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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
What is HF-REF?
The disease process affects contraction of the heart muscle
26
What are the main causes of HF-REF?
Myocardial injury or overload (increased preload or afterload) -> can be regional (e.g. MI) or global (e.g. dilated CM)
27
What happens to the Starling's law curve as a result of short-term and long-term changes?
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
Why does ventricular remodelling occur?
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
How does ventricular remodelling occur after myocardial injury i.e. acute infarction?
Initial infarct -> expansion of infarct (hrs-days) -> inside pressure pushing on fibrotic tissue -> global remodelling (dys-mnths)
30
How does ventricular remodelling after in long-term uncontrolled hypertension i.e. chronic overload?
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
What are the macroscopic features of ventricular remodelling?
- Lost muscle mass - Alteration in chamber size (dilation/hypertrophy) - Dys-synchronous contractions
32
What are the microscopic features of ventricular remodelling?
- Myocyte changes (cell thinning, lengthening, hypertrophy, necrosis + apoptosis) - Disorganised muscle fibre orientation - ECM alterations + inflammatory changes
33
What are the intracellular features of ventricular remodelling?
- Contractile protein structural + functional derangements - Disorganised cytoskeleton - Impaired cell-cell communication - Altered energy metabolism - Deranged excitation
34
What changes occur in the heart in a myocardial infarction?
Blocked epicardial artery -> ischaemia + death of territory myocardium -> regional wall motion abnormality -> reduced LVEF -> dilation LV -> functional mitral regurgitation/papillary muscle rupture
35
List a few causes of dilated cardiomyopathy.
Vascular: ischaemic Infective: virus e.g. HIV or bacterial e.g. lyme disease Autoimmune: SLE Drug-related: alcohol, cocaine
36
What are the consequences of right CHD?
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
What are the consequences of left CHD?
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
Explain class I heart failure.
No limitation of physical activity: ordinary physical activity does not cause undue breathlessness, fatigue or palpitations
39
Explain class II heart failure.
Slight limitation of physical activity: comfortable at rest but ordinary physical activity results in undue breathlessness, fatigue or palpitations
40
Explain class III heart failure.
Marked limitation of physical activity: comfortable at rest but less than ordinary physical activity results in undue breathlessness, fatigue or palpitations
41
Explain class IV heart failure.
Unable to do any physical activity w/o discomfort, symptoms at rest can be present + if any physical activity undertaken, discomfort is decreased
42
What does acute presentation of heart failure look like?
- Sudden trigger vs decompensation - Breathlessness (pulmonary oedema), cardiogenic shock (low CO + BP), arrhythmia, AKI + low GCS - Death Must look for cause
43
What does chronic presentation of heart failure look like?
- Left vs right - Breathlessness, fatigue + congestion - Peripheral oedema, liver congestion, anaemic, CKD + cardiac cachexia
44
Where is acute and chronic heart failure most common?
Acute: developing world Chronic: developed world
45
Why do you get oedema in heart failure?
Increased hydrostatic pressure thus increased filtration -> fluid moves out of vessels + retained in interstitial space
46
How is decreased renal perfusion in heart failure compensated for? Why is this bad?
Increased RAAS -> Na/H2O retention, interstitial fibrosis + vasoconstriction Vasoconstriction causes increased wall stress + ventricular remodelling
47
How is decreased blood pressure in heart failure compensated for? Why is this bad?
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
What other mechanisms are used by the body to compensate in heart failure?
``` Neurohormonal activation Cytokine activation Oxidative stress Apoptosis Altered gene expression ```
49
What does compensatory mechanisms do overall to the heart failure?
Progresses it further due to ventricular remodelling
50
How is acute decompensated heart failure treated?
``` ABCDE O2 via re-breath bag GTN (spray/infusion) Loop diuretics (fast) cPAP Inotropes Transplant (rarely) ```
51
What are the main drug choices for heart failure?
ACE inhibitors ARB's Anti-aldosterone drugs

Block 2 (45 decks)

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