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Block 2 > Pathophysiology Of Heart Failure > Flashcards

Pathophysiology Of Heart Failure Flashcards

1
Q

Describe the pressure difference in the cardiac cycle.

A
  1. Atria & ventricles in diastole; blood flowing from atria -> ventricles (low pressure)
  2. Atria systole; pressure rises in ventricles above atria so A-V valves close
  3. Isovolumnic contraction increases pressure in ventricles above aorta/PA so AV & PV open
  4. Blood flows from ventricles out of aorta/PA so ventricular pressure drops below aorta/PA closing the AV & PV valves
  5. At the point of blood ejection from ventricles, pressure in system increases so atria start passively filling from SVC/IVC/PV
  6. Blood volume will increase atria pressure above ventricles opening A-V valves again so cycle starts again
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2
Q

What is Starling’s law?

A

SV & contractility will increase with ventricular EDV until a certain point after which there is a decrease in SV & contractility

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3
Q

What does the SNS do to the heart?

A

Increased HR
Increased force of contraction
Increased rate of force development
Increased relaxation

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4
Q

How do you work out stroke volume?

A

EDV - ESV

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5
Q

What factors affect end diastolic volume (EDV)?

A

Preload (venous return + filling time)

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6
Q

What factors affect end systolic volume (ESV)?

A

Preload (venous return + filling time)

Afterload (vasodilation or vasoconstriction)

Contractility (hormones + ANS)

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7
Q

What is the structure of the veins and arteries?

A

Veins: THIN, elastic, muscular wall

Artery: THICK, elastic, muscular wall

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8
Q

What is the Starling equation?

A

Net filtration pressure = Hydrostatic pressure - osmotic force

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9
Q

What are the 3 ways capillary fluid movement occurs?

A
  1. Diffusion (passive)
  2. Filtration (hydrostatic pressure)
  3. Absorption (oncotic pressure)
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10
Q

How does the Starling equation explain the movement of fluid in capillary beds?

A

Arteriole: hydrostatic pressure higher than osmotic pressure so fluid moves into tissues (filtration)

Venules: osmotic pressure higher than hydrostatic pressure so fluid comes in to be taken to the heart (absorption)

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11
Q

Define heart failure clinically.

A

Syndrome in which patients have typical symptoms (e.g. breathlessness, ankle swelling + fatigue) + signs (e.g. elevated JVP, pulmonary crackles + displaced apex beat) resulting from abnormality of cardiac structure or function

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12
Q

Define heart failure pathophysiologically.

A

Abnormality of cardiac structure or function leading to failure of the heart to deliver O2 at a rate commensurate with the requirements of the metabolizing tissues

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13
Q

Summarise the epidemiology of heart failure.

A

More common in older age with 60-70% people dying within 5 years of diagnosis

Congenital abnormalities is the exception

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14
Q

Why is heart failure a heterogenous condition?

A

It is a syndrome rather than a complete diagnosis + the underlying cause of cardiac dysfunction should always be determined

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15
Q

What are the 4 main cardiac dysfunctions that underlie heart failure? Give some examples of each.

A
  1. Coronary artery disease e.g. MI, CM + HTN
  2. Valvular heart disease e.g. congenital + immunological (rheumatic fever or chagas disease)
  3. High-output cardiac failure e.g. anaemia, liver cirrhosis + pregnancy
  4. Arrhythmias + conduction e.g. tachy/brady arrhythmias + pericarditis
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16
Q

What are the 2 different types of heart failure?

A
  1. Heart failure with reduced ejection fraction (HF-REF)

2. Heart failure with preserved ejection fraction (HR-PEF)

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17
Q

What is required to diagnosis HR-REF?

A
  1. Typical HF symptoms
  2. Typical HF signs
  3. Reduced LVEF
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18
Q

What is required to diagnosis HR-PEF?

A
  1. Typical HF symptoms
  2. Typical HF signs
  3. Normal/mildly reduced LVEF + LV not dilated
  4. Relevant structural heart disease (LV hypertrophy/LA enlargement) AND/OR diastolic dysfunction
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19
Q

What is the equation for stroke volume?

A

EDV - ESV

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20
Q

What is the equation for ejection fraction?

A

SV/EDV = %

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21
Q

What is the main structure used to define heart failure?

A

Left ventricle

22
Q

What are the strengths and weakness of echocardiography?

A

S: cheap + robust
W: very subjective

23
Q

What does echocardiography do?

A

Defines cardiac structure + function

24
Q

What alternative imaging can you use to look at heart failure?

A

Cardiovascular magnetic resonance (CMR)

Nuclear

25
Q

What is HF-REF?

A

The disease process affects contraction of the heart muscle

26
Q

What are the main causes of HF-REF?

A

Myocardial injury or overload (increased preload or afterload) -> can be regional (e.g. MI) or global (e.g. dilated CM)

27
Q

What happens to the Starling’s law curve as a result of short-term and long-term changes?

A

Short-term e.g. exercise will increase SNS, contractility + HR efficiently shifting curve up as SV will increase more as VEDV increases

Long-term e.g. adverse remodelling in a damaged heart so curve flattens out as SV will decrease less as VEDV increases

28
Q

Why does ventricular remodelling occur?

A

Myocardial injury or chronic volume overload (preload), which often both co-exist, will cause ventricular dilation due to hypertrophy designed to preserve SV (CO reserve)

29
Q

How does ventricular remodelling occur after myocardial injury i.e. acute infarction?

A

Initial infarct -> expansion of infarct (hrs-days) -> inside pressure pushing on fibrotic tissue -> global remodelling (dys-mnths)

30
Q

How does ventricular remodelling after in long-term uncontrolled hypertension i.e. chronic overload?

A

Hypertrophy -> diastolic heart failure

Dilated heart -> systolic heart failure

Failure occurs as the heart cannot cope; although it has got bigger, there is no extra vasculature

31
Q

What are the macroscopic features of ventricular remodelling?

A
  • Lost muscle mass
  • Alteration in chamber size (dilation/hypertrophy)
  • Dys-synchronous contractions
32
Q

What are the microscopic features of ventricular remodelling?

A
  • Myocyte changes (cell thinning, lengthening, hypertrophy, necrosis + apoptosis)
  • Disorganised muscle fibre orientation
  • ECM alterations + inflammatory changes
33
Q

What are the intracellular features of ventricular remodelling?

A
  • Contractile protein structural + functional derangements
  • Disorganised cytoskeleton
  • Impaired cell-cell communication
  • Altered energy metabolism
  • Deranged excitation
34
Q

What changes occur in the heart in a myocardial infarction?

A

Blocked epicardial artery -> ischaemia + death of territory myocardium -> regional wall motion abnormality -> reduced LVEF -> dilation LV -> functional mitral regurgitation/papillary muscle rupture

35
Q

List a few causes of dilated cardiomyopathy.

A

Vascular: ischaemic

Infective: virus e.g. HIV or bacterial e.g. lyme disease

Autoimmune: SLE

Drug-related: alcohol, cocaine

36
Q

What are the consequences of right CHD?

A

Congestion of peripheral tissues causes:

  • Dependent edema + ascites
  • GI tract congestion -> anorexia, GI distress + weight loss
  • Liver congestion -> signs related to impaired liver function
37
Q

What are the consequences of left CHD?

A

Decreased CO -> activity intolerance + signs of decreased tissue perfusion

Pulmonary congestion causes:

  • Impaired gas exchange -> cyanosis + signs of hypoxia
  • Pulmonary edema -> cough with frothy sputum, orthopnea + paroxysmal nocturnal dyspnea
38
Q

Explain class I heart failure.

A

No limitation of physical activity: ordinary physical activity does not cause undue breathlessness, fatigue or palpitations

39
Q

Explain class II heart failure.

A

Slight limitation of physical activity: comfortable at rest but ordinary physical activity results in undue breathlessness, fatigue or palpitations

40
Q

Explain class III heart failure.

A

Marked limitation of physical activity: comfortable at rest but less than ordinary physical activity results in undue breathlessness, fatigue or palpitations

41
Q

Explain class IV heart failure.

A

Unable to do any physical activity w/o discomfort, symptoms at rest can be present + if any physical activity undertaken, discomfort is decreased

42
Q

What does acute presentation of heart failure look like?

A
  • Sudden trigger vs decompensation
  • Breathlessness (pulmonary oedema), cardiogenic shock (low CO + BP), arrhythmia, AKI + low GCS
  • Death

Must look for cause

43
Q

What does chronic presentation of heart failure look like?

A
  • Left vs right
  • Breathlessness, fatigue + congestion
  • Peripheral oedema, liver congestion, anaemic, CKD + cardiac cachexia
44
Q

Where is acute and chronic heart failure most common?

A

Acute: developing world

Chronic: developed world

45
Q

Why do you get oedema in heart failure?

A

Increased hydrostatic pressure thus increased filtration -> fluid moves out of vessels + retained in interstitial space

46
Q

How is decreased renal perfusion in heart failure compensated for? Why is this bad?

A

Increased RAAS -> Na/H2O retention, interstitial fibrosis + vasoconstriction

Vasoconstriction causes increased wall stress + ventricular remodelling

47
Q

How is decreased blood pressure in heart failure compensated for? Why is this bad?

A

Increases SNS activation + NA release -> increased HR + vasoconstriction

Causes direct myocardial toxicity, increased HR increases O2 demand of heart + vasoconstriction causes wall stress + ventricular remodelling

48
Q

What other mechanisms are used by the body to compensate in heart failure?

A 
Neurohormonal activation
Cytokine activation
Oxidative stress
Apoptosis
Altered gene expression
49
Q

What does compensatory mechanisms do overall to the heart failure?

A

Progresses it further due to ventricular remodelling

50
Q

How is acute decompensated heart failure treated?

A 
ABCDE 
O2 via re-breath bag
GTN (spray/infusion)
Loop diuretics (fast)
cPAP
Inotropes
Transplant (rarely)
51
Q

What are the main drug choices for heart failure?

A

ACE inhibitors
ARB’s
Anti-aldosterone drugs

Block 2 (45 decks)

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