Heart Failure

Objectives :
● Different classifications of heart failure.
● Causes and precipitating factors for heart failure decompensation.
● Pathophysiology, therapies that improve survival, and prognosis.
● Diagnostic tests of HF.
● Different treatment of HF.
● Side effects of medication of HF.
● Management of cardiac risk factors for HF.
● Role of devices and lifestyle in HF treatment.

Done by :
Team Leader: Hadeel Awartani
Team Members: Saad Al Haddab, Abdullah Al Zaid,
Balqees Al Rajhi, Lujain Al Zaid

Revised by: Aseel Badukhon

Resources :
437 slides, 436 team, Davidson.

Important Notes Golden Notes Extra Book

 Introduction

★ General principles: (watch this)

- (Only this was mentioned in the slides) Ejection Fraction (EF) is a measurement of
how much blood the left ventricle pumps out with each contraction, Normally between
50% and 70%. (EF= SV/EDV) An ejection fraction of 60 percent means that 60 percent of the
total amount of blood in the left ventricle is pushed out with each heartbeat.
EXTRA- Preload is the end-diastolic volume (EDV) at the beginning of systole. It‘s The amount
of ventricular stretch at the end of diastole.
- Afterload is the ventricular pressure at the end of systole (ESP). The amount of
resistance the heart must overcome to open the aortic valve and push the blood volume out
into the systemic Circulation.
- Cardiac output is simply the amount of blood pumped by the heart per minute.
Necessarily, the cardiac output is the product of the heart rate, which is the number of
beats per minute, and the stroke volume, which is amount pumped per beat: CO = HR X
SV (Note : SV = EDV - ESV). Cardiac output at rest is about 5 liters/minute (4900
ml/min). Cardiac output is determined by preload (the volume and pressure of blood in
the ventricles at the end of diastole), afterload (the volume and pressure of blood in the
ventricles during systole) and myocardial contractility; this is the basis of Starling’s Law.

Heart Failure:
Heart failure is bad , and its prognosis is bad. Even as worse as cancers. You have to treat probably.
Heart failure age among Saudis is lower 10-15 years in comparison to Europe because of DM, HT,
★ poor lifestyle and other comorbidities.
➔ Heart failure is a complex syndrome 1 that can result from any structural or functional
cardiac disorder that impairs the ability of the ventricle to fill with or eject blood (and
profuse tissues).
➔ 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
➔ Heart failure describes the state that develops when the heart cannot maintain an adequate
cardiac output or can do so only at the expense of elevated filling pressures.
➔ In mild to moderate forms of heart failure, cardiac output is normal at rest and only becomes
impaired when the metabolic demand increases during exercise or some other form of
stress.
➔ Almost all forms of heart disease can lead to heart failure. An accurate aetiological
diagnosis is important because treatment of the underlying cause may reverse heart failure

1
or prevent its progression. Approximately 50% of patients are dead within 5 years.
HF is a syndrome as a result of many diseases of the heart. Complex clinical syndrome: because there are many mechanisms that will result
in HF signs and Sx.
 Etiology:
The common cause differs regionally as in Asia ,Middle East and etc.
★ The common cause in SA is IHD but in Africa is Hypertension.

Main causes ★ First: Ischemic heart disease5, most common cause (35–40%)
Focus mainly ★ Second: Cardiomyopathy (dilated) Such as in Peripartum Cardiomyopathy (30–34%)
on these four
★ Third: Hypertension (15–20%)
major groups
★ Valvular heart disease (mitral, aortic, tricuspid).
Other causes ● Cardiomyopathies (other than dilated): hypertrophic, restrictive (amyloidosis,
sarcoidosis)
● Congenital heart disease (Atrial septal defect, ventricular septal defect).
● Drugs (chemotherapy – trastuzumab, imatinib, Doxorubicin2).
● Hyperdynamic circulation (anaemia*, sepsis, thyrotoxicosis*, pregnancy* and
Paget‘s disease3 AV fistula, Beriberi (alcohol abuse causes it)) ―High output
status^ǁ
● Hypervolemic state (Renal failure; Iatrogenic)
● Haemochromatosis4, radiation.
● Right heart failure (Cor pulmonale, right ventricular infarct, pulmonary
hypertension, pulmonary embolism, COPD, Pneumonia, Interstitial lung
disease).
● Tricuspid incompetence.
● Obesity* Any factor that increases myocardial work (*) may aggravate
existing HF or initiate failure.
● Arrhythmias* (atrial fibrillation, AV block, bradycardia (complete heart block,
sick sinus syndrome))
● Pericardial disease (constrictive pericarditis, pericardial effusion) if the
pericardium is calcified there will be impaired filling which in turn lead to
HF.
● Infections (e.g. myocarditis due to Chagas‘ disease), (Coxsackieviruses).
● Sleep apnea.
(not in slides)
HF could be caused
by:

1 3
Loss of muscles:
Restricted filling:
Post-MI (decreased blood supply),
chronic ischemia, connective tissue Pericardial diseases,
diseases, infections, poisons
Restrictive cardiomyopathy,
tachyarrhythmias.
(alcohol,cobalt and drugs).

2
Inappropriate workload:
- Volume overload: Regurgitate valve (Aortic,
mitral), High output status (mentioned
above^).
- Pressure overload: Systemic HTN, Outflow
obstruction (Aortic stenosis).
2
Echo is required before and during the treatment.
3
Paget disease is a cause of HF.
4
Storage disorder causes restrictive cardiomyopathies.
5 As IHD is the most common cause in SA, you have to know its risk factors: DM, HT, Hyperlipidemia, smoking and family history.
Pathophysiology of Heart Failure:
In patients without a valvular disease, the primary abnormality is impairment of ventricular myocardial
function, leading to a fall in cardiac output. This can occur because of impaired systolic contraction,
impaired diastolic relaxation, or both. This activates counter-regulatory neurohumoral mechanisms that, in
normal physiological circumstances, would support cardiac function but, in the setting of impaired
ventricular function, can lead to a deleterious increase in both afterload and preload . A vicious circle may be
established because any additional fall in cardiac output will cause further neurohumoral activation and
increasing peripheral vascular resistance.

In acute heart failure, this body’s response( Activation of RAS &

SNS)is essential for survival but for chronic heart failure it
would harmful, so we block RAS and SNS in management.

● Stimulation of the renin–angiotensin–aldosterone system (mediated by angiotensin II, a

potent constrictor of arterioles, in both the kidney and the systemic circulation) leads to:
1) Vasoconstriction
2) Sodium and water retention.
3) Sympathetic nervous system activation.

After MI, cardiac contractility is impaired and neurohumoral

activation causes hypertrophy of non-infarcted segments, with
thinning, dilatation and expansion of the infarcted segment
(remodelling). This leads to further deterioration in ventricular
function and worsening heart failure.

Initially: Promoted By:

Activation of the sympathetic nervous -Aldosterone
system may initially sustain cardiac -Endothelin-1 (a potent
output through increased myocardial vasoconstrictor peptide
contractility (inotropy) and heart rate
(chronotropy).
Activation of produced by the vascular

Prolonged Sympathetic Stimulation:

SNS endothelium with marked
effects on the renal
vasculature).
Negative effects :
-Antidiuretic hormone (ADH)
- Cardiac myocyte apoptosis
“in severe HF”.
- Hypertrophy and focal ADH = AVP = Vasopressin
myocardial necrosis. Sodium and Results in:
- Peripheral vasoconstriction water Pulmonary and peripheral oedema
- arrhythmias retention 5 occurs because of high left and
right atrial pressures.
 Cellular Changes:
Last thing to happen, irreversible.

Changes in Ca+2 Changes in

adrenergic
handling receptors:

(In heart failure, there is a ● Slight ↑ in α1 receptors

prolongation of the calcium current ● β1 receptors desensitization →
followed by down regulation
in association with prolongation of
● Changes in contractile proteins.
contraction and relaxation). ● Program cell death (Apoptosis).
● Increase amount of fibrous tissue.

★Neurohormonal Changes:
Neurohormonal changes Favorable effect Unfavorable effect
↑ Increased sympathetic ● ↑ HR and contractility ↑ Arteriolar constriction →
activity ● Vasoconstriction→ ↑ Venous After load → ↑ workload → ↑
return, ↑ filling O 2 consumption
↑ Renin-Angiotensin- Salt & water retention → ●Angiotensin-II will lead to
Aldosterone ↑ Venous return (preload). Arteriolar constriction ↑
Afterload.
●Increased salt & water retention →
peripheral and pulmonary edema.
↑ Vasopressin Same effect Same effect

↑ Interleukins & TNFα May have roles in myocyte Apoptosis

hypertrophy
↑ Endothelin Vasoconstriction→ ↑ Venous return ↑ Afterload

★ Natriuretic peptides are released from the atria in response to atrial stretch, and act as physiological antagonists to the fluid-conserving
effect of aldosterone. There are four different groups NPs identified till date [atrial natriuretic peptide (ANP), B-type natriuretic peptide
(BNP), C-type natriuretic peptide (CNP) and dendroaspis natriuretic peptide, a D-type natriuretic peptide (DNP)].

➔ Atrial natriuretic peptide (ANP) is released from atrial myocytes in response to

stretch. ANP induces diuresis, natriuresis, vasodilatation and suppression of the
renin–angiotensin system.
Levels of circulating ANP are increased in congestive cardiac failure and correlate
with functional class, prognosis and haemodynamic

state.
➔ Administration of synthetic natriuretic peptides has not improved outcomes in acute HF but
modulation of the natriuretic system through inhibition of the enzyme that degrades natriuretic (and
other vasoactive) peptides, neprilysin, has proven to be successful (ARN-is)
 6
reduced

Classifications of Heart Failure

7

preserved
HFrEF and HFpEF are the most and uptodate classification for heart
★ Diastolic/Systolic Failure: (MOST IMP. CLASS.) failure. The prognosis for each is different. You cannot differentiate
between them by clinical symptoms. You have to do an echo.

Systolic Dysfunction (HFr6EF) Diastolic Dysfunction (HFp7EF)

Owing to impaired contractility Owing to impaired ventricular filling during diastole, because
● The abnormality is decreased EF of either:
● Causes include: 1. Impaired relaxation
2. Increased stiffness of ventricle or both
1. Ischemic heart disease - EF is preserved
or after a recent
- Diastolic dysfunction is less common than
MI—infarcted cardiac
systolic dysfunction.
muscle does not pump
- HTN leading to myocardial hypertrophy is the most
blood (decreased EF)
common cause of diastolic dysfunction.
2. HTN resulting in
- All-cause mortality: similar to that of heart failure with
cardiomyopathy
reduced LVEF. Mortality is mostly due to non-cardiac
3. Valvular heart disease
causes
4. Myocarditis (postviral)
- Risk factors: Age; female; HTN; LVH; ischemia; DM;
5. Less common causes: Obesity; RCM; HCM.
Alcohol abuse,
- Factors associated with decompensation:
radiation,
uncontrolled / labile HTN; AF; ischemia; volume
hemochromatosis, overload; extracardiac cause.
thyroid disease whom have HFrEF will end up with HFpEF but not usually the
other way around.
● Usually both systolic and diastolic dysfunctions present simultaneously
● Around 20-33% of HF cases have normal EF

★ High/Low Output Heart Failure:

High Output Heart Failure8 Low Output Heart Failure9
Certain medical conditions increase demands on Cardiac output is inadequate to perfuse the
cardiac output, causing a clinical picture of heart body (ie ejection fraction <40%), or can only
failure due to an excessively high cardiac output.
be adequate with high filling pressures.
(ex; severe anemia, thyrotoxicosis or
pregnancy)

★ New York Heart Association Classification (VERY Important):

No limitation during ordinary activity.
Class I Normal physical exercise doesn‘t cause
symptoms (fatigue,dyspnea or palpitations).
Slight/Mild limitation during ordinary activity.
Class II Comfortable at rest but normal physical exercise
causes symptoms
Marked limitation. Comfortable at rest but gentle
Class III
physical activity produces symptoms
Symptoms of heart failure occur at rest, and
Class IV
exacerbated by any physical activity.
★ Acute/Chronic Heart Failure:
Acute heart failure (Acute Pulmonary edema) Chronic heart failure (More
Common)
This usually presents with sudden-onset dyspnoea at rest with This commonly follows a relapsing
acute respiratory distress, orthopnoea . A precipitant (e.g. acute and remitting course, with periods
MI, valvular disease, myocarditis, and cardiogenic shock ) may of stability interrupted by episodes
be apparent from the history. The peripheries are cool to the of decompensation. A low cardiac
touch, the pulse is rapid and there is JVD. The apex is not output causes fatigue, listlessness
displaced, as there has been no time for ventricular dilatation. and a poor effort tolerance; the
Auscultation may reveal S3 ‗gallop‘ and crepitations are peripheries are cold and BP is low
heard at the lung bases.
Clinical picture depends on:
A. Oxygen
1. The underlying heart disease
Loop diuretics (furosemide): Most
B.
Management of 2. Type of heart failure
Acute important drug that decreases the
3. Neurohormonal
Decompensated preload10
changes that
Heart Failure C. Nitrate (IV) : that decrease the afterload
developed.
D. Morphine can be used
Sometimes associated with:
Note: If pulmonary edema continuous despite - Weight loss (cardiac cachexia)
these 4 > dobutamine is added (increased - Poor tissue perfusion
contractility & decrease afterload) - Skeletal muscle atrophy
*ACE inhibitors and β-Blockers are not
used in acute settings.

★ Forrester Classification: Tx of Cold & Dry: Vasodilators/+ve inotropes (eg

dobutamine)
Warm & Wet most common presentation + tx
w/diuretics
You never give HF pt IV Fluids.
Dry and cold worse prognosis.

★ Dry: no congestion.
★ Wet: congestion.
★ Warm: no decrease in perfusion.
★ Cold: decrease in perfusion.

★ Left, right and biventricular heart failure:

The left side of the heart comprises the functional unit of the LA and LV, together with the mitral and aortic
valves; the right heart comprises the RA, RV, and tricuspid and pulmonary valves

10
Best initial therapy
 Left-sided Heart Failure Right-sided Heart Failure
(reduction in LV output) (reduction in RV output)11

Left-sided heart failure: Right-sided heart failure:

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 pressure. Causes of isolated right heart failure
or pulmonary oedema; a more gradual increase in left atrial include chronic lung disease (cor pulmonale),
pressure, as occurs with mitral stenosis, leads to reflex pulmonary embolism and pulmonary valvular
pulmonary vasoconstriction, which protects the patient from stenosis.
pulmonary oedema. This increases pulmonary vascular
resistance and causes pulmonary hypertension, which can, in
turn, impair right ventricular function.

❖ Dyspnea: Difficulty breathing ❖ Peripheral pitting edema: Pedal edema

secondary to pulmonary lacks specificity as an isolated finding. In
congestion/edema the elderly, it is more likely to be secondary
to venous insufficiency
❖ Orthopnea: Difficulty breathing in the ❖ Nocturia: Due to increased venous return
recumbent position; relieved by with elevation of legs
elevation of the head with pillows” the
Symptoms:
severity can be determined by number
of the pillows”
❖ Paroxysmal nocturnal dyspnea
(PND): awakening after 1 to 2 hours
of sleep due to acute shortness of
breath (SOB)
❖ Nocturnal cough (nonproductive):
worse in recumbent 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 PMI (usually to the left) ❖ Jugular venous distention (JVD)
due to cardiomegaly ❖ Painful Hepatomegaly/hepatojugular
Signs
❖ Pathologic S3 (ventricular gallop) “low reflux
pitched sound that is heard during rapid ❖ Ascites
filling of ventricle” ❖ Right ventricular heave
❖ S4 gallop
❖ Crackles/rales at lung bases 12

Biventricular failure (Both sides)

Example: dilated cardiomyopathy or ischaemic heart disease, affects both ventricles or because disease of the left
heart leads
→ chronic elevation of the left atrial pressure→ pulmonary hypertension → right heart failure

11 Most common cause of Right-sided HF is left-sided

HF.
12 Because of Pulmonary Edema
★Diagnosis of CHF:
Test: Findings:
★ Initial test of choice: should be performed whenever CHF is suspected based on
history, examination, or CXR.
- Useful in determining whether systolic or diastolic dysfunction predominates, and
determines whether the cause of CHF is due to a pericardial, myocardial, or valvular
Transthor process.
acic - Estimates EF (very important): Patients with systolic dysfunction (EF <40%) should
be distinguished from patients with preserved left ventricular function (EF >40%).
Echocardi
ogram - Shows chamber dilation and/or hypertrophy.
- Identify patients who will benefit from long-term drug therapy, e.g. ACE inhibitors.
High pulmonary venous pressure in left-sided heart failure
first shows on the chest X-ray as an abnormal distension of
the upper lobe pulmonary veins (with the patient in the erect
position). The vascularity of the lung fields becomes more
prominent, and the right and left pulmonary arteries dilate.
Subsequently, interstitial oedema causes thickened
interlobular septa and dilated lymphatics. These are evident as
horizontal lines in the costophrenic angles (septal or ‗Kerley
B‘ lines). More advanced changes due to alveolar oedema
cause a hazy opacification spreading from the hilar regions,
Chest and pleural effusions.
X ray
- Cardiomegaly
(CXR - 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
vessels
- Pleural effusion

- Nonspecific, but can be useful for detecting chamber enlargement and presence of
ECG ischemic heart disease or prior MI. Recommended to determine rhythm, heart rate, QRS
and to detect relevant abnormalities. A completly normal ECG makes systolic hf unlikely

- Precise valve diameter, septal defects (when CAD or valvular suspected or if heart transplant
Catheter
is indicated)

- CBC for→ anemia. --Blood glucose; HbA1c

- -Creatinine. -Urinalysis. -Lipids
- -If necessary: CK, Iron assessment, HIV, ANA, RF, Urine metanephrines, SPEP-UPEP, Uric
acid, CRP, troponin, polysomnography
Blood tests - Liver biochemistry(may be altered do to hepatic congestion)
- Brain natriuretic peptide (BNP) or (Pro BNP), if normal(<100pg/mL) exclude heart
failure (particularly pulmonary edema).
- T4 & TSH
- Electrolytes imbalance(including Ca / Mg)→ Chronic renal insufficiency

Others
-Radionuclide ventriculography, -Cardiac MRI, - Coronary Angiography,
(Selected
stress test / 6MWT / VO2 Max , -Biopsy
patients)
★Management of CHF:
What are the classes and what are the options to treat HF. No
need to memorize doses.

Management of any disease we think in three categories: 1- life modification. 2- Medical management. 3- Surgical intervention.

✦ Acute presentation treats only by 1- Diuretics. 2- Ventilator support if needed.

Systolic Failure Management
Aim of management? ❖ Sodium restriction (2 gram Na = 5 gram NaCl)
1.Improve quality of life: ❖ Fluid restriction (1.5 Liter = 6-8 cups)
-Reduce symptoms
-Reduce hospitalization ❖ Weight loss
-Improve functional class ❖ Daily weight (tailor therapy). (diuretics) ‫ةﻋﺮﺟﻨﺎ دوز داز ھﺘﻔﺶ اذا ﻛﻮزو ﺑﻘﺎر ﺿﯿﺮﻣﮭﻦ ﻟﻮﻗﻮ‬To check
-Prevent disease progression
2.improve quantity:
whether the diuretics are effective or not.
Improve survival. ❖ Smoking cessation
General ❖ Restrict alcohol use
lifestyle ❖ Exercise program (to increase heart contractility function)” Cardiac Rehab”
❖ Annual influenza vaccine and pneumococcal vaccine recommended because influenza
modification
virus has mortality in chronic diseases one of them chronic heart failure.
❖ Most effective means of providing symptomatic relief to patients with moderate to severe CHF
❖ Recommended for patients with systolic failure and volume overload
❖ Have not been shown to reduce mortality or improve prognosis, just for symptom control.
Goal is relief of signs and symptoms of volume overload (dyspnea, peripheral edema)
❖ Loop diuretics: Furosemide (Lasix)—most potent (Most common use. Sometimes
Diuretics we use (furosemide + metolazone (thiazide13) ‗work in distal convoluted tubule‘)
❖ Thiazide diuretics: Hydrochlorothiazide—modest potency
❖ Side effect of these drugs: Pre-renal azotemia, Skin rashes, Neutropenia,
Thrombocytopenia, Hyperglycemia, ↑Uric Acid, Hepatic dysfunction, ototoxicity”
Single high dose”
✦ High stage of heart failure needed high dose comparison to early stage of heart failure.
❖ The combination of B blockers and an ACE inhibitors required for patient with LVEF
less than 40% either symptomatic or asymptomatic
β-Blockers14 ❖ Proven to decrease mortality in patients with post-MI heart failure.
Has been traditionally ❖ β-Blockers also have antiarrhythmic and anti-ischemic effect.
contraindicated in pts with
CHF .Now they are the main
❖ Reported to improve symptoms of CHF; may slow progression of heart failure by slowing
stay in treatment on CHF & may
down tissue remodeling. The decrease in heart rate( antiarrhythmic) ar leads to decreased
be the only medication that oxygen consumption (anti ischemic effect)
shows substantial improvement ❖ Should be given to stable patients with mild to moderate CHF (class I, II, and III) unless
in LV function
there is a noncardiac contraindication.
❖ Not all β-blockers are equal. There is evidence only for metoprolol, bisoprolol, and carvedilo
❖ It is contraindicated in acute HF or in case of pulmonary edema.
❖ It reduces mortality
❖ Monitor serum potassium and renal function
❖ Prolong survival in CHF patients with subsequent effect on myocardial remodeling and
Spironolacto fibrosis.
ne
❖ Monitor serum potassium and renal function
(aldosterone
❖ Spironolactone is proven effective only for more advanced stages of CHF (classes III and IV)
antagonist)
❖ Eplerenone is an alternative to spironolactone (does not cause gynecomastia). If the
patient developed gynecomastia, impotence (cause its structurally similar to
progesterone) switch to eplerenone.
13
Not effective with GFR < 30/min
14
When a patient comes to ER with very high HR don't give him beta-blocker! Because you're blocking the mechanism that increase his cardiac output! Think, why he is
having tachycardia? because of activation of sympathetic NS, now you want him to relax so give him oxygen or diuretics > HF will improve > HR back to normal. (YOU
DON'T TREAT NUMBERS! YOU DEAL WITH PATHOPHYSIOLOGY).
 Cause venous and arterial dilation, decreasing preload and afterload.
❖
The combination of a diuretic and an ACE inhibitor should be the initial
treatment in most symptomatic patients.
❖ ACE inhibitors reduce mortality, prolong survival, and alleviate symptoms in mild,
moderate, and severe CHF.
❖ Indicated for left ventricular systolic dysfunction (LV ejection fraction less than 40%).
❖ All patients with systolic dysfunction should be on an ACE inhibitor even
ACE Inhibitors if they are asymptomatic.
❖ Side effects of ACE inhibitors: Angioedema”most serious” (rare occurring but when it
(Benazepril, happen it is scary we should stop this medication and start alternative one which is ARBs
Captopril, and give patient steroid), Hypotension, Renal insufficiency (afferent arteriole
Enalapril,
Fosinopril.
constriction), Rash , Cough”most common”(increase in Bradykinin)
Lisinopril) ❖ If patient developed hyperkalemia or renal impairment or is pregnant→ switch from
ACEI to Hydralazine (arterial dilator)(decrease afterload) with isosorbide dinitrate
(Venodilator)(decrease preload).
Always start at a low dose to prevent hypotension, Monitor BP, potassium, BUN, and creatinine.

Angiotensin II Used in patients unable to take ACE inhibitors due to side effects (eg, angioneurotic edema,
receptor cough) but do not replace ACE inhibitors if patient tolerates an ACE inhibitor.
blockers
(ARBs)
❖ Recent FDA approval (2015).
❖ The only product available (valsartan/sacubitril). Not used alone, it needs to be combined
ARBs.
Angiotensin ❖ Valsartan = ARB.
Receptor- ❖ Sacubitril = prodrug for sacubitrilat.
Neprilysin
❖ Inhibit neprilysin which breakdown the vasoactive peptides.
inhibitor (ARNi)
❖ Used if patient LVEF <= 35% and still symptomatic with ACE/ARB. In this
specific group of patients it improves mortality and morbidity. “HFrEF only”

❖ Ivabradine; Inhibit the Na inflow during the SA node action potential phase 4.
If - ❖ Decrease the heart rate.
Channel ❖ Only use it if HR not controlled by B-blocker and remains > 70 bpm and the
blocker15: patient has sinus rhythm. In this group if patients it improve Morbidity and
Mortality. Restrictive criteria for prescription.
Diabetic medication used in Heart Failure. Blocks SGLT2 transporter in the proximal renal
tubule and reduces glucose and Na+ reabsorption. It promotes diuresis, naturieses, HbA1c,
weight loss.
How does it promote diuresis and naturieses? During the reabsorption of of Na+ and glucose,
water is absorbed with them. By blocking the transporter you are promoting water and
sodium loss, thus reducing fluid retention.
SGLT2 Inhibitors
(Dapagliflozin)

15
Funnel channel Na in SA node.
Digitalis ❖ Positive inotropic16 agent. Has vagotonic17 & arrhythmatic effects.
We avoid digitalis ❖ Useful in patients with EF <40%, who continue to have symptoms despite optimal
because of its therapy (with ACE inhibitor, β-blocker, aldosterone antagonist, and a diuretic), severe
narrow therapeutic
CHF, or severe AFib.
index and mostly
❖ Provides short-term symptomatic relief (used to control dyspnea and will decrease
HF patients have
renal failure. frequency of hospitalizations) but has not been shown to improve mortality.
❖ Serum levels should be monitored (digoxin toxicity: yellow vision, nausea, vomiting)
❖ Neither works on RAAS nor improves patient survival. Potassium level has to be monitored
because digitalis can cause hypokalemia.

Diastolic Failure Management

Few therapeutic options available; patients are treated symptomatically (NO

medications have proven mortality benefit)
1.β-Blockers have clear benefit and should be used
Notes 2.Diuretics are used for symptom control (volume
overload) 3.ACE inhibitors and ARBs
(Digoxin and spironolactone should NOT be used).
➔ The standard treatment of systolic dysfunction is: Diuretics + ACE inhibitor + β blockers.

➔ The initial treatment for symptomatic patient is: Diuretics + Vasodilatation (ACEI, ARB or Hydralazine
with isosorbide18).
★The following medications are contraindicated in patients with CHF:
1. Metformin—may cause potentially fatal lactic acidosis. 5.CCB except amlodipine and felodipine(negative inotropic)
2. Thiazolidinediones—causes fluid retention. 6. Addition of an ARB or renin inhibitor is not recommended to
3. NSAIDs may increase risk of CHF exacerbation., ACE combo also mineralocorticoids antagonist bc of risk of renal failure
4. COX-2 inhibitors because they cause water sodium retention, worsening renal function

Some antiarrhythmic agents that have negative inotropic effect.

★Medications that have been shown to lower mortality in systolic heart failure: (imp.)
1. ACE inhibitors and ARBs β-Blockers
2. Aldosterone antagonists (spironolactone) Hydralazine and
3. nitrate (Nitroglycerin)

★ The following devices have been shown to reduce mortality in selected patients: “after you
consider all the treatment options”
1. An ICD19 lowers mortality by helping prevent sudden cardiac death (which is the most common cause of death in CHF). It is
indicated for patients at least 40 days post-MI, EF <35%, and class II or III symptoms despite optimal medical treatment.

2. Cardiac resynchronization therapy (CRT): This is biventricular pacemaker indications are similar to ICD except these
patients also have prolonged QRS duration >120 msec. Most patients who meet criteria for CRT are also candidates for ICD
and receive a combined device.

3. Revascularization.
★ Cardiac transplantation is the last alternative if the above do not control symptoms.
Advance stage of heart failure (stage D) management Cardiac Transplant (best)
There are criteria to be accepted as a candidate for Cardiac Transplantation such as young and no organs failure

16
Affect the strength of contraction of heart muscle (myocardial contractility).
17
Overactivity or irritability of the vagus nerve, adversely affecting function of the blood vessels, stomach, and muscles.
18
is in the class of drugs called nitrates that are used for treating and preventing angina.
19
An implantable cardioverter-defibrillator (ICD) or automated implantable cardioverter defibrillator (AICD) is a device implantable inside
the body, able to perform cardioversion, defibrillation, and (in modern versions) pacing of the heart
Precipitating Factors for Acute Decompensated HF

★
★

★
★

★ very common in our region

Management Of Heart Failure

1 Whether patient is symptomatic / asymptomatic, give Beta Blockers +ACE-i
Patient still symptomatic
and LVEF<35%?
2 Add Mineralocorticoid Receptor Antagonist
Patient still symptomatic
and LVEF<35%?
3 Add Neprilysin inhibitor (ARN-i)
Patient still symptomatic
and LVEF<35%?
4 Add SGLT2 inhibitor
Patient still symptomatic
and LVEF<35%?
5 Surgical Intervention (ICD/heart transplant)
Doctors` notes IMPORTANT

1st Lecture

● Cases of HF are very important

● When we don’t have s4 in patient with HF? patient with AF and atrial
flutter b/c we lose atrial kick
● Ca blocker is CI in patient with HF
● Investigation / you should start by cbc , electrolyte and creatinine
electrolyte= k and ca b\c you will treat patient with acei + mra->
hyperkalemia
● Creatinine =b\c you will treat patient with acei + mra
● How do we know if symptoms b/c Respiratory or cardio problem by
detect bnp in blood to if it is cardio
● Acei is CI in angioedema ,pregnancy and bilateral renal artery stenosis
● In patient who can not tolerate acei and arb -> use hydralazine and
isosorbide dinitrate as combo
● Depagliflozin -> new drug for HF

2nd Lecture
● Dilated cardiomyopathy ,valvular heart disease and alcohol are most in
young
● We could not actually differentiate between Right side and left side HF
by symptoms only but in case of acute HF we can
● In case of HHpEF the management is risk factor management
● SGLT 2 inhibitors slide is missing.
● SGLT 2 inhibitors Are used only for diabetic population.
● Positive inotropic agent slide is missing
● Anticoagulants were traditionally used for treating HF but currently is not
a part of HF management and used only for specific indications.
● Anticoagulation slides are missing.
● Most common cause of death in HF patients is arrhythmia.
● recurrent hospitalization due to HF is poor prognostic factor
Diuretics are not shown here because from the beginning it would be prescribed. Is
unethical to argue on diuretics because it is the most effective treatment in relieving
patients’ symptoms.

Diuretics, digoxin or positive inotropic agents(milrinone,amrinone and

dobutamine) haven’t been proven to lower or benefit mortality.
Summary
Definition: Complex clinical syndrome secondary to a functional or structural abnormality of the heart which impairs the
capacity of the ventricles to eject blood or to be adequately filled.

Signs and symptoms include:

- Orthopnoea
- JVD CAD : ischemic
- PND
- S3 sound heart disease
- Decreased exercise tolerance
- Crackles
- Peripheral edema ARRHYTHMIA
- Signs of pleural effusion
- Nocturnal cough
- Hepatomegaly
- Tachycardia
- Peripheral edema AV block
NYHA class:
HTN

CARDIOMYOPA
THY and
MYOCARDITIS

VALVULAR
heart disease “ETIOLOGIES”
PERICARDIAL
disease

CONGENITAL
pathophysiology Evaluation heart disease

PULMONARY
disease
High output
states Hypervole
mic states

Stages, phenotypes and treatment of HF

Summary
★ Heart Failure:
Any cardiac disorder that causes the heart to fail in ejection of blood or failure to adequately fill with blood (low cardiac
output).

★ Main Pathophysiologies:
1Sympathetic nervous system: makes cardiac output better at first, but then later causes vasoconstriction.
2RAS, Aldosterone (& vasopressin): cause sodium and water retention which eventually cause peripheral and pulmonary
edema. 3- Atrial Natriuretic Peptides: released from the atria to antagonize aldosterone, therefor decrease sodium and
water retention.
4- Cellular changes: Changes in calcium, adrenergic receptors, and contractile proteins.

★ Classifications:
1 Systolic or Diastolic:
a. Systolic dysfunction: impaired contractility, ejection fraction is decreased. (more common)
b. Diastolic dysfunction: impaired ventricular filling, ejection fraction is preserved.
2 High or Low Output:
a. High Output: increase in demands cause excessively high cardiac output
b. Low Output: inadequate tissue perfusion, unless there is high filling pressure.
3 Class I to IV of New York Heart Association:
Depends on whether the symptoms occur at rest, or at different intensities of physical activities.
4 Acute or Chronic:
b. Acute pulmonary edema: Usually a sudden presentation of SOB and orthopnea, with Jugular Venous
Distention, an S3 Gallop, but without apex beat displacement.

c. Chronic heart failure: Usually has a relapsing and remitting course, the signs and symptoms vary depending on
the
underlying pathologies.
5 Left sided or Right Sided or Biventricular:
b. Left sided heart failure: Reduction in Left Ventricle output, either with a sudden increase in Left Atrial
(pulmonary) venous pressure which causes pulmonary edema, or gradual increase in Left Atrial pressure
which protects from it. But still, this gradual increase causes pulmonary vasoconstriction which can
eventually lead to Right Ventricular failure. It presents with the same signs of acute pulmonary edema,
but the PMI here is displaced without JVD.
 b. Right sided heart failure: Reduction in Right Ventricle output and increase in Right atrial
(systemic) venous pressure. It presents with JVD, painful hepatomegaly, and ascites.

c. Biventricular heart failure: either due to a disease that affects both ventricles, or a disease of the left
heart which eventually affects the right.

★ Diagnosis:
1- Transthoracic Echocardiogram: Determines whether systolic or diastolic (&
determining EF). 2- Chest X Ray: Shows the important signs of pulmonary edema such
as Kerley B Lines.
3- ECG 4- Catheter 5- Blood tests: the levels of BNP can exclude the diagnosis of heart failure.

★ Management (main differences between systolic and diastolic):

🡪 Systolic: Drugs that decrease mortality (B-Blockers, ACE Inhibitors, ARBs, Spironolactone) and to improve
symptoms (Diuretics, Digitalis).
🡪 Diastolic: the drugs do not decrease mortality, they just treat the symptoms. (B-Blockers, ACE Inhibitors, ARBs,
Diuretics).

Questions:
1The term „orthopnoea‟ refers to breathlessness (dyspnoea) in a particular situation. Which answer
below describes that situation?
A. After several hours of sleep
B. Due to asthma
C. Immediately on lying flat
D. On exertion
E. On sitting upright

2Which of the following physical signs is associated with left ventricular failure?
A. A gallop rhythm with a fourth heart sound
B. A gallop rhythm with a third heart sound
C. A loud second heart sound
D. A quiet first heart sound
E. Fixed splitting of the second heart sound
3What relationship does Starling‟s Law of the heart describe?
A. Between blood pressure and cardiac output
B. Between cardiac filling and blood pressure
C. Between cardiac filling and cardiac output
D. Between heart rate and blood pressure
E. Between heart rate and cardiac output

4What underlying pathophysiological changes is chronic cardiac failure associated with?

A. Activation of the renin–angiotensin– aldosterone system (RAAS)
B. Inhibition of the RAAS
C. Inhibition of the sympathetic nervous system
D. Reduced production of brain natriuretic peptide (BNP)
E. Systemic vasodilatation

5Neuroendocrine system activation is a feature of heart failure. Abnormalities of which hormone can
cause heart failure rather than result from heart failure?
A. Aldosterone
B. Angiotensin II
C. Catecholamines
D. Thyroxine
E. Vasopressin (antidiuretic hormone, ADH)

6A 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
E. Atrial fibrillation

7A 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 oedema
E. Kerley B lines

8A 70 years old female presented to the ER with SOBOE, LL swelling for 2 weeks. BP 180/100. JVP
high. LL oedema. Chest crackles. ECO was done, EF = 55%. What is the patient expected to have?
A. HfpEF
B. HfrEF
C. LSHF
D. RSHF
 9. A 42 English man presented to the ER with shortness of breath, fatigue, lower limb swilling. A climical dignosis of
HF. on examination the patient was found to have hip pain, deafness, LL numbness, varus. What is the expected
underlying cause?
A. ASD
B. Pericarditis
C. Paget‘s disease
D. Anemia.

10A patient presented with dyspnea, fatigue, palpitations at rest. He is NYHA class..
A. I
B. II
C. IV
D. III

1150 year old man is note to have severe congestive heart failure what drug of the following can prolong survival:

A. Furosemide
B. Hydrochlorothyzide
C. Spironolactone.
D. Digitalis.

12What is the initial treatment for asymptomatic patients with systolic dysfunction?

A. β blockers and Diuretics

B. Diuretics + vasodilatation (ACEI or ARBs) + β blockers
C. Diuretics + vasodilatation (ACEI or ARBs)
D. β blockers and vasodilatation (ACEI or ARBs)

13What is the standard treatment for patients with diastolic dysfunction?

A. β blockers and Diuretics

B. Diuretics + vasodilatation (ACEI or ARBs) + β blockers
C. Diuretics + vasodilation (ACEI or ARBs)
D. β blockers and vasodilatation (ACEI or ARBs)

1445 years old known CHF, he‟s on ( Diuretics, ACE inhibitors, beta blockers ) Recently he develops a dry cough. Which
one of the following drugs caused this side effect?

A. Carvedilol (beta-blockers)
B. Enalapril (ACE inhibitors)
C. Losartan (AIIR blockers)
D. Furosemide (loop diuretic)

15Which one of the following drugs reduce the morbidity rate (hospitalization, HF symptoms) but does not affect
the mortality rate?

A. Ivabradine
B. Spironolactone
C. Digoxin
D. Captopril
 16. 55-year-old patient presents to you after a 3-day hospital stay for gradually increasing shortness of
breath and leg swelling while away on a business trip. He was told that he had congestive heart failure, but is
asymptomatic now, with normal vital signs and physical examination. An echocardiogram shows an
estimated ejection fraction of 38%. The patient likes to keep medications to a minimum. He is currently on
aspirin and simvastatin. Which would be the most appropriate additional treatment?

A. Begin an ACE inhibitor and then add a beta-blocker on a scheduled basis.

B. Begin digoxin plus furosemide on a scheduled basis.
C. Begin spironolactone on a scheduled basis.
D. Begin furosemide plus nitroglycerin.

17.56-year-old man, diagnosed with dilated cardiomyopathy with ejection fraction less than 25%, NYHA class II
dyspnea, BP: 112/68, HR:82, JVP: 7cm water [normal], soft S3 and grade 2 pansystolic murmur, chest is clear, no
lower limb edema, warm extremities.

1. According to perfusion and congestion, how do we classify this patient?

A. Warm and dry

B. Cold and dry
C. Warm and wet
D. Cold and wet

2. How do we treat this patient?

A. Diuretics
B. ACEI and beta-blockers
C. Inotropes
D. No treatment

18.You are caring for a 72-year-old man admitted to the hospital with an exacerbation of congestive heart failure.
Two weeks prior to admission, he was able to ambulate two blocks before stopping because of dyspnea. He has
now returned to baseline and is ready for discharge. His preadmission medications include aspirin, metoprolol,
and furosemide. Systolic blood pressure has ranged from 110 to 128 mm Hg over the course of his hospitalization.
Heart rate was in 120s at the time of presentation, but has been consistently around 70/minute over the past 24
hours. An echocardiogram performed during this hospitalization revealed global hypokinesis with an ejection
fraction of 30%. Which of the following medications, when added to his preadmission regimen, would be most
likely to decrease his risk of subsequent mortality?

A. Digoxin
B. Enalapril
C. Hydrochlorothiazide
D. Propranolol

19. A 75 year-old male presents to you with a gradual onset of symptoms suggestive of heart failure and sinus
rhythm and examination confirms the presence of biventricular failure. Following confirmation of the diagnosis by
chest x-ray and electrocardiography you should take the following steps:

a. Treat the heart failure with diuretics and ACE inhibitors

b. Treat the heart failure with digoxin and diuretics
c. Treat he patient with diuretics, ACE inhibitors and anticoagulants
d. Try to establish the cause of the heart failure with echocardiography, cardiac catheterisation and whatever other
investigations are appropriate
e. Use ACE inhibitor, vasodilator therapy and diuretic
 20-A 68-year-old man with a history of hypertension, diabetes, and urinary retention awoke feeling nauseated and
light-headed. He did not respond to questions from his wife. When the emergency medical technicians arrived, his
blood pressure was 60 by palpation. IV fluids and oxygen were administered. Vital signs obtained in the ER were
blood pressure 60, heart rate 120 and regular, temperature 38.9C (102F), and respiratory rate 30. A brief physical
examination revealed coarse rales approximately halfway up in the chest bilaterally and inaudible heart sounds. An
indwelling urinary catheter was placed with drainage of 10 to 20 mL of dark urine. Chest x-ray revealed bilateral
interstitial infiltrates; ECG was unremarkable except for sinus tachycardia. Antibiotics were administered, and the
patient was transferred to the ICU, where a right heart catheterization was performed. Pulmonary capillary wedge
pressure was 28 mmHg. Cardiac output was 1.9 L/min. Right atrial mean pressure was 10 mmHg. The most likely
cause of this man’s hypotension was:

(A) left ventricular dysfunction

(B) right ventricular infarction
(C) gram-negative sepsis
(D)gastrointestinal bleeding

21-A 65-year-old man with a long history of untreated hypertension complains of recurrent shortness of breath on
minimal exertion. Examination of the cardiovascular system is normal except for a prominent precordial impulse.
Chest x-ray is normal except for a prominent left ventricular shadow. An exercise tolerance test with thallium
scanning reveals no evidence of myocardial ischemia. Two-dimensional echocardiography reveals left ventricular
hypertrophy. Radionuclide ventriculography reveals normal right and left ventricular ejection fractions. What is the
most likely explanation for the patient’s symptoms?
(A) Chronic obstructive pulmonary disease
(B) Reactive airways disease
(C) Systolic congestive heart failure
(D) Diastolic congestive heart failure
(E) Myocardial ischemia

1-C 2-B 3-C 4-A 5-D 6-D 7-A 8-A 9-C 10-C 11-C 12-D 13-C 14-B 15-C 16-A 17(1)-A 17(2)-B 18-B 19- d 20-A 21- D