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
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
3
Q
what does the pulmonary circulation do?
A
- transp deoxygenated blood from r side of heart to lungs
- supported by r atrium/ventricle
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
5
Q
SA Node
A
- pacemaker
- generates electrical impulses
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
7
Q
excitation
A
generation of action potential, triggered by electrical impulse
8
Q
contraction
A
- shortening of muscle cells
- triggered by excitation
- intrinsic characteristic of heart
9
Q
diastole
A
- ventricles are relaxed
- at the end, both atria contract
10
Q
systole
A
- ventricles contract
- eject blood into aorta and pulmonary artery
11
Q
heart rate
A
- number of heart beats in 1 min
- normal is 60-100 bpm
12
Q
end diastolic volume (EDV)
A
- filled volume of ventricle prior to contraction (at the end of diastole)
13
Q
end systolic volume (ESV)
A
- residual volume of blood remaining in ventricle after ejection (after systole)
14
Q
stroke volume
A
- amount of blood pumped out by left ventricle in one contraction
- SV= EDV- ESV
15
Q
preload
A
- ventricular volume at end of diastole
- EDV
16
Q
Afterload
A
- ventricular wall tension during contraction
- depends on atrial blood pressure and vascular tone
- increased afterload = increased cardiac workload
17
Q
cardiac output
A
- amount of blood heart pumps in one minute
- depends on HR, contractility, preload, and afterload
- CO= SV X HR
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
19
Q
what is a normal EF?
A
50-70%
20
Q
what is the EF in heart failure?
A
less than 40%
21
Q
chronotropic effect
A
increase or decrease heart rate
22
Q
inotropic effect
A
force/strength of contraction
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
24
Q
what are the main mechanisms of controlling the heart?
A
nervous control or hormonal control
25
Nervous control of the heart
- medulla oblongata
- sympathetic NS
- parasympathetic NS
26
hormonal control of the heart
- ADH
- aldosterone
- epinephrine
- angiotensin II
27
factors that affect heart performance
- preload
- myocardial contractility
- afterload
28
general mechanisms of cardiovascular disease
- pump failure
- blood flow obstruction
- regurgitant flow
- shunted flow
- abnormal cardiac conduction
- rupture of heart or major vessel
29
what is heart failure?
- heart fails as a pump
| - any structural or functional cardiac disorder that impairs ability of ventricle to fill with or eject blood
30
what is the clinical significance of HF?
- 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
31
types of HF
- R sided HF (rare in isolation, usually occurs due to L side HF)
- L sided HF
- Congestive HF
32
what is congestive HF
- 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
33
what are the types of left- sided heart failure?
systolic dysfunction and diastolic dysfunction
34
systolic left sided HF
- contraction part of heart is failed
- HF with reduced EF
- HFrEF
- EF less than 40%
- most common cause- ischemic/coronary heart disease
35
diastolic left sided HF
- 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
36
pure right sided HF cause
- sytemic and portal venous congestion
- hepatic and splenic enlargement
- peripheral edema
- pleural effusion
- ascites
37
compensatory mechanisms of HF
- frank starling mechanism- increased EDV -> dilate the heart -> increased CO
- activation of neurohormonal systems
- myocardial adaptations - hypertrophy
38
what are the neurohormonal systems that are activated to compensate for HF?
- NE released -> increased HR, contractility, and vascular resistance
- renin-angiotensin- aldosterone system
- ANP
39
consequences of compensatory hypertrophy
- increased protein synthesis and O2 demand
| - altered gene expression
40
clinical significance of compensatory hypertrophy
- cardiomyocytes lost through apoptosis
- accumulation of excess ECM -> fibrosis
- prorhythmic phenotype
- hypertrophied heart vulnerable to ischemia
41
causes of cardiac hypertrophy
- HTN
- valvular disease
- MI- compensate for dead part of the heart
42
congenital heart disease (CHD)
- cardiac/ vessel abnormalities present at birth
- most result of defective embryogenesis during gestational weeks 3-8
- either shunts or obstructions
43
types of left to right shunts
- ASD
- VSD
- PDA
44
types of right to left shunts
- tetralogy of fallot
| - PFO
45
shunt
abnormal flow or abnormal opening of heart
46
what are some causes of CHD?
- genetic factors
- most common genetic factor is trisomy 21
- environmental factors
- maternal factors
- nutritional factors
47
clinical features of right to left shunt
- bypass lungs, causes hypoxia or cyanosis
- allow venus emboli to enter systemic circulation
- finger and toe clubbing
48
clinical features of left to right shunt
- pulmonary overload
| - increase volume and pressure in pulmonary circulation
49
atrial septal defect (ASD)
- abnormal opening in septum between atria
- shunts blood left to right
- most common congenital defects in adults
- usually asymptomatic
50
clinical features of ASD
- pulmonary vascular resistance much less than systemic
| - murmur
51
ventricular septal defect (VSD)
- opening in septum between ventricles
- most common form of congenital abnormalities
- shunts blood left to right
52
clinical features of VSD
- usually associated with tetralogy of fallot
| - large defects can cause right ventricular hypertrophy and pulmonary HTN
53
patent ductus arteriosus (PDA)
- blood flow between aorta and pulmonary artery
- normal during fetal development to bypass lungs
- should close 1-2 after birth
54
clinical features of PDA
- initially asymptomatic
| - "machine-like" murmur
55
tetralogy of fallot
- right to left shunt
- most common cause of cyanotic heart
- four heart defects at birth
56
what are the heart defects associated with tetralogy of fallot?
- VSD
- subpulmonary stenosis
- overriding aorta
- right ventricular hypertrophy
57
clinical features of tetralogy of fallot
- untreated pt can survive into adult life
- sx severity related to extent of pulmonary stenosis
- can result in cyanosis
58
patent foramen ovale (PFO)
- 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
what is a paradoxical embolism?
any emboli that enters venous circulation can get to systemic circulation
60
coarctation of aorta
- obstructive abnormality
- constriction of aorta
- mostly genetic link but some acquired links
61
clinical manifestations of coarctation of aorta
- depends on severity of narrowing and PDA
- HTN in upper extremities
- weak pulse/ hypotension in lower extremities -> claudication and coldness
62
ischemic heart disease (IHD)
- mismatch between cardiac demand and supply
- aka coronary heart disease
- atherosclerosis is most common cause
63
clinical presentations of IHD
- cardiac syndrome
- angina pectoris
- myocyte death due to stable/unstable/ or prinzmetal angina
- MI
- chronic IHD with CHF
- sudden cardiac death
64
acute coronary syndrome
- unstable angina
- MI
- sudden cardiac death
65
chronic IHD
- progressive heart failure
| - can result from ischemic myocardial damage and/or post MI
66
pathogenesis of IHD
- reduced coronary BF due to atherosclerosis
- thrombosis
- vasospasm
67
consequences of atherosclerosis
- inflammation
- thrombosis
- vasoconstriction
68
MI
- myocyte death caused by vascular occlusion
| - once cells die they cannot be replaced
69
pathogensis of MI
- coronary plaque undergoes erosion/ ulceration/ rupture and/or intraplaque hemorrhage
- platelet adhesion and aggregation
- activation of coagulation
- expansion of thrombus can occlude artery
70
area at risk
- area of heart where coronary artery was supposed to feed becomes occluded
71
what is the window of opportunity to avoid myocyte death
20-30 min of ischemia
72
what are the early biochemical changes associated with MI?
- loss of ATP
| - accumulation of lactate
73
MI clinical features
- chest pain: crushing, stabbing, or squeezing
- rapid or weak pulse
- sweating
- N/V
- 25% are asymptomatic
74
what are the lab tests for MI?
- cardiac- specific troponins T and I (best indicator) aka cTnT and cTnI
- MB fraction of creatine kinase (CK-MB)
75
complications of acute MI
- contractile dysfunction
- arrhythmias
- infarct expansion
- pericarditis
76
how many cusps/leaflets does the mitral valve have?
2 cusps, all other valves have 3
77
what does contraction of valves do?
opens the valve
78
types of valvular heart disease
- stenosis
- insufficiency
- combo of both
79
clinical significance of valve dysfunction depends on
- valve involved
- degree of impairment
- whether it is stenotic or regurgitant
80
what are the types of valvular heart disease?
- aortic stenosis
- aortic regurgitation
- mitral stenosis
- mitral regurgitation
81
what are the most common valvular heart disease types?
aortic and mitral stenosis
82
what is the common cause of mitral/aortic stenosis?
rheumatic heart disease
83
mitral valve prolapse
- prolapse- ballooning of leaflets
- prolapse and regurgitation can happen at same time
- abnormal systolic displacement of one or more leaflets into atrium
84
what is the pathology of mitral valve prolapse
- associated with CT disorders
| - excessive mitral valve leaflet tissue leading to folding
85
aortic valve stenosis
- 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
calcific aortic stenosis
- common degenerative age related
| - two stages are early phase and later propagation phase
87
early phase of calcific aortic stenosis
- lipid accumulation
- inflammation
- calcification
88
later phase of calcific aortic stenosis
- calcification predominating
- progressive stiffness
- narrowing of valve
89
clinical features of aortic stenosis
- obstruction of L ventricular outflow -> increasing pressure gradient
- L ventricular hypertrophy
- ischemia and angina
- HF
- onset of sx has extremely poor prognosis
90
rheumatic valvular disease
- 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
cardiomyopathy
- cardiac mechanical and/or electrical dysfunction
- heart muscle becomes enlarged, thick or rigid
- as worsens results in heart failure and arrhythmias
92
types of cardiomyopathies
- dilated
- hypertrophic
- restrictive
- arrhythmogenic (very rare)
93
dilated cardiomyopathy
- <40% LVEF
- due to impaired contractility/ systolic dysfunction
- result of genetics, alcohol, myocarditis, medication toxicity, idiopathic
94
hypertrophic cardiomyopathy
- 50-80% LVEF
- impaired compliance/ diastolic dysfunction
- due to genetics
