Heart Failure Flashcards

1
Q

Define heart failure

A
  • inability of the heart
  • to generate sufficient CO
  • to meet demands of body
  • without increased filling pressure
  • secondary to an underlying cause
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2
Q

Most common cause of HF

A

coronary artery disease

hypertension

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3
Q

Age group common HF

A

Over 70

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4
Q

Presentation of chronic HF

A
  • breathlessness with impaired exercise tolerance
  • slowly progressive
  • periods of acute decompensation
  • state of fluid retention and overload
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5
Q

Acute HF Presentation

A
  • flash pulmonary oedema
  • precipitating ischaemia, arrhythmia, intercurrent infection
  • OR gradual deterioration = fluid accumulates, exercise tolerance falls, orthopnoea, PND
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6
Q

Systolic HF alternative name

A

HFrEF

HF with mildly rEF

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7
Q

Severities of systolic HF

A
  • mild = 46-55% EF by Echo
  • moderate = 36-45%
  • severe = <35%
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8
Q

Diastolic HF alternative name

A

HFpEF

- stiffness of ventricular wall with impaired filling and reduced CO

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9
Q

Echo signs of diastolic HF

A
  • LVH
  • L atrial dilatation
  • abnormal relaxation
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10
Q

Right HF features

A
  • fluid overload

- secondary to L. heart disease, cor pulmonale, congenital heart disease, cardiomyopathy

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11
Q

Left HF Features

A

HFrEF

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12
Q

Low output HF

A
  • common
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13
Q

High Output HF

A
  • overworked heart

- physiological or pathophysiological

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14
Q

What does HF result in?

A
  • decreased SV and CO
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15
Q

What is the neurohormonal response to HF?

A
  • sympathetic system activated
  • RAAS system activated
  • both result in vasoconstriction and sodium and fluid retention
  • further stress of ventricular wall and dilatation (remodelling)
  • worsening ventricular function
  • further HF
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16
Q

Explain the RAAS mechanism?

A
  • liver, vessels and brain produce angiotensinogen
  • renin produced by JGA in kidney when blood flow to kidney is low
  • renin converts angiotensinogen to angiotensin I
  • ACE from lungs converts angiotensin I to II
  • angiotensin II = vasoconstriction and enhanced sympathetic activity as well as aldosterone release
  • aldosterone = salt and water retention
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17
Q

What does the sympathetic nervous system do?

A
  • RAAS
  • vasoconstriction
  • increased HR and contractility
  • direct cardiotoxicity
18
Q

What does direct cardiotoxicity result in?

A
  • myocyte damage
19
Q

What does increased HR and contractility result in?

A
  • increased myocardial oxygen demand = decreased contractility
20
Q

What does vasoconstriction and RAAS result in?

A
RAAS = fluid retention = increased wall stress = myocardial hypertrophy and decreased contractility as increased myocardial oxygen demand
Vasoconstriction = increased wall stress = myocardial hypertrophy and decreased contractility
21
Q

What does CO =?

A

SV x HR
HR increases via autonomic systemic
SV dependent on ventricular performance

22
Q

What is Starling’s Law of the heart?

A
  • contractile function depends on velocity of muscle contraction, load being moved and amount of stretch
  • pre-stretch improves relationship
23
Q

Main causes of HF?

A
  • IHD
  • Dilated cardiomyopathy
  • hypertensive heart disease
24
Q

Infectious causes of HF?

A

Viral mycoarditis

25
Q

Right HF causes

A

COPD

26
Q

Metabolic causes

A

Anaemia
Thyrotoxicosis
Haemochromatosis

27
Q

Arrhthmic causes

A

AF

bradycardia

28
Q

Drug causes of HF

A

EtOH

Chemo

29
Q

Other cardiac causes

A

Valvular heart disease

Primary heart muscle disease

30
Q

Symptoms

A
Breathlessness - on exertion or rest
Orthopnoea
PND
Tiredness and falling exercise tolerance
Peripheral oedema
Palpitations
Depression
Gout
31
Q

NYHA Classification of symptoms

A
1 = none
2= symptoms on exertion
3= symptoms on minimal exertion
4= symptoms at rest
32
Q

Signs

A
Raised JVP
3rd heart sound
pulmonary crepitations
hepatomegaly
peripheral or sacral oedema
cachexia
33
Q

Routine bloods

A
FBC
Iron studies
U&amp;E
Glucose
Cholesterol
LFTs
TFTs
BNP
Uric acid
Ferritin
CK
Immunoglobulins
Autoimmune profile
Viral titres
Genetics
34
Q

What diagnostic tests are done?

A

Routine bloods
ECG
CXR
Transthoracic echocardiography

Others = holter monitoring, lung function, cardiopulmonary exercise testing, cardiac catheterisation, perfusion imaging, cardiac MRI

35
Q

Management of acute pulmonary oedema

A
  • medical emergency
  • high flow oxygen
  • morphine and anti-emetic
  • IV GTN
  • furosemide if fluid overload
  • ECG monitor
  • ventilatory support
  • find cause
36
Q

Principles of chronic HF management

A
  • prevent decompensation
  • maintain or improve symptoms
  • increase longevity
37
Q

Types of management for chronic HF

A
  • drug therapy start low dose then uptitrate
  • device
  • surgical
  • exercise training through cardiac rehab
  • palliation
  • remove exacerbating factors
38
Q

Drugs used in HFrEF

A

1) Symptomatic = ACEi or ARB and Beta blocker
2) MR antagonist add
3) still symptomatic and LVEF <35% = ARNI replace ACEi/HR>70 = ivabradine
4) resistant symptoms = digoxin, heart transplant, LVAD

39
Q

Advanced Treatment

A

Implantable cardiac defibrillators
Cardiac Resynchronisation Therapy
LVAD
Extracorporeal Membrane Oxygenation

40
Q

Surgical Options

A

Valve Surgery
Revascularisation
Stem Cells
Heart Transplants