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Patho 1 > Chap 12- The Heart > Flashcards

Chap 12- The Heart Flashcards

1
Q

anatomy of the right side of the heart

A
  • sup/inf vena cava
  • r atrium
  • tricuspid valve
  • r ventricle
  • pulmonary valve
  • pulmonary artery
  • has deoxygenated blood
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2
Q

anatomy of left side of the heart

A
  • pulmonary vein
  • l atrium
  • bicuspid/mitral valve
  • l ventricle
  • aortic valve
  • aorta
  • pumps oxygenated blood to body
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3
Q

what does the pulmonary circulation do?

A
  • transp deoxygenated blood from r side of heart to lungs

- supported by r atrium/ventricle

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4
Q

what does the systemic circulation do?

A
  • carries oxygenated blood from l side of heart to tissues of body
  • removes waste
  • returns deoxygenated blood to r side of heart
  • supported by l atrium/ventricle
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5
Q

SA Node

A
  • pacemaker

- generates electrical impulses

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6
Q

where does the electrical impulse in the heart travel?

A

SA node (generated) -> AV node -> bundle of his -> purkinje fibers which stimulate R and L ventricles

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7
Q

excitation

A

generation of action potential, triggered by electrical impulse

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8
Q

contraction

A
  • shortening of muscle cells
  • triggered by excitation
  • intrinsic characteristic of heart
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9
Q

diastole

A
  • ventricles are relaxed

- at the end, both atria contract

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10
Q

systole

A
  • ventricles contract

- eject blood into aorta and pulmonary artery

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11
Q

heart rate

A
  • number of heart beats in 1 min

- normal is 60-100 bpm

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12
Q

end diastolic volume (EDV)

A
  • filled volume of ventricle prior to contraction (at the end of diastole)
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13
Q

end systolic volume (ESV)

A
  • residual volume of blood remaining in ventricle after ejection (after systole)
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14
Q

stroke volume

A
  • amount of blood pumped out by left ventricle in one contraction
  • SV= EDV- ESV
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15
Q

preload

A
  • ventricular volume at end of diastole

- EDV

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16
Q

Afterload

A
  • ventricular wall tension during contraction
  • depends on atrial blood pressure and vascular tone
  • increased afterload = increased cardiac workload
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17
Q

cardiac output

A
  • amount of blood heart pumps in one minute
  • depends on HR, contractility, preload, and afterload
  • CO= SV X HR
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18
Q

Ejection fraction

A
  • percentage of blood pumped out of a filled ventricle with each heartbeat
  • usually only measured in left ventricle
  • EF= SV/EDV
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19
Q

what is a normal EF?

A

50-70%

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20
Q

what is the EF in heart failure?

A

less than 40%

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21
Q

chronotropic effect

A

increase or decrease heart rate

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22
Q

inotropic effect

A

force/strength of contraction

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23
Q

frank starling law

A
  • relationship between force and stretch
  • SV rises in response to increase preload (EDV)
  • large volume of blood in ventricles -> more stretch -> more force
  • force on y axis
  • stretch on x axis
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24
Q

what are the main mechanisms of controlling the heart?

A

nervous control or hormonal control

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25
Q

Nervous control of the heart

A
  • medulla oblongata
  • sympathetic NS
  • parasympathetic NS
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26
Q

hormonal control of the heart

A
  • ADH
  • aldosterone
  • epinephrine
  • angiotensin II
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27
Q

factors that affect heart performance

A
  • preload
  • myocardial contractility
  • afterload
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28
Q

general mechanisms of cardiovascular disease

A
  • pump failure
  • blood flow obstruction
  • regurgitant flow
  • shunted flow
  • abnormal cardiac conduction
  • rupture of heart or major vessel
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29
Q

what is heart failure?

A
  • heart fails as a pump

- any structural or functional cardiac disorder that impairs ability of ventricle to fill with or eject blood

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30
Q

what is the clinical significance of HF?

A
  • blood and fluid backs up into lungs
  • build up of fluid in feet, ankles, and legs (edema)
  • tiredness and SOB
  • it is the common end stage of many forms of chronic heart disease
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31
Q

types of HF

A
  • R sided HF (rare in isolation, usually occurs due to L side HF)
  • L sided HF
  • Congestive HF
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32
Q

what is congestive HF

A
  • blood returning to heart gets backed up
  • congestion in bodys tissues
  • usually swelling in ankles and legs
  • fluid can collect in lungs -> SOB
  • kidneys have decreased ability to excrete Na/water -> edema in tissues
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33
Q

what are the types of left- sided heart failure?

A

systolic dysfunction and diastolic dysfunction

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34
Q

systolic left sided HF

A
  • contraction part of heart is failed
  • HF with reduced EF
  • HFrEF
  • EF less than 40%
  • most common cause- ischemic/coronary heart disease
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35
Q

diastolic left sided HF

A
  • when heart is relaxed so EF is not effected, it is preserved
  • HFpEF
  • EF is greater than 50%
  • most common cause- HTN and ischemic heart disease
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36
Q

pure right sided HF cause

A
  • sytemic and portal venous congestion
  • hepatic and splenic enlargement
  • peripheral edema
  • pleural effusion
  • ascites
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37
Q

compensatory mechanisms of HF

A
  • frank starling mechanism- increased EDV -> dilate the heart -> increased CO
  • activation of neurohormonal systems
  • myocardial adaptations - hypertrophy
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38
Q

what are the neurohormonal systems that are activated to compensate for HF?

A
  • NE released -> increased HR, contractility, and vascular resistance
  • renin-angiotensin- aldosterone system
  • ANP
39
Q

consequences of compensatory hypertrophy

A
  • increased protein synthesis and O2 demand

- altered gene expression

40
Q

clinical significance of compensatory hypertrophy

A
  • cardiomyocytes lost through apoptosis
  • accumulation of excess ECM -> fibrosis
  • prorhythmic phenotype
  • hypertrophied heart vulnerable to ischemia
41
Q

causes of cardiac hypertrophy

A
  • HTN
  • valvular disease
  • MI- compensate for dead part of the heart
42
Q

congenital heart disease (CHD)

A
  • cardiac/ vessel abnormalities present at birth
  • most result of defective embryogenesis during gestational weeks 3-8
  • either shunts or obstructions
43
Q

types of left to right shunts

A
  • ASD
  • VSD
  • PDA
44
Q

types of right to left shunts

A
  • tetralogy of fallot

- PFO

45
Q

shunt

A

abnormal flow or abnormal opening of heart

46
Q

what are some causes of CHD?

A
  • genetic factors
  • most common genetic factor is trisomy 21
  • environmental factors
  • maternal factors
  • nutritional factors
47
Q

clinical features of right to left shunt

A
  • bypass lungs, causes hypoxia or cyanosis
  • allow venus emboli to enter systemic circulation
  • finger and toe clubbing
48
Q

clinical features of left to right shunt

A
  • pulmonary overload

- increase volume and pressure in pulmonary circulation

49
Q

atrial septal defect (ASD)

A
  • abnormal opening in septum between atria
  • shunts blood left to right
  • most common congenital defects in adults
  • usually asymptomatic
50
Q

clinical features of ASD

A
  • pulmonary vascular resistance much less than systemic

- murmur

51
Q

ventricular septal defect (VSD)

A
  • opening in septum between ventricles
  • most common form of congenital abnormalities
  • shunts blood left to right
52
Q

clinical features of VSD

A
  • usually associated with tetralogy of fallot

- large defects can cause right ventricular hypertrophy and pulmonary HTN

53
Q

patent ductus arteriosus (PDA)

A
  • blood flow between aorta and pulmonary artery
  • normal during fetal development to bypass lungs
  • should close 1-2 after birth
54
Q

clinical features of PDA

A
  • initially asymptomatic

- “machine-like” murmur

55
Q

tetralogy of fallot

A
  • right to left shunt
  • most common cause of cyanotic heart
  • four heart defects at birth
56
Q

what are the heart defects associated with tetralogy of fallot?

A
  • VSD
  • subpulmonary stenosis
  • overriding aorta
  • right ventricular hypertrophy
57
Q

clinical features of tetralogy of fallot

A
  • untreated pt can survive into adult life
  • sx severity related to extent of pulmonary stenosis
  • can result in cyanosis
58
Q

patent foramen ovale (PFO)

A
  • small hole resulting in defective postnatal closure of flap
  • fetus blood goes from R atrium to L atria to bypass lung
  • flap normally closed right after birth
  • unsealed flap can open if R pressure is elevated and cause paradoxical embolism
  • R to L shunt
  • cyanosis not severe
59
Q

what is a paradoxical embolism?

A

any emboli that enters venous circulation can get to systemic circulation

60
Q

coarctation of aorta

A
  • obstructive abnormality
  • constriction of aorta
  • mostly genetic link but some acquired links
61
Q

clinical manifestations of coarctation of aorta

A
  • depends on severity of narrowing and PDA
  • HTN in upper extremities
  • weak pulse/ hypotension in lower extremities -> claudication and coldness
62
Q

ischemic heart disease (IHD)

A
  • mismatch between cardiac demand and supply
  • aka coronary heart disease
  • atherosclerosis is most common cause
63
Q

clinical presentations of IHD

A
  • cardiac syndrome
  • angina pectoris
  • myocyte death due to stable/unstable/ or prinzmetal angina
  • MI
  • chronic IHD with CHF
  • sudden cardiac death
64
Q

acute coronary syndrome

A
  • unstable angina
  • MI
  • sudden cardiac death
65
Q

chronic IHD

A
  • progressive heart failure

- can result from ischemic myocardial damage and/or post MI

66
Q

pathogenesis of IHD

A
  • reduced coronary BF due to atherosclerosis
  • thrombosis
  • vasospasm
67
Q

consequences of atherosclerosis

A
  • inflammation
  • thrombosis
  • vasoconstriction
68
Q

MI

A
  • myocyte death caused by vascular occlusion

- once cells die they cannot be replaced

69
Q

pathogensis of MI

A
  • coronary plaque undergoes erosion/ ulceration/ rupture and/or intraplaque hemorrhage
  • platelet adhesion and aggregation
  • activation of coagulation
  • expansion of thrombus can occlude artery
70
Q

area at risk

A
  • area of heart where coronary artery was supposed to feed becomes occluded
71
Q

what is the window of opportunity to avoid myocyte death

A

20-30 min of ischemia

72
Q

what are the early biochemical changes associated with MI?

A
  • loss of ATP

- accumulation of lactate

73
Q

MI clinical features

A
  • chest pain: crushing, stabbing, or squeezing
  • rapid or weak pulse
  • sweating
  • N/V
  • 25% are asymptomatic
74
Q

what are the lab tests for MI?

A
  • cardiac- specific troponins T and I (best indicator) aka cTnT and cTnI
  • MB fraction of creatine kinase (CK-MB)
75
Q

complications of acute MI

A
  • contractile dysfunction
  • arrhythmias
  • infarct expansion
  • pericarditis
76
Q

how many cusps/leaflets does the mitral valve have?

A

2 cusps, all other valves have 3

77
Q

what does contraction of valves do?

A

opens the valve

78
Q

types of valvular heart disease

A
  • stenosis
  • insufficiency
  • combo of both
79
Q

clinical significance of valve dysfunction depends on

A
  • valve involved
  • degree of impairment
  • whether it is stenotic or regurgitant
80
Q

what are the types of valvular heart disease?

A
  • aortic stenosis
  • aortic regurgitation
  • mitral stenosis
  • mitral regurgitation
81
Q

what are the most common valvular heart disease types?

A

aortic and mitral stenosis

82
Q

what is the common cause of mitral/aortic stenosis?

A

rheumatic heart disease

83
Q

mitral valve prolapse

A
  • prolapse- ballooning of leaflets
  • prolapse and regurgitation can happen at same time
  • abnormal systolic displacement of one or more leaflets into atrium
84
Q

what is the pathology of mitral valve prolapse

A
  • associated with CT disorders

- excessive mitral valve leaflet tissue leading to folding

85
Q

aortic valve stenosis

A
  • narrowing of aortic valve
  • thickened and calcific
  • most common cause of L ventricular outflow obstruction in kids and adults
  • limits BF from L ventricle to aorta
86
Q

calcific aortic stenosis

A
  • common degenerative age related

- two stages are early phase and later propagation phase

87
Q

early phase of calcific aortic stenosis

A
  • lipid accumulation
  • inflammation
  • calcification
88
Q

later phase of calcific aortic stenosis

A
  • calcification predominating
  • progressive stiffness
  • narrowing of valve
89
Q

clinical features of aortic stenosis

A
  • obstruction of L ventricular outflow -> increasing pressure gradient
  • L ventricular hypertrophy
  • ischemia and angina
  • HF
  • onset of sx has extremely poor prognosis
90
Q

rheumatic valvular disease

A
  • usually occurs in kids due to strep A pharyngitis
  • bacteria looks like protein on wall of heart
  • have autoreactive B and T cells
  • depends on severity of infection and repetition of exposure
91
Q

cardiomyopathy

A
  • cardiac mechanical and/or electrical dysfunction
  • heart muscle becomes enlarged, thick or rigid
  • as worsens results in heart failure and arrhythmias
92
Q

types of cardiomyopathies

A
  • dilated
  • hypertrophic
  • restrictive
  • arrhythmogenic (very rare)
93
Q

dilated cardiomyopathy

A
  • <40% LVEF
  • due to impaired contractility/ systolic dysfunction
  • result of genetics, alcohol, myocarditis, medication toxicity, idiopathic
94
Q

hypertrophic cardiomyopathy

A
  • 50-80% LVEF
  • impaired compliance/ diastolic dysfunction
  • due to genetics

Patho 1 (12 decks)

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