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Dr HARRIS HASAN SpPD,SpJP(K)DEPARTEMEN KARDIOLOGI FK USU MEDAN
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ACUTE LEFT VENTRICULAR
FAILURE
Acute LV failure can either occur de novo
or on a background of chronic cardiacfailure, i.e. acute-on-chronic cardiac
failure. This is important because the
aetiologies, clinical presentation and
management are quite distinct.
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CLASSIFICATION
Most cases of cardiac failure are
associated with reduced systolic function
and sometimes a low-output state.Diastolic dysfunction may also contribute
to cardiac failure in patients with large
infarct zones, cardiomyopathies,pericardial disease or mitral stenosis.
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AETIOLOGY
Acute de novocardiac failure
Acute MIAcute native valve failure (e.g.chordal
rupture, endocarditis) or acute VSD
Acute myocarditisHypertensive crisis
accelerated hypertension with background
essential hypertensionrenovascular disease (e.g.renal arterystenosis)
phaeochromocytoma
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Cardiac tamponade
Profound bradycardia or tachycardia
Myocardial depression due to drug toxicity
tricyclic antidepressants
blockers
calcium channel antagonists
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Acute-on-chronic cardiac failure
Non compliance with or reduction in
cardiac failure drug therapy (e.g.diuretic,
ACE inhibitor) a common precipitant
Myocardial depressant drug or drugs that
promote sodium / water retention(e.g.corticosteroids, NSAIDs)
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Intercurrent non-cardiac illness in a patients with
chronic cardiac failure
Progression of underlying cardiac disease
Myocardial ischaemia/infarction
Arrhythmias, especially atrial fibrillation
Increased metabolic demand : anaemia,pregnancy, thyrotoxicosis
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CLINICAL PRESENTATION
Acute de novoLV failure usually presents with
rapidly worsening fatigue, dyspnoea and
limitation of effort tolerance. Orthopnoea,
paroxysmal nocturnal dyspnoea and acuterespiratory distress may supervene. There may
also be prodormal symptoms which suggest an
underlying aetiology, e.g.chest pain or
palpitation. Physical signs of cardiac failure and
underlying cardiac diseases are described more
comprehensively.
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INVESTIGATION
Laboratory tests
U & Es - renal failure (predisposes to fluid retention)
- High or low K+ predisposes to arrhythmiasABGs - systemic hypoxia
- Acidosis (may be metabolic due to poortissue perfusion, or mixed due toadditional CO2 retention)
Virology - If viral myocarditis suspected(e.g.antecedentHxof flu-like illness), serology may helpidentify the culprit organism
TFTs
FBC - anaemia (exacerbates cardiac failure),
WCC(infection) ECG
acute or previous MI
ischaemic features
arrhythmia, e.g.atrial fibrillation
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CXR
pulmonary oedema
Pleural effusions, fluid in horizontal fissure
Septal (Kerley B) linesPulmonary pathology
Cardiac size
Echo
- LV function
- LVH (suggests hypertension, aortic stenosis
or hypertrophic cardiomyopathy)-associated with
diastolic dysfunction
- valve disease, e.g.mitral regurgitation, aortic stenosis
- pericardial effusion
- endocarditis
Right heart catheterization
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Key points : examination General - usually distressed or agitated
- tachypnoea
- semiconscious or unconscious insevere/protracted cases
- signs of sympathetic activation/lowcardiac output
pallorsweating
Cool peripheries
Peripheral cyanosis
- Cutaneous stigmata of endocarditis- Signs of non-cardiac ilness
clinical anaemia
Fever
Thyroid signs
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Pulse - usually tachycardic. Relativebradycardia can worsen cardiacfailure by limiting cardiac output
- may be irregular; suggests atrialfibrillation
- may be low ( output) or normal pulse
volume
Blood pressure - hypotension heralds poorprognosis
- hypertension may aggravatecardiac failure
- check for pulsus paradoxus
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JVP - often elevated, but notinvariably so
Precordium - apex usually not displaced in denovocardiac failure; may bedyskinetic in anterior MI
- apex often displaced in chronicheart failure
- murmur (may suggest valvepathology or acute VSD)
- gallop rhythm :S3S4-inspiratory crepitations
- pleural effusions in chroniccardiac failure
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Other - peripheral/sacral oedema,pulsatile hepatomegaly,
ascites, right parasternal lift
most often accompanychronic right-sided cardiac
failure, but are uncommon
in de novo cardiac failure
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MANAGEMENT
Acute cardiac failure should be managed in a high-
dependency or coronary care unit. Patients who are
unable to maintain adequate systemic oxygenation or
acid-base balance despite initial therapy need to be
managed in an intensive care unit with ventilationfacilities. ECG, blood pressure and O2 saturation
monitoring are mandatory.
Initial management
IV access
High-low O2(60-100%)
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Nitrates - this is at least as important as diureticRX.
- buccal GTN 2-5 mg OR- IVI GTN 0.6-12 mg min-1 OR
- IVI isosorbide dinitrate 2-10 mg h-1
- IVI sodium nitroprusside 10-200 g
min-1Opiate - IV morphine 5-20 mg
Loop - IV frusemide 50-100 mg bolus OR
diuretic - IVI frusemide 5-20 mg h-1
The acute effect of loop diuretic isvenodilation;intravascular volume reductionoccurs later
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Digoxin - useful for rate control in atrial
fibrillation; role in cardiacfailure in sinus rhythm controversial
- oral dose:0.5 mg, repeated after 6
hours
- IVI:0.5 mg over 20 min, repeated after
6 hours
Treat identifiable triggers, e.g.aspirin andthrombolysis for acute MI.
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An additional agent (e.g. ACE inhibitor) may be
needed if nitrate therapy fails to controlhypertension. Arrhythmias are often poorly
tolerated. Atrial fibrillation can cause
catastrophic haemodynamic collapse because of
the loss of atrial contribution to ventricular filling.
In these cases DC cardioversion IVI
amiodaronevia a central venous catheter (300
mg over 30 min, followed by 900 mg over 24 h)may be needed.
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Management of resistant cardiac failure
Advanced haemodynamic support
Hypotensive patients with cardiac failuremay benefit from inotropes
Dobutamine 5-20 g kg-1min-1
Dopamine 2.5-5 g kg-1min-1
Adrenaline 1-12 g min-1
Noradrenaline 1-12 g min-1
Intra-aortic balloon pumping
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Renal failure
Patients with fluid overload in whom diuresis isnot achieved may require extracorporealhaemofiltration.
Respiratory failure
If, despite medical management, the patientsremains in a state of repiratory compromise,mechanical ventilation should be considered.
Intubation, paralysis and intermittent positive-
pressure ventilationMask continuous positive airway pressure
ventilation
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CHRONIC CARDIAC FAILUREChronic cardiac failure is a major public health problem in the
UK, affecting between 1 and 2% of the general population. It isassociated with acute high morbidity and mortality and is a
major cause of recurrent hospitalization. Chronic cardiac failure
is characterized by diminished cardiac reserve and a complex
series of maladaptive neurohumoral responses, principallyinvolving the sympathetic and renin-angiotensin axes. The
resultant increased peripheral vascular resistance and sodium
and water retention serve to increase cardiac workload and
worsen LV failure. Current drug therapies in chronic cardiacfailure are directed at preventing sodium and water retention
and antagonizing the humoral responses that cause peripheral
vasoconstriction.
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CLASSIFICATION
Cardiac failure is classified in several ways : acute andchronic, left and right, high output and low output andsytolic and diastolic dysfunction. Cardia failuresymptoms are graded using the New York Heart
Association System.
Diagnosis of diastolic heart failure requires :
Symptoms or sign of heart failure
Normal or mildly abnormal LV systolic functionAbnormal LV relaxation, filling or diastolic distensibility
or stiffness
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AETIOLOGY
The main causes of chronic cardiac failure in westerncountries are :
Ischaemic heart disease
Hypertension
Valvular heart disease Toxic : alcohol, adriamycin, cobalt
Viral myocarditis : Coxsackie, HIV
Other cardiomyopathies : hypertrophic, restrictive, dilated
(sometimes familial)
Infiltrative : amyloidosis, sarcoidosis
Metabolic and nutritional : haemochromatosis, thyroid
dysfunction, beri-beri
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CLINICAL PRESENTATION
The most common cause of chronic cardiac failure is
IHD; cardiac failure usually follows presentation with
an acute MI. In some cases myocardial ischaemia or
infarction is silent and the first presentation may bewith cardiac failure itself. Conversely, some patients
with IHD have asymptomatic LV dysfunction.
However, most patients with chronic cardiac failurepresent with exertional fatigue and breathlessness
and/or symptoms of fluid retention (e.g.oedema), or
with an episode of acute LV failure.
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INVESTIGATIONS Laboratory tests
U & Es - may be concomitant renal failure (due to renovasculardisease, low cardiac output, or to diuretics, ACE inhibitor)
- K+ because of diuretics- Na+an ominous sign in advanced cardiac failure
glucose - prognosis for diabetics with cardiac failure very poor
LFTs - may be deranged because of liver congestion
TFTs - hypo- and hyperthyroidism may exacerbate failure
FBC - anaemia may exacerbate failure
cardiomyopathy screen - ferritin (haemochromatosis), Ca2+(sarcoidosis), viral screen (Coxsackie,enterovirus, HIV)
autoantibody screen - probably disease marker rather thancausitive factor; anti-- and -myosinantibodies
blood group and tissue type - if transplantation being considered
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ECG
Rarely normal in cardiac failure. Look for :
evidence of previous MILVH (large voltages seen both with LVH and cardiacdilatation)
conduction defects
atrial fibrillation
CXR
cardiomegaly
cardiac contour (e.g.left or right enlargement) maygive clue to aetiology
upper lobe venous diversion, interstitial oedema,pleural effusions, Kerley B lines may present.
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Echo
Radionuclide ventriculography
Stress testing
Cardiac catheterization
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MANAGEMENT
Drug therapy
Diuretics
Loop diuretics, e.g. frusemide (typically 40-120 mg d-1)orbumetanide(typically 1-4 mg d-1)
Nitrates
Nitrates, e.g.oral isosorbide mononitrate(30-120 mg d-1)
Vasodilators
Oral ACE inhibitors, e.g.captopril12.5-50 mg tid, enalapril10-20 mgbd or lisinopril10-20 mg d-1
Oral AT1 receptor antagonists, e.g.losartan50-100 mg d-1
In patients with renal dysfunction or intolerance of ACE inhibitorsand AT1 receptor antagonists, the combination of hydralazine, and anitrate is a suitable alternative. The regimen used in the VeHEFT-IItrial was hydralazine75 mg qid and isosorbide dinitrate40 mg qid,although different dosing intervals and nitrate preparations can beused to improve compliance.
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Inotropes
BlockersAntiarrhythmics
Anticoagulants
SurgeryRevascularization
Valve replacementCardiac transplantation
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Causes and precipitating factors in AHF
1. Decompensation of pre-existing chronic heartfailure (e.g.cardiomyopathy)
2. Acute coronary syndromes
a) Myocardial infarction/unstable angina with
large extent of ischaemia and ischaemic
dysfunction
b) Mechanical complication of acute myocardialinfarction
c) Right ventricular infarction
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3. Hypertensive crisis
4. Acute arrhythmia (ventricular tachycardia,ventricular fibrillation, atrial fibrillation or flutter,other supraventricular tachycardia)
5. Valvular regurgitation (endocarditis, rupture of
chordae tendinae, worsening of pre-existingvalvular regurgitation)
6. Severe aortic valve stenosis
7. Acute severe myocarditis
8. Cardiac tamponade
9. Aortic dissection
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10. Post partum cardiomyopathy
11. Non-cardiovascular precipitating factorsa. lack of compliance with medical treatment
b. Volume overload
c. Infections, particularly pneumonia or septicaemia
d. Severe brain insulte. After major surgery
f. Reduction in renal function
g. Asthma
h. Drug abusei. Alcohol abuse
j. phaeochromocytoma
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12. High output syndromes
a) Septicaemia
b) Thyrotoxicosis crisisc) Anaemia
d) Shunt syndromes
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Dyregulation of contractiliy
Frank Starling mechanism?
Force-frequency-relationship?
Catecholamine refractoriness
Neuroendocrine activation
Sympathetic nervous system
RAAS
ADH,endothelin,etcHypertrophy
Low cardiac output
Remodeling
Ischaemia
Fibrosis
Myocyte Death
Apoptosis
Necrosis
Acidosis, radical load
Coronary perfusionPeripheral perfusion? Myocardial oxygen consumption?
Reduced renal blood flowTachycardiaHypotension
Filling pressure?
Wall tension?Cardiac output? Blood volume ?
Vascular resistance?
Precipitating condition
Anaemia, thyroid disease,etc.Critical LV-Deterioration
Previous myocardial injury
Remodeling
Chronic heart failure
Afterload-Chronotropy/Inotropy/Lusitropy mismatch
Hypertensive crisis
Arrhythmias,etc.
Acute critical myocardial injury
Acute myocardial infarction
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Suspected Acute Heart Failure Assess Symptoms & Signs
Heart Disease?
ECG/BNP/X-ray?
Evaluate cardiac
function byEchocardiography/otherimaging
HEART FAILURE, assess by
Echocardiography
Characterize type and severity
Consider other diagnosis
Selected tests
(angio, haemodynamically
monitoring, PAC)
Normal
Abnormal
Abnormal
Normal
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Assessment of Ventricular Function Left
Ventricular Ejection Fraction
Reduced LVEF
Systolic LV dysfunction
Preserved LVEF
Error in evaluation, other causesof heart failure, Diagnostic error
(no heart failure
DiastolicDysfunctionTransientSystolic
Dysfunction
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Goals of treatment of the patient with AHF
Clinical
symptoms (dyspnoea and/or fatigue
clinical signsbody weight
diuresis
oxygenation
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Laboratory
Serum electrolyte normalizationBUN and/or creatinine
S-bilirubin
Plasma BNP
Blood glucose normalization
Haemodynamic
pulmonary capillary wedge pressure to
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Outcome
Length of stay in the intensive care unit
Duration of hospitalization
Time to hospital re-admission
Mortality
Tolerability
Low rate of withdrawal from therapeutic measures
Low incidence of adverse effects
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If moribund BLS, ALS
Analgesia or sedation
Immediate Resuscitation
Patient distressed or in painYES
NO
Increase FiO2, consider
CPAP, NIPPV
NO
YES
Arterial oxygen saturation >95%
Pacing, antiarrhythmics etc
YES
YES
YES
NONormal Heart Rate and rhythm
Vasodilators, consider diuresis
if volume overload
NO
Mean BP >70 mmHg
Fluid challengeNOAdequate preload
Consider inotropes or further
afterload manipulation
Reassess frequentlyYES
NOAdequate Cardiac Output:
reversal of metabolic acidosis,
SvO2>65%, clinical signs of
adequate organ perfusion
Invasive monitoring eg
PAC may be require
Definitive Treatment
Diagnosis algorithm
Definitive Diagnosis
Acute Heart Failure
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Acute heart failure with systolic dysfunction
Oxygen/CPAPFurosemide vasodilator
Clinical evaluation (leading to mechanistic theraphy)
SBP < 85 mmHg
Volume Loading? Inotrope
and/or dopamine > 5
g/kg/min and/ornorepinephrine
No response: reconsider
mechanistic therapy
Inotropic agents
SBP 85-100 mmHg
Good response Oral
therapy furosemide,
ACEI
Vasodilator and/or
inotropic (dobutamine,
PDEI or levosimendan)
Vasodilator (NTG,
nitroprusside, BNP)
SBP > 100 mmHg
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Immediate surgical correction
Pericardiocentesis
Fluids
Inotropes
Consider IABP
DIAGNOSIS
Free wall rupture
Echocardiography
Pericardial effusion (especially if>10 mm)
Echodensities in the effusion
Echo signs of tamponade
E h di h
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Immediate surgical correction
Coronary Angiography
Urgent surgical
correction
Coronary Angiography
Stable patient
Medical Therapy
Unstable patientConsider :
IABP
Mechanical ventilation
PAC
Echocardiography
DIAGNOSIS VSR
VSR
Site
Size
Qp:Qs
Diagnosis uncertain
PACOximetry
O2step up>5% RA-RV
E h di h
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Immediate surgical correction
Coronary Angiography
Urgent Surgical
Therapy
Coronary Angiography
Stable Patient
Medical Therapy
Unstable patient
Consider
IABP
Mechanical Ventilation
PAC
DIAGNOSIS Acute MR
If Diagnosis Uncertain
Consider TEE
If TEE non Diagnostic
Consider PAC
To exclude VSR
Echocardiography
Echo signs of acute severe MR +/-
Visualization of ruptured papillary
muscle
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Echocardiography
akinetic apex
Hyperdinamic basal IVS, SAM
Discontinue
positive inotropes
nitrates
IABP
Consider
-blockers
-agonists
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Medical therapy
Consider
IABP
Mechanical ventilation
PCI or CABG
VAD
Heart transplant
Cardiogenic shock fromm loss
of ventricular muscle mass
Low EF
No signs of mechanical complication
Echocardiography