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BMS200 > Week 6, Lec 3 > Flashcards

Week 6, Lec 3 Flashcards

1
Q

normal ventricles should be (2)

A

compliant and strong

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2
Q

compliant ventricles

A

diastolic filling occurs at low atrial pressures, and the atria do not have to undergo hypertrophy to fill the ventricle at the end of diastole

  • The ventricle should be able to relax quickly and most filling should take place in early diastole
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3
Q

strong ventricles

A

a ventricle should generate enough force at rest with low diastolic pressures/preload to meet the needs of the body

  • Calcium should be quickly released and re- sequestered each cycle
  • There should be a significant reserve of function for when activity increases
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4
Q

reasons for heart failure

A
  1. increased afterload
  2. reduced compliance
  3. impaired oxygen supply
  4. disorders that damage myocardial and effect contractility - cardiomyopathies
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5
Q

why does increased afterload of the ventricles over long period of time cause heart failure

A

Ventricles become hypertrophic, increasing wall thickness and eventually chamber size

  • Molecular changes→decreased contractility
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6
Q

why does impaired oxygen supply cause heart failure

A

in a setting of chronic ischemic
heart disease

  • May or may not involve sites of infarcted tissue
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7
Q

reduced compliance/ impaired ability to relax due to?

A

fibrosis or poorly-characterized molecular changes

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8
Q

cardiomyopathies

A

Disorders that damage the myocardium and impair compliance or contractility

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9
Q

biggest risk factors for heart failure

A

hypertension (like 40-60%)

myocardial infarction, diabetes, valvular disease etc.

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10
Q

2 major phenotypes of heart failure

A

systolic dysfunction

diastolic dysfunction

THERE ARE NEW NAMES

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11
Q

what is systolic dysfunction heart failure

A

impaired force of contraction/contractility→reliance on elevated preload for adequate cardiac output

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12
Q

what is diastolic dysfunction heart failure

A

elevated diastolic pressures are evident, but force of contraction/contractility is maintained

  • Despite elevated diastolic pressures, there maybe impaired EDV
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13
Q

what are systolic and diastolic dysfunction now known as

A

systolic dysfunction= HFrEF (heart failure with reduced ejection fraction)

diastolic= HFpEF (heart failure with preserved ejection fraction)

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14
Q

2 major problems in heart failure progressuon

A
  1. forward flow problems
  2. backward problems
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15
Q

forward flow problems in heart failure

A

impaired cardiac output to a range of tissues impairs function

▪ Major tissues that experience decreased perfusion include the brain, the heart, the kidneys, and the extremities
* Sometimes reduced flow to the viscera can lead to abdominal pain, but uncommon
▪ Impaired venous return from the pulmonary veins→LV

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16
Q

which important tissues have decreased perfusion from heart failure

A

brain, heart, kidneys

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17
Q

backwards problems/ congestion in heart failure

A

left ventricle cardiac output and right ventricle cardiac output decline

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18
Q

what happens when left ventricle cardiac output declines

A

As LV CO declines, blood congests in the pulmonary venous circulation→elevated pressures in pulmonary capillaries → development of pulmonary edema and thickening of arterioles/arteries in the lung

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19
Q

as right ventricle cardiac output declines what happens

A

blood congests in the systemic venous circulation→elevated pressures in systemic capillaries→edema
* Hepatic congestion & splenomegaly
* Dependent edema

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20
Q

RV vs LV come from

A

RV comes from systemic circulation

LV comes from pulmonary circulation

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21
Q

what part of the heart is usually the first to fail in heart failure and why

A

left ventricle bc has greatest afterload

▪ As pulmonary congestion increases, the afterload of the RV also increases→ development of RV failure

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22
Q

what is the situation in which the right ventricle will fail first in heart failure

A

▪ Lung disease → areas that are hypoxic/poorly ventilated→ pulmonary vasoconstriction

▪ Known as cor pulmonale – common causes include COPD and obstructive sleep apnea

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23
Q

what is cor pulmonale

A

right ventricle fails first

bc of COPD or obstructive sleep apnea

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24
Q

pulmonary microcirculation is controlled by

A

oxygen concentrations

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25
Q

the pulmonary microcirculation ____ in reseponse to decreased oxygen levels

A

constricts

helps redirect blood flow to regions with higher oxygen levels. This optimizes gas exchange, allowing for more efficient oxygen uptake and carbon dioxide removal.

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26
Q

in heart failure what happens to diastolic and systolic dysfunction

A

some reduction in both compliance (diastolic dysfunction) and force of contraction (systolic dysfunction)

▪ However, most cases of heart failure can be clearly dichotomized into HFrEF and HFpEF

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27
Q

two common patterns of heart hypertrophy (that is not the normal physiologic hypertrophy seen in athletes)

A

▪ Concentric hypertrophy ▪ Eccentric hypertropy

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28
Q

concentric hypertrophy vs eccentric hypertrohy

A

concentric- increase ventricular wall thickness

eccentric- myocytes increase in length and narrow

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29
Q

concentric hypertrophy

A

▪ Thought to be earlier in the
development of HF
▪ Thickened ventricular wall, no increase in chamber size
▪ Increased thickness is thought to minimize wall stress

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30
Q

eccentric hypertrophy

A

▪ Ongoing remodeling → eccentric hypertrophy as myocytes increase in length
▪ Usually associated with a decrease in ejection fraction and increased symptoms

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31
Q

ventricular remodelling (mycotyes structure altered to adapt to failing heart)

A

▪ Increased expression of fetal forms of myosin that use ATP more effectively but generate less force

▪ Increased expression of TGF-beta leads to deposition of extracellular matrix in the extracellular spaces

▪ Myocytes themselves enlarge, but the capillary network in the hypertrophic heart tends to be less extensive than in physiologic hypertrophy

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32
Q

which singling pathway for heart failure

A

angiotensin ii

beta adrenergic

endothelia 1

inflammatory cytokines

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33
Q

angiotensin ii pathway in heart failure

A
  • Angiotensin II – as cardiac output to the kidneys decreases→ increased AT II
    ▪ AT II can also be released by “stressed” cardiac cells
  • AT II can directly bind to myocyte and myofibroblast receptors→ hypertrophy, proliferation of myofibroblasts, and increased deposition of connective tissue
  • Increased AT II also increases volume and vasoconstriction→ worsened edema and afterload
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34
Q

beta adrenergic signaling increased in heart failure

A

Beta-adrenergic signaling is increased in early heart failure→ receptor downregulation

  • Long-term beta-adrenergic signaling also results in hypertrophy and fibrosis, and even eventually apoptosis of myocytes
    ▪ long-term activation of the SNS in the heart is maladaptive, even though short-term activation improves cardiac function
    ▪ Exact signaling mechanisms are currently being studied
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35
Q

other detreminetal pathways in heart failure

A

▪ Endothelin-1: potent vasoconstrictor that is also a growth factor for cardiomyocytes

▪ Inflammatory cytokines: activate JNK and MAPK pathways that seem to be linked to maladaptive remodeling and apoptosis

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36
Q

how does calcium homeostasis change in heart failure

A

▪ Ryanodine receptors release less calcium per AP
▪ SERCA calcium uptake is inhibited
▪ The net effect seems to be elevated diastolic calcium levels and impaired calcium spikes during contraction

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37
Q

what is a beneficial pathway in heart failure

A

Activation of IGF-1 and PI3K pathways seem to be the major routes that drive physiologic (healthy) hypertrophy

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38
Q

what does activation of SNS and RAAS lead to initially and then over time

A

initial: increase HR, BP, contractility, retention of water and sodium (increases preload and cardiac output)

overtime:
-excessive vasoconstriction and volume retention
-baroreceptor dysfunction —> elevated pressures and decrease PNS tone
▪ Increased ADH release → increased volume
▪ Excessive SNS activation → decreased renal perfusion… which leads to chronically elevated release of renin + AT2 to maintain blood flow to the kidney

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39
Q

what can renin release be casued by

A

decreased perfusion to kidneys and SNS activation

40
Q

if decreased perfusion to kidney then what

A

release renin; have AT1 into AT2 which has many effects

-vasoconstrict, increase BP, h20 and Na+ reabsorption (via aldosterone and ADH)

41
Q

what do atrial (ANP) and b type natriuretic peptide (BNP) do?

A

vasodilator, decrease angiotensin 2 and renin

natriuresis diuresisi

42
Q

what happens to BNP and ANP in heart failure

A

patients become resistant

no longer leads to sodium and water loss

43
Q

symtpoms of heart failure

A

fatigue

▪ “Left-sided” symptoms: orthopnea, dyspnea, angina, impaired cognitive function
* Can cause chronic kidney disease (CKD) and exacerbate ischemic heart disease

▪ “Right-sided” symptoms: dependent edema, RUQ pain

44
Q

signs of heart failure

A

▪ Pitting edema, hepatosplenomegaly

▪ Elevated JVP, displacement of the apical impulse, S3 or S4

▪ Crackles, wheezing, and sometimes pleural effusions depending on the extent of pulmonary edema

45
Q

what are the classes for heart failure

A

class 1- Ordinary physical activity does not cause undue fatigue, dyspnea, palpitations, or angina

class 2- Comfortable at rest. Ordinary physical activity (e.g., carrying heavy packages) may result in fatigue, dyspnea, palpitations, or angina

class 4- Symptoms of heart failure or angina are present at rest and worsened with any activity

46
Q

how to diagnose heart failure

A

echocardiography (cardiac ultrasound)

BNP

chest x ray

47
Q

what is found in echocardiography for heart failure

A

HFrEF- decreased ejection fraction; <40%

HFpEF is normal (>50%) but can see:
* Left ventricular hypertrophy
* Atrial enlargement, abnormal ventricular wall movement
* More challenging diagnosis than HFrEF

48
Q

what is normal echocardiography

A

HFpEF >50 %

49
Q

BNP is

A

a natriuretic factor that is released by the ventricle in response to increased strain

50
Q

chest x ray to identify

A

cardiomegaly and pulmonary edema

51
Q

what is the most common cause of heart failure (60%)

A
  • Chronic IHD (coronary artery disease)

the majority of the rest of the cases are due to hypertension (2nd most common), valvular abnormalities, or patients with congenital heart disease

52
Q

what are the clinic features of heart failure due to ischemic heart disease IHD

A

myocardial hypertrophy and fibrosis

HFrEF; left ventricle involved first

53
Q

atherosclerosis

A

Progression from fatty streak→deposition of oxidized LDL→migration and activation of macrophages →
▪ Calcification, accumulation of cholesterol, foam cell development
▪ Increased deposition of extracellular matrix under the intima
▪ A variably-stable fibrous cap with underlying necrotic tissue and immune cells
▪ Stenosis of the lumen and impaired blood flow

54
Q

risk factors for athersolsceorsi

A
  • Smoking, high blood pressure, oxidative stress increase endothelial damage
  • Lp(a) – (immune cell recruitment, plaque, endothelial damage)
  • Diabetes and dyslipidemia (including metabolic syndrome): LDL and AGEs into endothelium, oxidative stress
55
Q

chronic hypertesnion is the second most common cause of heart failure… which ventricle effected first? concentric or eccentric?

A

oncentric LV hypertrophy – wall thickens, but the chamber size does not tend to increase

  • Over time can proceed to eccentric hypertrophy
56
Q

medication for angina and CHF (congestive heart failure)

A

beta blockers

57
Q

medications for CHF (congestive heart failure)

A

cardiac glycoside (digoxin)

diuretics

58
Q

beta blockers for angina and CHF; what receptor? what effect?

A

beta-1 epi/norepinephrine receptor

▪ IHD: Reduce cardiac oxygen demand – thus effective prophylactic for angina, other complications of IHD

▪ CHF: reduces and even reverses cardiac remodeling (less fibrosis, hypertrophy, cell death)

59
Q

beta blocker effcet

A

block SNS, NE and E –> lower HR and contractions and oxygen demans

60
Q

cardiac glycosides (digoxin) inhibit what

A

sodium potassium pump

61
Q

cardiac glycoside (digoxin) increases what

A

Increase contractility by increasing intracellular calcium, but also increase vagal tone (resulting in a slower heart rate)

  • Increasing vagal tone helps decrease oxygen demand
62
Q

digoxin inhibits Na+/K+ pump why is this good?

A

bc calcium extrusion from cytosol is partially determined by sodium gradient (sodium calcium exchanged)

digoxin decreases this gradient so increases cytosolic calcium during systole

63
Q

duretics in CHF

A

diuretics reduce blood volume, usually by
increasing water and sodium loss at the kidney tubule

64
Q

types of diuretics

A
  • Loop and thiazide diuretics – inhibit sodium reabsorption by inhibiting particular sodium transporters earlier in the nephron
  • Spironolactone – blocks the aldosterone receptor→ loss of sodium and water in the distal nephron
  • ACE inhibitors (ACE-i) block angiotensin-converting enzyme that converts AT1 to AT2

▪ They likely also have beneficial impacts on heart remodeling, just like beta-blockers

65
Q

medications for angina

A

calcium channel blockers (nondihydropryridine and dihyrdorpyridine)

nitrates

66
Q

what do dihydropyridine calcium channel blocker do

A

Can cause vasodilation with limited impact cardiac conduction or contractility

67
Q

what do nondihydropyridine calcium channel blocker do

A

Can cause slowing of AV conduction (slows heart rate) and decreased contractility, but with variable effects on vasodilation

68
Q

dihydropyrdiine vs nondihydropyridine calcium channel blockers

A

dihydro= vasodilate

non= slow AV conduction (HR) and decrease contractility

69
Q

nitrates effect on angina

A

converted to nitric oxide= vasodilate

  • Decreased preload (through vasodilation of veins, decreased venous
    return)→decreased oxygen demand
  • Decreased afterload (through vasodilation of arterioles) → decreased
    oxygen demand
  • Coronary vasodilation → increased blood supply
70
Q

4 meds for dyslipidemia

A
  1. HMG CoA reductase inhibitors (statins)
  2. PCSK9 inhibitors

3.ezetimibe

  1. niacin
71
Q

what do HMG coa reductase inhibitors (statins) do? organ they act on?

A

reduce the hepatocyte’s ability to produce cholesterol→depletion of the hepatocyte’s “intracellular supply” of cholesterol→upregulation of the LDL receptor on the hepatocyte cell membrane
▪ This increases clearance of LDL from the circulation

▪ These medications also:
* Decrease circulating triglyceride levels
* Improve endothelial function
* Seem to also reduce oxidative stress and inflammation at the plaque

72
Q

PCSK9 inhibitors do what?

A

block a protease known as PCSK9 on the hepatocyte membrane

▪ This protease degrades the LDL receptor – if it is blocked, then there are more LDL receptors available to clear LDL

73
Q

ezetimibe does what in dyslipidemia

A

reduces the absorption of dietary and biliary cholesterol in the small intestine

▪ This leads to a decrease in cholesterol stores in the hepatocyte→increased LDL receptor expression

74
Q

what does niacin do in dyslipidemia

A

inhibits lipolysis in adipose tissue
▪ Therefore less release of FFAs → less production of VLDL by the liver
▪ This in turn leads to decreased circulating LDL, but main effect is decreased in TG (VLDL) synthesis
▪ Also increases HDL… however importance of this is not known

75
Q

what pathological processes damage valves

A

-congenital disorders

-wear and tear from chronic infalmmation/ calfcification

-infalmmatory; infection or autoimmune

-ischemia or aortic dissection

-idiopathic

76
Q

what is stenosis

A

the valve has a more narrow than normal orifice, and/or it is difficult to open

▪ Either way → increased strain across the wall of the heart proximal to the stenosis→hypertrophy and complications
▪ Can also initially result in impaired outflow to structures after the stenosis→physiologic adaptations to poor outflow

77
Q

what is regurgitation

A

backflow of blood across a valve

▪ Backflow of blood to chamber proximal to the regurgitation→BOTH increased EDV/preload + impaired outflow distal to the regurgitation→ eventual chamber enlargement

78
Q

what is incompetence (insufficiency) in a valve

causes regurgitation

A

the valve does not close completely

79
Q

what is prolapse in a valve

causes regurgitation

A

excessive (backwards) valve movement into the proximal chamber

80
Q

4 valvular pathologies

A
  • Aortic regurgitation
  • Bicuspidandcalcific
    aortic stenosis
  • Mitral valve prolapse and mitral regurgitation
  • Rheumatic heart disease
81
Q

how does aortic sclerosis progress to heart failure

A

aortic sclerosis→asymptomatic aortic stenosis→aortic stenosis with heart failure

82
Q

congenital cause of aortic stenosis

A

congenital bicuspid aortic valves account for about 5% of all congenital heart disease, and is one of the most common congenital valvular defects

83
Q

calcific aortic stenosis

A

Damage to the valvular endothelium→oxidized LDL and migration of chronic inflammatory cells→ calcification and sclerosis of tissue

▪ Some myofibroblasts actually differentiate into cells that are “bone-like”
(osteoblast-like)
▪ This process is accelerated in the presence of a bicuspid aortic valve

  • As the valve calcifies→ increased afterload→ concentric hypertrophy of the heart
84
Q

3 ethologies of aortic regurgiation

A
  1. related to aortic stenosis (most common) (valvular malformation)
  2. inflammatory disorders (ankylosing spondylitis and rheumatic heart disease)
  3. acute damage of the valve (thoracic aortic dissection, infective endocarditive)
85
Q

most common valvular abnormality

A

mitral valve prolapse

86
Q

pathologic findings in mitral valve prolapse

A

▪ Enlarged valve leaflets that are redundant and often “billow”
into the left atrium during systole

▪ The annulus and chordae tendinae can also be enlarged, and sometimes the chordae break

▪ Microscopy – lots of myxomatous connective tissue that massively increases the thickness leaflet – full of proteoglycans with a deficit in collagen
* Primary causes – not well-understood, some show a deficit in the cadherins
* Secondary causes – associated with disorders of connective tissue that impact other organs (Marfan’s syndrome, Ehlers-Danlos Syndrome)

87
Q

mitral valve regurgitation is usually do to? what is less common?

A

longer term mitral valve prolpase

less common:
▪Ischemia→dysfunction or actual rupture of papillary muscles
* Rupture can be acutely life-threatening
▪Infective endocarditis
▪ Rheumatic heart disease
▪ Enlargement of the left atrium or left ventricle

88
Q

acute mitral regurgitation causes left atrial pressures to ___ and pulmonary pressures to ____

A

increase

89
Q

mitral regurgitation caused by

A

chordae tendinae rupture, impaired papillary function, or papillary rupture

90
Q

rheumatic fever

A

auto-immune reaction to infection with Group A streptococcus
▪ Can occur with strep throat OR with strep skin infection (i.e. impetigo)

91
Q

what happens in rheumatic fever

A

The “M-protein” of streptococcal antigens stimulates an immune response→antibodies & T also recognize epitopes
c
on cardiac cells (particularly valves)

92
Q

who is rheumatic fever most common in

A

kids /teens

93
Q

rheumatic heart disease causes by rheumatic fever affects which part of heart wall

A
  • Canaffecteverylayeroftheheartwall–endocarditis(valves), myocarditis, pericarditis
94
Q

pathogenesis of rheumatic heart disease

A
  • GAS (group A strep) introduces streptococcal antigens into the body→antibodies and activated cytotoxic T cells
  • Immune responses can cross-react with cardiac antigens, including those from myocyte sarcolemma and valvular glycoproteins.
  • inflammation of the heart in acute rheumatic fever may involve all cardiac layers (endocarditis, myocarditis, pericarditis). Occurs 2-3 weeks after infection
  • Active inflammation of the valves may lead to chronic valvular stenosis or insufficiency
    ▪ These lesions involve mitral, aortic, and tricuspid valves, in that order of frequency.
95
Q

which valves are most effected in rheumatic heart disease

A

mitral and aortic valve (mitral and aortic stenosis)

96
Q

mitral stenosis and aortic stenosis in rheumatic heart disease

A

▪ RHD is the most common cause of mitral stenosis
▪ Often the scarring along the valve and the shortening of the chordae tendinae cause the valve to be incompetent as well

aortic stenosis;
▪ Often the aortic commissures are fused, making them resemble a bicuspid aortic valve
▪ The aortic valve can also become incompetent as well as stenotic

97
Q

SLIDE 52- 54 on lec 6 week 3 very important ****

A

GO LOOK

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