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Heart Failure Flashcards

1
Q

Heart failure

DEFINITION

A

• Heart failure (HF) is a clinical syndrome determined by any structural and functional impairment of the heart
• “The heart cannot pump enough blood to fulfill the metabolic needs of the body or perform that with increased diastolic filling pressures”
• “Impaired ability of the ventricle to fill with or eject blood”
• Final pathway of evolution common for any cardiovascular disease
• Natural history
→ progresive disorder
→ decreased life expectancy

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2
Q

EPIDEMIOLOGY

A
  • ↑ Incidence →population is aging (85% of HF cases → > 65 y)
  • prevalence depends on the definition ~ 1–2% of the adult population in developed countries, rising to ≥10% among people >70 years of age (2016 ESC guideline)
  • The lifetime risk of HF at age 55 years is 33% for men and 28% for women
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3
Q

PROGNOSIS = POOR

A

• ↑ Risk of death
5 -10% annually in patients with mild symptoms
30- 40% annually in patients with advanced disease
1 in 5 pt with CHF will die within 1 year of diagnosis
~ half of those diagnosed with HFrEF will be dead within 5 years
• the leading cause of hospitalization in patients older than 65 y

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4
Q

2016 ESC (European Society of Cardiology) definition

A

“HF is a clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema) caused by a structural
and/or functional cardiac abnormality, resulting in a reduced cardiac output and/ or elevated intracardiac pressures at rest or during stress.”

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5
Q

2013 American College of Cardiology (ACC)/American Heart Association (AHA) definition

A

“Heart failure is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood”.

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6
Q

Etiology

A
  1. Coronary artery disease 4. Valvular heart disease
  2. Hypertension 5. Cor pulmonale
  3. Cardiomyopathy 6. Other
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7
Q

Pathophysiological causes of HF

A
  1. Increased work load (HTN)
  2. Myocardial Dysfunction (MI, DCM)
  3. Decreased Ventricular Filling (Valvular, cardiomyopathy)
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8
Q

HF classification

Depending on EF

A
  1. Asymptomatic Systolic dysfunction (without HF symptoms)
  2. HF with Preserved LVEF (with HF symptoms)
  3. HF with Reduced LVEF (Systolic dysfunction) (EF<40%)
  4. HF with mid range EF (>40–50%)

PLVEF preserved left ventricular ejection fraction
LVEF left ventricular ejection fraction

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9
Q

Classification according to

Symptoms and the Stage of the disease

A

NYHA (functional classes)

Class Function 1 yr mortality
I Asymptomatic with ordinary activity 5%
II Slight limitation of normal function 15%
III Marked limitation of current physical activities 30%
IV Dyspnea at rest 60%
Compare the patient with himself !

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10
Q

Stage ACC/AHA Stages of heart failure

A

A High risk for heart failure without structural disease,
currently asymptomatic
B Heart disease with asymptomatic LV dysfunction
C Prior or current symptoms of Heart failure
D Advanced structural heart disease, severely
symptomatic or refractory heart failure therapy

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11
Q

Descriptive terms in HF

A
  1. Acute (New onset, transient, ADHF) vs Chronic HF
  2. Diastolic vs Systolic Heart Failure

 Systolic HF - reduced cardiac contractility
 Diastolic HF – impaired cardiac filling

the term “congestive” no longer used because
not all the patients have volume overload

  1. Other

• Left vs Right HF
Right ventricular systolic dysfunction
Consequence of LV dysfunction
Direct causes: RV Infarction, PAH, chronic. severe TR,

Arrhythmias, RV dysplasia
• High output vs Low output
High output HF
Thyrotoxicosis
Arteriovenous fistulae
Pregnancy
Severe anemia

• Etiology based : ischemic or nonischemic HF

ADHF- acute decompensated heart failure
LV- left ventricle
RV- right ventricle
TR- tricuspid regurgitation
PAH- pulmonary arterial hypertension
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12
Q

Mechanisms of heart failure

A
  1. Hemodynamics abnormalities
  2. Activation of neurohormonal systems
  3. Cardiorenal interactions
  4. Abnormal calcium cycling
  5. Alterations in myocite regeneration, cel death
    Replacement with fibrosis of extracellular matrix
    Beta-adrenergic desensitization
  6. Myocardial genetics (inherited, mutations)
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13
Q

Compensatory mechanisms

A

 Increased Heart Rate

Sympathetic mediated (Norepinephrine)

 Dilatation

Frank Starling (Contractility)
The Frank-Starling mechanism: by increasing
preload try to sustain cardiac performance
 Activation of neurohormonal systems

Activation of SNS
Activation of RAAS
Release of ADH
Release of atrial natriuretic peptide

→ Redistribution of Blood

 Myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented
→ impaired diastolic and systolic function

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14
Q

HF: Progressive Disorder

Due to:

A
  1. Ventricular dysfunction
    • begins with injury or stress to the myocardium
    • Is progressive
  2. Remodeling → heart chamber dilates, hypertrophies, and becomes spherical with increased walls stress
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15
Q

Remodeling (LV)

A

• factors that alter the ventricular size and function

  1. Mechanical
  2. Genetic
  3. Neurohormonal
    ↑ levels of
    Norepinephrine
    Angiotensin II, Aldosterone
    Endothelin, Vasopressin
    Cytokines
  • Hypertrophy, myocyte death, ↑ interstitial fibrosis
  • Consequences of Remodeling
  • Mitral Regurgitation
  • Arrhythmias
  • Bundle Branch Block
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16
Q

Consequences of Remodeling (LV)

MR- mitral regurgitation
SVT- supraventricular tachycardia
Afib- atrial fibrilation
VT- ventricular tachycardia
SCD- Sudden Cardiac Death
LBBB- left bundle branch block
A

• Mitral Regurgitation
- LV dilates → spherical heart with thinned walls
- distortion of the papillary apparatus → MR→further Progression
• Arrhythmias & Bundle Branch Block→ x 6-9 SCD

Arrhythmias (e.g.: SVT→ AFib; VT)
- consequence of Ischemia, Inflammation, Fibrosis,

Aging -
elevation in LVED volume → atrial stretch → electrical
instability

Abnormal myocardial conduction
LBBB → predictor of Sudden Cardiac Death (SCD)
- ventricular dyssynchrony -> abnormal ventricular
activation & contraction
- delayed opening and closure of the Ao and Mi valves
- abnormal diastolic function
- Lead to paradoxical septal motion, ↓EF, ↓cardiac
output, ↓arterial pressure

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17
Q

The progression of HF is favored by:

A

• Angiotensin system
• SNS activation in heart failure determine
 Dysfunction/death of cardiac myocytes
 Provokes myocardial ischemia
 Provokes arrhythmias
 Impairs cardiac performance
These effects are mediated via stimulation of beta and α1 receptors

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18
Q

Consequences of compensatory mechanisms

A

Catecholamines
• aggravate ischemia, determine arrhythmia
• induce cardiac remodeling, toxic to myocytes
Stimulated RAA system & sympathetic stimulation
• arteriolar constriction
• Na+ H20 retention
• ↑ aldosterone, fibrosis
• endothelial dysfunction

Baroreceptor and osmotic stimuli
• hypothalamic vasopressin →H20 reabsorption in collecting duct
• ↑ endothelin
• ↑ cytokines → cashecxia & apoptosis

Natriuretic peptides from cardiomyocytes
• vasodilatation
• enhanced Na +H20 excretion
• suppress neurohormones
Neurohormonal modulation is the basis of current treatment of HF
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19
Q

Heart failure – clinical diagnosis

A
  1. Dyspnea
  2. Orthopnea
  3. bendopnea
  4. paroxysmal nocturnal dyspnea PND
  5. Fatigue and weakness
  6. Decreased effort capacity
  7. Palpitations and Chest Pain/Pressure
  8. Nocturia and oliguria
  9. Cardiac Cachexia
  10. Right upper quadrant abdominal pain
  11. Cognitive Dysfunction and Mood Disorders
  12. Sleep Disorders
  13. Cheyne-Stokes respiration & Central sleep apnea
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20
Q 
Dyspnea (Shortness of Breath defined by NYHA classification)
with activity (at slight, moderate or current effort) DOE
A

 most common but nonspecific (exist in pts with lung disease or anemia)
 cause: pulmonary congestion that increases the accumulation of interstitial or intra-alveolar fluid,
reduces lung compliance, and increases the work of breathing

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21
Q

orthopnea=

A

dyspnea occurs at rest in the recumbent position→ NYHA IV
 specific symptom of heart failure
 characterized by the number of pillows a patient requires to sleep without
dyspnea
 intolerance of lying flat due to a rapid increase in filling pressure (results from the
increase in venous return from the extremities and splanchnic circulation to the
central circulation with changes in posture)
 Sleeping possible only sitting upright
 correlates well with the severity of pulmonary congestion → When ventricular
preload increases pulmonary venous and pulmonary capillary hydrostatic
pressures raises

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22
Q

bendopnea =

A

= dyspnea that occurs while bending over (Mechanism unknown,just presumed)

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23
Q

paroxysmal nocturnal dyspnea PND is

A

an acute dyspnea
 awakens the patient from sleep
 usually occurs ≥1 hour after the patient lies in dorsal decubitul and resolves with sitting or standing.
 Mechanism: increased venous return + mobilization of interstitial fluid from the splanchnic circulation and lower extremities, with accumulation of alveolar edema

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24
Q

Fatigue and weakness

A

 nonspecific

 Occur in > 90% of patients

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25
Cardiac Cachexia
 Secondary to: constitutional symptoms: nausea, vomiting, anorexia, abdominal pain, and /or muscle wasting  Characteristic to right-sided heart failure, ± tricuspid regurgitation
26
Cognitive Dysfunction and Mood Disorders particularly in elderly
 due to relative hypotension with cerebral hypoperfusion  memory impairment, limited attention .altered mentation.  Depression~25% of patients
27
Physical Examination General appearance and Vital signs
• Sitting upright or Feel uncomfortable when lying flat few minutes (NYHA IV) • Labored breathing • SBP- depending on stage (low when low cardiac output inadvanced HF) • The pulse: variable – if diminished reflect a ↓stroke volume • Increased heart rate (tachycardia=nonspecific ↑ adrenergic activity • Peripheral vasoconstriction – cold extremities + cyanosis of the lips and nail Increased adrenergic activity results in diaphoresis, pallor, peripheral cyanosis with pallor and coldness of the extremities
28
Jugular veins
* Jugular vein distension JVD * Provides an estimation of right atrial pressure * The jugular venous pressure (normal ≤8 cm of water ) = the height of the venous column of blood above the sternal angle in centimeters and then adding + 5 cm
29
Pulmonary examination
* Inspection: +/- tachypnea--Sitting upright or Feel uncomfortable (dyspnea, cough) when lying flat few minutes (NYHA IV) * Auscultation: Pulmonary congestion rales (wet crepitant rales) due to fluid transudation into the alveoli * Percussion: dullness due to Pleural effusions (Hydrothorax)  often bilateral basal dullness in HF  If unilateral occur more frequently in the right pleural space • Acute Pulmonary edema:  Expectoration of frothy, blood-tinged sputum  Rales may be heard widely over both lung fields and  May be accompanied by expiratory wheezing (cardiac asthma)
30
Physical Examination
1. Cardiac examination 2. Cardiac cachexia in advanced HF (anorexia from hepatic and intestinal congestion) 3. Abdomen and extremities 4. Peripheral edema
31
Cardiac examination
does not provide definitive information about HF severity • Palpation, Percussion, Auscultation ‒ Pulsus alternans (during pulse palpation an alternation of one strong and one weak beat without a change in the cycle length) Or ‒ The pulse may be weak, rapid, and thready; the proportional pulse pressure (pulse pressure/systolic pressure) may be markedly reduced ‒ If right heart =enlarged or hypertrophied -> sustained and prolonged left parasternal impulse extending throughout systole • If cardiomegaly present  point of maximal impulse (PMI) is displaced usuallybelow the 5th intercostal space and/or lateral to the midclavicular line  the impulse is palpable over 2 intercostal spaces  if Severe LV hypertrophy -> sustained PMI • S3 may be audible and palpable at the apex in advanced HF • Accentuation of the P2 heart sound is a cardinal sign of Pulmonary Artery Hypertension • Murmurs of Mitral and Tricuspid Regurgitation may appear if there is biventricular heart enlargement • Increased adrenergic activity results in Tachycardia • Systolic arterial pressure may be reduced if cardiac output has declined acutely,
32
Abdomen and extremities
1. Hepatomegaly = enlarged and tender liver that may pulsate during systole if tricuspid regurgitation is present 2. The hepatojugular reflux HJR = secondary to manual pressure over the liver JVD increases; the patient's torso should be positioned at a 45° angle. HJR occurs in patients with elevated left-sided filling pressures and reflects elevated capillary wedge pressure and congestive LV heart failure 3. Ascites, a late sign 4. Jaundice, also a late finding
33
Peripheral edema
= cardinal manifestation of HF But nonspecific • usually absent in patients treated adequately with diuretics • usually symmetric • ambulatory patients: predominantly in the ankles and the pretibial region • bedridden patients: the sacral area (presacral edema) and the scrotum • indurated and pigmented skin if Long-standing edema
34
Patterns of Presentation
• Left sided Heart Failure • Right sided Heart Failure Biventricular Heart Failure • Acute heart failure  Acute pulmonary edema  Cardiogenic shock !Pts with very low EF may be Asymptomatic while Patients with preserved EF may be disabled by symptoms
35
Left sided Heart Failure
``` Left HF Symptoms Fatigue (generalized weakness) Exercise intolerance Dyspnea on exertion Paroxysmal nocturnal dyspnea Orthopnea Anxiety, confusion, restlessness ```
36
Left HF Signs
``` Nocturia Palpitation due to Arrhythmia /Tachycardia Cough - Persistent +/- Pink sputum wheezing like (“cardiac asthma”) Increased respiratory rate-Tachypnea Cyanosis (late) Cardiomegaly Laterally displaced apical impulse Third heart sound (S3) Mitral regurgitation murmur ```
37
Right-sided Heart Failure | Systemic Signs & Symptoms
Jugular vein distension, hepato-jugular reflux Edema (pedal, pre-tibial, sacral) Hepatomegaly, Splenomegaly (20%) Anasarca (generalized edema) Fluid accumulation in body cavities (ascites, pleural, pericardial effusion) Weight gain Palpitation- Tachycardia Nausea, lack of appetite, early satiety, abdominal fullness
38
Classic Triad of pure Right Ventricular Failure:
1. JVD 2. Hypotension 3. Clear Lungs (without rales)
39
Causes of right heart failure:
* LV failure * Coronary artery disease (ischemia) * Pulmonary hypertension * Pulmonary valve stenosis * Pulmonary embolism * Chronic pulmonary disease * Neuromuscular disease
40
Complications of RHF
Hepatic Cirrhosis Effusive enteropathy Nefrotic Syndrome Renal Veins Thrombosis
41
HF- Framingham | Diagnostic criteria
For diagnosis: presence of • 2 major criteria OR • 1 major + 2 minor criteria
42
HF- Framingham | Major criteria comprise the following:
1. Paroxysmal nocturnal dyspnea 2. Weight loss of 4.5 kg in 5 days in response to treatment 3. Jugular vein distention 4. Hepatojugular reflux 5. Rales 6. Central venous pressure greater than 16 cm water 7. Acute pulmonary edema 8. S 3 gallop 9. Circulation time ≥ 25 seconds 10. Radiographic cardiomegaly 11. Pulmonary edema/visceral congestion/ cardiomegaly at autopsy
43
``` HF- Framingham Minor criteria (never related to to another medical condition) ```
1. Nocturnal cough 2. Dyspnea on ordinary exertion 3. A decrease in vital capacity by one third the maximal value recorded 4. Pleural effusion 5. Tachycardia (rate of 120 bpm) 6. Hepatomegaly 7. Bilateral ankle edema
44
Distinction between • pure right ventricular failure and • pure left ventricular failure
→ RV failure causes leg edema | → LV failure causes pulmonary congestion
45
ACUTE HEART FAILURE | Definition
New onset or gradual or rapidly worsening HF signs and symptoms requiring urgent therapy
46
ACUTE HEART FAILURE | Pathophysiology
 Structural substrate→ cardiac dysfunction  Neurohormonal activation  Renal dysfunction  Vascular and endothelial dysfunction  Inflammation and oxidative stress activated  Hemodynamic abnormalities
47
Classification models for AHF
European Society of Cardiology (ESC) - 6 patterns (1) Pulmonary edema (2) Cardiogenic shock (3) Worsening or decompensated chronic HF (4) Isolated right HF (5) Hypertensive HF (6) Acute coronary syndrome and HF The ACC/AHA describes – 3 patterns (1) Patients with volume overload (pulmonary and/or systemic congestion) (2) Patients with hypotension and severe reduction in CO (3) Patients with combination cardiogenic shock and congestion
48
Symptoms and signs in AHF
slide 18
49
Hemodynamic & clinical profiles in AHF
Profile A: Patients without congestion with adequate perfusion (“dry-warm”) Profile B: Patients with congestion but adequate perfusion (“wet-warm”) Profile C: Patients with congestion and hypoperfusion (“wet-cold”) Profile L: Patients without congestion, with hypoperfusion (“dry-cold”) *Congestion evaluated by orthopnea, jugular venous distention, rales, hepatojugular reflux, ascites, peripheral edema *Poor perfusion evaluated by presence of narrow pulse pressure, pulsus alternans, symptomatic hypotension, cool extremities, and/or decreased mentation.
50
Cardiogenic Shock | Definition:
Cardiogenic shock is characterized by a severe generally systolic dysfunction, most often with diminished cardiac output With inadequate tissue perfusion • Most extreme form of pump failure • Mortality is high even with treatment
51
Cardiogenic Shock | Mechanism:
myocardial dysfunction → the heart is unable to maintain adequate cardiac output.→ clinical signs of low cardiac output, with adequate intravascular volume
52
Signs/Symptoms
SBP < 90 mmHg systolic or > 30mmHg drop below baseline Cool, clammy skin Pallor Weak or absent extremity pulses Tachycardia Confusion, restlessness, anxiety, stupor, coma Slow or absent capillary refill • Evaluate signs of peripheral perfusion in addition to BP • BP is NOT the same as perfusion • Shock can be present with a “normal” BP
53
Acute Pulmonary Edema | Definition
Acute pulmonary edema is defined as the sudden | increase in pulmonary capillary wedge pressure (usually >25 mm Hg) as a result of acute LV failure
54
Acute Pulmonary Edema | Symptoms
* Orthopnea * Profound Dyspnea * Anxiety * Associated (prior) * DOE (dyspnea of effort * PND * Fatigue * Nocturia * GI Symptoms * Chest Pain a true life- threatening emergency
55
Acute Pulmonary Edema Physical Exam SLIDE 21!!!!! SOS
* Diaphoresis * Palor * Tachypnea * Confusion * Edema * Diaphoresis * ±Hypertension * Pink Frothy Sputum * Cyanosis * Specific Rales * Tachycardia * JVD * S3 Gallop * Rales –coarse rales, rhonchus * Displaced PMI (point of maximal impulse)* if cardiomegaly present
56
HF precipitating/aggravating factors
 Volume overload, Excessive fluid intake, Dietary sodium intake  Tachycardia, Arrhythmia (Atrial fibrillation, AV block)  Intercurrent illness (eg infection)  Anemia  Hypertension  Myocardial ischemia or acute infarction  Conditions associated with increased metabolic demand (e.g. pregnancy, thyreotoxicosis, ↑physical activity, Anemia, fever  Fluid retention (eg. NSAIDs, corticosteroids)  Medication noncompliance  Administration of drug with negative inotropic properties  Alcohol intake
57
Acute Pulmonary Edema | Other Useful tools for DIAGNOSTIC (I)
``` Labs BNP (↑sensitivity) NTproBNP • Diagnosis of heart failure • level correlates well with NYHA class. • Useful in assessing response to therapy • Helpful in discharge timing • Discharge BNP =prognostic value ```
58
Acute Pulmonary Edema | Other Useful tools for DIAGNOSTIC (II)
``` Chest X-Ray (CXR) Cardiomegaly Prominent upper lobe vessels Bats wing pulmonary edema, Kerley B lines Pleural effusions ``` EKG Arrhythmias ( Afib, VT); Conduction abnormalities Echo EF – helps distinguish systolic and diastolic HF Diastolic pattern Etiology: Regional wall motion abnormalities, Valvular disease Related conditions: Pulmonary artery pressures Coronary angiography- asses etiology MRI (Arrh. RV dysplasia, myocardial viability assessment, infiltrative cmp)
59
HF-conclusions HF is a clinical syndrome in which patients have the following features:
Symptoms typical of HF (breathlessness at rest or on exercise, fatigue, tiredness, ankle swelling) and Signs typical of HF (tachycardia, tachypnea, pulmonary rales, pleural effusion, raised jugular venous pressure, peripheral edema, hepatomegaly) and Objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heart sound, cardiac murmurs, abnormality on the echocardiogram, raised natriuretic peptide concentration)
60
Acute Pulmonary Edema | Goals of treatment
* To ↓ disease Progression * To ↓ Death risk and Hospitalization * To improve symptoms and quality of life QUANTITY OF LIFE is prolonged by: 1. Beta-blocker 2. ACE-Inhibitors 3. MRA (Mineralocorticoid receptors Antagonists) Doses based on clinical trials Only QUALITY OF LIFE is ameliorated by 1. Diuretics (loop diuretics) 2. Digoxin (rate control in Afib)

Semiology second semester (13 decks)

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