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Internal medicine Cardiovascular
lecture for 3rd year PHO students
AKLOG A.(MD)
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contents

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 heart failure and pulmonary edema
 Acute rheumatic fever
 Infective endocarditis
 Valvular heart disease
 Ischemic heart disease
 Cardiomyopathies
 Hypertension
 Shock
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Heart failure

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Definition
 The current American College of Cardiology Foundation
(ACCF)/American Heart Association (AHA) guidelines define HF as a
complex clinical syndrome that results from structural or functional
impairment of ventricular filling or ejection of blood, which in turn leads
to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF,
namely edema and rales
 Because many patients present without signs or symptoms of volume
overload, the term heart failure is preferred over the older term congestive
heart failure
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Epidemiology

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 HF is a huge problem worldwide, with more than 20 million people
affected
 The overall prevalence of HF in the adult population in developed
countries is 2%
 HF prevalence follows an exponential pattern, rising with age, and
affects 6–10% of people over age 65
 The overall prevalence of HF is increasing
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Current classification of heart failure
 HF patients are broadly categorized into HF with a reduced EF
(HFrEF) or HF with a pre- served EF (HFpEF)
 The terms systolic and diastolic heart failure are currently less often
used
 The etiologies of HF with HFpEF differs from that of patients with
HFrEF but there is a considerable overlap between this two
conditions
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etiology

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 Any condition that leads to an alteration in left ventricular structure
or function can predispose a patient to develop heart failure
 Coronary artery disease(CAD) is the predominant(60-75%) cause of
HF in developed countries whereas chronic rheumatic vulvular heart
disease(CRVHD) is the most common cause of HF in developing
countries

Etiologies of HF with depressed EF(<40%)
Non ischemic(idiopathic) dilated cardiomyopathy

Coronary artery disease
-Myocardial ischemia*
-Myocardial infarction *
chronic pressure overload
-Hypertension*
-Obstructive vulvular disease*
Chronic volume overload
-Regurgitant vulvular disease
-Intracardiac (left to right)shunting
-Extracardiac shunting
Chronic lung disease
-cor pulmonale
-pulmonary vascular disorders
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-Familial/genetic disorders
-Infiltrative disorders*
Toxic/drug induced damage

-Metabolic disorders*
-viral
Chagas’ disease

Disorders of rhythm

-Chronic bradyarrhythmias
-Chronic tachyarrhythmias
*indicates conditions that can also cause HFpEF
*Indicates conditions that can also lead to heart
failure with a preserved ejection fraction
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Etiologies of HF with preserved EF(>40-50%)

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 Pathologic hypertrophy  High-Output States
-Primary (hypertrophic cardiomyopathy)
-secondary(hypertension)
-Thyrotoxicosis
 Aging -beriberi
 Restrictive cardiomyopathy
-Systemic arteriovenous
-Infiltrative disorders (amyloidosis,
sarcoidosis) shunting
-Storage diseases (hemochromatosis) -Chronic anemia
 Fibrosis
 Endomyocardial disorders
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pathophysiology

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 HF may be viewed as a progressive disorder that is initiated after an index event
either
 Damages the heart muscle with a resultant loss of functioning cardiac
myocytes or
 Alternatively disrupts the ability of the myocardium to generate force, thereby
preventing the heart from contracting normally
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
In most instances
 Patients remain

asymptomatic or
 Minimally symptomatic

following the initial decline

in pumping capacity of the
heart, or
 Develop symptoms only

after the dysfunction has

been present for some time
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 The transition to symptomatic HF is accompanied by
 Increasing activation of neurohormonal (RAA), adrenergic, and

cytokine systems that lead to a series of adaptive changes within

the myocardium, collectively referred to as LV remodeling
 Ventricular remodeling
 Refers to the changes in LV mass, volume, shape, and
composition of the heart that occur following cardiac injury
and/or abnormal hemodynamic loading conditions
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 LV remodeling develops in response to a series of complex events
that occur at the cellular and molecular level:
(1) Myocyte hypertrophy
2) Alterations in the contractile properties of the myocyte
(3) Progressive loss of myocytes through necrosis, apoptosis, and
autophagic cell death
(4) Adrenergic desensitization
(5) Abnormal myocardial energetics and metabolism
(6) Reorganization of the extracellular matrix
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The list of compensatory mechanisms that have been described thus far include
 activation of the renin-angiotensin-aldosterone (RAA) and adrenergic nervous
systems,
↓
a-which are responsible for maintaining cardiac output through increased retention
of salt and water
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b- increased myocardial contractility
There is activation of a family of countervailing vasodilatory molecules, including
the atrial and brain natriuretic peptides (ANP and BNP), prostaglandins (PGE2
and PGI2), and nitric oxide (NO),
VS
That offset the excessive peripheral vascular vasoconstriction
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Activation of neurohormonal systems in heart failure
 The decreased cardiac output in HF patients results in an
"unloading" of high-pressure baroceptors in the left ventricle,
carotid sinus, and aortic arch
↓
 Stimulate the release of arginine vasopression (AVP) from the
posterior pituitary
↓
 Powerful vasoconstrictor that increases the permeability of the
renal collecting ducts
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 These afferent signals to the CNS also activate efferent sympathetic
nervous system pathways that innervate the heart, kidney, peripheral
vasculature, and skeletal muscles
 Sympathetic stimulation of the kidney leads to the release of renin,
with a resultant increase in the circulating levels of angiotensin II
and aldosterone
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The activation of the renin-angiotensin-aldosterone system
 promotes salt and water retention
 Vasoconstriction of the peripheral vasculature
 myocyte hypertrophy
 myocyte cell death
 myocardial fibrosis
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Clinical manifestations

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 Symptoms
 The cardinal symptoms of HF are fatigue and shortness of breath
 The origin of dyspnea in HF is multifactorial
-The most important mechanism is pulmonary congestion with
accumulation of interstitial or intra-alveolar fluid
-Other factors that contribute to dyspnea on exertion include reductions in
pulmonary compliance, increased airway resistance, respiratory muscle and/or
diaphragm fatigue, and anemia
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 Orthopnea, dyspnea occurring in the recumbent position, is usually a later
manifestation of HF than is exertional dyspnea
 Nocturnal cough is a common manifestation of heart failure associated with
orthopnea
 paroxysmal nocturnal dyspnea (PND)- refers to acute episodes of severe
shortness of breath and coughing that generally occur at night and awaken the
patient from sleep, usually 1–3 h after the patient retires
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 cheyne-stokes respiration
 a.k.a periodic respiration or cyclic respiration, is present in 40% of
patients with advanced HF and usually is associated with low
cardiac output
 Cheyne-Stokes respirations may be perceived by the patient or the
patient’s family as severe dyspnea or as a transient cessation of
breathing
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other Symptoms
Patients with HF also may present with gastrointestinal symptoms
Anorexia, nausea, and early satiety associated with abdominal pain and
fullness are common complaints and may be related to edema of the
bowel wall and/or a congested liver
 Congestion of the liver and stretching of its capsule may lead to right
upper quadrant pain
Cerebral symptoms such as confusion, disorientation, and sleep and
mood disturbances may be observed in patients with severe HF
 Nocturia is common in HF and may contribute to insomnia
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 Physical examination
 The purpose is to help determine the cause of HF as well as to assess the severity
of the syndrome
General Appearance and Vital Signs
 cardiorespiratory distress
 Systolic blood pressure may be normal or high in early HF, but it generally is
reduced in advanced HF because of severe LV dysfunction
 The pulse pressure may be diminished, reflecting a reduction in stroke volume
 Sinus tachycardia is a nonspecific sign caused by increased adrenergic activity
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Jugular Venous pressure(JVP)
 provides an estimation of right atrial pressure
 best appreciated with the patient lying recumbent, with the head tilted at 45°
 should be quantified in centimeters of water (normal ≤8 cm)
 In the early stages of HF, JVP may be normal at rest but may become abnormally
elevated with sustained (~15 seconds) pressure on the abdomen (positive
abdominojugular reflux)
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Pulmonary Examination

 Pulmonary crackles (rales or crepitations) result from the transudation of

fluid from the intravascular space into the alveoli.
 In patients with pulmonary edema, rales may be heard widely over both
lung fields and may be accompanied by expiratory wheezing
 When present in patients without concomitant lung disease, rales are
specific for HF
 pleural effusions are often bilateral in HF but when they are unilateral
they occur more frequently in the right pleural space
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Cardiac examination
 Precordium-active/ quiet, location and characteristics of PMI
 Thrills and heave
 S3 (or protodiastolic gallop)
 A fourth heart sound (S4) is not a specific indicator of HF but
is usually present in patients with diastolic dysfunction
 The murmurs of mitral and tricuspid regurgitation are
frequently present in patients with advanced HF
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Abdomen and Extremities
 liver may be enlarged, tender and may pulsate during systole
if tricuspid regurgitation is present
 Ascites
 Jaundice, also a late finding in HF, results from impairment of
hepatic function secondary to hepatic congestion and
hepatocellular hypoxia, and is associated with elevations of
both direct and indirect bilirubin.
 Peripheral edema
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Cardiac Cachexia
 With severe chronic HF, there may be marked weight loss and cachexia
 the mechanism of cachexia is not entirely understood
 it is likely multifactorial and includes:
- elevation of the resting metabolic rate
- anorexia, nausea, and vomiting due to congestive hepatomegaly and abdominal
fullness
-elevation of circulating concentrations of cytokines such as TNF
- impairment of intestinal absorption due to congestion of the intestinal veins
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Diagnosis

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 The diagnosis of HF is relatively straightforward when the patient presents with
classic signs and symptoms of HF; however, the signs and symptoms of HF are
neither specific nor sensitive
Framingham criteria
 Simultaneous presence of at least two major criteria or one major criterion in
conjunction with two minor criteria
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Framingham criteria

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Investigations

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 Laboratory-
 CBC, U/A,RFT, LFT,serum electrolytes
 ECG
 To assess cardiac rhythm,
 To determine the presence of chamber enlargement (LVH…)
 A prior MI (presence or absence of Q waves)
 To determine QRS width
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 Chest x-ray
 Provides useful information about cardiac size and shape, as well as the state of the
pulmonary vasculature
 May identify noncardiac causes of the patient's symptoms
 ECHO
 Diagnosing the cause/s of HF= >Regional wall motion abnormalits, Presence of VHD,
pericardial disease
 LV function , diastolic dysfunction
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 Biomarkers
 Both BNP and N-terminal pro-BNP are relatively sensitive markers for the presence of
HF with depressed EF
 They are also elevated in HF patients with a preserved HF
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Differential diagnosis of CHF
 CLD
 CKD
 nephrotic syndrome
 nephritic syndrome
 TB peritonitis
 TB pericarditis
 other pulmonary causes like COPD…
Precipitating factors of heart failure 34

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Can be remembered by the cardiac mnemonic “HEART FAILED”
 Hypertension
 Endocrine(thyrotoxicosis)
 Anemia
 Rheumatic heart disease(RF,IE)
 Toxins(e.g metal phosphide poisoning,drugs…)
 Failure to take medications
 Arrhythmia
 Infection
 Lung(PE,pneumonia)
 Electrolyte imbalance
 Dietary non-compliance
Principles of management of heart failure 35

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1-general Measures
2- treat the precipitating factors
3- treat the underlying causes
4- treat CHF
5- preventing Disease Progression
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 General principles
 Assess the etiology and severity of the disease
 Next therapeutic regimen aimed at the following factors:
 Correction of precipitating factors including lifestyle modification (eg, high salt intake,
alcohol cessation, medication compliance)
 Treatment of the cause of the heart disease
 Pharmacologic therapy directed at relieving symptoms, slowing the progression of the HF,
and improving patient survival
 Specialized management for HF that is refractory to maximal oral pharmacologic therapy
New York Heart Association (NYHA) classification 37

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Stages of heart failure

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 Stage A
 At high risk for heart failure but without structural heart disease or symptoms of HF
 Stage B
 Structural heart disease but without signs or symptoms of HF
 Stage C
 Structural heart disease with prior or current symptoms of HF
 Stage D
 Refractory HF requiring specialized interventions
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Diuretics

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 Control fluid and salt retention
 For Rx. of pulmonary/peripheral congestion
 These are relievers of symptoms
 Loop Diuretics - Furosemide, Torasemide, Bumetamide are preferred
 Thiazides
 Inhibit selective reabsorbtion of NaCl in the distal cortical diluting segment
 Decreased potency in patients with impaired renal function
 Side effects
 Hypokalemia
 Metabolic alkalosis
 Hyperurecemia
 Hyperglycemia
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 Loop diuretics
 Inhibits reabsorbtion of sodium chloride & potassium in the thick ascending limb of
loop of Henle
 Induces diuresis as high as ¼ of the GFR
 Potassium sparing diuretics
 Shouldn’t be used in state of
 Hyperkalemia
 Renal failure
 e.g spironolactone,triametrine & amiloride
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 Preventing disease progression
 ACE inhibitors and beta blockers have emerged as the cornerstones of modern therapy
for HF with a depressed EF
 Angiotensin Receptor Blockers (ARBs) are used in patients who are intolerant of ACE
inhibitors
 ACE-I & BB Decrease
- Myocyte necrosis
-Myocyte apoptosis
- Fibrosis
-LV Dilation
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Cardiac Glycosides

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 These increase the force of contraction (inotrops)
 Reduce the conduction with in the A-V Node
 Digoxin is the most commonly used glycoside
 it doesn’t have mortality benefit but it may decrease hospital stay
 It may be useful in patients such as those who
 Remain symptomatic despite maximal medical Rx.
 To provide rate control in patients with AF
 Should be avoided in ventricular arrhythmias
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prognosis

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 the development of symptomatic HF still carries a poor prognosis
 Community-based studies indicate that 30–40% of patients die
within 1 year of diagnosis and 60–70% die within 5 years, mainly
from worsening HF or as a sudden event
 functional status is an important predictor of patient outcome
 The most common cause of death is progressive heart failure, but sudden death may
account for up to 45% of all deaths.
Natural history of heart failure 45

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Cor pulmonale

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 Cor pumonale, often referred to as pulmonary heart disease, can be defined as
altered RV structure and/or function in the context of chronic lung disease and is
triggered by the onset of pulmonary hypertension
 Causes of chronic cor pulmonale
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pathophysiology

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 The common final pathway is pulmonary hypertension that is sufficient to
lead to RV dilation, with or without the development of concomitant RV
hypertrophy
 The severity of the PA hypertension and the onset of RV failure are
influenced by multiple factors including
 Hypoxia
 Hypercapnia
 Acidosis, and
 The alterations in RV volume overload that are affected by exercise, heart
rate, polycythemia, or increased salt and retention because of a fall in
cardiac output
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 Clinical manifestation
 Symptoms related to the pulmonary disorder
 Dyspnea, leg swelling, ascites
 Orthopnea and PND are rarely symptoms of isolated right side HF
 Diagnosis
 Rule out LV failure
 ECG
 Chest x-ray
 High resolution chest CT scan
 Echocardiography
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 The most common cause of right sided HF is not pulmonary parenchymal or
vascular disease but left sided HF
 Therefore, it is important to evaluate the patient for LV systolic and diastolic
dysfunction
 RV dysfunction is also an important sequela of HFpEF and HFrEF but this not
considered as cor pulmonale
 Treatment of cor pulmonale
 Primary treatment of underlying lung disease
 Adequate oxygenation, phlebotomy
 Diuretics
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Pulmonary edema

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 Acute pulmonary edema usually presents with the rapid onset of dyspnea at rest,
tachypnea, tachycardia, and severe hypoxemia
  Acute decompensated heart failure (ADHF) is a common and potentially fatal
cause of acute respiratory distress and it is mainly due to pulmonary edema
 cardiogenic pulmonary edema is characterized by the development of acute
dyspnea associated with the rapid accumulation of fluid within the lung's
interstitial and alveolar spaces which is the result of elevated cardiac filling
pressures
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 a variety of conditions can cause cardiogenic pulmonary edema in
the absence of heart disease, including primary fluid overload (eg,
due to blood transfusion), severe hypertension, renal artery stenosis,
and severe renal disease
 Noncardiogenic pulmonary edema is a distinct clinical syndrome
associated with diffuse filling of the alveolar spaces in the absence
of elevated pulmonary capillary wedge pressure
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Management of pulmonary edema

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The treatment of pulmonary edema depends on the specific etiology
 Support with oxygen and ventilation
-Patients with acute cardiogenic pulmonary edema generally have an identifiable
cause of acute LV failurethat can be rapidly treated, with improvement in gas
exchange
 In contrast, Noncardiogenic pulmonay edema usually resolves much less quickly,
and most patients require mechanical ventilation
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 Reduction of preload
 Positioning- sitting position
 loop diuretics
 Nitrates-nitroglycerin,isosorbide dinitrate
 Morphine
 ACEI-reduce both preload and afterload ,used in pulmonary edema
associated with hypertension
 Inotropic and ionodilator drugs- dopamine,dobutamine
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Thank u