dr.

Ilham Uddin, SpJP, FIHA

Tempat, tgl. Lahir : Tuban, 21 Desember 1968

Riwayat Pendidikan
• Fakultas Kedokteran Universitas Airlangga, Surabaya, Lulus 1994
• Spesialisasi Jantung dan Pembuluh Darah di Bagian Kardiologi dan
Kedokteran Vaskular FK Universitas Indonesia / Harapan Kita National
Cardiovascular Center, Jakarta, lulus 2006
• Fellow Cardiovascular Intervensi, Semarang, 2012-2014

Riwayat Pekerjaan
1. Kepala Puskesmas Compreng, Tuban 1995-1998
2. Sekretaris Bagian Kardiologi & Kedokteran Vaskular FK UNDIP.RSUP dr
Kariadi 2009-sekarang
 Pulmonary Edema :
Cardiac Vs Non Cardiac Origin

Ilham Uddin, MD, FIHA

Dept. of Cardiology and Vascular Medicine

Kariadi Hospital – Diponegoro University

 Terminology
• Heart Failure: The inability of the heart to
maintain an output adequate to maintain the
metabolic demands of the body.
• Pulmonary Edema: An abnormal
accumulation of fluid in the lungs.
• CHF with Acute Pulmonary Edema:
Pulmonary Edema due to Heart Failure
(Cardiogenic Pulmonary Edema)
 Pulmonary Blood Pressures
Gravity and Distance:
– Distance above or below the heart (arterial ,venous)
– Distance between Apex and Base
Gravity and Blood Flow
Physiology of Microvascular Fluid Exchange in the Lung

Ware, L. B. et al. N Engl J Med 2005;353:2788-2796

 Pulmonary Edema
• Excessive amounts of fluid collect in the
spaces between the alveoli and the capillaries.
• Cardiac (CPE) – increased LVEDP (PCWP);
increased pressure in the pulmonary veins
push fluid out of the capillaries.
• Noncardiac (NCPE) – inflammation, „leaky“
alveolocapillary membrane; destruction of
capillary beds causes fluid to leak out -> ARDS
– Inhaled toxins, aspiration, sepsis, oxygen toxicity,
pancreatits, traumatic shock
Ware, L. B. et al. N Engl J Med 2005;353:2788-2796
 Pathophysiology : CPE
Pulmonary edema
 Fluid first accumulates in interstitial space.

 Followed by alveolar flooding

 Impairs gas exchange and reduces lung compliance

Hydrostatic (cardiogenic) pulmonary edema (CPE)

 Fluid accumulation in interstitium raises hydrostatic

pressure rapidly and alveolar flooding follows.

 Flooding occur in “all or nothing” manner.
 Fluid filling alveoli is identical to interstitial fluid.

Increased Pressure in Pulmonary Vascular Bed

Mosby items and derived items © 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 9
Pulmonary Edema & Acute Heart Failure
Etiology CPE :

 Left ventricular failure

 Valvular heart disease
– Stenosis
– Insufficiency
 Hypertensive crisis (high afterload)
 Volume overload

Increased Pressure in Pulmonary Vascular Bed

Clinical Severity Classification
Warm/Dry
Warm/Wet

Cold/Dry

Cold/Wet

• PERFUSION
• CONGESTION
– Auscultation of the lungs
Ware, L. B. et al. N Engl J Med 2005;353:2788-2796
 Pathophysiology NCPE
Nonhydrostatic (noncardiogenic) pulmonary edema
 Fluid accumulates despite normal hydrostatic

pressure.
 Vascular endothelial injury alters permeability.
 Protein-rich fluid floods the interstitial space.
 Alveolar flooding occurs as osmotic pressures in capillaries
and interstitium equalize.
 Alveolar epithelium is also injured.
 There is also impaired pulmonary fluid clearance.
 The common mechanism for development of ARDS
appears to be lung inflammation.

Increased Permeability of Alveolar-Capillary Walls

Mosby items and derived items © 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 14
Mosby items and derived items © 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 15
 Pathophysiology NCPE
Gas exchange and lung mechanics during ARDS
 Restrictive changes with refractory hypoxemia

 Altered permeability floods the lung, resulting in

decreased lung compliance (CL) and consolidation.

 Impaired surfactant synthesis and function worsens

gas exchange and CL.

 Loss of normal vascular response to alveolar

hypoxemia
 Unaerated alveoli receive blood flow in excess of ventilation
so increased shunting occurs

Mosby items and derived items © 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 16
 Etiology
Cardiogenic vs. Noncardiogenic PE
• Cardiogenic pulmonary edema
– Heart failure
• Coronary artery disease with left
ventricular failure.
• Cardiomyopathy
• Obstructing valvular lesions -- for
example
– Fluid overload -- for example,
kidney failure.
• Non-cardiogenic pulmonary edema
-- due to changes in capillary
permeability
– LUNG
• Smoke inhalation
• Near-drowning
• Overwhelming aspiration
• Acute Respiratory Distress Syndrome
(ARDS)
• Acute lung re-expansion
• High altitude pulmonary edema
– CAPILLARY
• Overwhelming sepsis
• Disseminated intravascular coagulopathy
(DIC)
 Signs & Symptoms:
Pulmonary Edema
– Dyspnea and orthopnea, Severe respiratory
distress
– Frothy sputum & Crackles in lungs
– Cyanosis, or pale wet skins (if severe)
– JVD
– Swollen lower extemeties
– Severe apprehnsion, agitation, confusion
– Abnormal vital signs
 DDx
• History
• Physical examination
– Paleness (anemia), cyanosis
– Respiratory rate, heart rate, BP, body temperature
– Respiratory effort
– Lungs and heart auscultation
– Peripheral edema
• Pulse oximetry
• Chest x-ray
www.med.yale.edu/intmed/cardio/imaging/findin
gs/pulmonary_edema/index.html
Radiographic Features That May Help to Differentiate
Cardiogenic from Noncardiogenic Pulmonary Edema

Ware, L. B. et al. N Engl J Med 2005;353:2788-2796

 Algorithm for the Clinical Differentiation between
Cardiogenic and Noncardiogenic Pulmonary Edema

Ware, L. B. et al. N Engl J Med 2005;353:2788-2796

Pulmonary Edema & Acute Heart Failure
General Therapeutic Approach
Oxygen

• Class I, C
– Improves oxygen delivery and tissue
perfusion
– Goal Saturation should be 95-98%, beyond
that there is no indication for increased FIO2
– Always consider CPAP first or Non Invasive
Positive Pressure Ventilation First
– Endotrachial Intubation as a last resort
Pharmacotherapy

• Morphine
• Anticoagulation
• Vasodilators
• Diuretics
• Beta Antagonists
• Inotropic Agents
Morphine

• Class IIb, B
– Great Early in management
– Venodilation
– Mild Arterial Dilation
– Slows Heart rate
Anticoagulation

• No evidence to support anticoagulation for

Acute Heart Failure alone
• Yes in the case of Atrial Fibrillation
• Yes in the case of LV thrombus
 Anticoagulation: CPE & Non STEMI
 In Management of ACS, we need to consider the efficacy versus
safety of antithrombotic that we use, including anticoagulant
 Anticoagulant options in management of UA/NSTEMI:
1. UFH
2. LMWH
3. Fondaparinux
 Based on OASIS 5, Fondaparinux (Arixtra®) is a selective factor Xa
inhibitor which offers good efficacy with less bleeding risk compared
to enoxaparin for management UA/NSTEMI
 Fondaparinux 2.5 mg SC once daily is recommended by ESC
guideline for UA/NSTEMI patients as having favorable efficacy-
safety (Class I)
 Fondaparinux can be used for low to moderate renal impairment and
it’s contraindicated for sever renal impairment with CrCl < 20 ml/min
 Anticoagulation: CPE & STEMI
UNFRACTIONATED HEPARIN
► GOLD STANDARD for so many years
► contain the pentasaccharide sequence, which binds to
antithrombin and accelerates the rate at which antithrombin
inhibits factor Xa
► Disadvantages
 Heparin induced thrombocytopenia (HIT)

 Parenteral administration

 Nonspecific protein and cell binding

 Bleeding complications similar to VKA

 Indirect inhibition via anti thrombin

 Inability to inhibit clot bound thrombin

 Frequent monitoring & dose adjustment

 Adverse reactions – osteoporosis

The Need for Novel Anticoagulation Therapy in Acute Coronary Syndrome. Am J Thera 2011
 Anticoagulation: CPE & STEMI
LMWH
► Have balanced anti-Xa and anti-IIa activity,
depending on the molecular weight of the
molecule, with greater anti-IIa activity with
increasing molecular weight.

► Have different pharmacokinetic properties and

anticoagulant activities, and are not therefore
clinically interchangeable

► Most LMWHs are contraindicated in the case of

renal failure with CrCl <30 mL/min.

ESC guideline for STEMI 2012

 Anticoagulation: CPE & STEMI
Fondaparinux
• Selective activated factor X (factor Xa)
inhibitor available for clinical use
• Inhibits coagulation factor Xa by binding
reversibly and non-covalently to antithrombin,
with a high affinity
• 100% bioavailability after SQ injection, with
an elimination half-life of 17 h
• eliminated mainly by the kidneys, and is
contraindicated if CrCl is <20 mL/min
 Anticoagulation: CPE & STEMI
Role of Fondaparinux in STEMI
management:

•Adjunctive anticoagulant for STEMI

patients who are managed with
thrombolytics, OR
• Initially are to receive no other form
of reperfusion therapy.

Arixtra-BPOM approved on GDS12/IPI10 (24 November 2010)

Vasodilators
• Nitrates: Class I, B
– Improves Cardiac Output
and decreases PCWP
– Best with diuretics
– Low doses, venodilation
– High doses, arterial dilation
– Preload and Afteroad
– Good for 16-24 hours
• Sodium Nitroprusside:
Class I, C
– Severe Heart Failure with
Hypertension
– Primarily arterial dilation
– Need for arterial invasive
monitoring
– Stop if active ischemia due
to coronary steal
phenomenon
Summary of Vasodilators
 Diuretics
• Class I, B
 Diuretics
• Class I, B
Diuretic Resistance can be
associated with increased mortality.
Inotropic Agents

• Peripheral Hypoperfusion refractory to

vasodilators and diuretics, Class IIa, C
• Danger: May increase oxygen demand and
calcium loading
Dopamine and Dobutamine
• Dopamine: • Dobutamine, Class IIa, C
– Vasodilator of Renal,
Coronary, splanchnic and
Cerebral Vascular beds
– Hypotensive patients
– Drawbacks: arrhythmia,
increased pulmonary
vascular resistance and
increased afterload
– Hypotension and low Urine
output
– Beta 1 and 2 agonist
– At high doses increases
SVR
– Additive effect with
Phosphodiesterase
inhibitors
– Draw Backs- arrhythmia,
reflex decrease in
sympathetic tone
Pressors

• Vasopressin: Cardiogenic shock in

conjunction with inotropic therapy
• Epinephrine B1 and B2,
• Norepinephrine alpha receptors
• Cardiac Glycosides: Inhibit cardiac Na/K
ATPase, increases Ca/Na exchange
mechanism. Tachycardia induced
Cardiomyopathy.
 ARDS Management Principles

  ?

Brandstetter RD. Heart Lung 1997;26: 3-14

Thank You

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