L22. Cardiac Failure Flashcards

1
Q

What are four major factors that affect cardiac output?

A
  1. Input (preload)
  2. Rate (HR)
  3. Strength (contractility, SR)
  4. Resistance (afterload)
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2
Q

Describe the length-tension relationship of muslces. How does it apply to the heart?

A

The longer the sarcomere length (stretch)
The increased the sensitivity to calcium (of troponin)
The increase the force of muscle contraction

The higher the preload (EDV/filling), the higher the force of cardiac contraction leading to increased SV and CO

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3
Q

How do we measure right ventricular end diastolic pressure (EDP)?
- invasively vs. non-invasively

A

Catheter insertion into a VEIN into the right atrium and measuring the atrial pressure at the end of diasole as a measure of the ventricular pressure. This is an invasive procedure

Measurement of the JVP gives an estimate for the right atrial (and hence right ventricular) pressure

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4
Q

How do we measure left ventricular end diastolic pressure (EDP)?

A

Catheter insertion into an ARTERY and across the aortic valve and measure the left atrial pressure at the end of diastole as a measure of left ventricular pressure

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5
Q

What is the pulmonary artery wedge pressure?

A

Insertion of a catheter into a vein through the right heart and into the pulmonary artery.
Temporary balloon occlusion of the artery (blocks any pressure from behind) and will allow the sensor to measure the pulmonary venous pressure as an indication of the left atrium and ventricle.
- useful in measuring patient haemodynamics

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6
Q

What is oedema or ‘dropsy’?

A

The swelling of the peripheral limbs (especially ankles, legs, sacrum and scrotum) as a result of a build up of interstitial fluid in the tissue
Clinically: Indentations are left in the skin when pressed

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7
Q

What are the normal pressures or ‘Starling Forces’ occurring across the capillary wall?

A
Hydrostatic pressure 
Osmotic pressure (protein concentrations in the blood)

The balance of forces tends to force fluid out at the arterial end and back at the venous end. Any excess left in the tissue is drained by the lymphatics

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8
Q

Does the capillary wall experience more venous or arterial pressure?

A

Mainly VENOUS pressure (increases in venous pressure forces fluid out of the capillary).
Changes (increases) in arterial pressure tend to not affect the capillary because the arterioles are very good at blocking/filtering out the pressure

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9
Q

What are the causes of oedema?

A
  1. Increased Venous pressure
  2. Decreased osmotic pressure
  3. Blocked lymphatic drainage
  4. Increased vascular permeability
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10
Q

What are the main factors that can affect the EDP of the left vs. the right ventricles?

A

LVEDP is measured by Left atrial pressure or the pulmonary vein pressure
- Increased pressure can cause increased lung capillary pressures leading to oedema in the lungs

RVEDP is measured by right atrial pressure or JVP
- increased pressures leads to increased peripheral pressures and oedema

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11
Q

What happens to the EDP with failing CO?

A

Decreased CO leads to increase in HR and an increase in contractility of the heart. This overall leads to an increased EDP to eject more blood out (increase the SV)

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12
Q

What is the problem with the bodies compensatory mechanism for a decreased CO?

A

Increasing the EDP to compensate for CO is useful up until a point where the ventricular EDP gets too large that back pressures occur increases the atrial pressure and the pulmonary pressure leading to pulmonary congestion and stops oxygenation.
Thus occurs about 20-30 mmHg

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13
Q

What is meant by the term ‘Cardiac Failure’?

What are the normal causes of cardiac failure?

A

A relative term for when cardiac output is less than what is adequate for the body’s needs

It is usually due to a reduction in CO rather than an increase in body demand. And this is usually due to systolic failure as a result of lost contractility (reduced SV and EDP)

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14
Q

What is one of the body’s major adaptations to increase CO (by increasing blood volume)

A

Retention of fluid by the body (renin-angiotensin-aldosterone pathway) leads to increases in blood volume and thus an increased venous return which increases the EDV (EDP). This adaptation is usually asymptomatic until it isn’t enough to compensate.

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15
Q

How can this retention of blood volume become pathogenic?

A

The increase in blood volume may increase the EDP too much leading to eventual pulmonary oedema and shortness of breath (left heart failure)
In right heart failure, the EDP can increase too much to the point of peripheral oedema

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16
Q

How can high arterial pressure lead to oedema and then ventricular failure?

A

High arterial pressure (high afterload) puts a strain on the ventricle. This may eventually lead to ventricular failure then builds up pressure in the atrium and then into the pulmonary system to cause oedema

17
Q

What are the main mechanisms of cardiac failure?

A
Loss of viable myocardial muscle (MI, cardiomyopathy)
Pressure overload (aortic stenosis, hypertension)
Volume overload (regurgitation, shunts or septal defects)
18
Q

What are the clinical features of left and right heart failure?

A

Left: shortness of breath, fatigue, tachycardia, lung creps
Right: Peripheral oedema, liver congestion

19
Q

What is meant by inappropriate adaptations are made by the body in response to decreased CO?

  • fluid retention
  • sympathetic NS
A

Fluid retention and vasoconstriction to increase the CO leads to an eventual increase in the afterload of the heart meaning it is more difficult to get blood out of the heart and CO falls more

Sympathetic nerve activation increases noradrenaline and contractility in response to decreased CO. But long term this and the vasoconstriction can lead to ventricular arrhythmia. Additionally adrenaline is believed to have direct toxic effects on the tissue.

20
Q

What are the mechanisms of right heart failure?

A

Global heart disease (cardiomyopathies)
Specific right heart diseases (right sided valve and shunt diseases, pericardial disease or pulmonary hypertension: cor pulmonale or pulmonary embolism)
Severe Left heart failure leading to pulmonary venous hypertension and congestion to right heart

21
Q

Pulmonary congestion is a stimulus for hormone induced vasoconstriction. What hormones are involved?

A

Endothelin (ET receptor)

Angiopoietin (on Smooth Muscle)

22
Q

What is diastolic heart failure? What can cause it?

A

When systolic function is normal but there is a reduction in LV compliance meaning it is difficult to fill the heart (diastole)

  • can be caused by scarring from infarction or by stiffness caused by hypertrophy due to hypertension.
  • can lead to increased pulmonary venous pressure by increased LVEDP
23
Q

What are the main treatments used for cardiac failure?

A
Beta Blockers 
Diuretics (frusemide)
Aldosterone antagonists (spironolactone)
ACE inhibitors (captopril, ramipril)
Angtiotensin Receptor Antagonists (irbesartan, candesartan)

Digitoxin (conterversial drug that increases contractility)
Positive inotropic drugs: only used short tem

Treating the underlying cause and by artificial or surgical means