PBL 1 Flashcards

1
Q

what is heart failure?

A

a clinical syndrome that results when the heart is unable to provide sufficient blood flow to meet metabolic requirements or accommodate systemic venous return.

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2
Q

what are the compensatory mechanisms that occur as the failing heart attempts to maintain adequate function?

A

increasing cardiac output via the Frank-Starling mechanism, increasing ventricular volume and wall thickness through ventricular remodelling, and maintaining tissue perfusion with augmented mean arterial pressure through activation of neurohormonal systems. Although initially beneficial in the early stages of heart failure, all of these compensatory mechanisms eventually lead to a vicious cycle of worsening heart failure.

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3
Q

outline the pathophysiology of heart failure in the long term?

A

left ventricular pump failre leads to a fall in bp which activates the sympathetic system = vasoconstriction and an increase in afterload which increases bp
this drop in bp also decreases renal perfusion so RAAS is activated and this leads to Na+ and H2O retention, increasing preload and restoring renal perfusion

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4
Q

how do we diagnose heart failure?

A

blood test - B type natriuretic peptide
echocardiogram
xray

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5
Q

why do we do an echocardiogram to diagnose heart failure?

A

to estimate ejection fraction, measure ventricular wall and chamber size, assess heart valves and pulmonary arterial pressures

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6
Q

what would we see in an xray of heart failure?

A
cardiomegaly
pleural effusions
kerley b lines
upper lobe pulmonary venous congestion
interstitial oedema
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7
Q

what are causes of heart failure?

A
ischaemic heart disease
hypertension
diabetes
cardiomyopathies
valvular disease
arrhythmias
myocarditis
congenital heart disease
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8
Q

why can hypertension cause heart failure?

A

the increased pressure causes left ventricular hypertrophy which increases oxygen demands. This hypertrophy also causes squashing of coronary arteries which reduces the supply.
On top of this the hypertrophy reduces room for diastolic filling

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9
Q

how does dilated cardiomyoapthy lead to heart failure?

A

heart chambers dilate in an attempy to fill ventricles wth larger volumes of blood but overtime the walls weaken

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10
Q

what are the symptoms of heart failure?

A
dyspnoea
orthopnoea
paroxysmal noctural dyspnoea
fatigue
pitting oedema
tachycardia
cough/wheeze
ascites
loss of appetite
confusion
weight gain or loss
dizziness
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11
Q

why does heart failure cause orthopnoea?

A

as gravity isnt impairing venous return any more

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12
Q

what are risk factors for heart failure?

A
coronary artery disease
MI
heart valve disease
RA
hypertension
arrythmias
congenital heart diseases
diabetes
alcohol use
sleep apnoea
smoking
obesity
viruses
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13
Q

what are the types of heart failure?

A
systolic
diastolic
left
right
biventricular
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14
Q

what is systolic heart failure?

A

heart failure with reduced ejection fraction
left ventricles loses ability to contract normally so the heart cannot pump with enough force to push enough blood into the circulation

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15
Q

what is diastolic heart failure?

A

heart failure with preserved ejection fraction

left ventricle loses ability to relax normally so it cannot totally fill during diastole

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16
Q

which symptoms/signs are more closely associated with right sided heart failure?

A

raised JVP
hepatoegaly
ascites
pitting oedema

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17
Q

what is the Frank-Starling relationship?

A

the force or tension developed in a miscle fibre dependant on the extent to which the fibre is stretched

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18
Q

how do you calculate cardiac output?

A

stroke volume x heart rate

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19
Q

how do you calculate ejection fraction?

A

stroke volume / total volume

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20
Q

what is considered a normal ejection fraction? what is sugestive of systolic heart failure?

A

50-70% norm

<40% HF

21
Q

why does diastolic heart failure have a normal ejection fraction?

A

as stroke volume and total volume will be low

22
Q

how do we classify heart failure

A

with the New York Heart Association classification

class 1 = symptoms with extreme exertion
class 2 = symptoms with moderate exertion
class 3 = symptoms with mild exertion
class 4 = symptoms at rest
23
Q

what do we give first line for heart failure?

A

ACEi or beta blocker (ARB if ACEi not tolerated)

24
Q

what can you give in heart failure to reduce symptoms?

A

diuretics

25
Q

what do you give in heart failure if symptoms persists after ACEi, beta blocker and diuretics?

A
aldosterone antagonist 
hydralazine hydrochlorides with nitrate
amiodarone hydrochloride
digoxin
ivabradine
26
Q

why should calcium channel blockers be avoided in heart failure?

A

as they reduce cardiac contractility

27
Q

what are the 2 aspects we need to control in AF management?

A

rate and rhythm

28
Q

how do we control rate in AF?

A

beta blockers or a rate-limiting Ca2+ channel blocker

digoxin may be offered if these options are not suitable

29
Q

what scale is used to classify anti-arrythmic drugs?

A

Vaghaun Williams scale

30
Q

whats the MOA of class 1 anti-arrhythmias?

A

Na+ channel blockers

31
Q

whats the MOA of class 2 anti-arrythmics?

A

beta blockers

32
Q

whats the MOA of class 3 antiarrhythmics?

A

K+ channel blocker

33
Q

whats the MOA of class 4 anti arrythmics?

A

Ca2+ channel blockers

34
Q

what are examples of class 1a antiarrhythmics?

A

quinidine

procainamide

35
Q

what are examples of class 1b antiarrhythmics?

A

lidocaine

phenytoin

36
Q

what are examples of class 1c antiarrythmics?

A

flecainide

propafenone

37
Q

what are examples of classs 2 anti arrhythmics?

A

propanolol

metoprolol

38
Q

what are examples of class 3 anti arrhythmics?

A

amiodarone

sotalol

39
Q

what are examples of class 4 antiarrhythmics?

A

verapamil

diltiazem

40
Q

what are examples of class 5 anti-arrhythmic drugs?

A

digoxin
adenosine
megnesium sulphate
atropine

41
Q

whats the moa of digoxin?

A

inhibits Na+/K+ leading to a build up of Na+ intracellularly. This is then exchanged with Ca2+. An increase in Ca2+ within the cells increase contractility

42
Q

whats the moa of adenosine?

A

binds to A1 receptors which lets. an influx of K+ = hyperpolarisation

43
Q

whats the moa of magnesium sulphate?

A

competitively blocking intracellular calcium channels, decreasing calcium availability and thus inhibiting smooth muscle contractility.

44
Q

whats the moa of atropine?

A

competitiely inhibits ACh

45
Q

what are the 4 systolic murmurs?

A

aortic stensois
pulmonary stenosis
mitral regurgitation
tricuspid regurgitation

46
Q

what are the 4 diastolic murmurs?

A

mitral stensosi
tricuspid stenosis
aortic regurgitation
pulmonary regurgitation

47
Q

when are systolic murmurs heard?

A

between S1 and S2

48
Q

when are diastolic murmurs heard?

A

between S2 and S1 of the next cycle

49
Q

what are continuous murmurs and what are they usually caused by?

A

murmurs heard through systole and diastole that are usualy caused by patent ductus arteriosus