2.1 Dr. J. Nugroho Sp.jp - Edema Paru Akut

8/11/2019 2.1 Dr. J. Nugroho Sp.jp - Edema Paru Akut

1/34

Abraham Ahmad A.F.

J. Nugroho

Review Article

Department of Cardiology and Vascular Medicine

Faculty of Medicine, Airlangga University - Dr.Soetomo

General Hospital


2/34

CLINICAL PRESENTATION AHF

Acutely

DecompensatedChronic HF

Hypertensive AHF

ACS and HF

PULMONARY EDEMA

Cardiogenic Shock

Right HF

ACS = acute coronary syndrome; HF = heart failureAdapted from Filippatos G, et al. Heart Fail Rev. 2007;12(2):87-90


3/34

PULMONARY EDEMA

Life-threatening

Require immediate treatment

Mortality rate : High


4/34

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 interstitium and alveoli

Cardiac dysfunction

Deterioration of alveolar gas

exchange and respiratory failure


5/34

PATHOPHYSIOLOGY

Pathophysiologic mechanisms:

Imbalance of Starling forces - Ie, increased

pulmonary capillary pressure, decreased

plasma oncotic pressure, increased negativeinterstitial pressure

Damage to the alveolar-capillary barrier

Lymphatic obstruction Idiopathic (unknown) mechanism


6/34

MECHANISM OFCARDIOGENIC PULMONARY EDEMA


7/34

Elevated LA pressure distention and opening of

small pulmonary vesselsBlood gas exchange does not deteriorate

The progression

Fluid and colloid shift into the lung interstitium

Lymphatic outflow removes the fluid

Alveolar floodingAbnormalities in gas exchange

Vital capacity and respiratory volumes

Severe hypoxemia

Filling interstitial space (can contain up to 500mL)


8/34

DIAGNOSIS

History &

Physical

Examination1

Laboratory

Studies2Electrocardio

graphy3

Clinical features ofleft heart failure

Reflect evidence of

hypoxia and

increased

sympathetic tone History

to determine the

exact cause

Complete bloodcount

Electrolyte

Blood urea nitrogen

(BUN) and creatinine

Blood gas analysis

LA enlargement andLV hypertrophy

Chronic LV

dysfunction

Tachydysrhythmia or

bradydysrhythmia oracute myocardial

ischemia or

infarction


9/34

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 100 pg/mL


10/34

Radiography

Enlarged heart, Kerley lines, basilar edema,

pleural effusion (particularly bilateral andsymmetrical pleural effusions)


11/34

Echocardiography

Establish the etiology of pulmonary edema

Evaluate LV systolic and diastolic function, valvularfunction, and pericardial disease.

Non-invasive hemodynamic parameters appropriate

therapy


12/34

Pulmonary Arterial Catheter

Helps in differentiating CPE from Non CardiogenicPulmonary Edema (NCPE).

A PCWP exceeding 18 mm Hg indicates CPE

Monitor hemodynamic condition


13/34

DIFFERENTIAL DIAGNOSIS

Conditions to consider in the differentialdiagnosis of CPE include the following :

Pneumothorax

Pulmonary embolism

Respiratory failure

Acute Respiratory Distress Syndrome

Asthma

Chronic Obstructive Pulmonary Disease


14/34

MANAGEMENT


15/34

MainGoal

Reduction of

pulmonaryvenousreturn

(preload)

Reduction ofsystemicvascular

resistance(afterload)

Inotropicsupport (in

some cases)

Medical treatment


16/34

Vasodilators ( Nitroglycerin )

Preload reduction

Vasodilation effect lowers preloadreduce

pulmonary congestion

Should be avoided : Systolic blood pressure


17/34

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


18/34

Opiates

Reduce the anxiety associated with dyspnea

Venodilators reduce preload

Reduce sympathetic drive

Depress respiratory drive

Increasing the need for invasive ventilation


19/34

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


20/34

ACE inhibitor (ACEi)

Hemodynamic effects of ACEI :

Reduce afterload, improving stroke volume andcardiac output, and slightly reduce preload

improve renal perfusion diuresis

Caution in patients with :

Hypotension (systolic 3 mg / dl)

Bilateral renal artery stenosis Increased blood potassium levels (> 5 mEq / L)


21/34

Angiotensin II receptor blockers (ARBs)

ACEi intolerance

ACEI and ARBs Preventing remodeling,

reduce arrhythmias

The Valsartan Heart Failure (Val-HeFT) andCandesartan in Heart Failure: Assessment in

Reduction of Mortality and Morbidity(CHARM)

ARBs lowers the incidence of atrial fibrillation (AF)


22/34

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


23/34

Dopamine1 Dobutamine2Norepine

phrine3

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 todecreased

contractility

Positive chronotropic

& inotropic

Moderate or severe

hypotension

should be avoided

-receptorsvasoconstriction

Use in severe

hypotension

Combination with

dobutamine

improve

hemodynamic


24/34

Phosphodiesterase inhibitors ( milrinone )

Increase the level of intracellular cyclicadenosine 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


25/34

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


26/34

Ultrafiltration

Useful in patients with renal dysfunction

and diuretic resistance


27/34

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


28/34

Intra-Aortic Balloon Pumping ( IABP )

Reducing aortic impedance and systolicpressure

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, orrecent MI


29/34

Ventilatory Support


30/34

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


31/34

Mechanical ventilation

When : Remain hypoxic with noninvasive supplemental

oxygenation

Impending respiratory failure

Hemodynamically unstable

Maximizes myocardial oxygen delivery and

ventilation Increase alveolar patency


32/34


33/34

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 echocardiographyImportant diagnostic tools

Therapeutic goal :

Improve the patient's symptoms

Improves fluid status

Identification of causal factors


34/34

2.1 Dr. J. Nugroho Sp.jp - Edema Paru Akut

Documents

Transcript of 2.1 Dr. J. Nugroho Sp.jp - Edema Paru Akut