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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
Systolic HF
Cardiac contractility is impaired More prevalent in men vs. women
26
Diastolic HF
“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
27
Systolic failure and compensation - PV loop
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
28
Diastolic failure - PV loop
See figure AUC is smaller, so cardiac output is reduced
29
Signs and symptoms of heart failure
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)
30
Signs and symptoms of congestive heart failure
Pulmonary edema (detected as rales or crackles; reported by patients as dyspnea/orthopnea, pressure in chest) Jugular vein engorgement
31
Drugs used for HF - what are they effective for?
Symptomatic relief Effects on longevity are minor In some causes, surgical interventions are necessary
32
Examples of drugs used to treat heart failure
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
33
What happens to coronary blood flow when heart rate or metabolic rate increases?
Smooth muscle in arterioles supplying the heart muscle relax Vasodilation and increased blood flow
34
What causes local dilation of coronary arteries?
Metabolites produced by heart muscle Beta agonist stimulation Release of NO from vascular epithelium
35
How does the heart receive blood during diastole?
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
Effect of higher HR on perfusion of coronary arteries
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
Vasodilation by Local messengers
See figure
38
What determines the amount of blood delivered to the heart?
Amount of blood delivered is matched to myocardial oxygen demand Determined by heart rate, contractility, preload, and afterload (wall tension).
39
How can myocardial oxygen consumption be estimated?
rate-pressure product heart rate x systolic pressure
40
What can happen when an atherosclerotic plaque has reduced lumen size by 75%
Ischemia can occur during times of elevated myocardial oxygen demand (e.g. physical exertion, emotional stress, hot or cold exposure, large meal)
41
What can happen when an atherosclerotic plaque has reduced lumen size by 90%
Ischemia can occur at rest.
42
What causes ischemia?
Either increased demand or decreased supply or both.
43
What is the result of ischemia?
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
What is angina?
Cardiac pain resulting from ischemia.
45
What is silent ischemia?
Not everyone with ischemia develops angina
46
What does angina produce on the EKG?
ST segment depression
47
Distribution and sensation of pain in angina pectoris
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
What can occur alongside myocardial dysfunction?
Shortness of breath (dyspnea) due to pulmonary congestion
49
What is stable angina?
Effort or exertion angina Reproducible, often at a consistent rate-pressure product
50
What relieves stable angina?
Rest and/or nitroglycerin
51
Cause of stable angina
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
Duration of stable angina
Usually brief (< 5 minutes) as long as the person takes appropriate action
53
When does ST segment depression occur?
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
When does ST segment elevation occur?
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
Acute treatment of effort angina
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
Long term treatment of effort angina
Prevented by oral nitrate preparations or nitro-patches. However, tolerance is a problem.
57
Other drugs that prevent effort angina
β-blockade and calcium-channel blockers that lower the heart rate
58
What determines blood pressure?
Autonomic reflexes (baroreceptor, chemoreceptor, low pressure receptor) Blood volume Viscosity Fluid balance Ensure optimal perfusion of all tissues
59
What can dysregulation of normal BP lead to?
Hypertension Hypotension Can be acute or chronic Can lead to poor quality of life, impaired organ function and death
60
What can HTN lead to if untreated?
Heart attack Stroke/Memory loss Vision impairment or blindness Kidney damage
61
Cause of hypertension
Primary (essential) hypertension cause is unknown Secondary hypertension cause is known
62
What is a common hallmark of primary (essential) HTN?
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
What is afterload?
the force that impedes the movement of blood out of the ventricle.
64
Effect of HTN on after load
Hypertension increases afterload, forcing the heart to work harder to maintain cardiac output may result in hypertrophy
65
Pathological outcomes of HTN
See figure
66
Conventional therapies for HTN
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
What is hypotension
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
What causes hypotension?
Reduced blood volume (e.g. hemorrhage); may lead to shock Reduced vascular tone Reduced cardiac output A combination of the above
69
Symptoms of hypotension
Dizziness Lightheadedness Confusion Fainting or seizures due to under-perfusion of the brain Other symptoms can range from irregular heartbeat to indigestion.
70
Orthostatic hypotension
A drop in blood pressure when moving from a supine to a standing position Results in dizziness/lightheadedness (but possibly also recurrent fainting)
71
Vasovagal syncope - what and why?
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
What is circulatory shock? What can extended periods cause?
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
What causes drop in blood pressure?
Decreases in cardiac output and/or total peripheral resistance MAP = CO x TPR
74
What is hypovolemic shock?
due to loss of blood volume, e.g. hemorrhage, diarrhea
75
What is cariogenic shock?
due to decreased cardiac output/function
76
What is vasogenic shock?
Mass vasodilation, excluding a role of the sympathetic system e.g. release of vasodilator substances (histamine – anaphylaxis), bacterial infection (sepsis)
77
What is neurogenic shock?
Mass vasodilation, due to decreased sympathetic system activity e.g. crushing injuries, extreme pain
78
Overview of shock
See figure
79
Treatment of circulatory shock - main goal
Attempts to restore blood pressure, while supporting cardiovascular function of the patient
80
Treatment of circulatory shock - options
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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