claudication (pain in calf or buttocks when walking
Decreased renal blood flow
(ctivates the renin,angiotensin,aldosterone system
causing hypertension
v2 Development of collateral circulation
Collaterals develop between intercostal arteries above and below
the constriction.
Chest radiograph shows rib notching on the undersurface of ribs.
Due to increased blood flow through enlarged intercostal
arteries
Acquired Valvular Heart Disease
)heumatic fever
1. 'pidemiology
a. ?ccurs at 7 to 17 years of age
b. Develops 1 to 7 weeks after group ( streptococcal pharyngitis or scarlet fever
c. Possible relapses may occur leading to chronic valvular disease
2. Pathogenesis
a. :mmune,mediated disease that follows group ( streptococcal infection
b. (ntibodies develop against group ( streptococcal - proteins
i. (ntibodies cross,react with similar proteins in human tissue
ii. .ype :: hypersensitivity reaction
a. +ibrinous pericarditis
Precordial chest pain with friction rub
b. -yocarditis
i. -ost common cause of death in acute disease
ii. (schoff bodies are present.
Central area of fibrinoid necrosis surrounded by (nitschkow cells
(reactive histiocytes
b. 'ndocarditis
i. -ost commonly involves the mitral valve (then aortic valve
ii. Sterile& verrucoid,appearing vegetations develop along the line of closure
of the valve
'mbolism is uncommon.
iii. -itral valve regurgitation or aortic valve regurgitation
-ay result in C%+
iv. )ecurrent infection of the mitral and aortic valves leads to mitral stenosis
or aortic stenosis.
c. -igratory polyarthritis
i. -ost common initial presentation of acute rheumatic fever
ii. ?ccurs in large 1oints (knees and small 1oints (wrists
iii. No permanent 1oint damage
d. Subcutaneous nodules occur on e"tensor surfaces.
e. 'rythema marginatum
'vanescent circular ring of erythema that develops around normal skin
b. SydenhamDs chorea
i. )eversible rapid& involuntary movements affecting all muscles
ii. #ate manifestation of acute rheumatic fever
0. Diagnosis of acute rheumatic fever
f. :ncreased antistreptolysin ? ((S? titers
g. Positive throat culture
h. #eukocytosis& increased P) interval& increased C,reactive protein
)heumatic fever
1. 'pidemiology
a. ?ccurs at 7 to 17 years of age
b. Develops 1 to 7 weeks after group ( streptococcal pharyngitis or scarlet fever
c. Possible relapses may occur leading to chronic valvular disease
2. Pathogenesis
a. :mmune,mediated disease that follows group ( streptococcal infection
b. (ntibodies develop against group ( streptococcal - proteins
i. (ntibodies cross,react with similar proteins in human tissue
ii. .ype :: hypersensitivity reaction
a. +ibrinous pericarditis
Precordial chest pain with friction rub
b. -yocarditis
i. -ost common cause of death in acute disease
ii. (schoff bodies are present.
Central area of fibrinoid necrosis surrounded by (nitschkow cells
(reactive histiocytes
b. 'ndocarditis
i. -ost commonly involves the mitral valve (then aortic valve
ii. Sterile& verrucoid,appearing vegetations develop along the line of closure
of the valve
'mbolism is uncommon.
iii. -itral valve regurgitation or aortic valve regurgitation
-ay result in C%+
iv. )ecurrent infection of the mitral and aortic valves leads to mitral stenosis
or aortic stenosis.
c. -igratory polyarthritis
i. -ost common initial presentation of acute rheumatic fever
ii. ?ccurs in large 1oints (knees and small 1oints (wrists
iii. No permanent 1oint damage
d. Subcutaneous nodules occur on e"tensor surfaces.
e. 'rythema marginatum
'vanescent circular ring of erythema that develops around normal skin
b. SydenhamDs chorea
i. )eversible rapid& involuntary movements affecting all muscles
ii. #ate manifestation of acute rheumatic fever
0. Diagnosis of acute rheumatic fever
f. :ncreased antistreptolysin ? ((S? titers
g. Positive throat culture
h. #eukocytosis& increased P) interval& increased C,reactive protein
-itral stenosis
page 187
-itral stenosis is a problem with opening the valve. .he valve opens in
diastole& and thus& the murmur occurs in diastole. Sudden opening of the
thickened& nonpliable valve with left atrial contraction produces an opening
snap followed by a rumble caused by rapid entry of blood into the left
ventricle. .he murmur is best heard at the ape".
1. 'tiology
o -ost often caused by recurrent attacks of rheumatic fever
2. Pathophysiology
a. !arrowing of the mitral valve orifice
b. #eft atrium becomes dilated and hypertrophied
Due to increased work in filling the ventricle in diastole
2. Clinical findings
a. ?pening snap followed by mid,diastolic rumble
b. Dyspnea and hemoptysis with rust,colored sputum (heart failure cells
Due to pulmonary capillary congestion and hemorrhage into the alveoli
c. (trial fibrillation
22 Due to left atrial dilation and hypertrophy
222 :ntra,atrial thrombus develops due to stasis.
Danger of systemic emboli3ation
b. Pulmonary venous hypertension
22 Due to chronic backup of atrial blood into the pulmonary vein
222 )$% eventually develops
c. Dysphagia for solids
22 #eft atrium is the most posteriorly located chamber in the heart.
222 Dilation of the left atrium compresses the esophagus.
-itral regurgitation
page 187
page 18B
1. 'tiology
a. -itral valve prolapse (most common cause
b. #eft,sided heart failure
c. :nfective endocarditis& rupture or dysfunction of the papillary muscle
2. Pathophysiology
a. )etrograde blood flow into the left atrium during systole
Due to an incompetent mitral valve or dilated mitral valve ring
b. $olume overload in the left ventricle and left atrium leads to #%+.
a. Pansystolic murmur with radiation to the a"illa
b. Dyspnea and cough from #%+
-itral valve prolapse (-$P
page 18B
page 189
1. 'pidemiology
a. (utosomal dominant inheritance in some cases
b. -ore common in women
c. (ssociated with -arfan and 'hlers,Danlos syndrome
2. Pathophysiology
a. Posterior bulging of the anterior and posterior leaflets into the left atrium during
systole
b. )edundancy of valve tissue
i. -y"omatous degeneration of the mitral valve leaflets
ii. Due to e"cess production of dermatan sulfate
a. -ost patients are asymptomatic.
b. %eart murmur
i. -id,systolic click
Due to sudden restraint by the chordae of the prolapsed valve
ii. -id to late systolic regurgitant murmur follows the click.
iii. Decreased preload causes the click and murmur to move closer to the S1
heart sound; e"amples<
(n"iety
:ncreased heart rate decreases diastolic filling of left
ventricle.
Standing
Decreases venous return to the right side of the heart
$alsalva maneuver (holding breath with epiglottis closed
Positive intrathoracic pressure decreases venous return
to the heart.
iv. :ncreased preload causes the click and murmur to move closer to the S2
heart sound; e"amples<
)eclining
:ncreases venous return to the right side of the heart
S/uatting or sustained hand grip
:ncreases systemic vascular resistance& which impedes
emptying of the left ventricle
c. Palpitations& chest pain
(ortic stenosis
(ortic stenosis is a problem in opening the valve. 2ecause the aortic valve
opens in systole& the murmur occurs in systole. :t is an e1ection type of
murmur with murmur intensity initially increasing and then decreasing
(crescendo,decrescendo. :t is best heard in the second right intercostal
space and radiates into the carotid arteries. Decreasing preload lessens the
volume the left ventricle must e1ect; therefore& murmur intensity decreases.
:ncreasing preload increases the volume the left ventricle must e1ect;
therefore& murmur intensity increases.
page 189
page 188
1. 'tiology
a. Dystrophic calcification of a normal aortic valve or bicuspid aortic valve
b. (ge,related sclerosis of the aortic valve
c. Chronic rheumatic fever
2. Pathophysiology
a. ?bstruction to left ventricular outflow during systole
b. )eduction in the aortic valve orifice area produces concentric #$%.
a. Systolic e1ection murmur
b. (ngina with e"ercise
i. Decreased blood flow through the stenotic valve leads to less filling of the
coronary arteries during diastole.
ii. Subendocardium of concentrically hypertrophied heart receives less
blood.
c. Syncope with e"ercise
Decreased blood flow through the stenotic valve leads to decreased
blood flow to the brain.
b. %emolytic anemia with schistocytes
(ortic regurgitation
page 188
page 18E
(ortic regurgitation is a problem in closing the aortic valve. 2ecause the valve
closes in diastole& the murmur occurs in diastole. :t is characteri3ed by a high,
pitched >blowing> early diastolic murmur immediately following the S2 heart
sound. :t increases in intensity on e"piration and is heard best along the left
parasternal border.
1. 'tiology
a. :solated aortic valve root dilation
b. :nfective endocarditis
-ost common cause of acute aortic regurgitation
c. #ong,standing essential hypertension
d. Chronic rheumatic fever& aortic dissection& coarctation
2. Pathophysiology
a. )etrograde blood flow into the left ventricle
22 Due to an incompetent valve or dilated valve ring
222 Decreases diastolic pressure
Due to drop in arterial volume as blood flows back into the left
ventricle
2222 $olume overload of the left ventricle
:ncreases stroke volume (+rank,Starling mechanism
b. :ncreased pulse pressure (difference between systolic and diastolic pressure
Produces hyperdynamic circulation (e.g.& bounding pulses
a. 'arly diastolic murmur
b. 2ounding pulses (water hammer pulse& head nodding& pulsating uvula
c. (ustin +lint murmur
22 )egurgitant stream from incompetent aortic valve hits the anterior mitral
valve leaflet producing a diastolic murmur
222 Presence of this murmur indicates the need for replacement of the valve.
.ricuspid regurgitation
1. 'tiology
a. )ight,sided heart failure
b. :nfective endocarditis in intravenous drug abuse
c. Carcinoid heart disease
2. Pathophysiology
a. )etrograde blood flow into the right atrium during systole
i. Due to stretching of the valve ring or damage to the valve
ii. Causes right ventricular overload and )%+
b. Produces volume overload in the right atrium and right ventricle
a. Pansystolic murmur that increases in intensity with inspiration
b. Pulsating liver
2lood regurgitates into the venous system with systole.
Carcinoid heart disease
1. Due to liver metastasis from a carcinoid tumor of small intestine
2. Serotonin causes fibrosis of the tricuspid valve and pulmonary valve.
o Produces tricuspid valve regurgitation and pulmonary valve stenosis
:nfective endocarditis (:'
1. 'pidemiology
a. -icrobial pathogens
i. Streptococcus viridans
-ost common overall cause of :'
ii. Staphylococcus aureus
-ost common cause of :' in intravenous (:$ drug abuse
iii. Staphylococcus epidermidis
-ost common cause of :' due to prosthetic devices
iv. Streptococcus bovis
-ost common cause of :' in ulcerative colitis or colorectal
cancer
2. $alves involved in :'
a. -itral valve
-ost common overall valve involved in :'
b. .ricuspid valve and aortic valve
-ost common valves involved in :' due to :$ drug abuse
22 Pathogenesis
a. Streptococcus viridans infects previously damaged valves.
b. Staphylococcus aureus infects normal or previously damaged valves.
22 Pathology
a. $egetations emboli3e producing abscesses and infarctions in distant organ sites
b. $alve destruction leads to regurgitation murmurs.
a. :mmunocomple" vasculitis
'"amples,splinter hemorrhages in nail beds& glomerulonephritis
b. +ever& splenomegaly& positive blood cultures
#ibman,Sacks endocarditis
1. (ssociated with systemic lupus erythematosus (S#'
2. Sterile vegetations are located over the mitral valve surface.
o Produces valve deformity and mitral regurgitation
!onbacterial thrombotic endocarditis (marantic endocarditis
1. Paraneoplastic syndrome
2. Sterile& nondestructive vegetations on the mitral valve
o Procoagulant effect of circulating mucin from mucin,producing tumors of the
colon and pancreas
*. Complications
a. 'mboli3ation
b. -ay be secondarily infected
yocardial and !ericardial Disorders
-yocarditis
1. 'tiology
i. Co"sackievirus (most common cause
ii. Trypanosoma cruzi (ChagasD disease
#eishmanial forms infect cardiac muscle.
b. (cute rheumatic fever& diphtheria to"in& drugs (e.g.& do"orubicin& S#'
2. Pathology
a. 'ndocardial biopsy is sometimes performed if infection is suspected.
b. ( lymphocytic infiltrate is highly predictive of co"sackievirus
a. +ever& chest pain& C%+
b. :ncreased CF,-2 and troponins
-yocarditis
1. 'tiology
i. Co"sackievirus (most common cause
ii. Trypanosoma cruzi (ChagasD disease
#eishmanial forms infect cardiac muscle.
b. (cute rheumatic fever& diphtheria to"in& drugs (e.g.& do"orubicin& S#'
2. Pathology
a. 'ndocardial biopsy is sometimes performed if infection is suspected.
b. ( lymphocytic infiltrate is highly predictive of co"sackievirus
a. +ever& chest pain& C%+
b. :ncreased CF,-2 and troponins
Pericarditis
page 1E1
page 1E2
1. 'tiology
a. Similar to myocarditis
b. Co"sackievirus most common overall cause
2. Pathology
a. +ibrinous type of pericardial e"udate
?ften accompanied by an effusion
b. Dense scar tissue with dystrophic calcification may cause constrictive pericarditis.
a. Precordial chest pain
22 Pain is relieved when leaning forward.
222 Pain increases with inspiration.
b. Pericardial friction rub
Scratchy& three,component rub (systole& early& and late diastole
b. Pericardial effusion
22 -uffled heart sounds
+luid surrounds the heart.
222 %ypotension associated with pulsus parado"us
Drop in systolic blood pressure greater than 15 mm %g during
inspiration
2222 !eck vein distention on inspiration
2lood cannot enter the right atrium and reflu"es into the 1ugular
vein (FussmaulDs sign.
2v2 Chest radiograph shows a >water bottle> configuration.
b. Constrictive pericarditis
22 'tiology
.uberculosis is the most common cause worldwide.
-ost cases in the Anited States are idiopathic.
222 Pathophysiology
:ncomplete filling of the cardiac chambers due to thickening of
the parietal pericardium
2222 Pericardial knock
Due to the ventricles hitting the thickened parietal pericardium
Cardiomyopathy
Definition
=roup of diseases that primarily involve the myocardium and produce myocardial
dysfunction
Definition
=roup of diseases that primarily involve the myocardium and produce myocardial
dysfunction
.ypes of cardiomyopathy
1. Dilated (congestive
2. %ypertrophic
*. )estrictive
Dilated cardiomyopathy
1. 'pidemiology
a. -ost common cardiomyopathy
b. 'tiology
i. :diopathic (most common
ii. =enetic causes (27,*76
iii. -yocarditis (see section $:
iv. Drugs (e.g.& do"orubicin& cocaine
v. Postpartum state& thiamine deficiency (alcoholism
2. Pathophysiology
a. Decreased contractility with a decreased '+ (4056
b. Systolic dysfunction type of #%+
a. =lobal enlargement of the heart
i. (ll chambers are dilated.
ii. 'chocardiography shows poor contractility.
b. 2iventricular C%+
c. 2undle branch blocks and atrial and ventricular arrhythmias
%ypertrophic cardiomyopathy
1. 'pidemiology
a. -ost common cause of sudden death in young individuals
b. +amilial form (autosomal dominant in young individuals (ma1ority of cases
Due to mutations in heavy chain of I,myosin and in the troponins
c. Sporadic form in elderly people
2. Pathophysiology
a. %ypertrophy of the myocardium
Disproportionately greater thickening of the interventricular septum than
of the free left ventricular wall
b. ?bstruction of blood flow is below the aortic valve
(nterior leaflet of the mitral valve is drawn against the asymmetrically
hypertrophied septum as blood e"its the left ventricle
c. (berrant myofibers and conduction system in the interventricular septum
Conduction disturbances are responsible for sudden death.
d. Decreased diastolic filling
-uscle thickening restricts filling.
a. Systolic e1ection type murmur.
b. -urmur intensity increases (obstruction worsens with decreased preload
'"amples,standing up& use of inotropic drugs (e.g.& digitalis
c. -urmur intensity decreases (obstruction lessens with increased preload
'"amples,reclining& drugs decreasing cardiac contractility (e.g.& I,
blockers
)estrictive cardiomyopathy
1. 'tiology
a. .ropical endomyocardial fibrosis
-ost common cause worldwide
b. :nfiltrative diseases
'"amples,PompeDs glycogenosis& amyloidosis& hemochromatosis
c. 'ndocardial fibroelastosis in a child (thick fibroelastic tissue in the endocardium&
sarcoidosis
d. Pathophysiology
22 Decreased ventricular compliance
22 Asually secondary to infiltrative disease of the myocardium
22 Diastolic dysfunction type of #%+
b. Clinical findings
(rrhythmias (conduction defects& C%+
"umors o# the Heart
'pidemiology
1. -etastasis is more common than primary tumors
o '"ample,e"tension of a primary lung cancer
2. Pericardium is the most common site for metastasis.
o #eads to pericarditis and effusions
*. Primary tumors or tumor,like conditions
o Cardiac my"oma& rhabdomyoma
'pidemiology
1. -etastasis is more common than primary tumors
o '"ample,e"tension of a primary lung cancer
2. Pericardium is the most common site for metastasis.
o #eads to pericarditis and effusions
*. Primary tumors or tumor,like conditions
o Cardiac my"oma& rhabdomyoma
Cardiac my"oma
1. -ost common primary adult tumor
2. Pathology
a. 2enign primary mesenchymal tumor
b. (ppro"imately E56 arise from the left atrium
c. Sessile or pedunculated
d. >2all,valve> effect blocks the mitral valve orifice
2locks diastolic filling of the ventricle& simulating mitral valve stenosis
a. !onspecific findings
+ever& fatigue& malaise& anemia
b. Complications
'mboli3ation& syncopal episodes (blocks mitral valve orifice
0. Diagnosis
o .ransesophageal ultrasound (most useful study for viewing the left atrium
)habdomyoma
1. -ost common primary tumor of the heart in infants and children
o -a1or association with tuberous sclerosis
2. %amartoma (non,neoplastic arising from cardiac muscle

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