Abraham Ahmad A.F.

J. Nugroho
Review Article
Department of Cardiology and Vascular Medicine
Faculty of Medicine, Airlangga University - Dr.Soetomo
General Hospital
CLINICAL PRESENTATION AHF
Acutely
Decompensated
Chronic HF
Hypertensive AHF
ACS and HF
PULMONARY EDEMA
Cardiogenic Shock
Right HF
ACS = acute coronary syndrome; HF = heart failure
Adapted from Filippatos G, et al. Heart Fail Rev. 2007;12(2):87-90
PULMONARY EDEMA
Life-threatening
Require immediate treatment
Mortality rate : High
Defined as pulmonary edema due to increased capillary
hydrostatic pressure secondary to elevated pulmonary
venous pressure
McMurray JJ, 2012
Fluid accumulation with a low-protein content in the
lung interstitiumand alveoli
Cardiac dysfunction
Deterioration of alveolar gas
exchange and respiratory failure
PATHOPHYSIOLOGY
Pathophysiologic mechanisms:
Imbalance of Starling forces - Ie, increased
pulmonary capillary pressure, decreased
plasma oncotic pressure, increased negative
interstitial pressure
Damage to the alveolar-capillary barrier
Lymphatic obstruction
Idiopathic (unknown) mechanism
MECHANISM OF
CARDIOGENIC PULMONARY EDEMA
Elevated LA pressure distention and opening of
small pulmonary vessels
Blood gas exchange does not deteriorate
The progression
Fluid and colloid shift into the lung interstitium
Lymphatic outflow removes the fluid
Alveolar flooding
Abnormalities in gas exchange
Vital capacity and respiratory volumes
Severe hypoxemia
Filling interstitial space (can contain up to 500mL)
DIAGNOSIS
History &
Physical
Examination
1
Laboratory
Studies
2
Electrocardio
graphy
3
Clinical features of
left heart failure
Reflect evidence of
hypoxia and
increased
sympathetic tone
History
to determine the
exact cause
Complete blood
count
Electrolyte
Blood urea nitrogen
(BUN) and creatinine
Blood gas analysis
LA enlargement and
LV hypertrophy
Chronic LV
dysfunction
Tachydysrhythmia or
bradydysrhythmia or
acute myocardial
ischemia or
infarction
Brain-type
natriuretic peptide
(BNP)
4
High negative predictive
value
Cutoff value : 100 pg/mL
BNP value of under 100
pg/mL heart failure is
unlikely
The level of BNP increase:
age, renal dysfunction
N -terminal pro BNP
(NT-pro BNP)
5
Well correlated with BNP
levels
NT-proBNP > 450 pg/mL
(in patients <50 years) ~
BNP > 100 pg/mL
Radiography
Enlarged heart, Kerley lines, basilar edema,
pleural effusion (particularly bilateral and
symmetrical pleural effusions)
Echocardiography
Establish the etiology of pulmonary edema
Evaluate LV systolic and diastolic function, valvular
function, and pericardial disease.
Non-invasive hemodynamic parameters appropriate
therapy
Pulmonary Arterial Catheter
Helps in differentiating CPE from Non Cardiogenic
Pulmonary Edema (NCPE).
A PCWP exceeding 18 mm Hg indicates CPE
Monitor hemodynamic condition
DIFFERENTIAL DIAGNOSIS
Conditions to consider in the differential
diagnosis of CPE include the following :
Pneumothorax
Pulmonary embolism
Respiratory failure
Acute Respiratory Distress Syndrome
Asthma
Chronic Obstructive Pulmonary Disease
MANAGEMENT
Main
Goal
Reduction of
pulmonary
venous
return
(preload)
Reduction of
systemic
vascular
resistance
(afterload)
Inotropic
support (in
some cases)
Medical treatment
Vasodilators ( Nitroglycerin )
Preload reduction
Vasodilation effect lowers preload reduce
pulmonary congestion
Should be avoided : Systolic blood pressure
<110 mmHg
Diuretics
Loop diuretics : Furosemide
Affect the ascending loop of Henle
Diminished renal perfusion
Delay the onset of effects of loop diuretics
Long-term use electrolyte disturbances,
hypotension and worsening renal function
Opiates
Reduce the anxiety associated with dyspnea
Venodilators reduce preload
Reduce sympathetic drive
Depress respiratory drive
Increasing the need for invasive ventilation
Nesiritide
Reduce :
Left ventricular filling pressure
Pulmonary arterial pressure
Right atrial pressure
Systemic vascular resistance
Reduce levels of :
Renin, Aldosterone
Norepinephrine, and endothelin-1
Ventricular tachycardia
May cause hypotension
ACE inhibitor (ACEi)
Hemodynamic effects of ACEI :
Reduce afterload, improving stroke volume and
cardiac output, and slightly reduce preload
improve renal perfusion diuresis
Caution in patients with :
Hypotension (systolic <80 mmHg)
Increased serum creatinine (> 3 mg / dl)
Bilateral renal artery stenosis
Increased blood potassium levels (> 5 mEq / L)
Angiotensin II receptor blockers (ARBs)
ACEi intolerance
ACEI and ARBs Preventing remodeling,
reduce arrhythmias
The Valsartan Heart Failure (Val-HeFT) and
Candesartan in Heart Failure: Assessment in
Reduction of Mortality and Morbidity (CHARM)
ARBs lowers the incidence of atrial fibrillation (AF)
Inotropes
When :
Reduction in preload and afterload still has not
improved
Impaired systolic function
Perfusion disturbances and/or congestion
Associated with increased long-term
mortality
Used only in heart failure patients with low
cardiac index and stroke volume
Dopamine
1
Dobutamine
2
Norepine
phrine
3
Cardiogenic shock
Low dose
dopaminergic
receptors
increasing diuresis
Moderate dose
-receptors
Cardiac
contractility and
Heart rate
High dose
-receptors
Vasoconstriction
(increased
afterload), Blood
pressure
Hypotension due to
decreased
contractility
Positive chronotropic
& inotropic
Moderate or severe
hypotension
should be avoided
-receptors
vasoconstriction
Use in severe
hypotension
Combination with
dobutamine
improve
hemodynamic
Phosphodiesterase inhibitors ( milrinone )
Increase the level of intracellular cyclic
adenosine monophosphate (cAMP)
Positive inotropic effect on the myocardium
Peripheral vasodilation (decreased afterload)
Reduction in pulmonary vascular resistance
(decreased preload)
Improvements in stroke volume, cardiac output,
PCWP (preload), and peripheral vascular
resistance (afterload)
increased incidence of arrhythmias
Calcium sensitizers ( Levosimendan )
Inotropic, metabolic, and vasodilatory effects
Binding to troponin C
Not increase myocardial oxygen demand
Not a proarrhythmogenic agent
Effective and safe alternative to dobutamine
Ultrafiltration
Useful in patients with renal dysfunction
and diuretic resistance
Ultrafiltration should be considered in acute heart failure with volume overload who
do not respond to high doses of diuretics or in patients with impaired renal function
Intra-Aortic Balloon Pumping ( IABP )
Reducing aortic impedance and systolic
pressure
In cardiogenic shock :
decreases LV filling pressures by 20-25%
improves cardiac output by 20%
Provide hemodynamic support in perioperative
and postoperative period in high-risk patients
severe coronary disease, severe LV dysfunction, or
recent MI
Ventilatory Support
Noninvasive pressure-support ventilation (NPSV)
Consider in severe CPE
Two types :
CPAP and BiPAP
Improves air exchange
Increases intrathoracic pressure reduction
preload & afterload
Several studies :
Decreased length of stay in the ICU
Decreased need for mechanical ventilation
Mechanical ventilation
When :
Remain hypoxic with noninvasive supplemental
oxygenation
Impending respiratory failure
Hemodynamically unstable
Maximizes myocardial oxygen delivery and
ventilation
Increase alveolar patency
Summary
Common cause of acute heart failure, life-threatening
and require immediate action
Defined as pulmonary edema due to increased capillary
hydrostatic pressure secondary to pulmonary venous
pressure
High mortality rate
Acute myocardial infarction, hypotension and a history
of frequent acute attacks increase the risk of mortality
BNP and echocardiography Important diagnostic tools
Therapeutic goal :
Improve the patient's symptoms
Improves fluid status
Identification of causal factors