ACUTE HEART

FAILURE

Georgios Pantelakis
6th year General Medicine A2
Chief Consultant: Prof. MUDr. Rokyta Richard Ph.D

Definitions of Heart Failure

Heart failure can be defined as an abnormality of cardiac structure

or function leading to failure of the heart to deliver oxygen at a
rate commensurate with the requirements of the metabolizing
tissues, despite normal filling pressures

In guidelines, HF is defined, clinically, as a syndrome in which

patients have typical

symptoms e.g.breathlessness, ankle swelling, and fatigue

signs

e.g. elevated jugular venous pressure, pulmonary

crackles, and displaced apex beat resulting from an
abnormality of cardiac structure or function.

Acute heart failure (AHF)

is

the term used to describe the rapid onset of, or change

in, symptoms and signs of HF, which causing elevated
cardiac filling pressures this will lead severe dyspnoea and
fluid accumulates in the interstitium and alveolar spaces of
the lung (pulmonary oedema)

It

is a lifethreatening condition that requires immediate

medical attention and usually leads to urgent admission to
hospital

Epidimiology

Worldwide, the incidence of heart failure is variable but increases

with advancing age.

Approximately 23 million people worldwide have heart failure,

Approximately 12% of the adult population in developed countries

has HF, with the prevalence rising to 10% among persons 70 years
of age or older

AHF has a poor prognosis with a 60-day mortality rate of nearly 10%
and a rate of death or rehospitalization of 35% within 60 days. In
patients with acute pulmonary oedema the in-hospital mortality rate
is 12% and by 12 months this rises to 30%

Types Of Heart Failure

Acute VS Transient VS Chronic

Systolic VS Diastolic
(HFPEF,

Right VS Left

HFNEF,HFPSF)

Causes of acute heart failure

Acute MI

Unstable AP

Hypertension

Acute myocaditis

Mitral valve stenosis

Aortic valve stenosis

Acute aortic valve regurgitation

Worsening of chronic heart failure

Massive pulmonary embolisation

Compensatory mechanisms

Neurohumoral activation
Heart dysfunction
RAS
Angiotensin
II
Aldosteron

sympaticus
Norepynephri
n

vasopresin, endotelin ..
Plasmatic
vasopresin ..

Na retention,
vasoconstriction
preload

congestion

afterloa
d
Myocardial
function

Classification of heart failure

Class

Patient Symptoms

Class I (Mild)

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue,
palpitation, or dyspnea (shortness of breath).

Class II (Mild)

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in
fatigue, palpitation, or dyspnea.

Class III (Moderate)

Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes
fatigue, palpitation, or dyspnea.

Class IV (Severe)

Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency
at rest. If any physical activity is undertaken, discomfort is increased.

Clinical Syndromes of AHF

Acute

decompensated HF mild features of HF (e.g: dyspnea)

Hypertensive

AHF high BP, preserved LV function, pulmonary

edema
Acute

pulmonary edema tachypnea, orthopnea, pulmonary

crackles, oxygen saturation <90%, pulmonary edema; mortality rate
12% (in-hospital) and 30% (2months)

Cardiogenic

shock systolic BP<90mmHg, MAP drop >30mmHg,

HR>60bpm, urine output<0,5mL/kg/h

High

output HF warm peripheries, pulmonary congestion, low BP

(e.g: septic shock)

Right

HF low CO, elevated JVP, hepatomegaly, hypotension

Initial assessment and monitoring of

patients

(i) Does the patient have HF or is there an alternative cause for their
symptoms and signs (e.g. chronic lung disease, anaemia, kidney
failure, or pulmonary embolism)?

(ii) If the patient does have HF, is there a precipitant and does it require
immediate treatment or correction (e.g. an arrhythmia or acute
coronary syndrome)?

(iii) Is the patients condition immediately life-threatening because of

hypoxaemia or hypotension leading to underperfusion of the vital
organs (heart, kidneys, and brain)?

Diagnosis
Initial

investigation performed in the emergency room should

include
ECG

12-lead acute coronary sy, LV hypertrophy, atrial fibrillation,

valvular heart disease, LBBB

CXR

cardiomegaly, pulmonary edema, pleural effusion, non-cardiac

disease

Blood

investigations: serum creatinine, electrolytes, FBC, blood

glucose, cardiac enzymes, troponin, CRP, d-dimers

Plasma

BNP or NTproBNP BNP>100pg/ml or NTproBNP>300pg/ml

indicates HF

Transthoracic

echocardiography

Treatment

The main problem in acute heart failure is that we have not evidence based for the benefits of the drugs as in
chronic heart failire

So for the treatment we must always try to find the etiology and to treat the symptoms and very often we put
patients in ICU

The goals of treatment in a patient with AHF include:

Immediate relief of symptoms and stabilization of haemodynamics (short-term benefits)

Reduction in length of hospital stay and hospital readmissions

Reduction in mortality from heart failure

Key drugs are

Oxygen

Diuretics

Vasodilators

Opiates and inotropes are used more selectively,

Non-invasive ventilation is used commonly

Treatment

Oxygen Oxygen may be given to treat hypoxaemia (SpO2 ,90%), which is associated with an
increased risk of short-term mortality

Diuretics Most patients with dyspnoea caused by pulmonary oedema obtain rapid symptomatic
relief from administration of an i.v. diuretic, as a result of both an immediate venodilator action and
subsequent removal of fluid

Opiates Opiates such as morphine may be useful in some patients with acute pulmonary oedema
as they reduce anxiety and relieve distress associated with dyspnea, May also reduce sympathetic
drive

In patients with resistant peripheral oedema (and ascites), a combination of a loop and a thiazide (e.g.
bendroflumethiazide)

opiates induce nausea may need administration of an antiemetic

Vasodilators Although vasodilators such as nitroglycerine reduce preload and afterload and increase
stroke volume, there is no robust evidence that they relieve dyspnoea or improve other clinical
outcomes

most useful in patients with hypertension and should be avoided in patients with a systolic blood pressure

Treatment

Nesiritidea human BNP that acts mainly as a vasodilatorwas recently shown to reduce
dyspnea

inotrope such as dobutamine should usually be reserved for patients with such severe reduction
in cardiac output that vital organ perfusion is compromised

Inotropes cause sinus tachycardia and may induce myocardial ischaemia and arrhythmias

Drugs with prominent peripheral arterial vasoconstrictor action such as norepinephrine are
sometimes given to severely ill patients with marked hypotension

are given to raise blood pressure and redistribute cardiac output from the extremities to the vital organs

Dopamine In large doses (.5 mg/kg/min) dopamine has inotropic and vasoconstrictor activity. At
lower doses (,3 mg/kg/min) dopamine may have a selective renal arterial vasodilator activity
and promote natriuresis, although this is uncertain. Dopamine may cause hypoxaemia.

Thrombo-embolism prophylaxis with heparin or another anticoagulant should be used, unless

contraindicated or unnecessary

After stabilization TREATMENT

Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker In patients with reduced

EF not already receiving an ACE inhibitor (or ARB), this treatment should be started as soon as
possible,blood pressure and renal function permitting

Beta-blocker In patients with reduced EF not already receiving a beta-blocker, this treatment
should be started as soon as possible after stabilization, blood pressure and heart rate
permitting

Mineralocorticoid (aldosterone) receptor antagonist In patients with reduced EF not already

receiving an MRA, this treatment should be started as soon as possible, renal function and
potassium permitting

Digoxin In patients with reduced EF, digoxin may be used to control the ventricular rate in AF,
especially if it has not been possible to up-titrate the dose of beta-blocker. Digoxin may also
provide symptom benefit and reduce the risk of HF hospitalization in patients with severe
systolic HF

Non-pharmacological/non-device
therapy

Restrict sodium intake to ,2 g/day and fluid intake to ,

1.52.0 L/day

Ventilation-Non-invasive ventilation Continuous

positive airway pressure (CPAP) and non-invasive
positive pressure ventilation (NIPPV) relieve dyspnoea
and improve certain physiological measures (e.g.
oxygen saturation) in patients with acute pulmonary
oedema.

Endotracheal intubation and invasive ventilation in

respiratory failure

References
1)European

Society of Cardiology guidline

2012
2)Kumar

and clark clinical internal medicine

8th edition

3)lectures

of faculty of medicine plzen