Heart Failure Flashcards

1
Q

What is cardiac output?

A

The volume of blood leaving EITHER side of the heart per minute (usually in the context of the left ventricle)

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2
Q

What is heart failure and what is this reliant on?

A

CO is inadequate in heart failure.
This is dependant on:
-Preload ( strech of that cardiomyocyte): Inadequate venous return can compromise SV
-Afterload ( force the ventricles have to contract against to eject blood) : Excessive resistance compromises ejection volume
-Contractility (intrinsic muscle strength): Inadequate contractility can compromise SV.

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3
Q

How to work out stroke volume?

How to work out ejection fraction?how to work cardiac output?

A

Stroke volume= End diastolic volume (EDV) - End systolic volume (ESV)

Stroke volume/ End-diastolic volume x 100 = Ejection fraction.

Cardiac output= stroke volume x heart rate

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4
Q

what can lead to a low SV?

A

Low Preload  low venous return
High Afterload  high peripheral resistance
Low Contractility  ionic imbalance

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5
Q

How to measure ejection fraction?

A

Using a transthoracic echocardiogram.

- ultrasound of the chest

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6
Q

Define heart failure.

A

Syndrome that arises when the heart is unable to maintain an appropriate blood pressure without support. - P. Harris
Definition of heart failure in man - a clinical syndrome caused by an abnormality of he heart and recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses.

  1. Inability of the heart to keep up with demand
  2. Inadequate perfusion of organs (e.g. brain, liver, kidneys)
  3. Congestion in lungs and legs
  4. Collection of signs and symptoms
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7
Q

What other organ normally fails as a result of heart failure?

A

Kidneys - they receive around 35-40% of cardiac output

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8
Q

State some causes of heart failure.

A
Arrhythmia
Valve disease 
Pericardial disease 
Congenital heart disease 
Cardiomyopathy
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9
Q

What happens to the structure of the heart following myocardial infarction?

A

Part of the heart muscle will be weaker due to the formation of fibrous tissue, which leads to infarct expansion. The heart muscle will remodel and dilate in an attempt to maintain normal pumping activity.

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10
Q

What is cardiomyopathy? What are the main types?

A

Heart disease in the absence of a known cause. The muscle becomes enlarged, thickened and/or stiffened.
Dilated, Hypertrophic, Restrictive and Arrhythmic Right Ventricular Cardiomyopathy.

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11
Q

State some causes of dilated cardiomyopathy.

A
Congenital causes 
Idiopathic 
Infectious causes - HIV, rickettsia 
Toxins/Poisons - ethanol and cocaine 
Chemotherapeutic agents, antiviral agents
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12
Q

What is restrictive cardiomyopathy? State some causes.

A

The heart is unable to relax easily so the relaxation is very slow and there is diastolic dysfunction.
Causes: infiltrative disease e.g. sarcoidosis and amyloidosis
Storage disease - haemochromatosis and haemosiderosis

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13
Q

What is the commonest cause of death in heart failure?

A

Opportunistic arrhythmia

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14
Q

What is the hormonal response to heart failure?

A

Increased sympathetic firing - increase in noradrenaline and adrenaline (because your body thinks that it is bleeding to death)
RAS system is switched on - try to retain more sodium and water
Vasoconstrictors are produced by endothelial cells (e.g. endothelin-1)

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15
Q

What drugs are given to counteract these effect?

A

ACE inhibitors - block the RAS system
Beta blockers - MOST EFFECTIVE - they block the sympathetic drive
Aldosterone receptor antagonists (aldosterone receptors are high in heart failure)

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16
Q

Other than troponin I and T, what other hormone is elevated in heart failure?

A

Atrial Natriuretic Peptide

17
Q

What is a clear sign of heart failure in a chest X-ray?

A

Massively increased cardio: thoracic ratio

The widest part of the heart should be no more than 50% the width of the thorax

18
Q

What is the system used to classify heart failure patients based on functional capacity?

A

New York Heart Association Classification (PPQ!)
1 = barely any symptoms
4 = can’t get out of chair or in bed

19
Q

What are the different syndromes of heart failure and what symptoms are they associated with?

A

Pitting Oedema
Fluid accumulation leads to pitting effect when pushed

Raised JVP
Increased right-sided heart pressure backs up blood to jugular vein, causing it to bulge

Ascites
Fluid accumulation in PERITONEAL cavity

20
Q

What do you give immediately if someone has pulmonary oedema?

A

Diuretics - to get rid of the fluid (increase urinary output)

21
Q

State some common drugs used in heart failure.

A
ACE inhibitors 
Beta blockers 
Aldosterone antagonist - spironolactone 
Digoxin (for atrial fibrilation) 
Devices (cardiac resynchronisation, implanted cardioverter defibrillator)
22
Q

What is the mechanism for left and right heart failure?

A

Left heart failure:
Insufficient contractility  Blood backs up in lungs causing PULMONARY CONGESTION

Respiratory Symptoms: Breathlessness, Coughing, Wheezing
Dizziness
Cyanosis

Right heart failure:
PULMONARY HYPERTENSION  High afterload
Increased afterload of the pulmonary circulation (pulmonary hypertension), this increases afterload on the right ventricle which has to pump with a greater pressure to contract.
-Ventricles need to work harder, leads to cardiomyocytes cell death and so right hear failure
Often secondary to left heart failure.

23
Q

what is the difference between chronic HF and acute HF?

A

Chronic HF:
Slow onset.
Infection, pulmonary embolism, myocardial infarction or surgery.

Acute HF.
Rapid onset.
Symptoms similar to chronic HF, except the timing of onset is quicker and worsening is much more severe.

24
Q

What is the difference between HF with reduced and preserved ejection fraction?

A

Reduced:~ 32%

  • HF with reduced EF (HFrEF)
  • Abnormal systolic function, i.e. ventricle is unable to pump blood into the aorta, this could be due to dilated cardiomyopathy, or valve stenosis
  • Impaired contraction of the ventricles = increase in HR results in decreased cardiac output
  • Typically, weakness is caused by damage or destruction of the ventricular myocytes
  • Weaker ejection leads to higher diastolic pressures
  • causes left ventricular end systolic volume to increase, as more blood left.
  • Stroke volume decreases
  • ejection fraction decreases

Preserved:50%

  • HF with preserved EF (HFpEF)
  • Abnormal diastolic function
  • Normal contraction of the ventricle
  • Increased stiffness of ventricle, impaired relaxation or impaired filling, lower preload
  • Because EDV is inherently reduced, the stroke volume is also reduced so ejection function is preserved.
25
Q

What are the causes heart failure?

A
  1. Valve disease
    Hardening of valve reduces ventricular filling (AV) or ejection (semilunar), this then causes congestion in the lungs
    2.ischaemic Heart Disease (IHD)
    Narrowing of coronary arteries cause ischaemia in heart muscle.
    -Cardiomyocytes start to die, so heart has to work harder.
    3.Myocardial infarction
    Significant occlusion leads to death of heart muscle
    4.Hypertension
    Ventricles have to work harder to work against the force.
    Hypertension increases afterload which means ventricle must work harder
    CO decreases.
    5.Dilated cardiomyopathy
    Dilated LV reduces generatable pressures which reduces ejection, (blood is there but can’t eject it out)
    6.Hypertrophic cardiomyopathy
    Increased LV thickness reduces internal ventricular volume & impedes filling.
26
Q

What is positive inotropy of the heart?

A

When the heart beats harder.

27
Q

How can we categorise heart failure?

A
  1. Left vs right
  2. Chronic vs acute
  3. HR reduced EF vs HF preserved EF
28
Q

what is Dilated myopathy?

A

Wall is thinner, so less able to produce enough pressure to eject enough blood.

HEART failure

29
Q

At what age is heart failure most common?

A

Mainly from 60-84: most of the cases for heart failure.

30
Q

What is the most common cause of heart failure?

A

Coronary artery disease

31
Q

What are the clinical features of heart failure?

A

Patient

  • Exertional breathlessness
  • Fatigue
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Anorexia
  • Weight loss

Clinical:

  • Tachycardia
  • Reduced pulse volume
  • Pitting oedema
  • Increased JVP
  • Hepatomegaly
  • Ascites
32
Q

What investigations can you do to find out about heart failure?

A
  • X-ray
  • Echocardiogram
  • Ambulatory ECG
  • Exercise test
  • Angiogram
  • BNP
33
Q

What are the hallmark signs of heart failure?

A

Raised jugular venous pressure:
Increased pressure in right side of heart leads to pressures backing up into systemic veins, especially visible in jugular vein.
Pitting oedema:
Fluid accumulation in tissue (especially of lower extremities) leads to a pitting effect when physically depressed. The indentation is visible for a short period.
Ascites:
Fluid accumulation in peritoneal cavity

34
Q

What is Gold standard in diagnosing Heart Failure

A

BNP: B-type Natriuretic Peptide

Natriuresis is ‘sodium excretion’

  1. Released from ventricular myocytes in response to stretch.
    - Vasodilation of microvessels
    - Reduced aldosterone secretion
    - Reduced sodium reabsorption
    - Inhibits renin secretion

THEREFORE Reduced ECF—–> Reduced pressure

Greater than 100pg/ml (300pg/mL in people over age of 70) indicates heart failure

35
Q

what medications do we give?

A

ACE Inhibitor: blocks aldosterone production, so less sodium and water re-absorption.

Beta blocker: reduce heart rate
Diuretic: gets rid of excess fluid, so pressure goes down, afterload goes down e.g. spironolactone

36
Q

What is the Law of LaPlace?

A

Laplace’s Law: wall stress = Pressure x Radius/ 2 x Wall thickness.

In compensatory hypertrophy: the wall thickness increases, and the wall stress decreases but pooling of blood is decreased.

In Dilated cardiomyopathy: the wall thickness is dilated, so wall stress increase.

37
Q

What is the response to heart failure?

A

Positive Beneficial Physiological response:
-Natriuretic peptides, BNP released when ventricular myocytes/wall are stretching,
causes naturesis and diuresis release, so sodium and excretion, reducing the pressure, reducing the afterload.
which allows vasodilation, and lowers BP, it reduces aldosterone level.

Pathophysiological response:
Heart is beating less effectively, reduction in renal perfusion, this activates RAAS ( Renin angiotensin aldosterone system), this causes the rise in aldosterone production (aldosterone causes vasoconstriction, which will increase BP, sodium retention and water retention.

we don’t like the pathophysiological response for heart problems.
so when this balance balances thw wrong way it worsens heart problems.

38
Q

when is the ejection fraction reduced OR preserved?

A

Ejection fraction is reduced if the heart is unable to generate adequate force (HFrEF)
Ejection fraction is preserved if the heart is unable to fill adequately (HFpEF)

39
Q

What are the clinical features for right and left HF?

A

Left ventricular HF is majorly associated with breathlessness
Right ventricular HF is majorly associated with peripheral oedema