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CVS > Heart failure > Flashcards

Heart failure Flashcards

1
Q

Cardiac Output meaning

A

Volume of blood leaving EITHER side of the heart per minute

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2
Q

Heart failure

Measured by?

A

Inability of the heart to keep up with demand= inadequate perfusion of organs (e.g. brain, liver, kidneys)= congestion in lungs and legs and

Measured by:
Inadequate Cardiac Output
Which is dependent on SV x HR
SV is dependent on preload, afterload, contractility (CVS Mechanics)

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3
Q

Normal ejection fraction

A 
>= 55%
45-54= mildly reduced
30-44%= moderately reduced
<30%= severely reduced
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4
Q

How to measure ejection fraction?

A 
Transthoracic echocardiogram (echo)
Ultrasound of chest
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5
Q

Features of poor heart function

A

On echo, dialated cardiomyopathy, wall is thinner= ventricle is less able to produce enough pressure to push blood out

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6
Q

Types of heart failure

A

Left vs. right
Chronic vs. acute
HFrEF (Heart failure with reduced ejection fraction) vs. HFpEF (Heart failure with preserved ejection fraction)

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7
Q

Left vs. right heart failure

A

Left:
Dysfunction associated with the left ventricle
Ejection or filling issue
Blood backs up into the lungs causing congestion
Breathlessness, couging , wheezing - increased pressure in lungs= pulmonary hypertension= increased hydrostatic pressure
Also dizziness and cyanosis

Right:
Dysfunction associated with the right ventricle
Ejection or filling issue
Increased afterload of the pulmonary circulation (pulmonary hypertension)- congestion increases the afterload on RV- has to pump against a greater pressure to push the blood out= cardiac myocytes require more oxygen but they don’t have that-= cell death= heart failure
Often secondary to left heart failure

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8
Q

Acute vs Chronic heart failure

A

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

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

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9
Q

HFrEF vs HFpEF heart failure

Calculation of EF with both?

A

HF with reduced EF (HFrEF):
Abnormal systolic function-ventricle unable to push blood into aorta (for LV) could be due to dialated cardiac myopathy (ventricle is much thinner), aortic stenosis (valve problem)
Impaired contraction of the ventricles which despite an 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

HF with preserved EF (HFpEF):
Abnormal diastolic function
Normal contraction of the ventricle (but the issue is a filling issue)
Increased stiffness of ventricle= impaired relaxation or impaired filling
Because EDV is inherently reduced, the reduced stroke volume is masked when looking at ejection fraction

HFrEF: EDV= normal, SV= reduced, EF= low
HFpEF: EDV is already reduced, so SV= reduced (less blood there in the first place), so EF= higher than HFrEF

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10
Q

Causes of heart failure

A
  1. Valve disease
    Hardening of valve reduces ventricular filling (AV) or ejection (semilunar)
    Mitral/ tricuspid valves issue= ventricles unable to fill up with blood (diastolic problem) OR Aortic/ pulmonary valves= ventricles unable to squeeze blood out/ eject (systolic problem)= congestion in lungs/ legs
  2. IHD
    Narrowing of coronary arteries cause ischaemia in heart muscle
    Iscahemic heart disease, less O2 to cardiac myocytes= cell death= less of the heart has to perform the same function= needs more o2 etc (cycle)
  3. Myocardial infarction
    Significant occlusion leads to death of heart muscle
    Leads to same effect as IHD
  4. Hypertension
    Hypertension increases afterload which means ventricle must work harder
    Ventricles have to work against a greater force= increased afterload= ventricular hypertrophy which always happens inwards= less space for the blood to pool in the ventricles in diastole= decreased cardiac output because less blood ejected round the body
  5. Dilated cardiomyopathy
    Dilated LV reduces generatable pressures which reduces ejection
    Wall of ventricle is thinner= ventricle isn’t able to create as much force to push the blood out (systolic dysfunction)
  6. Hypertrophic cardiomyopathy
    Increased LV thickness reduces internal ventricular volume & impedes filling
    Similar to hypertension, (diastolic dysfunction)
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11
Q

Clinical features of heart failure

A

Breathlessness: orthopnoea (SOB when lying), fatigue, poroxysmal nocturnal dyspnoea (falls asleep+ wakes up feeling out of breath)
Anorexia
Weight Loss
Pitting oedema
Fluid accumulation: increased JVP (jugular venous pressure), ascites, pitting oedema
Reduced pulse volume
Tachycardia

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12
Q

Fluid accumulation implications to heart failure

A

Raised jugular venous pressure:
Increased pressure in right side of heart (RA) leads to pressures backing up into systemic veins, especially visible in jugular vein.

Pitting oedema
Fluid accumulation in tissue (especially of lower extremities). fluid backs up into superior vena cava= raised hydrostatic pressure= leaks into tissue= pitting effect when physically depressed. The indentation is visible for a short period.

Ascites
Fluid accumulation in peritoneal cavity

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13
Q

Investigations of heart failure

A 
X ray
Echo
ECG
Angiogram
BNP- B-type natriuretic peptide
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14
Q

Natriuresis meaning

A

‘Na excretion’

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15
Q

BNP
released from?
Effect of BNP?
What range is suggestive of heart failure?

A

Released from ventricular myocytes in response to stretch

1) Vasodilation of microvessels
2) Reduced aldosterone section= Reduced sodium reabsorption
3) Inhibits renin secretion
1+ 2+ 3= Reduced ECF= Reduced blood pressure= decreased afterload for ventricles
BNP > 100 pg/mL (<70y) or >300 (>70y) suggestive of heart failure

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16
Q

Medication to initiate

A

1) ACE inhibitor (reduce Aldosterone production) OR Beta blocker (bisoprolol or carvedilol;
NOT atenolol or metoprolol) (slow the heart down and require less O2 and energy)
2) As EF<35% if still symptomatic, Diuretics get rid of the excess fluid= less pressure= less afterload, e.g. spironolactone or eplerenone
If still symptomatic,
3) Ivabradine if
HR >70 bpm in SR, causes vasodilation
4) ARNI: Sacubitril (inhibits an enzyme that breaks down BNP) in conjuction with valsartan (Angiotensin receptor blocker (ARB)= prevents aldosterone production)
if ACE I tolerated well
5) Consider CRT if
QRS >130ms and LBBB or QRS >150 and RBBB (cardiac resynchronization therapies= helps the ventricles beat more efficiently in synchronization)

17
Q

General action of
Duretics
ACE inhibitors
Beta blockers

A

Diuretics and ACE inhibitors reduce the load

Beta-blockers reduce the speed, which saves energy and makes it easier

18
Q

Non-pharmalogical treatment of heart failure

A

Fluid control:
Haemofiltration
Oeriotneal dialysis
Haemodialysis

Devices:
Intra-aortic balloon pumping
Resynchronisation
VAD/ Total artificial heart

Surgical:
Coronary artery bypass graft
Valve surgery
Transplantation

19
Q

Primary target of heart failure therapy

A

Reduce LV stress
Law of LaPlace:
Wall stress= (Pressure x Volume)/ LV Mass
Pressure x Volume= Wall stress

20
Q

Compensatory hypertrophy

A

wall thickness has increased so wall stress has gone down but there is less space for blood to pool

21
Q

Dilated cardiomyopathy

A

wall thickness decrease= increased wall stress, ventricles can’t contract as much

22
Q

Neural+ hormonal changes in heart failure

Diagram (slide 30+ 31, lecture 19)

A

Natiuretic peptides= BNP
Beneficial physiological response:
BNP released when the ventricular myocytes are stretched= allows vasodiaation= lowers BP= reduces aldosterone= positive response

Pathophysiological response:
Because heart is beating less effectively, less renal perfusion= activates RAAS= rise in aldosterone= bad because causes vasoconstriction+ increased BP+ sodium retention= water retention

Need balance between the two

23
Q

NYHA classification of heart failure

A

Classes 1 to 4 (4= worst)

Based on patients physical limitations

CVS (10 decks)

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