Dr Md Seebat Masrur Indoor Medical Officer Cardiology Dept Bangladesh

1. Dr Md Seebat Masrur
IMO at Cardiology at TMC & RCH

2. • Generally defined as a complex clinical syndrome in
which an abnormality of cardiac function and
connected system is responsible for failure of the
heart to move blood forward at a rate commensurate
with the requirement of the metabolizing tissues.
Ref.1.Braunwald`s Heart Disease
2.Hurts`s the heart

3. • A clinical syndrome in which the dominant feature is
fluid congestion in the lung(pulmonary oedema)
rather in the systemic circulation
• If left atrial pressure rises acutely it may cause
pulmonary oedema and if rises gradually there will
be reflex pulmonary vesoncstriction.

4. • Approximatly 5.1 million persons in the USA have
clinically manifest HF, and the prevalance continues
to rise
• The lifetime risk of developing HF is 20% for
Americans more or equal 40 years of age.
• Acute Heart Failure syndromes constitue the most
common indication for hospitalization in adults over
the age of 65 years.
• There are no available data for HF in Bnagladesh.

5. • Overall, the prevalence of heart failure in Asia is
1.26% to 6.7%.In Bangladesh, rheumatic heart
disease still plays an important role in the incidence
of heart failure, complicating the scenario. In a study
conducted in National Institute of Cardiovascular
Diseases and different medical colleges of
Bangladesh revealed that IHD was responsible for
65% of chronic heart failure, rheumatic heart disease
for 18% cases, hypertension for 12% cases and
idiopathic cardiomyopathy for 5% cases.

6. Loss of Muscles Volume overload Pressure overload Restricted Filling
• Post MI
• Chronic Ischemia
• Connective
Tissue Disease
• Infection
• Poisons(Alcohol,
cobalt,doxorubic
in)
• Regurgitative
Valve
• High Output
Status
• Systemic
Hypertension
• Outflow
obstruction
• Pericardial
Diseases
• Restrictive
Cardiomyopathy
• Tachyarrhythmia
s

8. several key factors play varying roles in the initiation
and propagation of AHF, including but not limited to
(1) Acute or subacute worsening of cardiac dysfunction,
either systolic or diastolic
(2) Neurohormonal activation
(3) The cardiorenal syndrome resulting from the
complex interplay between the kidney and the heart
(4) Impaired vascular/endothelial function
(5) Inflammation and oxidative stress and
(6) Hemodynamic Factors

14. ACC/AHA Stage Symptoms
A At high risk for heart failure but without structural heart
disease or symptoms of heart failure.
B Structural heart disease but without signs or symptoms of heart
failure.
C Structural heart disease with prior or current symptoms of
heart failure.
D Refractory heart failure requiring specialized interventions.

15. Killip class I Includes individuals with no clinical signs of heart failure
Killip class II Includes individuals with rales or crackles in the lungs, an S 3 gallop,
and elevated jugular venous pressure
Killip class III Describes individuals with frank acute pulmonary edema
Killip class IV Describes individuals in cardiogenic shock or hypotension (measured
as systolic blood pressure <90 mmHg), and evidence of low cardiac
output (oliguria, cyanosis, or impaired mental status).

17. Subset PCWP Cardiac Index Mortality Rate
I <18 >2.2 3
II >18 >2.2 9
III <18 <2.2 23
IV >18 <2.2 51

18. Systolic Diastolic Both
Impaired contractility of
the left ventricle(EF%)
Associated with chamber
dilation
Poor Ventricular Filling and
high LV end diastolic
pressure
Left ventricular
hypertrophy-stiff
noncompliant ventricle
Often coexist particularly in
patients with CAD.

19. Acute Chronic Acute on Chronic
1.Acute MI
2.Acute native valve failure
e.g Chordal rupture,
Endocarditis
3.Acute myocarditis
1.ICM
2.DCM
3.Hypertensive & diastolic
cardiomyopathy
4.Valvular disorders
5.Thiamine deficiency
Infection(Viral,Bacterial)

20. • The Acute Decompensated Heart Failure National
Registry (ADHERE) “risk tree”.
• The Enhanced Feedback for Effective Cardiac
Treatment (EFFECT) risk index.
• Get With the Guidelines–Heart Failure (GWTGHF) risk
score.
• The ESCAPE discharge risk score
• PROTECT risk score

21. • History taking and general examination
• Functional and haemodynamic assessment
• Diagnostic investigations
• Management plan
 Lifestyle modification
 Phamrmacological management
 Device therapy
 Revascularization
 Vaccination

22. A patient with AHF typically presents with some combination of increased
congestion and, less frequently, decreased peripheral perfusion. In addition to
disturbances in oxygenation due to pulmonary edema, renal dysfunction is a
frequent manifestation of AHF and reflects the multisystem nature of this
disease.
• The mean age of patients with AHF is in the mid-70s, with about half of
each sex and the majority with normal or elevated blood pressure.
• Most frequent symptoms at presentation:
• Dyspnea (including increasing dyspnea on exertion, dyspnea at rest,
orthopnea, and paroxysmal nocturnal dyspnea)
• Fatigue (including confusion)
• Cough
• Abdominal discomfort (including early satiety, bloating, anorexia)
• Leg pain (secondary to tense peripheral edema)
• Sleep disturbances

23. • The typical patient presents with signs and symptoms of
congestion, usually with some combination of lower extremity
edema and pulmonary congestion, normal or elevated blood
pressure and heart rate, and compromised oxygenation
proportional to the extent of the pulmonary edema. A significant
minority of patients may manifest worsening of their heart failure
with predominantly abdominal congestion symptoms and signs,
rather than lower extremity edema.
• Other patients, often elderly with hypertension, can present with
rapid, if not fulminant, pulmonary edema with no or mild increase
in total body fluid. Patients with recurrent heart failure
exacerbations tend to recapitulate their clinical presentations in
subsequent episodes, so obtaining a history of the time course,
triggers, signs and symptoms, and response to therapy of prior
events can increase the sensitivity to early decompensation.

24. Left Sided Heart failure

25. Most frequent signs at
presentation
• Edema (legs, abdomen, sacral)
• Pulmonary rales, pleural effusion
• Elevated jugular venous pressure
• Positive abdominojugular reflux
(hepatojugular reflux)
• Increased body weight
• Increased abdominal girth
• Normal or elevated blood
pressure
• Tachypnea
• Increased heart rate
• Third heart sound
Less common signs at presentation,
suggestive of low cardiac output
• Cool extremities
• Hypotension
• Narrow pulse pressure
• Pulsus alternans
• Impaired end organ
function, such as decreased
urine output

26. • There are no physical exam findings that individually establish a definitive
diagnosis of AHF, but relevant findings may be considered in two main categories.
First, there are findings that suggest the presence of underlying cardiac
dysfunction that provides the substrate for the AHF episode.
• These findings include evidence of left ventricular systolic dysfunction (laterally
displaced and/or diffuse PMI, S3, decreased stroke volume on carotid pulse),
diastolic dysfunction (S4), or both.
• Second, physical exam signs can support the diagnosis of AHF by suggesting the
predominant pathophysiologic process involved in the decompensation, such as
volume overload (peripheral edema, pleural effusions, rales, ascites, elevated
jugular venous pressure, hepatojugular reflux), vascular redistribution (elevated
jugular venous pressure, hepatojugular reflux, often elevated blood pressure), or
low cardiac output (cool extremities, low blood pressure, often narrow pulse
pressure, pulsus alternans).
• Note that patients with chronic heart failure may have markedly elevated
pulmonary venous pressure causing significant dyspnea with relatively mild rales.
Patients with AHF due to vascular redistribution frequently have rapid onset of
symptoms that can occur in the absence of signs of marked volume overload.

27. 12 Leads ECG CXR(P/A) Blood
It may reveal
• MI
• LVH
• Arrhythmia
• IHD
• Enlarged hilar vessels
• Ground glass/reticular
shadowing of alveolar
oedema
• Prominance of upper
lobe vessels
• Septal or kerley`s B line
• Pulmonary oedema
• NT Pro BNP
• Complete Blood Count
o Blood urea
o Serum Electrolytes
o Serum Creatinine
o Blood Sugar
o TSH

28. Class I In patient with dyspnea, measurement of BNP or NT-pro BNP is
useful to support a diagnosis or exclusion of HF
Class I Measurement of BNP or NT-ProBNP is useful for establishing
prognosis or disease severity in chronic HF
Class I Measurement of baselione levels of Natriuretic peptide biomarkers
and/or cardiac troponin on admission to the hospital is useful to
establish a prognosis in acutely decompensated HF.

35. • Most useful diagnostic test in the evaluation of
patients with heart failure.
• Provide information about aetiology and prognosis of
heart failure.
• Regional wall abnormalities, EF, LV dimensions, LV
mass, the myocardial performance index(Tei
index),measures of diastolic dysfunction all can be
done by ECHO.

40. Immediate management:The first step in management of the patient
with AHF is to address life-threatening issues, including, but not limited to:
• Respiratory failure: The most common presenting symptom of
subjects with AHF is dyspnea and respiratory failure is the most
frequent life-threatening condition for these patients. Immediate
administration of the following is recommended:
• Reposition the patient: If it is safe to do so, support the patient in
assuming an upright, sitting posture. Many patients will do this on
their own to optimize their ventilator efficiency
• Oxygen: Although no randomized study has been performed,
immediate administration of supplemental oxygen is the most
readily available means to increase end organ oxygen delivery.
• Ventilatory support: If the above measures remain inadequate

41. • Nitrates: Sublingual or intravenous nitrates can be very effective as
vasodilators, decreasing pulmonary venous pressure and relieving
dyspnea. Rapid administration of intravenous nitrates in patients with
severe pulmonary edema decreased the need for mechanical ventilation
and myocardial infarction compared to a high-dose furosemide strategy in
a randomized study.
• Diuretic: Most patients will also have significant volume overload
contributing to the respiratory insufficiency, so if there is evidence of
volume overload (as opposed to volume redistribution), rapid
administration of intravenous loop diuretics is recommended. Although it
has remained controversial, one early study suggested that furosemide
also directly dilates pulmonary veins.

42. Immediate management
• Opiates (morphine) in the setting of AHF have been associated with
increased rates of mechanical intubation, prolonged hospitalization, more
frequent ICU admissions, and higher mortality. While this association may
be reflective of the greater disease severity of patients receiving
morphine, these findings argue against routine use of morphine in
patients with dyspnea, as well as for careful monitoring in the select
patients who receive opiates.
• Beta-blocker therapy in particular should be continued during the hospital
course, unless there is cardiogenic shock, symptomatic bradycardia, or
advanced heart block. IVABRADIN can be beneficial to reduce HF
hospitalization for patients with symptoms(NYHA Class II-III) stable chronic
HFrEF9LVEF<35%) who are receiving a beta blocker at maximum tolerated
dose, and who are in sinus rhythm with a heart rate of &) bpm or greater
at rest(2016 ACC/AHA/HFSA focused update for HF)

43. Immediate management
• Circulatory failure: Surprisingly few (approximately 5%)
patients present with low output syndromes in the
general HF population, but these patients require
aggressive management of their shock to mitigate or
prevent the related end organ damage.
• Positive inotropes: To date, there are no “pure”
inotropes, since all of the currently available agents also
have some vascular effects, and the selection of the
specific agent should account for these differences. All of
these agents increase cAMP and intracellular calcium,
with the related increases in heart rate, myocardial
oxygen consumption, and arrhythmias, potentially
resulting in myocardial ischemia, infarction, or death.

44. • Blood pressure
• Peripheral perfusion
• Respiratory status
• Urine output
• Mental status and
• other end organ function.
Laboratory Tests to Monitor Response To, and
Adjustments in, Management
• Serial evaluation of electrolytes and renal function

45. 1. Intraaortic balloon pumps (IABP)
2. Ventricular assist devices (VADs)
3. Extracorporeal membrane oxygenation (ECMO)

46. • The long-term management of a patient admitted for AHF is directed to three main issues (also see
section on chronic heart failure):
• First, establishing the etiology of the heart failure is important, so that measures may be taken to
address potentially reversible causes. Selected patients with ischemic cardiomyopathies may
benefit from revascularization; patients with hypertensive cardiomyopathy should have an
aggressive antihypertensive regimen. Alcoholic cardiomyopathies may resolve with cessation of
alcohol consumption.
• Second, identification of precipitating factors for the AHF episode and intensive education to avoid
future hospitalizations (see later section).
• Third, optimization of therapies with demonstrated long-term benefits (see section on Chronic
heart failure). In patients with heart failure and reduced ejection fraction, these pharmacologic
therapies include beta-blockers, ACE inhibitors, possibly angiotensin receptor blockers,
mineralocorticoid receptor antagonists (spironolactone, eplerenone), possibly isosorbide
dinitrate/hydralazine, and possibly digoxin.
• It is absolutely imperative that these therapies be initiated as much as possible during the
hospitalization and not be left to the outpatient setting. In addition, consideration and scheduling of
device therapy, such as cardiac resynchronization therapy (CRT)/biventricular pacemaker and
implantable defibrillator device (ICD), should be done while the patient is still hospitalized, if
appropriate.
• The hospitalization for AHF is one of the most potent “teachable moments” and care providers are
strongly encouraged to take advantage of the patient as a captive audience.

47. • Treatment of Atrial fibrillation.
• In patients with preserved ejection fraction, beta-blockers and
calcium channel blockers are often effective.
• In any patient presenting with AHF, it is important to consider
the diagnosis of an ACS with an ECG for the evaluation of
myocardial ischemia/infarction.
• Treatment of Chronic obstructive pulmonary disease (COPD).
• Renal insufficiency: In patients who present with renal failure
as evidenced by an elevated creatinine (i.e., >3.0 mg/dL),
consideration should be given to withholding ACE inhibitors,
ARBs, and mineralocorticoid receptor antagonists
(spironolactone, eplerenone). Diuretic doses need to be
adjusted upward in the setting of renal failure, with doubling
of initial doses until a diuretic effect is achieved or until
concerns of toxicity arise.

48. • This education should include, but not be limited to, instruction on:
• Low-salt and weight loss diets (as appropriate)
• Daily use of a scale and a mechanism to record body weights,
including directions on the specific actions to take in the event of a
change in body weight
• Self-titration of diuretics, in appropriate patients. For example, if
weight increases by 3 to 5 lb above baseline, double the diuretic
dose for 3 to 5 days. If body weight returns to baseline, resume
prior dose of diuretics. If symptoms of hypotension ensue, hold
diuretics, and if the symptoms of hypotension do not resolve, call
care provider. If weight does not improve or if increasing symptoms
of dyspnea or other symptoms of congestion, call a care provider.
• Chronic heart failure management programs, if available
• Exercise or rehabilitation program
• Other health-related issues such as smoking cessation