Heart Failure Flashcards

notes

1
Q

Define heart failure

A

clinical syndrome caused by the inability of the heart to supply sufficient blood flow to meet the body’s needs

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2
Q

Classification of heart failure?

A
Reduced EF (Ejection Fraction) or Preserved EF (HFrEF, HFmrEF, HFpEF)
Acute or Chronic heart failure
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3
Q

Describe the NYHA Functional Class

A

4 : breathless at rest

1 : heart muscle damaged/abnormal but no symptoms

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4
Q

Describe heart failure epidemiology

A
  • Prevalence 1-2% (6-10% in >65yo)
  • In 2030 50% increase due to increasing prevalence rather than increasing incidence
  • Commonest cause for emergency admission >65y
  • 2% total NHS health care costs
  • 70% of cost = hospital admissions
  • Quality of life affected most
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5
Q

Prevalence in over 85?

A

1/7

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6
Q

Compensatory mechanisms of failing heart?

A
Ventricular dilatation
Increased myocardial contractility
Myocardial hypertrophy
Sympathetic stimulation
Renin-Angiotensin-Aldosterone-System (RAAS)
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7
Q

What’s the Frank-Starling Law?

A

-increased filling of the ventricle
-increased force of contraction
SV α LVEDV (left ventricular ejection end diastolic volume)

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8
Q

How does heart failure affect the Frank-Starling Law?

A

ventricle is over-stretched reducing ability to cross-link actin + myosin filaments.

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9
Q

Long term effects of compensatory mechanisms?

A
Continuous sympathetic activation
Increased HR
Increased preload
Increased TPR
Continuous neurohumoral activation
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10
Q

Describe the effect of continuous sympathetic activation

A

β-adrenergic downregulation + desensitization (less inotropic response)

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11
Q

Describe the effect of increased HR

A

Increased metabolic demands+myocardial cell death

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12
Q

Describe the effect of increased preload

A

Beyond limits of Starling’s law, pressure is transmitted to pulmonary vasculature –> pulmonary oedema

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13
Q

Describe the effect of increased TPR

A

Higher afterload –> decreased SV + CO

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14
Q

Describe the effect of continuous neurohumoral activation

A
  • chronically elevated Ang II + aldosterone
  • production of cytokines
  • stimulate macrophages + fibroblasts
  • myocardial remodelling
  • loss of contractility
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15
Q

Equation of CO?

A

CO = SV x HR

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16
Q

Effect of ventricular dilation?

A
  • maintains SV but exhausted
  • pressure in stretched ventricle steadily increases
  • restriction to filling + increased venous pressures
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17
Q

Why was β-blocker last option for HF?

A

negatively iontropic so reduce contractility of muscle but decreases afterload

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18
Q

Effect of increased sympathetic drive?

A
  • decreased CO detected by baroreceptors
  • central + peripheral chemoreflex activation induce A, NA, VP release
  • adrenergic activation increases HR + contractility via vasoconstriction
  • increased afterload
  • increased cardiac work
  • myocyte damage
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19
Q

Effect of β-blocker?

A

decrease BP, afterload, HR, contractility

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20
Q

Effect of renin-angiotensin cctivation?

A

-decreased CO
-renin-angiotensin activation:
vaoconstriction increases afterload
Na + H2O retention increases preload
-increases cardiac work
-myocyte damage via myocyte fibrosis, + eccentric ventricular hypertrophy

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21
Q

What are ACE inhibitors+ARBs?

A

angiotensin converting enzyme inhibitors

angiotensin-receptor blockers

22
Q

Effect of ACE + ARBs?

A

decrease Na + H2O retention which by decreasing:

systemic vascular resistance (SVR), afterload venous p, preload

23
Q

Effect of ACE + ARBs?

A

decrease Na + H2O retention by decreasing:

systemic vascular resistance (SVR), afterload venous p, preload

24
Q

Clinical signs of HF?

A
Peripheral oedema (right HF)
Pulmonary oedema (left HF)
Congestive Cardiac Failure (left + secondary right ventricular failure)
25
Q

Mechanical causes of pump failure?

A
Impaired ventricular function
Pressure overload of ventricle
Inflow obstruction of ventricle
Valvular disease 
Volume overload of ventricle
26
Q

eg of impaired ventricular function?

A

Myocardial infarction or cardiomyopathy

27
Q

eg of pressure overload of ventricle?

A

Systemic or pulmonary hypertension

28
Q

eg inflow obstruction of ventricle?

A

Restrictive cardiomyopathy
Diastolic heart failure
Mitral stenosis

29
Q

eg of valvular disease?

A

Aortic, Mitral or Tricuspid stenosis/regurgitation

30
Q

eg of volume overload of ventricle?

A

Ventricular + Atrial Septal defect (VSD + ASD)

31
Q

What’s right ventricular failure?

A
  • back pressure in RA
  • pressure in SVC + IVC
  • increases JVP
  • causes oedema, right and left pleural effusion, ascites (swelling in abdomen)
32
Q

What’s left ventricular failure?

A
  • back pressure into LA

- pulmonary veins causes pulmonary oedema (leak of fluid into alveoli)

33
Q

Symptoms of left ventricular failure?

A

Dyspnoea (Shortness Of Breath)
Orthopnoea (SOB lying flat)
Paroxysmal nocturnal dyspnoea (Sudden SOB at night)

34
Q

Signs of left ventricular failure?

A

Pulmonary oedema

35
Q

Associated features of HF?

A

Renal dysfunction – low perfusion + high venous pressure
Iron def – changes in iron handing
Gout
Cardiac cachexia – skeletal muscle wasting, neurohormonal + immunologically mediated

36
Q

Causes of left ventricular dysfunction?

A

CHD, hypertension

37
Q

Primary diagnosis of HF?

A
ischaemic heart disease
dilated cardiomyopathy
valvular heart disease
HF w preserved ejection fraction
hypertensive cardiomyopathy
tachycardia cardiomyopathy
pul hypertension
cardiac amyloidosis
38
Q

Causes of heart failure with preserved ejection fraction (HFpEF) EF>50% ?

A

Aging heart
Hypertension
Secondary hypertension:
Restrictive/Obliterative cardiomyopathy

39
Q

Causes of heart failure with preserved ejection fraction (HFpEF) EF>50% ?

A

Aging heart
Hypertension
Secondary hypertension
Restrictive/Obliterative cardiomyopathy

40
Q

What’s essential hypertension?

A

85%

41
Q

What’s secondary hypertension?

A

Pre-eclampsia, glomerulonephritis, pheochromocytoma, Conn’s syndrome, Acromegaly,
Drugs –steroids, sympathomimetics

42
Q

What’s restrictive/obliterative cardiomyopathy?

A
PRIME
Primary: Idiopathic
Radiation
Infiltrative: Amyloidosis, Sarcoidosis
Metabolic: Glycogen storage disease, Fabry’s disease
Endomyocardial fibrosis
43
Q

Why’s there re-classification of HFpEF?

A

No treatment yet proven to convincingly reduce morbidity or mortality
Often highly symptomatic, poor QOL
Heterogenous pathophysiology.

44
Q

Clinical diagnosis of HF?

A

GPs correctly diagnose heart failure about 35% of the time + diagnosis is correct in about 70% of hospital admissions

45
Q

What’s NTproBNP?

A

biomarker
BNP = Brain Natriuretic Peptide
released from heart muscle when it’s strained

46
Q

What’s the diagnostic algorithm?

A

-suspect HF
-test for BNP:
normal = test for other causes of breathlessness
elevated = echo to confirm

47
Q

Importance of NTproBNP when diagnosing HF?

A

Sensitive BUT not specific because raised in atrial fibrillation + hypertension
Prognostic importance
Diff cut-offs in acute + chronic HF

48
Q

Importance of echocardiography when diagnosing HF?

A

-Confirm diagnosis
-Points to aetiology of:
Ischaemic CM
Valvular CM
Hypertensive CM
Tachycardiomyopathy
Infiltration

49
Q

Why diagnose HF?

A

Prognosis

Treat underlying cause

50
Q

What’s Left Bundle Branch Block (LBBB)?

A

RV contracts before LV
30% with severe HF
Progresses over time

51
Q

What’s biventricular pacemaker

A

RA lead
LV lead
RVA lead - thread backwards via coronary sinus onto LV which paces both ventricles simultaneously
treats LBBB

52
Q

Other options for HF?

A

Cardiac resynchronisation therapy
Heart transplant
Left ventricular assist devices
Palliative care