10 heart disorders

8/11/2019 10 Heart Disorders

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10 Heart Disorders

Ventricular Hypertrophy

Pathogenesis of left and right ventricular hypertrophy

1. Sustained pressure increases wall stress.

a. Causes duplication of sarcomeresi. 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 commonii. ortic stenosis

b. Causes of concentric right ventricular hypertrophy ()$%

i. Pulmonary hypertensionii. Pulmonary artery stenosis

*. $olume overload (increased preload

c. Causes dilation and hypertrophy (eccentric hypertrophy of ventricular walli. +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 ventriclei. -itral valve or aortic valve regurgitationii. #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


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 (afterloada. 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 (#$%&


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i. 'ssential hypertension (most commonii. ortic stenosis

b. Causes of concentric right ventricular hypertrophy ()$%i. Pulmonary hypertensionii. Pulmonary artery stenosis


c. Causes dilation and hypertrophy (eccentric hypertrophy of ventricular walli. +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 ventriclei. -itral valve or aortic valve regurgitationii. #eft,to,right shunting of blood (e.g.& ventricular septal defect





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 (#$%&c. 'ssential hypertension (most common

i. ortic stenosisb. Causes of concentric right ventricular hypertrophy ()$%

i. Pulmonary hypertensionii. Pulmonary artery stenosis


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 regurgitationii. #eft,to,right shunting of blood (e.g.& ventricular septal defect





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Conse/uences of ventricular hypertrophy

1. #eft, or right,sided heart failure

2. ngina (primarily #$%*. S0heart 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 eect blood delivered to it by the venous system

'pidemiology

1. -ost common hospital admission diagnosis in elderly patients2. ypes of C%+

a. #eft,sided heart failure (most common typeb. )ight,sided heart failurec. iventricular heart failure (left, and right,sided heart failure

d. %igh,output heart failure

#eft,sided heart failure (#%+Systolic dysfunction is characteri3ed by a low eection fraction ('+ (4056.he '+ e/uals the stroke volume divided by the left ventricular end,diastolicvolume. he normal value ranges from 776 to 856. Diastolic dysfunction ischaracteri3ed by normal to high '+ (stiff ventricle and an S0gallop due toincreased resistance to filling in late diastole. here is an increase in left atrialpressure. he '+ is normal.

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-itral regurgitation is a problem in closing the mitral valve. he mitral valvenormally closes in systole. lood entering the left atrium during systole

produces a pansystolic murmur that increases in intensity on e"piration. hemurmur is best heard at the ape".

1. +orward failurea. #eft side of the heart cannot eect blood into the aortab. :ncrease in left ventricular end,diastolic volume and pressurec. ackup of blood into the lungs causing pulmonary edema

2. Pathogenesis


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a. Decreased ventricular contraction (systolic dysfunction; causesrteriali3ation> of the vessels& fibrosis& and occlusion common

after 15 years

Chronic ischemic heart disease


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1. Progressive C%+ resulting from long,term ischemic damage to myocardial tissue2. )eplacement of myocardial tissue with noncontractile scar tissue*. Clinical findings

a. iventricular C%+b. ngina pectoris

c. -ay develop dilated cardiomyopathy

Sudden cardiac death

1. Ane"pected death within 1 hour after onset of symptoms2. Diagnosis of e"clusion after other causes are ruled out*. Pathogenesis

a. Severe atherosclerotic coronary artery diseaseb. Disrupted fibrous pla/uesc. bsence of occlusive vessel thrombus (@856 of cases

0. Cause of death is ventricular fibrillation.

-yocardial infarctionpage 19E

1. Pathogenesisa. Se/uenceSilent> acute -:si. -ay occur in the elderly and in individuals with diabetes mellitusii. Due to high pain threshold or problems with nervous system

B. Complications

h. rrhythmiasi. $entricular premature contractions (most commonii. -ost common cause of death is ventricular fibrillation.

+re/uently associated with cardiogenic shock

i. Congestive heart failure

Asually occurs within the first 20 hoursb. )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


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Produces a left,to,right shunt causing )%+

. -ural thrombusi. -ost often associated with #D coronary artery thrombosisii. Danger of emboli3ation

k. +ibrinous pericarditis with or without effusioni. 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 aneurysmi. Clinically recogni3ed within 0 to 8 weeksii. Precordial bulge during systole

lood 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 thrombosisii. Clinical findings

%ypotension& )%+& and preserved left ventricle function

9. #aboratory diagnosis of acute -:

n. Creatine kinase isoen3yme - (CF,-i. CF,- appears within 0 to 8 hours; peaks at 20 hours; disappears within

1.7 to * days.ii. )einfarction

)eappearance of CF,- after * days

o. Cardiac troponins : (cn: and (cni. !ormally regulate calcium,mediated contractionii. cn: and cn 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,- and last longer

p. #actate dehydrogenase (#D%1,2>flip>i. !ormally& #D%2is higher than #D%1.

:n acute -:& #D%1in cardiac muscle is released causing the >flip.>

ii. #D%1,2

ppears within 15 hours; peaks at 2 to * days; disappears within9 days

8. Correlation of 'C= changes with microscopic changes

/. :nverted waves

Correlate with areas of ischemia at the periphery of the infarctc. 'levated S segment


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Correlate with inured myocardial cells surrounding the area of necrosisd. !ew G waves

Correlate with the area of coagulation necrosis

Congenital Heart Disease

+etal circulation

1. Chorionic villus in the placentaa. +etus,derivedb. Primary site for gas e"change in the fetusc. Chorionic villus vessels become the umbilical vein.

2. Ambilical vein

o $essel with the highest amount of o"ygen (?2 in the fetal circulation2. :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 atrium2. Descending aorta

a. lood flows toward the placenta via two umbilical arteries.b. hese vessels have the lowest ?2concentration.

*. Changes at birtha. Ductus arteriosus closes (becomes ligamentum arteriosumb. =as e"change occurs in the lungs.

c. +oramen ovale closes.

+etal circulation

1. Chorionic villus in the placentaa. +etus,derivedb. Primary site for gas e"change in the fetusc. Chorionic villus vessels become the umbilical vein.

2. Ambilical vein


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o $essel with the highest amount of o"ygen (?2 in the fetal circulation2. :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 aortaa. lood flows toward the placenta via two umbilical arteries.b. hese vessels have the lowest ?2concentration.

*. Changes at birtha. Ductus arteriosus closes (becomes ligamentum arteriosum

b. =as e"change occurs in the lungs.

c. +oramen ovale closes.

Congenital heart disease

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page 18*

1. ?2saturation (Sa?2 in shuntsa. #eft,sided to right,sided heart shunts

:ncreased Sa?2from 976 to 856 in affected chambers and vessels

b. )ight,sided to left,sided heart shunts Decreased Sa?2from E76 to 856 in affected chambers and vessels

2. #eft,sided to right,sided heart shuntsa. $olume overload occurs in the right side of the heart; complications

10 heart disorders

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