CVS L1: Heart Failure

Question 1

LVF Sx

Answer 1

• Breathlessness (dyspnea) - particularly when lying down (orthopnea) or at night [paroxysmal nocturnal dyspnea (PND)]
• Blood-tinged sputum (hemoptysis)
• Chest pain (occasional)
• Fatigue, nocturia, and confusion

Question 2

LVF Etiology

Answer 2

• Inappropriate workloads placed on the LV: -Volume overload (example: MR or AR) -Pressure overload (example: systemic hypertension)
• Restricted filling of the LV (example: constrictive pericarditis)
• Myocardial loss - as in MI
• Decreased myocardial contractility – as in poisoning or infections

Question 3

Pathophysiologic changes associated with heart failure:

Answer 3

• Hemodynamic changes
• Neurohumoral changes
• Cellular changes

Question 4

Causes of Systolic Dysfunction

Answer 4

• Coronary artery disease
• Valvular heart disease
• Hypertension
• Aging
• Dilated cardiomyopathy

Question 5

Normal Left ventricular pressure-volume loop

Answer 5

• 1 to 2 : Isovolumetric ventricular contraction
• 2 to 3 : Left ventricular ejection
• 3 to 4 : Isovolumetric ventricular relaxation
• 4 to 1 : Left ventricular filling
• Note: systole is 1 to 3

Question 6

Changes in left ventricular P-V loop in Systolic Dysfunction:

Answer 6

• Example: Patient with acute Myocardial Infarction (Loss of myocardium)
• Decrease in ventricular pressure during systole
• Increase in ventricular diastolic p
• Decrease in SV
• Increase in ESV

Loop A: Normal
Loop B: Loss of myocardium

Question 7

Hemodynamic Changes in Systolic dysfunction

Answer 7

• To maintain cardiac output, the heart responds with the following compensatory mechanisms:
• i) Increased preload (Frank-Starling relationship) Heart operates at a larger end-diastolic volume & pressure
• ii) Increased release of catecholamines
• iii) Cardiac muscle hypertrophy and ventricular volume increases
• When each of these mechanisms reach certain limit, the heart ultimately fails

Question 8

Compensated LV failure

Answer 8

SV is partially restored due to increased preload (EDV) shown by the PV loop C:

Question 9

Diastolic dysfunction

(aka HF with preserved systolic function or HF with preserved EF)

Answer 9

• Causes: Any disease that produces
• Decreased relaxation (Eg:constrictive pericarditis)
• Increased stiffness of ventricle (Eg:hypertrophic cardiomyopathies)

Question 10

Hemodynamic Changes in Diastolic dysfunction

Answer 10

• ventricular filling is impaired, resulting in reduced ventricular end-diastolic volume OR increased end-diastolic pressure, OR both
• Diastolic pressure-volume curve is shifted to the left, with an accompanying increase in left ventricular end-diastolic pressure
• Contractility and ejection fraction (EF) remain normal
• Markedly reduced LV filling can produce low CO and systemic symptoms
• Elevated left atrial pressures can produce pulmonary congestion

Question 11

Ejection Fraction (EF)

Answer 11

• EF is the fraction of end diastolic volume that is ejected in one beat
• It is an index of myocardial contractility
• Increase in EF indicates positive inotropic effect •Decrease in EF indicates negative inotropic effect

Question 12

Neurohumoral Changes in Heart Failure:

Answer 12

• Increased sympathetic activity
• Activation of Renin-Angiotensin-
• Aldosterone System (RAAS)
• Increased release of ADH (vasopressin)
• Release of cytokines and peptides

Question 13

Neurohumoral Changes (continued): Increased sympathetic activity:

Answer 13

• Occurs early in the heart failure
• Elevated plasma norepinephrine levels
• Increased cardiac contractility and rate
• Initially it may be helpful to improve SV
• Continued effect leads to increased preload and afterload which can worsen heart failure

Question 14

Neurohumoral Changes (Continued): Activation of RAAS

Answer 14

• Release of renin due to reduced renal blood flow
• Fluid and salt retention causing increase in preload
• Consequence of continued hyperactivity of RAAS initiates a vicious circle:
• Severe vasoconstriction combined with increased plasma volume → Increased both preload & afterload → Further reduction in cardiac output → Further reduction in glomerular filtration rate → RAAS activation (cycle repeats)

Question 15

Neurohumoral Changes (Continued): Other cytokines/peptides in heart failure

Answer 15

• IL-1 accelerates myocyte hypertrophy
• TNF-α – causes myocyte hypertrophy and cell death (apoptosis)
• Endothelin – stimulates vasoconstriction in pulm vasculature, myocyte growth, myocardial fribrosis
• ANP and BNP – cause natriuresis and vasodilatation

Question 16

BNP

Answer 16

• Secreted by ventricular myocytes when stretched
• Level in circulation is increased during CHF
• Measurement of this peptide in circulation is important in differential diagnosis and evaluation of heart failure
• BNP imp in monitoring HF

Question 17

Cellular Changes

Answer 17

• Inefficient intracellular calcium handling
• Adrenergic desensitization
• Myocyte hypertrophy
• Cell death (apoptosis)
• Myocardial fibrosis
• The cellular changes in ventricular myocardium in heart failure is collectively known as ventricular remodeling

Question 18

Basis for dyspnea in patient with CHF due to LVF

Answer 18

Dyspnea mechanism 1

Elevated pulmonary capillary pressures due to an elevated left ventricular and atrial pressures

↓
pulmonary venous congestion and pulmonary edema

↓
Stimulation of juxtacapillary J receptors resulting in reflex shallow and rapid breathing.

Edema of the bronchial walls can lead to small airway obstruction and produce wheezing known as “cardiac asthma”

Dyspnea mechanism 2

Replacement of air in the lungs by blood or interstitial fluid

↓
Reduction of vital capacity, restrictive pulmonary changes and closure of the small airways \

↓

Increased “work of breathing” as the patient tries to distend stiff lungs

↓
Respiratory muscle fatigue and dyspnea** **

Dyspnea mechanism 3

Ventilation-perfusion mismatch

↓

Widening of the alveolar-arterial O2 gradient, hypoxemia and increased dead space

↓

Dyspnea

Question 19

Basis for orthopnea

Answer 19

From erect to recumbent position

↓

Blood pooling in the pulmonary circulation coming from the extremities and abdomen

↓
Marked elevation in LV pressure

↓

Orthopnea

Question 20

Basis for PND

Answer 20

• Changes during sleep such as:
  
  • -Reduced adrenergic support
  • -Increased vagal activity
  • -Normal nocturnal depression of resp center
• These changes aggravate pulmonary pooling of blood causing sudden onset of severe respiratory distress at night called paroxysmal nocturnal dyspnea (PND)

Question 21

Physical examination findings in CHF due to LVF & pathophysiological basis:

Answer 21

• Elevated respiratory rate and heart rate
• Peripheral pulse may reveal “pulsus alternans”
• Pale & cold extremities is due to peripheral vasoconstriction to maintain blood flow to the vital organs
• Sweating: Increased sweat gland activity as a part of thermoregulation when body heat cannot be dissipated through the constricted vascular bed of the skin
• Bibasilar Rales, Pleural Effusion:
• Increased fluid in the alveolar spaces can be heard as rales in bilateral lower lung fields.
• Increased capillary pressures can also cause fluid accumulation in the pleural spaces
• S3 and S4

Question 22

Third Heart Sound (S3) pfizz basis

Answer 22

• vibration of blood and ventricular wall
• S3 is a low-pitched sound that is heard during rapid filling of the ventricle in early diastole.
• Increased end-systolic volumes and pressures characteristic of the failing heart are responsible for the prominent S3
• S3 is a consistent physical finding in CHF
• When it arises because of left ventricular failure, the third heart sound is usually heard best at the apex

Question 23

Fourth Heart Sound (S4) pfizz basis

Answer 23

• vibration due to stiffness
• It is a low-pitched sound at the end of diastole that corresponds to atrial contraction
• S4 can be heard if the ventricles are stiff
• Best heard laterally over the apex, particularly when the patient is partially rolled over onto the left side
• S4 is commonly heard in any patient with heart failure resulting from diastolic dysfunction or Ischemic heart disease (IHD)

Question 24

Causes of RVF

Answer 24

• Secondary to LVF because of an increased afterload placed on the right ventricle
• Increased flow from a congenital shunt can cause reactive pulmonary artery constriction, increased right ventricular afterload
• As a sequel of pulmonary disease (cor pulmonale) because of destruction of the pulmonary capillary bed or hypoxia-induced vasoconstriction of the pulmonary arterioles
• Right ventricular ischemia or infarction

Question 25

reversed Bernheim effect

Answer 25

**How LVF possible in a patient with RVF** High afterload on the right ventricle ↓ Increased RV pressure and volume ↓ Interventricular septum bowing to the left ventricular chamber ↓ Insufficient filling of the left ventricle ↓ Pulmonary congestion Rarely, the bowing can be so severe that left ventricular outflow can be partially obstructed. This phenomenon is termed a "reversed Bernheim effect.

Question 26

Clinical Presentation of RVF:

Answer 26

* Shortness of breath * Pedal edema (pitting type) * Abdominal pain

Question 27

Basis for shortness of breath in RVF:

Answer 27

i) LVF → pulmonary edema → dyspnea ii) Existing pulmonary diseases such as pulmonary embolus, chronic obstructive pulmonary disease iii) Congestion of the hepatic veins → ascites → restricted diaphragmatic movements → dyspnea iv) Reduced right-sided cardiac output → reduced pulmonary circulation and left-sided output → Acidosis and hypoxia → air hunger (dyspnea)

Question 28

Basis for Pedal Edema, Anasarca, Ascites

Answer 28

Right ventricular failure ↓ Elevated right-sided pressure ↓ Accumulation of fluid in the systemic veins and venous congestion ``` ↓ Dependent edema (swelling of the feet and legs), Generalized edema (anasarca), Ascites (fluid in peritoneal cavity) ```

Question 29

Physical examination in RVF:

Answer 29

* Elevated jugular venous pressure & Hepatojugular reflux * Sustained systolic heave of the sternum (due to right ventricular hypertrophy) * Right-sided S3 heard best at the sternal border * Additional signs of left ventricular failure such as bibasilar rales (if the primary cause is LVF)

Question 30

Elevated Jugular Venous Pressure

Answer 30

Elevated RAP indicates that the fluid is accumulating in the venous system due to a decreased right ventricular function incr in pressure in the mastoid area is an indication of RVF Other causes of elevated jugular pressures: - Pericardial tamponade - Constrictive pericarditis - Massive pulmonary embolism

Question 31

Hepatojugular reflux:

Answer 31

* Pressing on the liver for a short while (approximately 5 sec) leads to displacement of blood into the vena cava and an increase in jugular venous pressure * Sign of right ventricular failure

Question 32

P-V loop in progressive LVF

Answer 32

* Curve A: Normal * Curve B: Immediate effect of reduced contractility following AMI; Compensation not started * Curve C: Compensated LV failure - SV is partially restored due to increased preload * Curve D: Decompensated LV failure despite increase in preload, SV remains low and heart is over stretched