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Heart Failure Flashcards

1
Q

ventricular stroke volume is dependent on which three factors

A

preload
afterload
contractility

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2
Q

how is preload approximated

A

by measuring ventricular end-diastolic volume

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3
Q

what is preload

A

ventricular wall tension at the end of DIASTOLE

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4
Q

what is afterload

A

ventricular wall tension during SYSTOLE

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5
Q

how is afterload approximated

A

systolic arterial/ventricular pressure

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6
Q

what is ventricular end-systolic volume dependant on/

A

afterload and contractility but not preload

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7
Q

how is ventricular wall stress estimated and what is its relationship to wall thickness and chamber radius

A

Laplace’s relationship

wall tension is proportional to radius and inversely proportional to wall thickness

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8
Q

besides the side of heart failure, heart failure can be divided into two categories. Name them and briefly describe them

A

PRESERVED ejection fraction or DIASTOLIC dysfunction- abnormality in ventricular filling

REDUCED ejection fraction or SYSTOLIC dysfunction - an abnormality in ventricular filling from impaired contractility or increased afterload

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9
Q

name 5 conditions which impair ventricular filling

A

conditions which impair early diastolic relaxation (as this is an active process) or increase the stiffness of the ventricular wall

  1. left ventricular hypertrophy
  2. restrictive cardiomyopathy
  3. transient myocardial ischaemia
  4. myofibrosis
  5. pericardial constriction or tamponade
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10
Q

name three things which impair contractility of the ventricles

A

coronary artery disease (MI/transient ischaemia)
chronic volume overload (mitral or aortic regurg)
dilated cardiomyopathies

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11
Q

name two conditions which can increase afterload in heart failure

A

aortic stenosis

uncontrolled HTN

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12
Q

describe two conditions which are non-cardiac in origin which cause heart failure

A

inadequate perfusion (severe haemorrhage)

increased metabolic demand (hyperthyroid)

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13
Q

outline three pathophysiological processes which occur in cardiac muscle leading to decrease in contractility

A
  • change in gene expression (from adult to foetal)
  • less efficient energetics
  • impaired calcium handling (impair calcium release –> systolic dysfunction; impaired pumping of calcium outside of the cell impairs relaxation)
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14
Q

name three mechanisms of heart failure compensation

A

the Frank-Starling mechanism
neurohormonal adaptations
ventricular hypertrophy and remodelling

all of these mechanisms eventually become maladaptive

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15
Q

how does the Frank-Starling compensatory mechanism restore cardiac output

A

reduced stroke volume leads to incomplete ventricular emptying
on the next cardiac cycle this means the diastolic volume is increased.
This means that there is an increased stretch in the heart muscle and therefore increased contraction

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16
Q

which three neurohumoral alterations help compensate heart failure

A
  1. the adrenergic nervous system
  2. RAAS
  3. incr production of ADH
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17
Q

what are the three immediate effects from activation of the sympathetic nervous system in the context of heart failure compensation

A

increased contractility
increased heart rate
increased vasoconstriction (via alpha receptors in arteries and veins)

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18
Q

how does venous vasoconstriction increase cardiac output

A

it increases the venous return to the heart (increasing preload) which leads to increased stroke volume

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19
Q

what are the stimuli for renin release from the juxtaglomerular cells in the kidney in heart failure patients

A

1) decreased renal perfusion following reduced CO
2) decreased salt delivery to macula densa
3) direct stimulation of beta-2 receptors in juxtaglomerular apparatus via the sympathetic nervous system

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20
Q

name two ways angiotensin II increases the intravascular volume

A

1) at the hypothalamus it stimulates thirst

2) increases aldosterone secretion at the adrenal cortex

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21
Q

when is BNP released

A

it is not normally detected but is released when the ventricular myocardium undergoes haemodynamic stress

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22
Q

what is endothelin-1 and what is its significance in heart failure

A

a potent vasoconstrictor from endothelial cells

in heart failure endothelin-1 levels correlate with adverse outcomes

23
Q

how does chronic volume overload alter the ventricular musculature

A

it results in ECCENTRIC hypertrophy - addition of new sarcomeres in series

this impairs filling as the wall become stiffer

24
Q

how does chronic pressure overload alter the ventricular musculature

A

it results in CONCENTRIC hypertrophy - addition of new sarcomeres in parallel

this alters the wall tension owing the Laplaces law as the ventricle becomes thicker

25
Q

what causes constant fatigue in heart failure

A

mishandling of calcium in skeletal muscle

26
Q

list some factors which precipitate symptoms in patients with chronic compensated heart failure

A

increased metabolic demand (fever, infection, anaemia, tachycardia, hyperthyroidism, pregnancy)

increased circulating volume (XS Na, XS fluid administration, renal failure)

Increased afterload (HTN, AS, PE)

impaired contractility (negative ionotropic medications, MI, ethanol ingestion)

medication non-compliance

Bradycardia

27
Q

list some of the symptoms of left sided heart failure

A

dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
fatigue

28
Q

list some of the symptoms of right sided heart failure

A

peripheral oedema

RUQ discomfort from hepatomegaly

29
Q

how might aortic regurg develop in heart failure

A

from cardiomegaly distorting the valve orifice but the valve leaflets remain unchanged

30
Q

what is the first symptom of pulmonary oedema

A

paroxysmal nocturnal dyspnoea- respiratory chemoreceptors are less responsive during sleep

31
Q

at which pulmonary pressure can transudation of fluid into the pulmonary interstitium occur

A

20mmHg

32
Q

what is PND

A

severe breathlessness which awakens the patietn from sleep 2-3 hours after going to bed

33
Q

how does haemoptysis occur in heart failure

A

from engorged bronchial veins

34
Q

what causes anorexia in heart failure

A

oedema in the gastrointestinal tract

35
Q

what are the clinical signs of left sided heart failure

A 
diaphoresis (sweating)
tachycardia and tachypnoea
pulmonary rales
loud P2
S3/4 gallop
36
Q

which gallop rhythm is associated with systolic dysfunction

A

S3 gallop (early diastolic sound) caused by abnormal filling of a dilated chamber

37
Q

which gallop rhythm is associated with diastolic dysfunction

A

S4 gallop (late diastolic sound) cuased by forceful atrial contraction into a stiff ventricle

38
Q

which type of diuertic would be used immediately in acute heart failure

A

loop as they have a strong effect and quicker onset

they work by inhibiting reabsorption from the loop of Henle

39
Q

how do thiazide diuretics work

A

inhibit Na reabsorption in the DCT

40
Q

what are the side effects of thiazide (and related diuretics)

A

electrolyte disturbance (decr Na and K)
Gout (incr urate)
Hyperglycaemia
Derranged lipids

41
Q

how does nitroglycerine work in the treatment of acute heart failure

A

reduces preload, afterload and increases stroke volume

42
Q

what are the commonest causes of heart failure

A

IHD
HTN
valve disease
Cardiomyopathy

43
Q

what is cardiac cachexia

A

weightloss and anorexia commonly seen in HF

Caused by metabolic changes, gut congestion, reduced intake, inflammation

is a predictor of survival

44
Q

which heart sound is pathognomonic of heart failure

A

gallop rhythm

45
Q

What is Osler-Weber-Rendu disease also known as and what does it cause

A

hereditary haemorrhagic telangiectasia

there is vascular dysplasia and AVMs in the lungs liver and CNS

46
Q

what are the main differential diagnoses for heart failure

A

liver disease

nephrotic syndrome

47
Q

what is Eisenmenger’s syndrome

A

left to right shunt causing pulmonary hypertension leading to a cyanotic heart defect

48
Q

which two drugs used in the treatment of heart failure can cause gynaecomastia

A

spironolactone

digoxin

49
Q

which is the only ACEI used in paediatric cardiology

A

Captopril

50
Q

which protein is lacking in hereditary angioedema and why is this relevant to heart failure

A

C1esterase inhibitor is lacking

can’t tolerate ACEI or ARBs

51
Q

Kerley’s B lines are a specific sign of what

A

pulmonary oedema

can be caused by anything causing lymphatic obstruction eg sarcoidosis

52
Q

what is the bat wing appearance

A

a sign of pulmonary oedema on CXR

53
Q

would what a giant v-wave on jugular venous pressure be suggestive of

A

tricuspid regurgitation

54
Q

what would cannon a-waves in a jugular venous pressure be suggestive of

A

complete heart block

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