heart failure Flashcards

1
Q

what is definition of heart failure?

A

insufficient cardiac output to meet body’s requirements despite adequate filling pressures
leads to decreased organ perfusion

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2
Q

what classification is used to describe heart failure?

A

New York Heart Association - 5 classes

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3
Q

what are the 5 classes of NYHA for heart failure?

A

class 1- no limitation to physical activity
class 2- slight limitation of activity - dyspnoea + fatigue w moderate activity (climbing stairs)
class 3- marked limitation of activity + dyspnoea with minimal activity
class 4- severe limitation of activity + symptoms at rest
class 5- bed confinement

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4
Q

what system is used to diagnose chronic cardiac failure?

A

framingham criteria- 2 major criteria + 2 minor

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5
Q

what investigations would you do for heart failure?

A

bedside- ECG
bloods- FBC UE BNP TFT glucose lipids
imaging- CXR, ECHO

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6
Q

what is the general management of chronic heart failure?

A

primary/secondary cardiovascular risk
- stop smoking, decrease salt intake, optimise weight
- aspirin, statins, cardio rehab

treat precipitants/cause
- underlying cause- valve disease, arrhythmias, ischaemia
- exacerbating factors- anaemia infection, high BP

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7
Q

what is first line medical management of chronic heart failure?

A

ACE-I + beta blocker + loop diuretic

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8
Q

what is second line medical management of chronic heart failure?

A

get specialist advice

spironolactone/eplerenone

ACE-i and ARB

vasodilators- hydralazine + ISDN

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9
Q

what is third line medical management in chronic heart failure?

A

digoxin
cardiac resynchronisation therapy +/- ICD

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10
Q

what are invasive therapies you can consider for chronic heart failure?

A

cardiac resynchronisation +/- ICD
intra-aortic balloon counterpulsaiton
LVAD- left ventricular assist device- helps pump
heart transplant

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11
Q

how to treat acute pulmonary oedema?

A

PODMAN
P- position- sit up
O- oxygen
D- diuretic
M- morphine + anti-emetic
A-
N- nitrate- if SBP>100- IV nitrate (ISMN 2-10mg IV) or GTN 2 puffs or 2x300ug tabs SL unless sbp<90. if SBP<100 treat as cardiogenic shock + consider inotropes

if worsens- consider CPAP, nitrate infusion, haemodialysis

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12
Q

what are the causes of severe pulmonary oedema?

A

cardiogenic- MI, arrythmia, fluid overload (renal, iatrogenic)

non-cardiogenic- ARDS (sepsis, post-op, trauma), upper airway obstruction, neurogenic (HI)

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13
Q

what are clinical signs of severe pulmonary oedema?

A

distressed, sweaty, cyanosed
tachycardic, tachypnoeic
raised JVP
S3/Gallop Rythm
bibasal creps
pleural effusion
wheeze- cardiac asthma

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14
Q

how does morphine help in pulmonary oedema?

A

pulmonary venodilators -> decrease preload -> optimise position on starling curve

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15
Q

what blood tests would you do in severe pulmonary oedema?

A

FBC UE troponin BNP ABG

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16
Q

how would you treat cardiogenic shock?

A

oxygen
morphine/anti-emetic
consider need for dobutamine
treat underlying cause
bloods- FBC UE ABG troponin

17
Q

what is cardiogenic shock?

A

inadequate tissue perfusion primarily due to cardiac dysfunction

18
Q

what are the causes of cardiogenic shock?

A

MI HEART
MI
hyperkaelaemia
endocarditis- valve destruction
aortic dissection
rhythm disturbance
tamponade

obstructive- tension pnthx, massive PE

19
Q

what are the causes of cardiac tamponade?

A

trauma
lung/breast ca
pericardiits
MI
bacteria eg TB

20
Q

what are the signs fo tamponade?

A

becks triad- low bp, raised jvp, muffled heart sounds
kussmaul’s sign- raised JVP on inspiration
pulsus paradoxus- pulse fades on inspiration

21
Q

what is the management of cardiac tamponade?

A

pericardiocentesis - under ECHO guidance

22
Q

what are the 3 compensatory mechanisms of heart failure?

A

franks-starling law/mechanism
myocardial hypertrophy
neurohormonal system

23
Q

how does the frank-starling mechanism compensate in heart failure?

A

increased preload -> increased stroke vol

incomplete chamber emptying -> increased preload -> increases CO by increasing SV

detremental in long-term - severe HF, frank-starling curve is flatter than normal, so even large increase in end-diastolic vol has little effect on SV/CO.

increased ventricular end diastolic vol -> increased atrial pressure -> increased pulmonary pressure

24
Q

how does myocardial hypertrophy compensate in heart failure?

A

increased ventricular mass = cell hypertrophy (size) + hyperplasia (numbers)

  1. pressure overloaded hypertrophy
    if CO is due to higher afterload/higher arterial pressure
    concentric hypertrophy- muscle thickens due to synthesis of sarcomeres in parallel -> decreased compliance -> increased end systolic vol-> increased atrial pressure -> increased pulmonary pressure
  2. volume overloaded hypertrophy
    increased end diastolic vol -> ventricle stretches/dilates -> cannot generate enough force to pump blood

eccentric hypertrophy- heart balloons out due to synthesis of sarcomeres in series

25
Q

how does neurohormonal system compensate in heart failure?

A
  1. nor-adrenaline
  2. atrial natriuretic peptide
  3. RAAS
26
Q

how does noradrenaline release by neurohormonal system help in heart failure?

A

baroreceptors sense decreased CO as decreased perfusion-pressure so stimulates sympathetic NS

  • HR
  • Contractility
  • vessel tone-> increased venous return
  • preload (so more SV, more CO)
27
Q

how does atrial natriuretic peptide release by neurohormonal system help in heart failure?

A

released due to high filling pressures within heart via L-atrial + arterial barorecptors

  • reduces fluid retention ie diuretic
  • vasorelaxation
  • lowers BP
  • increases renal extretion (Na+water)
    so inhibits RAAS
28
Q

how does RAAS by neurohormonal system help in heart failure?

A

Due to ↓Renal Perfusion-Pressure → Stimulates Renin Secretion from Juxtaglomerular Cells.

  • →Vasoconstriction (Angiotensin-II = Potent Vasoconstrictor)
  • →↑Fluid Retention (Increases Intravascular Volume)
  • →↑Blood Pressure
  • →↑Preload (→SV →CO)
29
Q

why are these compensatory mechanisms bad for the heart?

A

heart responds by remodelling, leads to ventricular dysfunction and gets weaker