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Block 31 Cardio-respiratory > heart failure diagnosis, investigation and management > Flashcards

heart failure diagnosis, investigation and management Flashcards

1
Q

what is the commonest cause of heart failure in the west?

A

coronary artery disease

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2
Q

how does heart failure affect the heart?

A

impairs the ability of the heart to function as a pump to support physiological circulation

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3
Q

describe the pathophysiology of heart failure?

A
  • changes to heart and peripheral vascular system due to haemodynamic changes associated with heart failure
  • these are compensatory to maintain cardiac output and peripheral perfusion
  • as disease progresses the mechanisms are overwhelmed and become pathophysiological
  • development of pathological peripheral vasoconstriction and sodium retention by activation of RAAS are a loss of beneficial compensatory mechanisms and represent cardiac decompensation
  • factors involved in this are venous return, outflow resistance, contractility of myocardium and salt and water retention
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4
Q

what affect does myocardial failure have on venous return (preload)?

A
  • reduction in volume of blood ejected with each heart beat and increase in blood remaining after systole
  • Increased diastolic volume stretches myocardial fibres and myocardial contraction is restored (starlings law) yet in failing myocardium it results in depression of ventricular function curve
  • In heart failure the proportion of blood ejected with each heart beat is reduced
  • Sinus tachycardia ensures that any reduction of stroke volume is compensated for by increased heart rate and cardiac output is maintained
  • In severe myocardial dysfunction, the CO can only be maintained by a large increase in venous pressure and/or marked sinus tachycardia. This contributes to dyspnoea due to accumulation of interstitial and alveolar fluid and also to hepatic enlargement, ascites and dependent oedema due to increased systolic venous pressure. A normal increase in CO during exercise cannot be produces
  • In severe heart failure CO at rest is depressed despite high venous pressures and CO is redistributes to maintain perfusion of vital organs such as heat, brain, kidneys at expense of skin and muscle
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5
Q

what is after load (outflow resistance) and what is it formed by?

A

the load or resistance against which the ventricle contracts
formed by
-pulmonary and systemic resistance
-physical characteristics of the vessel walls
-volume of blood that is ejected

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6
Q
  1. what affect does increased after load have on the heart

2. how can this be expressed?

A
  1. decreases cardiac output -> further increase in end-diastolic volume and dilation of ventricle ->exacerbation
  2. laplace’s law
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7
Q

how is myocardial contractility (ionotropic state) affected in heart failure?

A
  • sympathetic NS-activated via baroreceptors as early compensatory mechanism to give ionotropic support and maintain CO
  • chronic sympathetic activation-increase neurohormonal activation leading to myocyte apoptosis. compensated by down regulation of beta receptors. increased contractility can result from increased sympathetic drive and this is a normal part of frank-starling relationship. myocardial depressants (hypoxia) decrease myocardial contractility
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8
Q

what pathophysiological changes are seen in heart failure?

A 
ventricular dilatation
myocyte hypertrophy
increased collagen synthesis
altered myosin gene expression
altered sarcoplasmic calcium ATPase density
increased ANP secretion
salt and water retention
sympathetic stimulation
peripheral vasoconstriction
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9
Q

what are the main causes of heart failure?

A

ischaemic heart disease
cardiomyopathy (dilated)
hypertension

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10
Q

name some other causes of heart failure?

A
  • cardiomyopathy (undilated)
  • valvular heart disease
  • congenital heart disease
  • alcohol and drugs
  • hyperdynamic circulation (anaemia, thyrotoxicosis, haemochromatosis, Paget’s disease)
  • right heart failure
  • tricuspid incompetence
  • arrythmias
  • pericardial disease
  • infections (chagas disease)
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11
Q

describe how heart failure causes neuohormonal and sympathetic activation (salt and water retention?

A
  • Increase in venous pressure when ventricles fail leads to retention of salt and water and their accumulation in interstitium
  • Reduced cardiac output leads to diminished renal perfusion activating RAAS and enhancing salt and water retention which increases venous pressure. The retention of sodium is partly compensated by circulating atrial natriuretic peptides and antidiuretic hormone
  • Increased ventricular wall stress promotes ventricular dilation and further worsens contractile efficiency. Prolonged activation of the sympathetic nervous and RAA systems exerts direct toxic effects on myocardial cells
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12
Q

describe myocardial remodelling in heart failure?

A

Left ventricular remodelling is a process of progressive alteration of ventricular size, shape and function owing to the influence of mechanical, neurohormonal and genetic factors in clinical conditions such as MI, cardiomyopathy, hypertension, valvular heart disease. Hallmarks include hypertrophy, loss of myocytes and increased interstitial fibrosis. Remodelling continues for months and eventually leads to change in ventricles and impairment of function of the heart as a pump. In cardiomyopathy the process of progressive ventricular dilation or hypertrophy occurs without ischaemic myocardial injury or infarction.

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13
Q

describe changes in myocardial gene expression in heart failure?

A

Haemodynamic overload of ventricle stimulates change in cardiac contractile protein gene expression. Increases protein synthesis but many proteins also switch to fetal and neonatal isoforms

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14
Q

describe abnormal calcium homeostasis in heart failure?

A
  • Calcium ion flux within myocytes regulates contractile function.
  • Excitation of myocyte cell membrane causes rapid entry of calcium from extracellular space and triggers the release of intracellular calcium from sarcoplasmic reticulum and initiates contraction.
  • Relaxation results from uptake and storage of calcium by sarcoplasmic reticulum controlled by changes in nitric oxide. In heart failure there is prolongation of calcium current association with prolongation of contraction and relaxation
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15
Q

describe ventricular remodelling after an acute infarction?

A
  • initial infarct
  • expansion of infarct (hours to days)
  • global remodelling (days to months)
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16
Q

describe ventricular remodelling in diastolic and systolic heart failure?

A 
hypertrophied heart (diastolic heart failure)
dilated heart (systolic heart failure)
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17
Q

describe apoptosis of myocytes in heart failure?

A

Apoptosis of myocytes is associated with irreversible congestive heart failure and the spiral of ventricular dysfunction, characteristic of heart failure, results from initiation of apoptosis by cytokines, free radicals and other triggers

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18
Q

what is ANP?

A

ANP is released from atrial myocytes in response to stretch. It induces diuresis, natriresis, vasodilation and suppression of RAAS. Levels are increased in congestive heart failure. Renal response to ANP is attenuated in heart failure.

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19
Q

name natriuretic peptides implicated in heart failure?

A

ANP
BNP
C-type

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20
Q

what is BNP?

A

BNP is mainly secreted by the ventricles and has similar action to ANP but is of greater diagnostic and prognostic value

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21
Q

what Is C type peptide?

A

C-type peptide-limited to vascular endothelium and CNS and has similar effects to ANP and BNP

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22
Q

what are the therapeutic benefits of natriuretic peptides?

A
  • BNP (nesritide) has no effect on dysponea and no longer recommended
  • NEP involved in degradation of variety of vasoactive peptides.
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23
Q

describe endothelial function in heart failure?

A

Central role in regulation of vasomotor tone
In patients with heart failure, endothelium-dependent vasodilation in peripheral blood vessels is impaired and one mechanism of exercise limitation
Abnormal endothelial responsiveness is due to abnormal release of nitric oxide and vasoconstrictor substances (endothelin)
Activity of nitric oxide is a potent vasodilator is blunted in heart failure
ET has actions contributing to pathophysiology of heart failure; vasoconstriction, sympathetic stimulation, RAAS activation and left ventricular hypertrophy

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24
Q

describe the role of antidiuretic hormone (vasopressin) in heart failure?

A

ADH is raised in severe chronic heart failure especially in patients on diuretics.
High ADH conc. Precipitates hyponatraemia which is ominous prognostic indicator

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25
Q

what are the different clinical syndromes of heart failure?

A
  • left ventricular systolic dysfunction
  • right ventricular systolic dysfunction
  • diastolic heart faiure
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26
Q

what causes left ventricular systolic dysfunction?

A

caused by ischaemic heart disease but can also occur with valvular heart disease and hypertension

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27
Q

what causes right ventricuar systolic dysfunction?

A

may be secondary to chronic LVSD but can occur with primary and secondary pulmonary hypertension, right ventricular infarction, arrythmogenic right ventricular cardiomyopathy and adult congenital heart disease

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28
Q

what is diastolic heart failure?

A

syndrome consisting of symptoms and signs of heart failure with preserved left ventricular ejection fraction above 45-50% and abnormal left ventricular relaxation assessed by echo. There is increased stiffness in ventricular wall and decreased left ventricular compliance leading to impairment of diastolic ventricular filling and decreased cardiac output. It is more common in elderly hypertensive patients but may occur with primary cardiomyopathies

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29
Q

what are the common symptoms of heart failure?

A

Exertional dyspnoea
Orthopneoa
Paroxysmal nocturnal dyspnoea
Fatigue

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30
Q

what are the common signs seen in a patient with heart failure?

A 
Cardiomyopathy
Third and fourth heart sounds
Elevated JVP
Tachycardia
Hypotension
Bi-basal crackles 
Pleural effusion
Peripheral ankle oedema
Ascites
Tender hepatomegaly
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31
Q

describe how a diagnosis of heart failure should be made?

A

Diagnosis relies on evidence of cardiac dysfunction usually via echo. The underlying cause should be established

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32
Q

what classification system can be used in heart failure?

A

New York heart association (NYHA) classification of heart failure

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33
Q

describe the features of class I NYHA?

A

no limitation

normal physical exercise doesn’t cause fatigue, dyspnoea or palpitations

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34
Q

describe the features of class II NYHA?

A

mild limitation

comfortable at rest but normal physical activity produces fatigue, dyspnoea or palpitations

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35
Q

describe the features of class III NYHA?

A

marked limitation

comfortable at rest but gentle physical activity produced marked symptoms of heart failure

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36
Q

describe the features of class IV NYHA?

A

symptoms of heart failure occur at rest and are exacerbated by any physical activity

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37
Q

describe the algorithm for the diagnosis of heart failure?

A
  • signs and symptoms
  • ECG, CXR, natriuretic peptides (if normal HF unlikely)
  • Echo (if normal HF unlikely)
  • assess aetiology, degree, precipitating factors, type of cardiac dysfunction
  • choose treatment
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38
Q

what investigations are useful in a patient with suspected heart failure?

A
  • bloods
  • CXR
  • ECG
  • echo
  • stress echo
  • nuclear cardiology
  • cardiac MRI
  • cardiac catheterisation
  • cardiac biopsy
  • cardiopulmonary exercise testing
  • ambulatory ECG
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39
Q

what blood tests are useful to perform in a patient with suspected heart failure?

A

FBC, liver biochem, U&E, cardiac enzymes, BNP or NTproBNP, thyroid function

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40
Q

what may CXR show in a patient with heart failure?

A

cardiomegaly, pulmonary congestion with upper lobe diversion, fluid in fissures, kerley B lines, pulmonary oedema

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41
Q

what is the purpose of doing an ECG in a patient with heart failure?

A

for ischaemia, hypertension or arrythmia

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42
Q

what is the purpose of doing echo in patients with heart failure?

A

cardiac chamber dimension, systolic and diastolic function, regional wall motion abnormalities, valvular heart disease, cardiomyopathies

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43
Q

what is the purpose of doing stress echo in patients with heart failure?

A

assessment of viability of dysfunctional myocardium-dobutamine identifies reserve in stunned or hibernating myocardium

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44
Q

what is the purpose of doing nuclear cardiology tests In patients with heart failure?

A

quantify ventricular ejection fraction, single photon emission tomography or positron emission tomography can demonstrate myocardial ischaemia and viability in dysfunctional myocardium

45
Q

what is the purpose of cardiac MRI in patients with heart failure?

A

assess viability in dysfunctional myocardium with use of dobutamine for contractile reserve or with gadolinium for delated enhancement

46
Q

what is the purpose of cardiac catheterisation in patients with heart failure?

A

diagnosis of ischaemic heart failure

47
Q

what is the purpose of cardiac biopsy in patients with heart failure?

A

diagnosing cardiomyopathies

48
Q

what is the purpose of CPET in patients with heart failure?

A

peak O2 consumption (VO2) is predictive of hospital admission and death in heart failure

49
Q

what is the purpose of ambulatory ECG in patients with heart failure?

A

in patients with suspected arrythmia. May be used in patients with severe heart failure or inherited cardiomyopathy to determine if defib is needed

50
Q

what are the aims in treating heart failure?

A

Treatment is to relieve symptoms, prevention and control of disease leading to cardiac dysfunction.

51
Q

what lifestyle changes can be suggested in management of heart failure?

A
  • Cessation of smoking, alcohol and illicit drugs, treat hypertension, diabetes, hypercholesterolaemia
  • Any factor making heart failure worse should be identified and treated
  • Education-weight, dose adjustment of diuretics
  • Obesity control
  • Dietary modification – large meals avoided. Salt restriction. -Fluid restriction. Increase omega 3 polyunsaturated fatty acids
  • Smoking
  • Physical activity
  • Vaccination-against pneumococcal disease and flu
  • Sexual activity-don’t take sildenafil
52
Q

what methods can be used to monitor heart failure patients?

A 
Functional capacity (vo2 max, exercise tolerance, echo)
Fluid status (Body weight, U&E)
Cardiac rhythm (ECG)
53
Q

what healthcare professionals should be involved in the MDT for a patient with heart failure?

A

MDT should involve specialist healthcare professionals, heart failure nurse, dietician, pharmacist, occupational therapist, physiotherapist and palliative care adviser

54
Q

what drugs can be used in the management of heart failure?

A 
diuretics
ACE inhibitors
ARB
beta blockers
aldosterone antagonists
cardiac glycosides
vasodilators and nitrates
inotropic and vasopressor agents 
prophylactic anticoagulation in hospital
oral anticoagulants for patients in AF
55
Q

what is the role of diuretics in treating heart failure?

A

Promote renal excretion of salt and water

56
Q

what is the role of beta blockers in treating heart failure?

A

improve functional status and reduce morbidity and mortality

57
Q

what is the role of aldosterone antagonists in treatment of heart failure?

A

reduce mortality (RALES), spironolactone, eplerenone. Gynaecomastia or breast pain in 1 in 10 men

58
Q

what are the role of cardiac glycosides in treating heart failure?

A

digoxin. For patients with heart failure in AF. Add on therapy for patients already on ACE and beta blockers

59
Q

what are the roles of vasodilators and nitrates in treatment of heart failure?

A

reduce either preload or afterload and used in patients intolerant of ACE or ARB

60
Q

what are the roles of inotropic and vasopressor agents in treating heart failure?

A

IV inotropes and vasopressors in patients with chronic heart failure not responding to oral medication. Don’t improve long term mortality when compared to placebo

61
Q

name the non pharmacological treatments of heart failure?

A
  • revascularisation
  • hibernating myocardium
  • hibernating myocardium and myocardial stunning
  • biventricular pacemaker or implantable cardioverter-defibrillator
  • cardiac transplantation
62
Q

when may cardiac transplantation be considered in treatment of heart failure?

A

for younger patients with severe intractable heart failure

63
Q

what is hibernating myocardium?

A

reversible left ventricular dysfunction due to chronic CAD that responds positively to inotropic stress and indicates the presence of viable heart muscle that may recover after revascularisation. It occurs from repetitive episodes of cardiac stunning that occur eg repeated exercise in a patient with coronary artery disease.

64
Q

in what patients can biventricular pacemaker or implantable cardioverter defibrillator be used in?

A 
patients not responding to the following therapy;
Systolic heart failure 
Non-reversible cause
NYHA class III/IV
Optimal medical therapy 
Ventricular dys-synchrony-LBBB
Sinus rhythm and AF
Mitral regurgitation
65
Q

name some ACE inhibitors/ARBs that can be used in heart failure treatment?

A 
captopril
enalapril
ramipril
candesartan
valsartan
losartan
66
Q

what are the precautions of using ACE inhibitors/ARBs in patients with heart failure?

A

captopril - monitor renal function

67
Q

give examples of beta blockers used in heart failure treatment?

A

bisoprolol
carvedilol
nebivolol

68
Q

what are the precautions of using beta blockers in heart failure treatment?

A
  • bisoprolol- caution in obstructive airway disease, bradyarrhythmias
  • carvedilol - avoid in acute heart failure until cardiovascular stable
69
Q

give examples of diuretics used in treatment of heart failure?

A

furosemide
bumetanide
bendroflumethiazide
metolazone

70
Q

what are the precautions of using diuretics in patients with heart failure?

A

furosemide-monitor renal function

metolazoxne-for severe heart failure

71
Q

give examples of aldosterone antagonists used in treatment of heart failure?

A

spironolactone

epirenone

72
Q

what are the precautions of aldosterone antagonists to treat heart failure?

A

spironolactone-monitor renal function, hyperkalaemia, gynacomastea

73
Q

what are the precautions for using digoxin in patients with heart failure?

A

renal impairment

if also on amiodarone

74
Q

give examples of vasodilators used in treatment of heart failure?

A

isosorbide dinitrate
hydralazine
ivabradine

75
Q

what are the precautions for vasodilators in heart failure treatment?

A

ivabradine-sick sinus syndrome, AV block

76
Q

Describe stage A systolic heart failure and treatments used?

A
  • high risk with no symptoms
  • risk factor reduction
  • treat hypertension, diabetes, dyslipidaemia, ACE inhibitors
77
Q

Describe stage B systolic heart failure and treatments used?

A
  • structural heart disease with no symptoms
  • ACE inhibitors in all patients
  • beta blockers in selected patients
78
Q

Describe stage C systolic heart failure and treatments used?

A
  • structural disease, previous or current symptoms
  • ACE inhibitors and beta blockers in all
  • sodium restriction, diuretics, digoxin
  • cardiac resynchronisation if bundle branch block
  • revascularisaton, mitral valve surgery
  • MDT
  • aldosterone antagonist-nesiritidine
79
Q

Describe stage D systolic heart failure and treatments used?

A
  • refractory symptoms requiring special intervention
  • inotropes
  • VAD, transplantation
  • hospice
80
Q

what is acute heart failure?

A

Rapid onset of symptoms and signs of heart failure secondary to abnormal cardiac function causing elevated cardiac filling pressures.
Severe dyspnoea and fluid accumulates in interstitium and alveolar spaces of lung
Poor prognosis

81
Q

what is the aetiology of acute heart failure?

A

Ischaemic heart disease
Valvular heart disease-valvular regurgitation
Hypertension-episodes of flash pulmonary oedema despite preserved left ventricular systolic function
Acute and chronic kidney disease-pulmonary oedema
AF-may require emergency cardioversion

82
Q

describe the pathophysiology of acute heart failure?

A

Similar to chronic heart failure with activation of RAAS and sympathetic nervous system. Prolonged ischaemia results in myocardial stunning that exacerbates myocardial dysfunction. If ischaemia persists it may exhibit hibernation that may recover with revascularisation

83
Q

how is a diagnosis of acute heart failure made?

A
  • 12 lead ECG (for ACS, left ventricular hypertrophy, AF, valvular heart disease, LBBB)
  • Chest X-ray (cardiomegaly, pulmonary oedema, pleural effusion, non cardiac disease)
  • Blood (serum creatinine and electrolytes, FBC, glucose, cardiac enzymes, troponin, CRP, D-dimer
  • Plasma BNP or NTproBNP (high levels indicate heart failure)
  • Transthoracic echo (confirm diagnosis and identify cause)
84
Q

what are the aims of treating acute heart failure?

A

Relief of symptoms and stabilise haemodynamics
Reduction in length of hospital stay and readmissions
Reduction in mortality

85
Q

how is acute heart failure managed?

A
  • Patients should be monitored, may require arterial lines, central venous cannulation pulmonary artery cannulation
  • Initial therapy (Oxygen, Diuretics (furosemide 50mg), Vasodilator therapy (glyceryl trinitrate infusion 10-200ug/min), Inotropic support with dobutamie, phosphodiesterase inhibitors or leosimendan , If low BP-noradrenaline (inotropes and vasopressors may be needed))
  • mechanical assist devices
86
Q

describe the use of mechanical assist devices in treatment of acute heart failure?

A
  • Used in patients who fail to respond to standard medical therapy but in whom there is either transient myocardial dysfunction with likelihood of recovery or a bridge is needed to cardiac surgery
  • Ventricular assist devices-replace or help failing ventricles in delivering blood around the body. A left ventricular assist device receives (LVAD) receives blood from left ventricle and delivers it to the aorta. A right ventricular assist devide receives blood from right ventricle and delivers it to the pulmonary artery
  • Main problems are thromboembolism, bleeding, infection and device malfunction
87
Q

give examples of clinical syndromes of acute heart failure?

A
  • acute decompensated heart failure
  • hypertensive AHF
  • acute pulmonary oedema
  • cardiogenic shock
  • high output heart failure
  • right heart failure
88
Q

what are the clinical features of acute decompensated heart failure?

A

mild features of heart failure such as dyspnoea

89
Q

what are the clinical features of hypertensive AHF?

A

high BP
preserved left ventricular function
pulmonary oedema on CXR

90
Q

what are the clinical features of acute pulmonary oedema?

A 
tachypnoea
orthopnoea
pulmonary crackles
oxygen saturations <90% on air
pulmonary oedema on CXR
91
Q

what are the clinical features of cariogenic shock?

A

systolic BP <90
mean arterial pressure drop >30
urine output <0.5mL/kg
HR>60

92
Q

what are the clinical features of high output heart failure?

A

warm peripheries
pulmonary congestion
BP may be low

93
Q

what are the clinical features of right heart failure?

A

low cardiac output
elevated JVP
hepatomegaly
hypertension

94
Q

what are the most common causes of left heart failure?

A

coronary artery disease and hypertension. Hypertension causes left heart failure via left ventricular hypertrophy

95
Q

what are the risk factors for left heart failure?

A

diabetes, smoking, male, sedentary lifestyle

96
Q

describe the pathophysiology of left ventricular heart failure?

A

Chronic or poorly controlled hypertension can cause an increased afterload and increased cardiac workload leading to hypertrophy of the left ventricle. Initially this is a compensatory mechanism to maintain cardiac output but long term can inhibit relaxation of the myocardium leading to impaired cardiac filling and decrease in left ventricular output. Coronary artery disease causes direct ischaemic damage to the myocardium, leading to remodelling and scar formation decreasing contractility and cardiac output. Arrythmias can cause remodelling, but in general, decrease cardiac output by impaired ventricular filling and decreased ventricular relaxation

97
Q

what would you expect in a history of a patient with left ventricular failure?

A 
Shortness of breath
Orthopnea 
Paroxysal nocturnal dysnoea
Symptoms of volume overload (leg swelling, weight gain, increased abdominal girl, right upper quadrant pain due to liver congestion
Weight loss-cardiac cachexia
98
Q

what examination findings would you expect to get in a patient with left ventricular failure?

A

Rales on lung auscultation (Pulmonary oedema)
Decreased breath sounds (pleural effusion)
S3 gallop (elevated left ventricular end diastolic pressure)
Point of maximal impulse displaced laterally on palpation (increased heart size)
Jugular venous distension (elevated right atrial pressure)
Positive hepatojugular efflux
Increased abdominal girth due to ascites
Swelling of scrotum
Low blood pressure and rapid heart rate

99
Q

what is the role of laboratory tests in a patient with left ventricular failure?

A

BNP or NT-proBNP is useful as it can differentiate between acute heart failure from other causes of shortness of breath. They lack specificity. Troponin T (MI). Blood count, basic metabolic panel (low sodium-indicate advanced disease. Liver function tests (liver injury due to volume overload)

100
Q

what ECG findings might be expected in a patient with left ventricular failure?

A

non specific findings. Ischemic changes, left ventricular hypertrophy or arrythmias

101
Q

what is the purpose of echo in patients with left ventricular failure?

A

distinguish between heart failure with or without preserved ejection fraction

102
Q

what is the role of coronary angiography in patients with left ventricular failure?

A

in patients with anginal symptoms or patients with worsening heart failure

103
Q

what are the potential complications in a patient with left ventricular failure?

A

Severe volume overload leading to respiratory distress and anasarca and arrythmias, cardiogenic shock

104
Q

Describe the NICE pathway for patients with acute heart failure?

A
  1. start treatment
  2. EITHER initial pharmacological OR non pharmacological treatment
  3. treatment after stabilisation
  4. management after acute phase
  5. valvular surgery and percutaneous intervention
  6. follow chronic heart failure guidelines
105
Q

what are the initial non pharmacological treatments in patients with acute heart failure?

A

-Ventilation
If patient has cardiogenic pulmonary oedema with severe dyspnoea and acidaemia consider non invasive ventilation.
Consider invasive ventilation in people with acute heart failure that despite treatment is leading to respiratory failure or reduced consciousness or physical exhaustion

-Ultrafiltration
not routine but consider in patients with diuretic resistance

106
Q

what is the initial pharmacological treatment in a patient with acute heart failure?

A

IV diuretics and monitor renal function, weight and urine output

107
Q

what treatment is given after stabilisation of acute heart failure?

A

Continue beta blockers unless heart rate is less than 50bm, second or third degree AV block or shock
ACE inhibitor or ARB and aldosterone antagonist for patients with acute heart failure and reduced left ventricular ejection fraction
Monitor renal function, electrolytes, heart rate, BP and clinical status

108
Q

describe how acute heart failure would be managed in an emergency department?

A
  • stabilise and treat life threatening complications
  • improve congestion and haemodynamics
  • vasodilators and diuretics
  • observation
109
Q

what is the early hospital management for acute heart failure?

A
  • early initiation of IV diuretics and vasoactive agents
  • prevent long hospital stay and improve long term outcomes
  • initiate/titrate ACE, ARB, BB etc

Block 31 Cardio-respiratory (15 decks)

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