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Learning Objectives
1. Delineate the different pathophysiologic patterns in acute heart failure.
2. Identify the major causes of acute heart failure.
3. Recognize the different clinical presentations and prognosis of acute heart failure.
4. Determine the indications and application of different management modalities in acute heart failure.
Definition and clinical classification of AHF
Definition:
Acute heart failure is defined as the rapid onset of symptoms and signs secondary to abnormal cardiac
function. May occur with or without previous cardiac disease. The cardiac dysfunction can be related to
systolic or diastolic dysfunction, to abnormalities in cardiac rhythm, or to pre‐load and after‐load
mismatch. It is often life threatening and requires urgent treatment.
AHF can present itself as acute de novo (new onset of acute heart failure in a patient without previously
known cardiac dysfunction) or acute decompensation chronic heart failure
The prevalence rate of AHF is 1‐2%.
Prevalence is greater in males than in females in patients aged 40‐75 years. No sex predilection is noted
among patients older than 75 years.
Prevalence of CHF increases with increasing age and affects about 10% of the population older than 75
years.
Pathophysiology of AHF
• AHF is a clinical syndrome, with reduced cardiac output, tissue hypoperfusion, increase in the
pulmonary capillary wedge pressure (PCWP), and tissue congestion.
• The underlying mechanism may be cardiac or extra‐cardiac, and may be transient and reversible
with resolution of the acute syndrome, or may induce permanent damage leading to chronic
heart failure.
• The cardiac dysfunction can be related to systolic or diastolic myocardial dysfunction (mainly
induced by ischaemia or infection), acute valvular dysfunction, pericardial tamponade,
abnormalities of cardiac rhythm, or pre‐load/after‐load mismatch.
• Multiple extra‐cardiac pathologies may result in acute heart failure by changing the cardiac
loading conditions for example
(i) increased after‐load due to systemic or pulmonary hypertension or massive pulmonary
emboli
(ii) increased pre‐load due to increased volume intake or reduced excretion due to renal
failure or endocrinopathy
(iii) high output state due to infection, thyrotoxicosis, anaemia, Paget’s disease.
• Heart failure can be complicated by co‐existing end‐organ disease. Severe heart failure can also
induce multi‐organ failure, which may be lethal. Appropriate long‐term medical therapy and, if
possible, anatomical correction of the underlying pathology may prevent further AHF syndrome
‘attacks’ and improve the poor long‐term prognosis associated with this syndrome.
• The clinical AHF syndrome may be classified as predominantly left or right forward failure, left or
right backward failure, or a combination of these. See table 1 anf figure 1.
• The vicious circle in the acute failing heart : The final common denominator in the syndrome of
AHF is a critical inability of the myocardium to maintain a cardiac output sufficient to meet the
demands of the peripheral circulation. Irrespective of the underlying cause of AHF, a vicious
circle is activated that, if not appropriately treated, leads to chronic heart failure and death.
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Table1.Classification and Common Clinical Characteristics of Patients with Acute Heart Failure
Symptom Signs and
Clinical Classification Onset Symptoms Hemodynamics Other Diagnostics
I Acute decompensated Usually Peripheral SBP: Low CXR: Normal or mild
congestive heart failure gradual edema (often normal/high interstitial edema, possible
significant), pleural effusion
CI: Low
dyspnea, usually
normal/high
well-perfused
extremities PCWP: Mildly
increased
II Acute heart failure with Often Dyspnea, altered SBP: High CXR: Normal or interstitial
hypertension/hypertensive very mental status, (>180/100 mm edema
crisis rapid possible Hg)
oliguria/anuria
CI: Usually
normal
PCWP: >18 mm
Hg
III Acute heart failure with Rapid or Severe dyspnea, SBP: Low SaO2: <90%
pulmonary edema gradual tachypnea, normal
CXR: Alveolar edema
tachycardia
IVa Cardiogenic shock/low Usually Evidence of SBP: Low
output syndrome gradual hypoperfusion; normal
oliguria
CI: Low, <2.2
liters/min/m2
PCWP: >16 mm
Hg
IVb Severe cardiogenic shock Often Marked SBP: <90 mm Usually in presence of severe
rapid hypoperfusion; Hg
oliguria/anuria
CI: Very low, < LV systolic dysfunction
1.8
liters/min/m2
PCWP: >18 mm
Hg
V High output failure Rapid or Well-perfused SBP: Variable
gradual extremities;
CI: Increased
often
tachycardic PCWP: Normal
or increased
VI Right-sided acute heart Rapid or Edema, SBP: Low CXR: often clear lung fields
failure gradual markedly with evidence of pulmonary
CI: Low
elevated neck hypertension; BNP may be
veins, often poor PCWP: Low elevated in pulmonary embolus
perfusion, but
clear lungs
BNP=B‐type natriuretic peptide. PCWP=Pulmonary Capillary Wedge Pressure.
CI=Cardiac Inde SBP=Systolic Blood Pressure. CXR=Chest X‐Ray.
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Figure 1. Clinical classification of acute heart failure
Diagnosis of AHF
The diagnosis of AHF is based on the symptoms and clinical findings, supported by appropriate
investigations such as ECG, chest X‐ray, biomarkers, and Doppler echocardiography. See table 2 for
causes and precipitating factors in acute heart failure.
History
• Apprehension
• Dyspnea at rest
• Dyspnea upon exertion: This has been found to be the most sensitive symptom reported, yet the
specificity for dyspnea is less than 60%.
• Orthopnea and paroxysmal nocturnal dyspnea (PND): These symptoms are observed; however,
the sensitivity for orthopnea and PND is only 20‐30%.
• Cough: Cough that produces pink, frothy sputum is highly suggestive of congestive heart failure
(CHF).
• Edema
• Nonspecific symptoms
o Lightheadedness
o Abdominal pain
o Malaise
o Wheezing
o Nausea
• Past medical history
o Cardiomyopathy
o Valvular heart disease
o Alcohol use
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o Hypertension
o Angina
o Prior myocardial infarction
o Familial heart disease
Physical signs
• Findings such as peripheral edema, jugular venous distention, and tachycardia are highly
predictive of CHF. Overall specificity of physical examination has been reported at 90%; however,
this same study reported a sensitivity of only 10‐30%.
• Tachypnea, using accessory muscles of respiration, has been observed.
• Hypertension may be present.
• Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle [LV]
function) may be observed.
• The skin may be diaphoretic or cold, gray, and cyanotic.
• Jugular venous distention (JVD) is frequently present.
• Wheezing or rales may be heard on lung auscultation.
• Apical impulse is frequently laterally displaced.
• Cardiac auscultation may reveal aortic or mitral valvular abnormalities (S3 or S4).
• Lower extremity edema may also be noted, especially in the subacute process.
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Algorithm for diagnosis of acute heart failure
Figure 2.Algorithm for diagnosis of acute heart failure
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Treatment of Acute Heart failure
Oxygen and ventilatory assistance
Oxygenation with face‐mask , CPAP (continuous positive airway pressure breathing , or mechanical
ventilation (SPO2 target of 94–96%)
Ventilatory support without endotracheal intubation (non‐invasive ventilation)
Two techniques are used for ventilatory support: CPAP or non‐invasive positive pressure ventilation
(NIPPV). NIPPV is a method of providing mechanical ventilation to patients without the need for
endotracheal intubation. There is a strong consensus that one of these two techniques should be used
before endotracheal intubation and mechanical ventilation. Utilization of non‐invasive techniques
dramatically reduces the need for endotracheal intubation and mechanical ventilation.
Mechanical ventilation with endotracheal intubation in AHF
Invasive mechanical ventilation (with endotracheal intubation) should not be used to reverse
hypoxaemia that could be better restored by oxygen therapy, CPAP, or NIPPV, but rather to reverse
AHF‐induced respiratory muscle fatigue. The latter is the most frequent reason for endotracheal
intubation and mechanical ventilation. Respiratory muscle fatigue may be diagnosed by a decrease in
respiratory rate, associated with hypercapnia and confused state of mind.
Morphine and its analogues in AHF
Morphine is indicated in the early stage of the treatment of a patient admitted with severe AHF,
especially if associated with restlessness and dyspnoea. Morphine induces venodilatation and mild
arterial dilatation, and reduces heart rate. In most studies, iv boluses of morphine 3 mg were
administered as soon as the intravenous line was inserted. This dosing can be repeated if required.
Diuretics
Administration of diuretics is indicated in patients with acute and acutely decompensated
heart failure in the presence of symptoms secondary to fluid retention . First‐line therapy generally
includes a loop diuretic such as furosemide, which inhibits sodium chloride reabsorption in the
ascending loop of Henle. A reasonable approach for furosemide might be as follows:
40‐80 mg IV for patients as an initial dose. Higher doses and more rapid redosing may be appropriate
for the patient in severe distress
Anticoagulation
Anticoagulation is well established in acute coronary syndrome with or without heart failure. The same
is true in atrial fibrillation. Unfractionated heparin is mostly used.Careful monitoring of the coagulation
system is mandatory in AHF as there is often concomitant liver dysfunction.
Vasodilators in the treatment of AHF
Vasodilators are indicated in most patients with acute heart failure as first line therapy, if hypoperfusion
is associated with an adequate blood pressure and signs of congestion with low diuresis, to open the
peripheral circulation and to lower pre‐load (Table 5).
Inotropic agents
Inotropic agents are indicated in the presence of peripheral hypoperfusion (hypotension, decreased
renal function) with or without congestion or pulmonary oedema refractory to diuretics and
vasodilators at optimal doses (Table 6). Principal inotropic agents include dopamine, dobutamine,
amrinone), milrinone and digoxin. In patients with hypotension presenting with CHF, dopamine and
dobutamine are usually used. Amrinone or milrinone inhibit phosphodiesterase, resulting in an increase
of intracellular cyclic adenosine monophosphate (AMP) and alteration in calcium transport. As a result,
they increase cardiac contractility and reduce vascular tone by vasodilatation.
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5
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Table 6. Postive inotropic agents in AHF
Cardiac glycosides.
Digoxin has no role in the emergency management of CHF due to delayed absorption and diminished
efficacy at times of increased sympathetic tone. Digoxin use in patients following myocardial infarction
with heart failure has shown adverse effects on outcome Therefore, inotropic support with cardiac
glycosides cannot be recommended
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Arrhythmias in acute heart failure
See table 7.
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Mechanical assist devices
Temporary mechanical circulatory assistance may be indicated in patients with AHF who are not
responding to conventional therapy and where there is the potential for myocardial recovery, or as a
bridge to heart transplant or interventions that may result in significant recovery of the heart function .
1.Intra‐aortic balloon counterpulsation (IABC).
Counter‐pulsation has become a standard component of treatment in patients with cardiogenic shock or
severe acute left heart failure that does not respond rapidly to fluid administration, vasodilatation, and
inotropic Support is complicated by significant MR or rupture of the interventricular septum, to obtain
haemodynamic stabilization for definitive diagnostic studies or treatment.
Synchronized IABC is performed by inflating and deflating a 30–50‐mL balloon placed in the thoracic
aorta through the femoral artery. The inflation of the balloon in diastole increases aortic diastolic
pressure and coronary low while the deflation during systole decreases
after‐load and facilitates LV emptying.
2. Ventricular assist devices.
Ventricular assist devices are mechanical pumps that partially replace
the mechanical work of the ventricle. They unload the ventricle, thereby decreasing myocardial work,
and pump blood into the arterial system increasing
peripheral and end‐organ flow.
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Cardiac disorders and AHF requiring surgical treatment
See table 8.
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MCQ
1. Factors that may precipitate acute decompensation of chronic heart failure include al l of the
following except
a.Arrhythmias
b.Infection
c. Poor compliance with medication regimen
d. Transfusion
e. Salt restriction
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2. In patients with heart failure, the following antiarrhythmic drug options are
Contraindicated except:
a. Amiodarone
b. Flecainide
c. procainamide
d. Disopyramide
e. All of the above
3. What type of lung sound would most likely be heard in a patient with severe left‐sided heart
failure?
a. Stridor
b. Rales
c. Wheeze
d. Stertor
e. Normal
4. Which of the following classes of medication have been proven to reduce mortality in heart failure
due to left ventricular systolic dysfunction?
a) Calcium‐channel blockers
b) NSAIDS
c) ACE inhibitors
d) Class I antiarrhythmics
e) Loop diuretics
5. Which of the following diuretics could cause fatal dysrhythmias due to hyperkalemia?
a) Furosemide
b) Hydrochlorothiazide
c) Spironolactone
d) Mannitol
6. Etiologies of acute heart failure include:
a. Acute mitral or aortic regurgitation
b. Rupture of valve leaflets or supporting structures
c. Infective endocarditis with valve incompetence
d. Extensive myocardial infarction
e. Rapid atrial fibrillation
f. All of the above
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