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Physiology > Lecture 16: Cardiovascular Dysfunction > Flashcards

Lecture 16: Cardiovascular Dysfunction Flashcards

1
Q

What is heart failure?

A

When the output of the heart is insufficient to meet the demands of the body.

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2
Q

How does heart failure occur?

A

Usually due to impairment of heart function (e.g. due to damage)

May also occur if demands of body increase (hypertension, anemia, reduced blood volume)

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3
Q

What is high output failure? Low output failure

A

When cardiac output is normal or even elevated in situations where body demands increase

yet the heart still fails to meet these increased demands

Low output failure (low cardiac output) is more common

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4
Q

How many cardiovascular related death is HF responsible for? Mortality of HF

A

34%

One year motrality: 33%

5 year mortality: 50+%

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5
Q

New York Heart Association classes of HF

A

Class I (mild)

Class II (mild)

Class III (moderate)

Class IV (severe)

See table

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6
Q

Classes of heart failure and hazard ratios for mortality and hospitalization

A

Risk of mortality and hospitalization go up with increased class

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7
Q

Frank Starling curve in low output HF

A

Failing heart ejects lower SV for a given EDV

Hallmark = impaired contractility

See figure

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8
Q

Compensation in heart failure & Frank Starling curve

A

Elevated SNS activity

Increased EDV

Both try to recover SV in initial stages of HF

See figure

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9
Q

What causes heart to enter a decompensated state?

A

Overtime, SNS stimulation becomes insufficient to compensate for failing heart

This happens because…

Sympathetic drive becomes diminished

Heart loses ability to respond to SNS (down regulation and/or decoupling of receptors)

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10
Q

What do kidneys do during HF

A

Cardiac output is diminished, so kidneys retain extra salt and water

This increases blood volume and elevates EDV

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11
Q

What happens to heart as HF progresses

A

Heart is unable to pump normal SV

Progressively less blood is pumped out

Cardiac muscle fibers become stretched and ventricles become dilated

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12
Q

What are backward and forward failure?

A

In HF, there is higher EDV due to kidneys, heart cannot pump normal SV, and ventricles are dilated

This causes backward failure, as blood is unable to enter the heart and it also cannot be pumped out. So it accumulates in venous system

Forward failure will follow, as heart cannot pump sufficient blood to body (diminished SV)

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13
Q

What causes hypertrophy of the heart?

A

Conditions that increase the workload of the heart (high arterial pressure, defective valve)

Conditions make the heart generate extra pressure to overcome the problem

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14
Q

What is hypertrophy?

A

Heart becomes larger due to increased size of muscle fibres

This enables heart to maintain normal SV

Similar to hypertrophy of skeletal muscles in exercise

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15
Q

Short term hypertrophy

A

Due to physical activity or pregnancy

Heart adjusts to workload, and returns to normal afterward

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16
Q

Sustained hypertrophy

A

Due to sustained workload

Causes deleterious changes to the heart leading to failure

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17
Q

Types of hypertrophy

A

Physiological (exercise, pregnancy, developement)

Pathophysiological (Hypertension, infarct)

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18
Q

What is cardiac dilatation? Impaired systolic function?

A

Chamber lumen increases in size

Results in impaired systolic function

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19
Q

Does cardiac dilatation accompany changes in wall thickness?

A

Dilatation may or may not accompany changes in wall thickness

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20
Q

What is the effect of dilatation on the cardiac wall?

A

Increase in chamber diameter results in increased outward stress exerted on the cardiac wall

Follows Law of LaPlace

Wall stress = (Ventricular pressure x chamber radius)/( 2x chamber wall thickness)

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21
Q

What phenomena contribute to dilatation?

A

Myocyte death

Myocyte slippage

hypertrophy via end to end assembly of sarcomeres (cells elongate)

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22
Q

Ventricular hypertrophy vs dilatation

A

See figure

In HF, heart usually goes normal, hypertrophy, dilatation

Can also go from normal to dilatation

Does not go from dilatation to hypertrophy

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23
Q

Left sided HF

A

left-side output is reduced

blood backs up into the respiratory vasculature

results in pleural edema – “congestive heart failure”

kidney blood flow is reduced, resulting in fluid retention

Generally more serious than right sided

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24
Q

Right sided HF

A

Right-side output is reduced

Blood backs up into the systemic venous system - results in ascites and/or peripheral edema

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25
Q

Systolic HF

A

Cardiac contractility is impaired

More prevalent in men vs. women

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26
Q

Diastolic HF

A

“Heart Failure with Preserved Ejection Fraction”

filling of the heart is impaired, reducing output

may be due to increased cardiac stiffness (fibrosis), or due to impaired relaxation

more prevalent and severe in women vs. men

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27
Q

Systolic failure and compensation - PV loop

A

A) Systolic dysfunction. Contractility curve shifts down, ventricles do not contract as strongly

B) Compensation (increased LV volume and elasticity). Drop of loop because pressure in ventricles is lower. More filling but less contractility than normal.

C) Compensation (increased contractility).. Contractility curve becomes more steep.

D) Compensation (increased filling/preload)

B, C and D will probably all occur at once in a person with HF

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28
Q

Diastolic failure - PV loop

A

See figure

AUC is smaller, so cardiac output is reduced

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29
Q

Signs and symptoms of heart failure

A

Pulmonary edema (detected as rales or crackles; reported by patients as dyspnea/orthopnea, pressure in chest)

Jugular vein engorgement

Peripheral edema, e.g. swollen ankles, pitting - Ascites

Lethargy/fatigue (heart can’t get enough oxygen to body)

Nausea, lack of appetite, cardiac cachexia

Cheyne-Stokes respiration (breathing pattern)

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30
Q

Signs and symptoms of congestive heart failure

A

Pulmonary edema (detected as rales or crackles; reported by patients as dyspnea/orthopnea, pressure in chest)

Jugular vein engorgement

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31
Q

Drugs used for HF - what are they effective for?

A

Symptomatic relief

Effects on longevity are minor

In some causes, surgical interventions are necessary

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32
Q

Examples of drugs used to treat heart failure

A

Diuretics – reduce blood volume to reduce cardiac workload

ACE inhibitors – promote vasodilation, decreased afterload

ARBs – promote vasodilation, decreased afterload

Beta blockers – reduce blood pressure and heart rate

Digitalis/digoxin – increases force of contraction

Aldosterone inhibitors – reduce salt/water retention

Nitroglycerin – causes vasodilation, reduced afterload

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33
Q

What happens to coronary blood flow when heart rate or metabolic rate increases?

A

Smooth muscle in arterioles supplying the heart muscle relax

Vasodilation and increased blood flow

34
Q

What causes local dilation of coronary arteries?

A

Metabolites produced by heart muscle

Beta agonist stimulation

Release of NO from vascular epithelium

35
Q

How does the heart receive blood during diastole?

A

Due to the high pressures during systole.

This is achieved in part by the ‘aortic recoil’ which aids cardiac perfusion through the coronary arteries.

36
Q

Effect of higher HR on perfusion of coronary arteries

A

A high HR decreases the diastolic time more than the systolic time.

This decreases the perfusion time of the coronary arteries, which may contribute to ischemia in an individual with narrowed coronary arteries.

37
Q

Vasodilation by Local messengers

A

See figure

38
Q

What determines the amount of blood delivered to the heart?

A

Amount of blood delivered is matched to myocardial oxygen demand

Determined by heart rate, contractility, preload, and afterload (wall tension).

39
Q

How can myocardial oxygen consumption be estimated?

A

rate-pressure product

heart rate x systolic pressure

40
Q

What can happen when an atherosclerotic plaque has reduced lumen size by 75%

A

Ischemia can occur during times of elevated myocardial oxygen demand

(e.g. physical exertion, emotional stress, hot or cold exposure, large meal)

41
Q

What can happen when an atherosclerotic plaque has reduced lumen size by 90%

A

Ischemia can occur at rest.

42
Q

What causes ischemia?

A

Either increased demand or decreased supply or both.

43
Q

What is the result of ischemia?

A

Diastolic and systolic dysfunction (i.e. failure of the heart to relax and fill, and failure of the heart to properly contract).

Angina pectoris.

ST segment changes in the ECG.

44
Q

What is angina?

A

Cardiac pain resulting from ischemia.

45
Q

What is silent ischemia?

A

Not everyone with ischemia develops angina

46
Q

What does angina produce on the EKG?

A

ST segment depression

47
Q

Distribution and sensation of pain in angina pectoris

A

Typically the pain is located in the sub- sternal region and may radiate to the arm (T1-T4 dermatome)

Other radiation patterns are considered atypical.

Often described as pressure, aching, heaviness or squeezing.

See figure

48
Q

What can occur alongside myocardial dysfunction?

A

Shortness of breath (dyspnea) due to pulmonary congestion

49
Q

What is stable angina?

A

Effort or exertion angina

Reproducible, often at a consistent rate-pressure product

50
Q

What relieves stable angina?

A

Rest and/or nitroglycerin

51
Q

Cause of stable angina

A

Thought to be caused by an advanced plaque that is highly fibrotic, and contains little lipid

Rarely, angina is caused by vasospasms. This is called variant or Prinzmetal’s angina, and can also occur with smoking or cocaine use.

52
Q

Duration of stable angina

A

Usually brief (< 5 minutes) as long as the person takes appropriate action

53
Q

When does ST segment depression occur?

A

With ischemia caused by partial occlusion of a coronary artery.

The ischemic region on the inside of the myocardium rapidly loses K+, making it relatively negative compared to non-ischemic myocardium during the resting state.

A current flows towards the non-ischemic muscle, resulting in the baseline of the ECG becoming elevated, or the ST segment becoming depressed.

See figure

54
Q

When does ST segment elevation occur?

A

With complete occlusion of a coronary artery, the entire thickness of the myocardium becomes ischemic.

During the resting state a current flows towards the non-ischemic muscle on the opposite side of the chamber, resulting in baseline depression, or ST segment elevation.

See figure

55
Q

Acute treatment of effort angina

A

Nitroglycerin (No donor)

Causes relaxation of smooth muscle in the vessels

Dilates coronary arteries and arterioles to improve blood supply to myocardium

Dilates systemic arteries to reduce afterload

Dilates veins to reduce myocardial preload and oxygen demand

56
Q

Long term treatment of effort angina

A

Prevented by oral nitrate preparations or nitro-patches.

However, tolerance is a problem.

57
Q

Other drugs that prevent effort angina

A

β-blockade and calcium-channel blockers that lower the heart rate

58
Q

What determines blood pressure?

A

Autonomic reflexes (baroreceptor, chemoreceptor, low pressure receptor)

Blood volume

Viscosity

Fluid balance

Ensure optimal perfusion of all tissues

59
Q

What can dysregulation of normal BP lead to?

A

Hypertension

Hypotension

Can be acute or chronic

Can lead to poor quality of life, impaired organ function and death

60
Q

What can HTN lead to if untreated?

A

Heart attack

Stroke/Memory loss

Vision impairment or blindness

Kidney damage

61
Q

Cause of hypertension

A

Primary (essential) hypertension cause is unknown

Secondary hypertension cause is known

62
Q

What is a common hallmark of primary (essential) HTN?

A

Decreased arterial lumen diameter

May result from increased vascular tone or an impairment in vasodilation (or both).

The net result is increased total peripheral resistance (TPR).

Increased blood volume can also be a contributor (water retention).

63
Q

What is afterload?

A

the force that impedes the movement of blood out of the ventricle.

64
Q

Effect of HTN on after load

A

Hypertension increases afterload, forcing the heart to work harder to maintain cardiac output

may result in hypertrophy

65
Q

Pathological outcomes of HTN

A

See figure

66
Q

Conventional therapies for HTN

A

Lifestyle changes (exercise, improve diet, lose weight, stop smoking, reduce stress)

Reduce salt/water retention and thus blood volume (diuretics)

Reduce renin/angiotensin axis activation (angiotensin-converting enzyme (ACE) inhibitors; angiotensin II receptor blockers (ARBs); renin inhibitors)

Reduce adrenergic drive (alpha-, beta-blockers)

Reduce excitation-contraction coupling (calcium channel blockers)

Vasodilators to increase vascular lumen diameter

Aldosterone antagonists

Endothelin receptor blockers

67
Q

What is hypotension

A

When SBP drops below 90 and/or DBP drops below 60

Usually transient although non-symptomatic chronic hypotension may occur in individuals who regularly exercise and are in peak physical condition.

68
Q

What causes hypotension?

A

Reduced blood volume (e.g. hemorrhage); may lead to shock

Reduced vascular tone

Reduced cardiac output

A combination of the above

69
Q

Symptoms of hypotension

A

Dizziness

Lightheadedness

Confusion

Fainting or seizures due to under-perfusion of the brain

Other symptoms can range from irregular heartbeat to indigestion.

70
Q

Orthostatic hypotension

A

A drop in blood pressure when moving from a supine to a standing position

Results in dizziness/lightheadedness (but possibly also recurrent fainting)

71
Q

Vasovagal syncope - what and why?

A

Fainting due to activation of the vagus nerve, leading to decreased cardiac rate/output, possibly with generalized loss of sympathetic vascular tone and rapid hypotension

The primary cause of fainting due to “stage fright”

72
Q

What is circulatory shock? What can extended periods cause?

A

Precipitous drop in blood pressure, leading to under-perfusion of tissues and organs.

Extended periods of low perfusion can lead to widespread organ damage and failure.

73
Q

What causes drop in blood pressure?

A

Decreases in cardiac output and/or total peripheral resistance

MAP = CO x TPR

74
Q

What is hypovolemic shock?

A

due to loss of blood volume, e.g. hemorrhage, diarrhea

75
Q

What is cariogenic shock?

A

due to decreased cardiac output/function

76
Q

What is vasogenic shock?

A

Mass vasodilation, excluding a role of the sympathetic system

e.g. release of vasodilator
substances (histamine – anaphylaxis), bacterial infection (sepsis)

77
Q

What is neurogenic shock?

A

Mass vasodilation, due to decreased sympathetic system activity

e.g. crushing injuries, extreme pain

78
Q

Overview of shock

A

See figure

79
Q

Treatment of circulatory shock - main goal

A

Attempts to restore blood pressure, while supporting cardiovascular function of the patient

80
Q

Treatment of circulatory shock - options

A

Oxygen – boosts oxygenation of blood (i.e. higher O2/ml)

Transfusion – blood may be provided in cases of hemorrhage, or saline solutions otherwise, in order to boost blood
volume and increase blood pressure

Vasopressors – drug administration to induce vasoconstriction, e.g. norepinephrine

Antibiotics – for cases of septic shock

Physiology (19 decks)

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