Dr HARRIS HASAN SpPD,SpJP(K)

DEPARTEMEN KARDIOLOGI FK USU MEDAN

ACUTE LEFT VENTRICULAR
FAILURE

Acute LV failure can either occur de novo

or on a background of chronic cardiac
failure, i.e. acute-on-chronic cardiac
failure. This is important because the
aetiologies, clinical presentation and
management are quite distinct.
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.
AETIOLOGY
Acute ‘de novo’ cardiac failure
 Acute MI
 Acute native valve failure (e.g.chordal
rupture, endocarditis) or acute VSD
 Acute myocarditis
 Hypertensive crisis
accelerated hypertension with background
essential hypertension
renovascular disease (e.g.renal artery
stenosis)
phaeochromocytoma
 Cardiac tamponade
 Profound bradycardia or tachycardia
 Myocardial depression due to drug toxicity
tricyclic antidepressants
β –blockers
calcium channel antagonists
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)
 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
CLINICAL PRESENTATION
Acute de novo LV failure usually presents with
rapidly worsening fatigue, dyspnoea and
limitation of effort tolerance. Orthopnoea,
paroxysmal nocturnal dyspnoea and acute
respiratory 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.
 INVESTIGATION
 Laboratory tests
U & Es - renal failure (predisposes to fluid retention)
- High or low K+ predisposes to arrhythmias
ABGs - systemic hypoxia
- Acidosis (may be metabolic due to poor
tissue perfusion, or mixed due to
additional CO2 retention)
Virology - If viral myocarditis suspected(e.g.antecedent
Hx of flu-like illness), serology may help
identify the culprit organism
TFTs
FBC - anaemia (exacerbates cardiac failure),
↑ WCC(infection)
 ECG
acute or previous MI
ischaemic features
arrhythmia, e.g.atrial fibrillation
 CXR
pulmonary oedema
Pleural effusions, fluid in horizontal fissure
Septal (Kerley B) lines
Pulmonary 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
Key points : examination
 General - usually distressed or agitated
- tachypnoea
- semiconscious or unconscious in
severe/protracted cases
- signs of sympathetic activation/low
cardiac output
pallor
sweating
Cool peripheries
Peripheral cyanosis
- Cutaneous stigmata of endocarditis
- Signs of non-cardiac ilness
clinical anaemia
Fever
Thyroid signs
 Pulse - usually tachycardic. Relative
bradycardia can worsen cardiac
failure by limiting cardiac output
- may be irregular; suggests atrial
fibrillation
- may be low ( ↓output) or normal pulse
volume

 Blood pressure - hypotension heralds poor

prognosis
- hypertension may aggravate
cardiac failure
- check for pulsus paradoxus
 JVP - often elevated, but not
invariably so

 Precordium - apex usually not displaced in de

novo cardiac failure; may be
dyskinetic in anterior MI
- apex often displaced in chronic
heart failure
- murmur (may suggest valve
pathology or acute VSD)
- ‘gallop’ rhythm :S3 ± S4
- inspiratory crepitations
- pleural effusions in chronic
cardiac failure
 Other - peripheral/sacral oedema,
pulsatile hepatomegaly,
ascites, right parasternal lift
most often accompany
chronic right-sided cardiac
failure, but are uncommon
in de novo cardiac failure
 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 ventilation
facilities. ECG, blood pressure and O2 saturation
monitoring are mandatory.

Initial management
 IV access
 High-low O2 (60-100%)
 Nitrates - this is at least as important as diuretic
R X.
- 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 μg
min-1
 Opiate - 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 is

venodilation;intravascular volume reduction
occurs later
 Digoxin - useful for rate control in atrial
fibrillation; role in cardiac
failure 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 and

thrombolysis for acute MI.
An additional agent (e.g. ACE inhibitor) may be
needed if nitrate therapy fails to control
hypertension. 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
amiodarone via a central venous catheter (300
mg over 30 min, followed by 900 mg over 24 h)
may be needed.
Management of resistant cardiac failure

Advanced haemodynamic support

Hypotensive patients with cardiac failure
may benefit from inotropes
 Dobutamine 5-20 μg kg-1 min-1
 Dopamine 2.5-5 μg kg-1 min-1
 Adrenaline 1-12 μg min-1
 Noradrenaline 1-12 μg min-1
 Intra-aortic balloon pumping
 Renal failure
Patients with fluid overload in whom diuresis is
not achieved may require extracorporeal
haemofiltration.

Respiratory failure
If, despite medical management, the patients
remains in a state of repiratory compromise,
mechanical ventilation should be considered.
 Intubation, paralysis and intermittent positive-
pressure ventilation
 Mask continuous positive airway pressure
ventilation
 CHRONIC CARDIAC FAILURE
Chronic cardiac failure is a major public health problem in the
UK, affecting between 1 and 2% of the general population. It is
associated 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, principally
involving 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 cardiac
failure are directed at preventing sodium and water retention
and antagonizing the humoral responses that cause peripheral
vasoconstriction.
 CLASSIFICATION
Cardiac failure is classified in several ways : acute and
chronic, left and right, high output and low output and
sytolic and diastolic dysfunction. Cardia failure
symptoms 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 function
 Abnormal LV relaxation, filling or diastolic distensibility
or stiffness
AETIOLOGY
The main causes of chronic cardiac failure in western
countries 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
 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 be
with cardiac failure itself. Conversely, some patients
with IHD have asymptomatic LV dysfunction.
However, most patients with chronic cardiac failure
present with exertional fatigue and breathlessness
and/or symptoms of fluid retention (e.g.oedema), or
with an episode of acute LV failure.
INVESTIGATIONS
 Laboratory tests
U & Es - may be concomitant renal failure (due to renovascular
disease, 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 than

causitive factor; anti- - and β -myosin
antibodies

blood group and tissue type - if transplantation being considered

 ECG
Rarely normal in cardiac failure. Look for :
evidence of previous MI
LVH (large voltages seen both with LVH and cardiac
dilatation)
conduction defects
atrial fibrillation

 CXR
cardiomegaly
cardiac contour (e.g.left or right enlargement) may
give clue to aetiology
upper lobe venous diversion, interstitial oedema,
pleural effusions, Kerley B lines may present.
 Echo
 Radionuclide ventriculography
 Stress testing
 Cardiac catheterization
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.captopril 12.5-50 mg tid, enalapril 10-20 mg
bd or lisinopril 10-20 mg d-1
 Oral AT1 receptor antagonists, e.g.losartan 50-100 mg d-1
 In patients with renal dysfunction or intolerance of ACE inhibitors
and AT1 receptor antagonists, the combination of hydralazine, and a
nitrate is a suitable alternative. The regimen used in the VeHEFT-II
trial was hydralazine 75 mg qid and isosorbide dinitrate 40 mg qid,
although different dosing intervals and nitrate preparations can be
used to improve compliance.
Inotropes
β –Blockers
Antiarrhythmics
Anticoagulants

Surgery
Revascularization
Valve replacement
Cardiac transplantation
Causes and precipitating factors in AHF
1. Decompensation of pre-existing chronic heart
failure (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 myocardial
infarction
c) Right ventricular infarction
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-existing
valvular regurgitation)
6. Severe aortic valve stenosis
7. Acute severe myocarditis
8. Cardiac tamponade
9. Aortic dissection
10. Post partum cardiomyopathy

11. Non-cardiovascular precipitating factors

a. lack of compliance with medical treatment
b. Volume overload
c. Infections, particularly pneumonia or septicaemia
d. Severe brain insult
e. After major surgery
f. Reduction in renal function
g. Asthma
h. Drug abuse
i. Alcohol abuse
j. phaeochromocytoma
12. High output syndromes
a) Septicaemia
b) Thyrotoxicosis crisis
c) Anaemia
d) Shunt syndromes
Acute critical myocardial injury Previous myocardial injury
Afterload-Chronotropy/Inotropy/Lusitropy mismatch
•Acute myocardial infarction •Hypertensive crisis
Remodeling
•Arrhythmias,etc.

Chronic heart failure

Precipitating condition
Critical LV-Deterioration
•Anaemia, thyroid disease,etc.

Filling pressure? Blood volume ?

Cardiac output?
Wall tension? Vascular resistance?

Hypotension Tachycardia Reduced renal blood flow

Peripheral perfusion? Coronary perfusion Myocardial oxygen consumption?

Remodeling Acidosis, radical load

•Ischaemia
•Fibrosis
•Myocyte Death Low cardiac output

Apoptosis
Necrosis
Neuroendocrine activation Dyregulation of contractiliy
•Sympathetic nervous system •Frank Starling mechanism?
•RAAS •Force-frequency-relationship?
Hypertrophy •ADH,endothelin,etc •Catecholamine refractoriness
 Suspected Acute Heart Failure Assess Symptoms & Signs

Normal
Heart Disease?
ECG/BNP/X-ray? Consider other diagnosis

Abnormal

Evaluate cardiac Normal

function by
Echocardiography/other imaging

Abnormal

HEART FAILURE, assess by

Selected tests
Echocardiography
(angio, haemodynamically
monitoring, PAC)
Characterize type and severity
 Assessment of Ventricular Function Left
Ventricular Ejection Fraction

<40%>
Reduced LVEF “Preserved” LVEF

Systolic LV dysfunction

Transient Diastolic
Error in evaluation, other causes
Systolic Dysfunction
of heart failure, Diagnostic error
Dysfunction (no heart failure
Goals of treatment of the patient with AHF

Clinical
↑symptoms (dyspnoea and/or fatigue
↓clinical signs
↓body weight
↑diuresis
↑oxygenation
Laboratory
Serum electrolyte normalization
↓BUN and/or creatinine
↓S-bilirubin
↓Plasma BNP
Blood glucose normalization

Haemodynamic
↓pulmonary capillary wedge pressure to<18 mmHg
↑cardiac output and/or stroke volume
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
 Acute Heart Failure

Definitive Diagnosis Immediate Resuscitation If moribund BLS, ALS

YES
Analgesia or sedation
Diagnosis algorithm Patient distressed or in pain
NO

NO
Increase FiO2, consider
Arterial oxygen saturation >95%
CPAP, NIPPV
Definitive Treatment YES

NO
Pacing, antiarrhythmics etc
Normal Heart Rate and rhythm

YES

YES Vasodilators, consider diuresis

Mean BP >70 mmHg if volume overload
NO

NO Fluid challenge
Adequate preload

Invasive monitoring eg YES

PAC may be require

NO Consider inotropes or further

Adequate Cardiac Output: afterload manipulation
reversal of metabolic acidosis,
SvO2>65%, clinical signs of
adequate organ perfusion YES Reassess frequently
 Acute heart failure with systolic dysfunction

Oxygen/CPAP
Furosemide ± vasodilator
Clinical evaluation (leading to mechanistic theraphy)

SBP > 100 mmHg SBP 85-100 mmHg SBP < 85 mmHg

Vasodilator (NTG, Volume Loading? Inotrope

Vasodilator and/or and/or dopamine > 5
nitroprusside, BNP) inotropic (dobutamine, µg/kg/min and/or
PDEI or levosimendan) norepinephrine

Good response Oral

therapy furosemide, No response: reconsider
ACEI mechanistic therapy
Inotropic agents
 Echocardiography

•Pericardial effusion (especially if>10 mm)

•Echodensities in the effusion
•Echo signs of tamponade

DIAGNOSIS
Free wall rupture

Pericardiocentesis
Fluids
Inotropes
Consider IABP

Immediate surgical correction

Echocardiography

VSR Diagnosis uncertain

• Site PAC

• Size Oximetry

• Qp:Qs O2 step up>5% RA-RV

DIAGNOSIS VSR Unstable patient

Consider :
Medical Therapy • IABP
• Mechanical ventilation

Stable patient • PAC

Coronary Angiography Coronary Angiography

Urgent surgical
Immediate surgical correction
correction
 Echocardiography

Echo signs of acute severe MR +/-

Visualization of ruptured papillary
muscle
If Diagnosis Uncertain
Consider TEE
DIAGNOSIS Acute MR If TEE non Diagnostic
Consider PAC
•To exclude VSR
Medical Therapy
Unstable patient
Consider

Stable Patient •IABP

•Mechanical Ventilation
•PAC
Coronary Angiography
Coronary Angiography
Urgent Surgical
Therapy Immediate surgical correction
 Echocardiography

• akinetic apex
•Hyperdinamic basal IVS, SAM

Discontinue
• positive inotropes
• nitrates
• IABP
Consider
• β-blockers
• α-agonists
 Echocardiography

Low EF
No signs of mechanical complication

Cardiogenic shock fromm loss

of ventricular muscle mass

Medical therapy
Consider
• IABP
• Mechanical ventilation
• PCI or CABG
• VAD
• Heart transplant