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
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 CO
2
retention)
Virology - If viral myocarditis suspected(e.g.antecedent
H
x
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 :S
3
S
4

-

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 O
2
saturation
monitoring are mandatory.

Initial management
IV access
High-low O
2
(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 g
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 g kg
-1
min
-1
Dopamine 2.5-5 g kg
-1
min
-1
Adrenaline 1-12 g min
-1
Noradrenaline 1-12 g 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), Ca
2+

(sarcoidosis), viral screen (Coxsackie,
enterovirus, HIV)

autoantibody screen - probably disease marker rather than
causitive factor; anti- - and -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 AT
1
receptor antagonists, e.g.losartan 50-100 mg d
-1
In patients with renal dysfunction or intolerance of ACE inhibitors
and AT
1
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
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

Dyregulation of contractiliy
Frank Starling mechanism?
Force-frequency-relationship?
Catecholamine refractoriness
Neuroendocrine activation
Sympathetic nervous system
RAAS
ADH,endothelin,etc Hypertrophy
Low cardiac output
Remodeling
Ischaemia
Fibrosis
Myocyte Death
Apoptosis
Necrosis
Acidosis, radical load
Coronary perfusion
Peripheral perfusion?
Myocardial oxygen consumption?
Reduced renal blood flow
Tachycardia Hypotension
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
Suspected Acute Heart Failure Assess Symptoms & Signs
Heart Disease?
ECG/BNP/X-ray?
Evaluate cardiac
function by
Echocardiography/other imaging
HEART FAILURE, assess by
Echocardiography
Characterize type and severity
Consider other diagnosis
Selected tests
(angio, haemodynamically
monitoring, PAC)
Normal
Abnormal
Abnormal
Normal
Assessment of Ventricular Function Left
Ventricular Ejection Fraction
Reduced LVEF
Systolic LV dysfunction
<40%>
Preserved LVEF
Error in evaluation, other causes
of heart failure, Diagnostic error
(no heart failure
Diastolic
Dysfunction
Transient
Systolic
Dysfunction
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
If moribund BLS, ALS
Analgesia or sedation
Immediate Resuscitation
Patient distressed or in pain
YES
NO
Increase FiO
2
, consider
CPAP, NIPPV
NO
YES
Arterial oxygen saturation >95%
Pacing, antiarrhythmics etc
YES
YES
YES
NO
Normal Heart Rate and rhythm
Vasodilators, consider diuresis
if volume overload
NO
Mean BP >70 mmHg
Fluid challenge
NO
Adequate preload
Consider inotropes or further
afterload manipulation
Reassess frequently YES
NO
Adequate Cardiac Output:
reversal of metabolic acidosis,
SvO
2
>65%, clinical signs of
adequate organ perfusion
Invasive monitoring eg
PAC may be require
Definitive Treatment
Diagnosis algorithm
Definitive Diagnosis
Acute Heart Failure
Acute heart failure with systolic dysfunction
Oxygen/CPAP
Furosemide vasodilator
Clinical evaluation (leading to mechanistic theraphy)
SBP < 85 mmHg
Volume Loading? Inotrope
and/or dopamine > 5
g/kg/min and/or
norepinephrine
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
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
Immediate surgical correction
Coronary Angiography
Urgent surgical
correction
Coronary Angiography
Stable patient
Medical Therapy
Unstable patient
Consider :
IABP
Mechanical ventilation
PAC
Echocardiography
DIAGNOSIS VSR
VSR
Site
Size
Qp:Qs
Diagnosis uncertain
PAC
Oximetry
O
2
step up>5% RA-RV
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
Echocardiography
akinetic apex
Hyperdinamic basal IVS, SAM
Discontinue
positive inotropes
nitrates
IABP
Consider
-blockers
-agonists

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