ADAMA HOSPITAL MEDICAL COLLEGE

DEPARTMENT OF EMERGENCY MEDICINE & CRITICAL CARE

SEMINAR ON APPROACH TO ACUTE HEART FAILURE AND

PULMONARY EDEMA
By: SAMUEL SHIFERAW ( C-II )

MODERATOR:
DR. SHIMELIS K. (MD, EMERGENCY MEDCINE & CRITICAL CARE SPECIALIST).
JUNE,2022 GC
1
01/22/2023
 OUTLINE

• Definition
• Causes
• Classification
• Differential Diagnosis
• Patient Approach- Hx, P/E & Investigations
• Manegement
 Acute Heart Failure
Defnition

 Acute heart failure (AHF) is a clinical syndrome of

new or worsening signs and symptoms of HF

 often leading to hospitalization or a visit to the

emergency department

 Covers a wide spectrum of illness severity

 Alternative terms Acute decompensated heart
failure, acute heart failure syndrome, or
hospitalized with heart failure

• 70% - due to worsening chronic HF

• 15 - 20% - present for the first time
• 5% with advanced or end-stage HF

 the prevalence of heart failure is expected to

increase with increased survival from chronic HF

 Heart failure has a poor prognosis, with ~ 50% of

patients dying within 5 years of diagnosis.
causes
For new onset AHF

1. Coronary artery disease ( ACS, MI)

2. Myocarditis
3. Acute valve syndromes (IE, ruptured chordae, ischemic
papillary muscle rupture, or aortic
dissection),thrombosed valve, Tear or perforation
4. Progressive valve disease
5. Cardiomyopathic states (Hypertrophic , recent onset
dilated, tachycardia mediated, stress/takotsubo )
6. Poorly controlled hypertension
 For Decompensation of chronic HF

 can occur without known precipitant factors but

more often occurs with one or more factors such as

infection
uncontrolled hypertension
rhythm disturbances and
nonadherence with drugs and diet.
Classification
There are six phenotypes

1. Those with acute heart failure and hypertension

(Hypertensive HF)

• characterized by the rapid onset of symptoms or signs

of HF (~10% of AHF )

• defined as rapid onset of HF with systolic blood

pressure >140 mmHg (frequently >180 mmHg)
• Commonly in older adults, particularly women

• frequently have a history of poorly controlled

hypertension

• usually predominant pulmonary rather than systemic

congestion - minimal weight gain prior to admission

• treatment initially focuses on antihypertensive

therapy
2. Patients with pulmonary edema

 in 15% or more of patients, Severe form in <3%

 typically experience a sudden and overwhelming

sensation of suffocation and air hunger

 extreme anxiety, cough, expectoration of a pink

frothy liquid, and a sensation of drowning
 patient sits upright, unable to speak in full
sentences, increased RR

 Signs of RD ,noisy, audible inspiratory and

expiratory sounds

 profuse sweating, cool skin, and cyanotic, reflecting

increased sympathetic outflow (PR also increased )

 SPO2 is usually < 90%

 obtundation in severe hypoxemia

 Coarse creptition, wheeze – on chest auscultation ,

 Cardiac auscultation - difficult in the acute situation, but

S3 & S4 may be present

 The chest radiograph cardiomegaly, upper zone

redistribution of blood flow interstitial edema, alveolar
edema
3. Acute heart failure accompanied by hypotension or
poor perfusion

• SBP is <90 mmHg in ~8% of patients

• characterized by symptoms and signs related to

decreased end-organ perfusion

• fatigue, altered mental status, or signs of organ

hypoperfusion
prerenal azotemia or abnormal hepatic enzymes
• tachypnea at rest, tachycardia, and a cold and cyanotic
periphery, poor capillary refill, diminished PP, (due to
decrased SV)

• with decompensated end-stage HF - present in occult

shock

• The only parameter differentiating occult shock patients

from nonshock patients is a significantly elevated lactic
acid level

4. Patients with acute decompensation of chronic heart

failure
5. High-output heart failure

• uncommon cause of AHF

• generally presents with warm extremities, pulmonary

congestion, tachycardia, and a wide pulse pressure

• has a relatively normal ejection fraction

• and is often caused by anemia or thyrotoxicosis

6. Those with isolated right sided heart failure

 occurs commonly in patients with

severe isolated tricuspid regurgitation,

right ventricular dysfunction, and
chronic lung disease,(COPD, interstitial lung
disease, or long-standing pulmonary
hypertension)

 patients are often oxygen dependent and present

with signs and symptoms of right-sided HF
Differential Diagnosis

1. Pulmonary embolism – sudden onset of dyspnea,

pleuritic chest pain, and cough (ECG, CXR)

2. Pneumonia -- acute SOB, hypoxemia, and an

inconclusive pulmonary examination ( CXR may help)
• Fever and leukocytosis may suggest an infection

3. Asthma –acute SOB, cough,fatigue,& wheezing (CXR)

 Patient Approach
History

• No single historical or physical examination finding

with excellent sensitivity and specificity

• initial clinical judgment has a sensitivity of 61% and

specificity of 86%

• A history of heart failure - most useful historical

parameter, but has a sensitivity of only 56% and
specificity of 80%
• Risk factors - HTN, DM, VHD, old age, male sex

• dyspnea on exertion - The symptom with the highest

sensitivity for diagnosis (84%)

• most specific symptoms - PND , orthopnea, and edema

(76% to 84%)

• Symptoms of abdominal and peripheral congestion ,

nausea and anorexia
• Other symptoms include

nocturia and
neurologic symptoms such as confusion,
headaches, insomnia, anxiety, disorientation, and
impaired memory.

• Evaluation for precipitating factors may aid diagnosis.

Physical examination
 G/A – Acutely sick looking
 Respiratory –
• Decreased air entry at the lung bases (pleural
effusion), (more frequent in the right pleural
cavity than in the left)
• Rales (crackles) and wheezing

 Cardiac examination –
• may be entirely normal or advanced systolic
dysfunction exhibit S3 and a laterally displaced
apex beat
• A murmur of MR when LV is markedly enlarged

• A TR murmur - when the right ventricle is volume

or pressure overloaded

• An elevated JVP

• An S3 has the highest positive likelihood ratio for

acute heart failure but its absence is not useful
 Gastrointestinal system--

positive hepatojugular reflux

tender, enlarged liver are frequent findings

 Musculoskeletal --

Leg edema (frequently evident in both legs)

• pretibial region and ankles in ambulatory
patients.
• Sacral edema in patients who are bedridden.
Investigations
Electrocardiogram 

• to assess for evidence of ACS (myocardial ischemia or MI) and

arrhythmias (eg , atrial fibrillation)

• other predisposing or precipitating conditions for HF such as left

ventricular hypertrophy or left atrial abnormalities

Chest radiograph 

• findings in AHF can range from mild pulmonary vascular redistribution

to marked cardiomegaly and extensive bilateral interstitial markings

• The presence of bilateral perihilar alveolar edema may give the typical
"butterfly" appearance
• Unilateral cardiogenic pulmonary edema is
infrequent

• Pleural effusions - often absent with de novo AHF but

are frequently present in acute decompensation of
chronic HF

• Up to 20 percent of patients with AHF may have

normal chest radiographs
Laboratory data 

•  Initial laboratory data - obtained when feasible but

are generally not needed for Dx or Tx

• treatment should NOT be delayed while waiting for

the results of laboratory tests

• Pulse oximetry and ABG analysis - to assess

ventilatory and acid-base status

• Routine chemistries - serum electrolytes,

bicarbonate, BUN, and serum creatinine
• A decline in renal function is commonly found in
advanced HF (cardiorenal syndrome) -may be due to
a low-output state

• Increased BUN and serum creatinine - underlying

renal disease, bilateral renal artery stenosis.

• B-type natriuretic peptide and N-terminal pro-B-

type natriuretic peptide - in the setting of
undifferentiated dyspnea , improving diagnostic
discrimination
• lactic acid level in shock as well as in those with
marked weakness and/or uncertain peripheral
perfusion

• Serum troponin (T or I) levels in any patient with

possible ACS

• CBC - to identify the presence of infection or anemia

that may have precipitated the event
Echocardiography
• is recommended for new or prior history of HF with
suspected change in cardiac function

• The urgency of echocardiography varies with the

acuity of presentation

• Should be done early in cardiogenic shock or low-

output syndrome & suspected valvular heart disease
 MANEGEMENT

• initial approach is depend on the acuity of the

presentation , hemodynamics, and volume status

• Airway management - first priority to In critically ill

patients

• less acutely ill, a focused evaluation followed by

treatment
• supplemental oxygen to keep SPO2 at or above 95%

• In extreme findings, use endotracheal intubation

• Other standard initial care measures include - cardiac

monitoring, IV access, and frequent vital sign
assessments.

• A urinary drainage catheter - monitoring fluid status in

the severely ill or incontinent (best reserved for
extreme illness or an inability to void)
HYPERTENSIVE ACUTE HEART FAILURE

• The failing heart - sensitive to increases in afterload

• some patients develope pulmonary edema with a

systolic BP as low as 150 mm Hg

• Prompt recognition and afterload reduction with

vasodilators can avoid the need for intubation
Nitroglycerin
 A short-acting, rapid-onset, systemic venous and
arterial dilator
 decreases mean arterial pressure by reducing
preload at high doses ,initially, it reduces afterload.

 may have coronary vasodilatory effects, decreasing

myocardial ischemia and improving cardiac function

 routes—IV, sublingual, or transdermal—based on

symptom severity
 Sublingual nitroglycerin spray is easily
administered, rapidly bioavailable, and titratable
• Initially sublingual 0.4 milligrams (400 micrograms),
1-2 sprays or tablets every 5 minutes until relief or
replacement with IV nitroglycerin

• A starting dose of 0.5 to 0.7 microgram/kg/min IV is

common and titrated every few minutes up to 200
micrograms/min based on the blood pressure
tolerance and symptoms

• High doses aid in the acute setting, and adverse

events are uncommon
• Apply transdermal nitroglycerin (0.5–2 inches to the
chest wall)

only after initial therapy has improved conditions

or if the symptoms are minor, because it has a
slow onset of action

• The most important nitroglycerin complication is

hypotension ( often transient & usually resolves after
cessation )
Nitroprusside
 When further afterload reduction is required

 (i.e., continued high systemic vascular resistance

manifested by persistent elevated BP and
continued symptoms despite nitroglycerin doses
>200 micrograms/min)

use IV nitroprusside.

 This is a potent arterial vasodilator

 Its hemodynamic effects include

decreased blood pressure

left ventricular filling pressure reduction, and
increased cardiac output

 initial dose is 0.3 microgram/kg/min, titrated upward

every 5 to 10 minutes based on BP and clinical
response (maximum 10 micrograms/kg/min)
Diuretics

 After vasodilator therapy or with near-normal blood

pressure and symptoms

 based on continued symptoms after blood pressure is

controlled

 Loop diuretics (furosemide is the most commonly used)

 administered alone without vasodilators for

hypertensive heart failure may increase mortality and
worsen renal dysfunction.
NORMOTENSIVE HEART FAILURE

• Shortness of breath, orthopnea, jugular venous

distention, rales, and an S3 may exist in the presence
of normal vital signs, oxygenation, and ventilation

• In this situation, diuresis should occur first, with

further treatment based on response to therapy
Loop diuretics

 provide rapid symptomatic relief of congestive

symptoms and improve the effects of ACEI by
decreasing intravascular volume

 dose based on symptoms and prior usage

 In general, dose loop diuretics at the lowest possible

dose that relieves congestion.

 After initial relief, a fixed maintenance dose helps

prevent recurrence.
 The DOSE trial

 Higher doses create more rapid symptom

improvement but also a slight decrease in renal
function or worsens and create hypokalemia.

 Potassium-sparing diuretics, such as spironolactone

(25 to 50 milligrams PO)

 these are used more for their mortality benefit than

diuretic effect
Morphine

 not a good choice for acute heart failure b/c of need

for mechanical ventilation, prolonged hospitalization,
intensive care unit admission, and mortality

 If desired for its venodilation properties or pain

control, use morphine in small, titrated doses (2 to 4
milligrams IV) and with monitoring.
Oral angiotensin-converting enzyme inhibitors and
angiotensin receptor blockers

 given for hypertension and chronic heart failure, no

solid data to recommend use for acute heart failure

 Ongoing use decrease mortality and hospitalizations

in patients with reduced ejection fraction

 IV enalaprilat appears safe and perhaps efficacious

in patients with acute heart failure
β-Blockers
 are not usually initiated in the acute setting except
to control rate-related heart failure

 Norepinephrine levels are elevated in heart failure,

contribute to myocardial hypertrophy, increase
afterload and coronary vasoconstriction, and are
associated with mortality

 β-Blockers reduce sympathetic nervous system

activity and are used for mortality reduction and
symptom relief.
Oral calcium channel blockers
 have myocardial depressant activity and are not
routine treatment for acute heart failure

 trials demonstrate either no benefit or worse

outcomes

Avoid selective or nonselective NSAIDs in patients

with acute heart failure

 They can cause sodium and water retention and

blunt the effects of diuretics and may increase
morbidity and mortality.
 Referrences

1. Tintinally ninth edition

2. UpToDate 2018.
THANK YOU !!!!