Heart failure (1)

(Etiology & Diagnosis) Editing file

No.5

Objectives :

★ Know different classifications of heart failure.

★ Know the causes and precipitation factors for heart failure
decompensation.
★ Describe the Pathophysiology, therapies that improve
survival, and prognosis.
★ To demonstrate and understand the most recent AHA/ACC
Color index
and ESC HF guidelines and the literature supporting their
recommendations Original text
Females slides
Males slides
Doctor’s notes 438
Doctor’s notes 439
Doctor’s notes 442
New text in slides 442
Text book
Important
Golden notes
Extra
EXTRA Review of basics 2

◄ CO variables and Starling curve

● Cardiac output is determined by SV and HR; SV is determined by the following:
○ Preload (the volume and pressure of blood in the ventricles at the end of diastole)
○ Afterload (The pressure that the heart must overcome to eject blood)
○ Myocardial contractility
SV increases with ↑Contractility, ↑preload and ↓afterload

● What is Starling curve?

○ Starling’s law states that the stroke volume is directly proportional to the
diastolic filling (i.e. the preload or ventricular end-diastolic pressure). As
the preload is increased, the stroke volume rises (normal). Increasing
contractility (e.g. increased with sympathetic stimulation) shifts the curve
upwards and to the left . If the ventricle is overstretched the stroke volume
will fall . In heart failure the ventricular function curve is relatively flat
(Shift to the right) so that increasing the preload has only a small effect on
cardiac output.

◄ What happens when CO is decreased?

● Activation of the SNS Improves ventricular function by increasing heart rate and myocardial contractility.
Constriction of venous capacitance vessels redistributes flow centrally, and the increased venous return to
the heart (preload) further augments ventricular function via the Starling mechanism . Sympathetic
stimulation, however, also leads to arteriolar constriction, this increasing the afterload which would eventually
reduce cardiac output.
● Activation of RAAS It is very imp to know how RAAS being activated ,The fall in cardiac output and increased
sympathetic tone lead to diminished renal perfusion, activation of the renin–angiotensin system, and hence
increased fluid retention. Salt and water retention further increases venous Cardiovascular disease pressure
and maintains stroke volume by the Starling mechanism . As salt and water retention increases, however,
peripheral and pulmonary congestion causes oedema and contributes to dyspnoea. Angiotensin II also causes
arteriolar constriction, thus increasing the afterload and the work of the heart.
● Natriuretic peptides These are released from the atria (atrial natriuretic peptide, ANP), ventricles (brain
natriuretic peptide, BNP – so called because it was first discovered in the brain) and vascular endothelium
(C-type peptide). They have diuretic, natriuretic and hypotensive properties. The effect of their action may
represent a beneficial, albeit inadequate, compensatory response leading to reduced cardiac load (preload
and afterload).

◄ Ejection Fraction (EF)

● The effectiveness of the ventricles in ejecting blood is described by the ejection fraction, which is the
fraction of the end-diastolic volume that is ejected in one stroke volume. Normally, ejection fraction is
approximately 0.55, or 55%. The ejection fraction is an indicator of contractility, with increases in
ejection fraction reflecting an increase in contractility and decreases in ejection fraction reflecting a
decrease in contractility. Thus EF= stroke volume/end-diastolic volume
 Introduction to HF 3

◄ Definition of heart failure ‫ﻓﺷل اﻟﻘﻠب‬

● Heart failure is, complex (because it has many types) clinical syndrome (not a disease, its a collection of
symptoms and signs that resulted from a disease) that can result from any structural (valvular heart
disease, coronary artery disease) or functional ( vitamins deficiency, thyroid disease) cardiac disorder that
impairs the ability of the ventricle to fill (impaired filling{diastolic HF}) (e.g. LVH) and/or eject (impaired
contractility{systolic HF}) blood to meet the body demand.

● An abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a rate
commensurate with the requirements of the metabolizing tissues (the patient will feel clammy, fatigued and
cold), despite normal filling pressures (or only at the expense of increased filling pressures) ( the patient will
usually present with fluid overload (peripheral pitting edema, SOB, ascites))
● HF is characterized by signs and symptoms of intravascular and interstitial volume overload and/or
manifestations of inadequate tissue perfusion.
● “A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the
heart to pump blood at a rate commensurate with the requirements of the metabolising tissues” (E
Braunwald, 1980)
● It leads to fluid overload ( fluid collection) in the lung, leg, or abdomen that results from cardiac disease.

we could also classifies them according to symptoms

Classification of heart failure and AHA classifcation

(it’s important to differentiate between them because they have different management)
Related to EF - HFrEF (reduced ejection fraction: EF<40%)
(phenotypes) - HFmEF (mildly impaired ejection fraction: EF 40-49%)
- HFpEF (preserved ejection fraction: EF≥50%)“If EF is >60% it doesn't mean that the patient
“Most Used classification is normal”
nowadays” - A normal heart’s ejection fraction may be between 50 and 70 percent.
You can have a normal ejection fraction measurement and still have heart failure (called HFpEF or heart failure with preserved ejection fraction).

Related to time-course - New onset - Transient - Chronic

Related to progression - Acute - Stable - Worsening - Acute on chronic (he is known to have HF
and he come with decompensation “sth wrong happened)

Related to location - Left heart - Right heart - Combined

◄ The burden of heart failure

● Number of patients: 21 million adults worldwide are living with HF, this number is expected to rise.
● Economic burden: in 2012, the overall worldwide cost of HF was nearly $108 billion.
● Mortality:50% of HF patients die within 5 years from diagnosis.
● Rehospitalization: HF is the number one cause of hospitalization for patients aged >65 years (increase
with age due to development of HF risk factors such as hypertension, diabetes and coronary artery disease)
● Comorbidities: the vast majority of HF patients has 3 or more comorbidities.

◄ Prevalence of heart failure

● Prevalence 0.4-2% overall, 3-5 % in over 65s, 10% of over 80s and > 10% also have AF
● Commonest medical reason for admission with an annual mortality of 60% over 80s
● Progressive condition (worsen with time, since HF is incurable, we need a management team to treat risk factors
because medications alone are not enough)- median survival 5 years after diagnosis
● Family history is usually positive for patients with HF
● REMEMBER: Left ventricular failure is a true life threatening emergency (always assume HF is an
emergency until proven otherwise)
● An estimated 6.2 million Americans currently live with HF, with increasing incidence and
prevalence over the years
 Introduction cont. 4

◄ Etiology of heart failure Very IMP..

● It is a common endpoint for many diseases of cardiovascular system.
● It can be caused by Inappropriate workload (volume or pressure overload) or Restricted filling or
Myocyte loss
● Heart failure is usually as a result from a chronic process but it may also result from an acute
insult to cardiac function, such as a large myocardial infarction, valvular disease, myocarditis, and
cardiogenic shock.
What are the most common causes of left HF? (can be dependant on the region. In south america, chagas disease is one of the
most common causes. Alcohol or toxic cardiomyopathy is common in western regions and hypertension is the most common cause in Africa).
- When a patient come to you with fluid overload think of HF by looking at the etiology
1. Most common: Coronary artery disease (IHD) ‫ﻣرض اﻟﺷراﯾﯾن اﻟﺗﺎﺟﯾﺔ‬
2. 2nd: Hypertension
3. 3rd: VHD (e.g. AS) ‫( ﻣرض ﺻﻣﺎم اﻟﻘﻠب‬Regurgitating valve patients are more prone to develop HF)
4. 4th: Dilated cardiomyopathy ‫ا‬ ‫ا‬ ‫( ا ل‬it is a genetic disorder),
5. Chagas disease in South America
6. Viral myocarditis (due to covid-19) can cause HF
We can classify the causes of HF into four main categories according to their pathophysiological alterations/ abnormalities

Pressure
Volume overload Loss of muscles Restricted filling
overload

1. Regurgitate valve 1. Systemic 1. Coronary artery 1. Pericardial disease: constrictive

(MR,AR) hypertension disease pericarditis(stiff pericardium),
pericardial effusion.
2. High output status: 2. Outflow 2. cardiomyopathy
anaemia, sepsis, obstruction 2. Restrictive cardiomyopathy
thyrotoxicosis, paget’s 3. Post MI
3. Valvular Heart disease: mitral,
disease, arteriovenous
aortic, tricuspid, pulmonary.
fistula 4. Chronic ischemia
4. Arrhythmia: tachyarrhythmia,
3. Renal failure 5. Connective tissue atrial, ventricular,
diseases bradyarrhythmia, sinus node
4. Iatrogenic: dysfunction.
postoperative fluid 6. Poisons
infusion (alcohol, cobalt, 5. Endocardial disease: with/without
Doxorubicin) hypereosinophilia, endocardial
fibroelastosis

6. Conduction disorders:
atrioventricular block

◄ Background of HF pathophysiology
Heart failure pathophysiology:
1. Index event (The first thing happens “ IHD, HTN, valvular heart disease”)
2. Compensatory mechanisms
3. Maladaptive mechanisms ( the time the patient comes to the hospital and it’s too late)

Heart failure usually begins after an index event (etiology) such as MI that produces a decline in the pumping capacity of the heart, in response to
this decline, a variety of compensatory mechanisms are activated that are designed to maintain cardiovascular homeostasis for periods of months
to years; during that period, patients tend to remain asymptomatic. When these compensatory mechanisms are excessively activated, they
themselves can cause secondary damage to the heart and circulation. It is this secondary damage that drives the disease process of heart failure
forward, Largely through the mechanism of cardiac remodeling. As the heart remodels, it not only gets bigger, but the cardiac walls get thinner
and the pumping capacity of the heart declines. With the transition from a small heart to a big heart, patients at this stage generally go from
asymptomatic to symptomatic( such as orthopnea, SOB, PND, lower limb edema, ascites) heart failure .
 Introduction cont. 5

◄ Changes in HF
● Injury to myocytes due to MI or other cause (index event) will cause ventricular remodeling by dilating
the ventricle which will lead to electrical instability (AF,VT) and reduced EF ultimately causing
neurohumoral imbalance.

● An imbalance occurs in three key neurohumoral systems:

1. Renin-Angiotensin- Aldosterone system
2. Sympathetic nervous system
3. natriuretic peptide system

● The systemic responses in the renin–angiotensin–aldosterone and sympathetic nervous systems cause further
myocardial injury, and have detrimental effects on the blood vessels, and various organs, thereby creating a
pathophysiological ‘vicious cycle’. The natriuretic peptide (specific indication in the blood for HF) system has a
protective function, which can counterbalance these detrimental effects.

11) Hemodynamic changes:

Hemodynamic changes associated with HF: MAP, CO( HR*SV) and systemic vascular resistance
Hemodynamic changes= vital signs
● From hemodynamic stand point HF can be secondary to systolic dysfunction or
diastolic dysfunction.
● The initial manifestations of hemodynamic dysfunction are a reduction in stroke
volume and a rise in ventricular filling pressures under conditions of increased
systemic demand for blood flow. This stimulates a variety of interdependent
compensatory responses involving the cardiovascular system, neurohormonal
systems, and alterations in renal physiology.

2 Neurohormonal changes: In the short term, these 'neurohormonal' systems induce a number of changes in
the heart, kidneys, and vasculature that are designed to maintain cardiovascular homeostasis. However, with chronic activation,
these responses result in haemodynamic stress and exert deleterious effects on the heart and the circulation. (RAAS)

N/H changes Favorable effect Unfavorable effect

↑ Increased - ↑ HR and contractility - ↑ Arteriolar constriction → ↑Afterload

sympathetic activity - Vasoconstriction→ ↑ Venous return, ↑ filling → ↑ workload → ↑ O2 consumption

- Salt & water retention (total body sodium will - Angiotensin-II will lead to ↑ Arteriolar
increase but we will also retain water which will constriction → ↑ Afterload.
↑ Renin-Angiotensin-
dilute the sodium (the concentration won’t - Increased salt & water retention →
Aldosterone change). So if we see low sodium concentration it peripheral and pulmonary edema.
will be a bad sign) → ↑ Venous return

↑ Vasopressin - Same effect - Same effect

↑ Interleukins & TNFα - May have a role in myocyte hypertrophy - Apoptosis

↑ Endothelin - Vasoconstriction → ↑ Venous return - ↑ Afterload

33) Cellular changes:

● Hypertrophy, loss of myocytes, remodeling and increased interstitial fibrosis.
 6
Forms of heart failure
HF has different effects on different parts of the heart, there are many types of HF resulting in different symptoms, onsents, etc. For this reason
different terms are used to describe HF but the commonest one used nowadays is HFrEF vs HFpEF.

◄ Systolic VS Diastolic Dysfunction HFpEF: HF with preserved ejection fraction

HFrEF: HF with reduced ejection fraction

Systolic dysfunction Diastolic dysfunction

‫( ﻓﺷل اﻟﻘﻠب اﻻﻧﻘﺑﺎﺿﻲ‬HFrEF)1 ‫( ﻓﺷل اﻟﻘﻠب اﻻﻧﺑﺳﺎطﻲ‬HFpEF)1
● Owing to impaired contractility ● Owing to impaired ventricular filling during
● EF is reduced (<45%) diastole (hence decreased cardiac output),
● Causes include: because of either: Impaired relaxation or
○ Ischemic heart disease or after a recent
Increased stiffness of ventricle or both.
MI—infarcted cardiac muscle does not
pump blood. Infarction → Dilation → Regurgitation ● EF is preserved (>45-50%)
→ CHF ● Diastolic dysfunction is less common than
○ HTN resulting in cardiomyopathy systolic dysfunction.
○ Valvular heart disease ● HTN leading to myocardial hypertrophy is the
○ Myocarditis (postviral)
most common cause of diastolic dysfunction.
○ Less common causes: Alcohol abuse,
radiation, hemochromatosis, thyroid ● Risk factors: Age, female, HTN, LVH, ischemia,
disease DM, Obesity, RCM and HCM.
Have more worse prognosis than HFpEF ● Factors associated with decompensation:
uncontrolled / labile HTN, AF, ischemia, volume
Systolic Dysfunction=dilated cardiomyopathy= Low EF overload and extracardiac cause.
ALL CAN BE USED INTERCHANGEABLY

What is decapitated blood pressure?

● Once HF is established and, especially, in patients with advanced HF, SBP is usually low (but high
diastolic blood pressure), even in those who presented initially with HTN. This phenomenon has
been called ‘decapitated hypertension’, that is, patients who have had HTN at the outset,
progressively develop normal and even low BP as HF worsens and becomes more severe.

Note: Usually both systolic and diastolic dysfunctions present simultaneously

Based on echo we can differentiate between HFrEF and HFpEF

◄ High VS Low output HF

High Output HF ‫ﻓﺷل اﻟﻘﻠب ﻋﺎﻟﻲ اﻟﻧﺗﺎج‬ Low Output HF ‫ﻓﺷل اﻟﻘﻠب ﻣﻧﺧﻔض اﻟﻧﺗﺎج‬

Certain medical conditions increase demands on Cardiac output is inadequate to perfuse the body
cardiac output, causing a clinical picture of heart (i.e ejection fraction <40%), or can only be
failure due to an excessively high cardiac output. adequate with high filling pressures.
(e.g. severe anemia, thyrotoxicosis or pregnancy,
A/V fistula, Beriberi and Paget's disease)

1- Scenario from doctor:

● HFPEF: old 70 year old lady with high BP (190/80) presents with symptoms and signs of heart failure. Echo shows normal EF. we measure the septum
and it’s 12-13 mm and LV hypertrophy with impaired relaxation. ecg and enzymes will be normal and relatives say she always had this high BP
● HFREF: 60 years old, chest pain, shortness of breath physical examination will show edema, crackles and raised JVP, ECG will show STEMI. Patient will
be cold bc of vasoconstriction. Echo will show reduced EF Diagnosis will be acute HFREF.
● Total body Na and water are high in HF patient not only water
 Right and Left HF 7

◄ Left VS Right sided HF (Females slides)

Left heart failure ‫ﻓﺷل اﻟﻘﻠب اﻻﯾﺳر‬ Right heart failure ‫ﻓﺷل اﻟﻘﻠب اﻻﯾﻣن‬

There is a reduction in left ventricular output and an increase There is a reduction in right ventricular output and
in left atrial and pulmonary venous pressure. An acute an increase in right atrial and systemic venous
increase in left atrial pressure causes pulmonary congestion or pressure. The most common cause of right Hf is left
pulmonary oedema; a more gradual increase in left atrial
HF (present as congestive HF), other causes include:
Patho

pressure, as occurs with mitral stenosis, leads to reflex

● Pulmonary HTN and chronic lung disease (cor
pulmonary vasoconstriction, which protects the patient
pulmonale)
from pulmonary oedema. This increases pulmonary vascular
● Pulmonary embolism and RV infarction
resistance and causes pulmonary hypertension, which in turn
● Mitral stenosis and Pulmonic valve stenosis
impairs right ventricular function. (Causes were discussed
Hallmark: increased RVEDP and RA
earlier)
Hallmark: Increased LVEDP

● Dyspnea2: Difficulty breathing secondary to pulmonary ● Peripheral pitting edema (legs\ankle edema + sacral
congestion/edema. Dyspnea (shortness of breath) is the edema in bed bound patients): Pedal edema lacks
indispensable clue to the diagnosis of HF specificity as an isolated finding. In the elderly, it is more
● Orthopnea: Difficulty breathing in the recumbent position; likely to be secondary to venous insufficiency
relieved by elevation of the head with pillows” the severity ● Nocturia: Due to increased venous return with elevation
Symptoms1

can be determined by number of the pillows” of legs

● Paroxysmal nocturnal dyspnea (PND): awakening after 1 ● Abdominal symptoms: anorexia, Nausea, abdominal
to 2 hours (time required for the fluid to shift from lower to fullness(ascites), right hypochondrial pain (The pain
upper lobe) of sleep due to acute shortness of breath (SOB), fibers of Glisson’s capsule are stimulated when the
usually caused by pulmonary edema. capsule is stretched. Thus any diseases that stretches the
● Nocturnal cough (nonproductive): worse in recumbent capsule such as an enlarged liver can cause liver pain.
position (same pathophysiology as orthopnea)
● Confusion and memory impairment: occur in advanced
CHF as a result of inadequate brain perfusion
● Diaphoresis and cool extremities at rest: Occur in
desperately ill patients (NYHA class IV)

● Displaced and sustained PMI3 (usually to the left) due to ● Jugular venous distention (JVD)
cardiomegaly (Normally, the apical impulse is located in the 5th ● Painful Hepatomegaly/hepatojugular reflux
intercostal space, but do to cardiomegaly/LVH it will be displaced to the 6th ● Ascites
intercostal space)
● Cardiac cirrhosis (on the long run)
● Pathologic S3 (ventricular gallop): low pitched sound that ● Right ventricular heave
Signs1

is heard during rapid filling of ventricle, usually due to ● Hepatic congestion

sudden deceleration of blood as elastic limits of the
ventricles are reached leading to vibration of the ventricular
wall by blood filling, it’s common in children.
● S4 gallop (at the end of diastole)Exact mechanism is not
known, could be due to (forceful) contraction of atrium
against stiff (noncompliant) ventricle
● Crackles/rales (inspiratory) at lung bases (Bibasal
crepitations)

Biventricular Heart failure

● In biventricular failure, both sides of the heart are affected. This may occur because the disease process, such as
dilated cardiomyopathy or ischaemic heart disease, affects both ventricles: ↑LVEDP → ↑LA pressure → ↑pulmonary
capillary pressure → ↑PA pressure → ↑RV pressure → ↑RA pressure → CHF

1- You cannot differentiate between different heart failure classifications using signs and symptoms alone, you need investigations to confirm which type it is
2- Due to pulmonary edema→fluid bulge out of lungs vasculature into alveoli→accumulation of fluid in alveoli will prevent oxygen enter the alveoli
3- Point of maximal impulse, the location at which the cardiac impulse can be best palpated on the chest wall. Frequently, this is at the fifth intercostal space
at the midclavicular line. When dilated cardiomyopathy is present, this can be shifted laterally.
 Acute and Chronic HF 8

◄ Acute VS Chronic HF (Females slides)

Acute heart failure ‫ﻓﺷل اﻟﻘﻠب اﻟﺣﺎد‬ Chronic heart failure ‫ﻓﺷل اﻟﻘﻠب اﻟﻣزﻣن‬
● Acute left heart failure presents with a sudden onset of ● Patients with chronic heart failure commonly follow a
dyspnoea at rest that rapidly progresses to acute relapsing and remitting course, with periods of
respiratory distress, orthopnoea and prostration. stability and episodes of decompensation*, leading to
● Often there is a clear precipitating factor (e.g. large MI, worsening symptoms that may necessitate
aortic valve dysfunction, myocarditis, and cardiogenic hospitalisation
shock ) which may be apparent from the history. ● The clinical picture depends on:
● Patients receive IV diuretics ○ The nature of the underlying heart disease
● SIgns & Symptoms: ○ The type of heart failure that it has evoked (e.g.
○ Rales Left/Right HF)
○ JVD ○ The changes in the SNS and RAAS that have
○ S3 gallop (Most specific) developed
○ Edema ● Low cardiac output causes fatigue, listlessness and a
○ Orthopnea poor effort tolerance; the peripheries are cold and the
BP is low. To maintain perfusion of vital organs, blood
flow is diverted away from skeletal muscle and this
may contribute to fatigue and weakness. Poor renal
perfusion leads to oliguria and uraemia.

*What are the factors that may precipitate acute decompensation of chronic heart failure?
Infection, ischemia and non compliant patients to dietary regimens ,uncontrolled HTN

Other factors:
● Dietary indiscretion (eating
salty food)
● Iatrogenic volume overload
(transfusion, fluid
administration)
CCB, BB and antiarrhythmics
● Pregnancy
● Exposure to high altitude
● Worsening mitral or tricuspid
regurgitation
● COVID-19

Click here for Boston criteria

◄ Modified Framingham criteria (Present in females slides only)

Major Minor

1) PND 1) Bilateral leg edema

2) Orthopnea 2) Nocturnal cough
3) Elevated JVP 3) Dyspnea on ordinary exertion
4) Pulmonary rales 4) Hepatomegaly
5) S3 5) Pleural effusion
6) Cardiomegaly on CXR 6) Tachycardia (heart rate ≥120bpm)
7) Weight loss ≥4.5kg in 5 days in response to 7) Weight loss ≥4.5kg in 5 days
treatment of presumed heart failure.

Diagnosis

The diagnosis of HF requires that 2 major OR 1 major and 2 minor criteria cannot be attributed to another disease.
 Diagnosis 9

◄ Differential diagnosis of HF signs and symptoms *

What are differential diagnosis of lower limb edema (fluid overload)?
1. Pericardial diseases
2. Liver diseases (common in pediatrics)
3. Nephrotic syndrome
4. Protein losing enteropathy (not very common)

◄ Principles of diagnosis of HF
➢ Consider: Medical history, signs, symptoms, CXR, ECG (IHD and Arrhythmia )
➢ Confirm: Natriuretic peptides, Echocardiography (If the patient has normal EF in echo but he has fluid retention that doesn’t mean he doesn't have HF)

➢ Assess clinical phenotype: HFrEF vs. HFpEF

➢ Assess etiology: Angiography, cMRI, Biopsy
➢ Risk stratification
➢ Workup for targeted therapies

◄ Diagnosis of HFrEF vs HFpEF

● The diagnosis of HFpEF is more difficult than the diagnosis of HFrEF1

HFrEF HFpEF
Symptoms typical of HF Symptoms typical of HF

Signs typical of HF Signs typical of HF

Reduced LVEF Normal or only mildly reduced LVEF and LV not dilated

Measurement of Natriuretic peptide Measurement of Natriuretic peptide

Relevant structural heart disease (LV hypertrophy/LA

--
enlargement) and/or diastolic dysfunction

◄ When we examine CHF patient:

1- Vital signs: Heart rate, blood pressure, temperature and oxygen.
- blood pressure in HF patients can be high and low. High blood pressure is a positive cause of heart failure. Low blood pressure can occur in
patient who have MI, cardiomyopathy and aortic stenosis.

2- JVP. If there’s a high pressure in the ventricles it will backflow to the atria. In HF the pressure of the RA will be high which will result in raised JVP.
3-Rales ‘crepitations” . It can be heard in the chest during inspiration and it is an additional sound. In normal conditions, the lung has no air
therefore no sound will be heard. fluid+air = crepitation
4- Displaced apical membrane.
5- Abnormal 3rh heart sound

1- The diagnosis of HFpEF can be challenging, because symptoms are nonspecific and can be explained by several alternative non-cardiac conditions, such
as chronic lung disease, anemia, and chronic kidney disease
 Diagnosis cont’ 10

◄ Investigations for ALL patients

Transthoracic echocardiography

● Echo is unquestionably the most important of all tests and should be performed whenever CHF
is suspected based on history, examination, or CXR.
● Asses function of both ventricles and motion abnormality that may signify CAD
● Useful in determining whether systolic or diastolic dysfunction predominates, and
determines the cause of CHF e.g. pericardial, myocardial, valvular process or Intracardiac shunts.
● Estimates EF: Patients with systolic dysfunction (EF <45%) should be distinguished from
patients with preserved left ventricular function (EF >45-50%). (Those patients in the grey
zone with an LVEF of 40–50% have recently been classified as having heart failure with mid- range
ejection fraction (HFmrEF).)
● Assist in planning and monitoring of treatment and to obtain prognostic information.
● Identify patients who will benefit from long-term drug therapy, e.g. ACE inhibitors.
● TEE is more accurate in evaluating heart valve function and diameter. TTE is the best initial test for CHF

Chest X-ray (CXR) (For fluid overload)

● Has low sensitivity and specificity.

● A CXR should be performed in all cases. It’s used to detect/exclude
certain types of lung disease e.g. cancer (does not exclude asthma/COPD).
It’s more useful in patient with suspected HF in acute setting
● To check the size and shape of heart (cardiomegaly in Left HF)
● Kerley B lines are short horizontal lines near periphery of the lung near the costophrenic angles,
and indicate pulmonary congestion secondary to dilation of pulmonary lymphatic vessel.
● Pleural effusion
● Upper lobe diversion: indicative of HF
● Findings that are seen: (fluid overload, upper lobe redistribution, venous congestion,
cardiomegaly)
● Stages of HF seen in X-ray (1- redistribution 2-interstitial edema 3-alveolar edema) Dr said: someone
might ask you about it

Electrocardiogram (ECG)

● Has low sensitivity and specificity , but can be useful for detecting chamber enlargement and
presence of ischemic heart disease, prior MI, arrhythmia, LBBB (may help in management) and
some forms of cardiomyopathy are tachycardia related.
● Recommended to determine rhythm, heart rate, QRS morphology, and QRS duration, and to
detect other relevant abnormalities. The information also assist in planning of treatment and is of
prognostic importance.
● A completely normal ECG makes systolic HF unlikely.

Abnormal ECG showing: Abnormal ECG showing:

Regular = not AF Wide QRS= bundle branch block
Tachycardia and Irregularity= AF
Peaked T wave = ischemia or electrolyte imbalance
Prominent Q wave= old MI (the combination of abnormal T wave and wide QRS favors ischemia) Wide QRS= left bundle branch block
 Diagnosis cont’ 11

◄ Investigations for ALL patients cont’

Blood tests

● Measurement of Natriuretic peptide (Natriuretic peptides can be used as diagnostic , prognostic and
follow up .BNP levels are not specific for HF as they can be increased in any condition where atrial pressure is
elevated.) (BNP, NT-proBNP or MR-proANP):
○ BNP >100pg/ml or NT-proBNP >300pg/ml is suggestive of heart failure. (Normal is
<100pg/mL). BNP is ordered when the etiology of acute dyspnea is not clear and you
cannot wait for echo to be done.
○ Normal or reduced BNP level will make HF less likely (VERY HIGH SENSITIVITY, less specificity)
● Liver biochemistry (may be altered do to hepatic congestion).
● Electrolytes imbalance (including Na, K+, Ca and Mg)→ to detect chronic renal insufficiency or
hypocalcemia
● CBC to look for anemia (causes high output HF) which may exacerbate HF or be an alternative cause
of the patient S&S.
● Blood glucose, HbA1C. (For diabetes)
● Lipids, Creatinine and check serum ferritin/TIBC level (to detect hemochromatosis or iron
deficiency)
● Urea and electrolytes (as a baseline before starting diuretics and ACE inhibitors)
● Thyroid function tests to detect hyperthyroidism (in the elderly and those with atrial
fibrillation).
● Pre-renal azotemia
● Hemochromatosis Iron overload (mainly seen in heart and kidney)

◄ Investigations for SELECTED patients

Cardiovascular magnetic resonance (CMR) imaging (AKA cardiac MRI)

● CMR imaging is recommended to evaluate cardiac structure and function, to measure

LVEF, and to characterize cardiac tissue, especially in subjects with inadequate
echocardiographic images or where the echocardiographic findings are inconclusive or
incomplete (but taking account of cautions/contraindications to CMR)

Myocardial perfusion/ischemia imaging

● Myocardial perfusion/ischemia imaging (echocardiography, CMR, SPECT or PET) should

be considered in patients though to have CAD, and who are considered suitable for
coronary revascularization, to determine whether there is reversible myocardial
ischemia and viable myocardium
 Diagnosis cont’ 12

◄ Investigations for SELECTED patients

Cardiac Catheterization ‫ﻗﺳطرة اﻟﻘﻠب‬

● To evaluate right and left heart function and pulmonary arterial resistance
● Can clarify the cause of CHF if noninvasive test results are equivocal.
● Used when CAD or VHD are suspected
● Recommended in patients being evaluated for heart transplant or mechanical circulatory
support.
● Gives precise valve diameter, and detects any septal defects

Exercise testing

● Exercise testing should be considered:

○ To detect reversible myocardial ischemia
○ As part of the evaluation of patients for heart transplantation and mechanical
circulatory support
○ To aid in the prescription of exercise training
○ To obtain prognostic information.

Other tests: Metanephrines, endomyocardial biopsy (if infiltrative disease (e.g. sarcoid, amyloid) is
considered)

Summary of diagnosis (From Dr slides)

Click here for an algorithm from Kumar
 Classification 13

ACC: American College of Cardiology

◄ ACC/AHA Classification AHA: American Heart Association
(based on structure and damage to heart)

At risk of HF HF

Stage Stage A Stage B Stage C Stage D

At high risk for HF but Structural heart Structural heart

Refractory HF
without structural heart disease but without disease with prior or
Description disease or symptoms of signs or symptoms of current symptoms of
requiring specialized
interventions
HF HF HF

E.g. Patients who

have marked
E.g. Patients with:
symptoms at rest
- Hypertension
E.g. Patients with: E.g. Patients with: despite maximal
- Atherosclerosis
- Previous MI - Known structural medical therapy (e.g.
- DM
- LV remodeling heart disease and those who are
- Obesity
Who? - Metabolic syndrome
including LVH and SOB, fatigue and recurrently
low EF reduced exercise hospitalized or
Or patients
- Asymptomatic tolerance cannot be safely
- Using cardiotoxins
vascular disease discharged from the
- With family history of
hospital without
CM
specialized
interventions)

Goals: Goals:
- All measures under - Appropriate
stage A and B measures under
- Dietary restriction stages A, B, C
Goals:
Drugs for routine use: - Decisician re:
- Treat hypertension
Goals: - Diuretics appropriate level of
- Encourage smoking
- All measures under - ACEI care
cessation
stage A - BB Options:
- Treat lipid disorders
Drugs: Drugs in selected - Compassionate
- Encourage regular
- ACEI or ARB patients: end-of-life
Therapy exercise
- BB - Aldosterone care/hospice
- Discourage alcohol
Devices in selected antagonist - Extraordinary
intake, illicit drug use
patients: - ARBs measures e.g. heart
- Control metabolic
- Implantable - Digitalis transplant, chronic
syndrome
defibrillators - Hydralazine/nitrates inotropes,
Drugs:
Devices in selected permanent
- ACEI or ARB
patients: mechanical
- Biventricular pacing support or
- Implantable experimental
defibrillators surgery or drugs
 Classification cont’ 14

◄ New York Heart Association (NYHA) Classification

(based on symptoms or physical activity) Used to assess severity

No limitations of activities. Symptoms only occur with vigorous activities, such as playing a
Class I sport. Patients are nearly asymptomatic.

Slight or mild limitation of activity. Symptoms occur with prolonged or moderate exertion,
such as climbing a flight of stairs or carrying heavy packages. Slight limitation of activities.
Class II Ordinary physical activity does not cause fatigue, palpitation or dyspnea

Marker limitation if activity.Symptoms occur with usual activities of daily living, such as
Class III walking across the room or getting dressed. Comfortable at rest.
Less than ordinary activity results in fatigue, palpitation or dyspnea

Unable to carry on any physical activity without discomfort

Symptoms occur at rest. Incapacitating.
Class IV
Discomfort increases in any physical activity

◄ Forrester Classification1 Not used clinically anymore

Other signs: Congestion at rest?

Low perfusion at rest?

- Narrow pulse pressure No Yes

- Pulsus alterations A B
- Declining serum Na level
- ACEI-related symptomatic
No

And valsalva square wave

hypotension And ascites
Class I Class II And Loud P2
L C
Yes

Class III Class IV

Dry: No congestion
Wet: Congestion
Warm: No decrease in perfusion
Cold: Decrease in perfusion

1- first, we look at the congestion state which is the fluid status (is he hypovolemic or overloaded?) and the BP (which is the perfusion status) if he’s not
congested with normal BP we call him warm & dry, and if he’s the opposite then he’s Cold & wet (cardiogenic state) . when he’s warm & wet when he’s
perfusing well he’s usually hypertensive. If they’re not having enough oral intake they’re Dry & cold
 Summary

Heart failure

Systolic dysfunction (HFrEF) Diastolic dysfunction (HFpEF)

● Impaired contractility, EF is reduced. ● Impaired ventricular filling, EF is

● Causes: IHD, HTN, VHD etc preserved.
● Causes: HTN leading to myocardial
hypertrophy.

High Output HF Low Output HF

Conditions that increase demand on CO, Cardiac output is inadequate to perfuse the
causing a clinical picture of heart failure due body (i.e. EF <40%), or can only be adequate
to an excessively high CO e.g. Severe with high filling pressures.
anemia, thyrotoxicosis, pregnancy, A/V
fistula, Beriberi and Paget’s disease

Acute HF Chronic HF

● Acute left heart failure presents with a ● Patients with chronic heart failure
sudden onset of dyspnoea at rest that commonly follow a relapsing and
rapidly progresses to acute respiratory remitting course, with periods of stability
Classification distress, orthopnoea and prostration. and episodes of decompensation*, leading
● Often there is a clear precipitating factor to worsening symptoms that may
(e.g. large MI, aortic valve dysfunction, necessitate hospitalisation
myocarditis, and cardiogenic shock )
which may be apparent from the history.

Left sided HF Right sided HF

● Reduction in left ventricular output ● Reduction in right ventricular output

and an increase in left atrial and and an increase in right atrial and
pulmonary venous pressure. This systemic venous pressure.
increases pulmonary vascular ● The most common cause of right Hf is
resistance and causes pulmonary left HF other causes include: Pulmonary
hypertension, which in turn impairs HTN and chronic lung disease (cor
right ventricular function. pulmonale)
● Hallmark: Increased LVEDP ● Symptoms: Peripheral edema,
● Symptoms: Dyspnea, Orthopnea, Nocturia, Abdominal symptoms
PND ● Signs: JVD, Hepatomegaly and Ascites
● Signs: Displaced PMI, Cardiomegaly,
S3, S4 and crackles at lung bases.
Figures from the male dr slides

HFmrEF: mid-range
Figures from the male dr slides
Dr said that it is imp for your future
Figures from the male dr slides
Epidemiology and prevalence
EXTRA Helpful figures
 Lecture Quiz
Q1: A 78-year-old woman is admitted with heart failure. The underlying cause is determined to be aortic stenosis. Which
sign is most likely to be present?
A- Pleural effusion on chest x-ray
B- Raised jugular venous pressure (JVP)
C- Bilateral pedal oedema
D- Bibasal crepitations

Q2: A 78-year-old woman is admitted to your ward following a 3-day history of shortness of breath and a productive
cough of white frothy sputum. On auscultation of the lungs, you hear bilateral basal coarse inspiratory crackles. You
suspect that the patient is in congestive cardiac failure. You request a chest x-ray. Which of the following signs is not
typically seen on chest x-ray in patients with congestive cardiac failure?
A- Lower lobe diversion
B- Cardiomegaly
C- Pleural effusions
D- Alveolar edema

Q3: A 71-year-old man is being treated for congestive heart failure with a combination of drugs. He complains of nausea
and anorexia, and has been puzzled by observing yellow rings around lights. His pulse rate is 53/minute and irregular and
blood pressure is 128/61mmHg. Which of the following medications is likely to be responsible for these symptoms?
A- Lisinopril
B- Spironolactone
C- Digoxin
D- Furosemide

Q4: A 71-year-old woman presents to ambulatory clinic with a chief complaint of dyspnea upon exertion. Over the past
few weeks, she has had a chronic cough and shortness of breath when walking more than two city blocks. She has a long
history of hypertension that has been poorly controlled in recent years. On physical examination, she has an elevated
jugular venous pulse and rales are evident on lung examination. Cardiac enzymes are negative. Which modality is the most
appropriate next step in distinguishing systolic from diastolic heart failure?
A- Cardiac catheterization
B- Clinical judgment based on physical examination
C- CT scan of the chest
D- Echocardiography

Q5: A 65-year-old woman with chronic systolic heart failure (left ventricular ejection fraction, 30%) comes for a routine
clinic visit. She reports that she is dyspneic climbing one light of stairs and uses two pillows to sleep at night. She has
intermittent lower extremity edema, especially after eating a salty meal. Her medications include lisinopril 20 mg daily,
carvedilol 25 mg twice daily, spironolactone 25 mg daily, and torsemide 40 mg daily. On examination, she has a heart rate
of 70 beats per minute, blood pressure of 110/70 mm Hg, no jugular venous dis- tention, normal heart sounds, a II/VI
holosystolic murmur at the apex, and trace-1+ peripheral edema. Her laboratory values are notable for sodium 140 mEq/L,
potassium 4.8 mEq/L, blood urea nitrogen 20 mg/dL, and creatinine 1.2 mg/dL. What is the next most appropriate step in
her management?
A- Continue her current medications.
B- Increase lisinopril to 30 mg daily.
C- Stop lisinopril and start sacubitril/valsartan 49/51 mg twice daily after 36-hour washout.
D- Increase torsemide to 60 mg daily.

Q6: A 74-year-old man with hypertension, coronary artery disease, GERD, and osteoarthritis presents for follow-up. He
had an ST segment myocardial infarction 2 years prior and underwent successful stenting of a complete LAD arterial
occlusion. For the past 3 weeks, he has noted worsening dyspnea on light exertion coupled with lower extremity swelling.
He has had no recurrent chest pain. His medications include metoprolol, nifedipine, aspirin, and rosuvastatin. On
examination, his blood pressure is 126/80 mm Hg. His heart rate is 70 beats per minute. His jugular venous pressure is 14
cm H2O. The first and second heart sounds are normal, and a third heart sound is appreciated. here is lower extremity
edema to the knee bilaterally. A stress echocardiogram reveals mild anterior wall hypokinesis at rest, and all walls augment
appropriately with stress. he left ventricular ejection fraction at rest is estimated at 40%. In addition to diuresis and
discontinuation of nifedipine, what is the most appropriate management?
A- Add hydralazine and isosorbide mononitrate.
B- Add clopidogrel.
C- Add lisinopril.
D- Add spironolactone..

Answers: Q1:D | Q2:A | Q3:C | Q4:D | Q5:C | Q6:C Answers Explanation File!
 Our Team

This work was originally done by 438 Medicine team.

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Note taker : Mohammed Beyari

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