CVS L1: Heart Failure Flashcards
LVF Sx
- 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
LVF Etiology
- 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
Pathophysiologic changes associated with heart failure:
- Hemodynamic changes
- Neurohumoral changes
- Cellular changes
Causes of Systolic Dysfunction
- Coronary artery disease
- Valvular heart disease
- Hypertension
- Aging
- Dilated cardiomyopathy
Normal Left ventricular pressure-volume loop
- 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
Changes in left ventricular P-V loop in Systolic Dysfunction:
- 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
Hemodynamic Changes in Systolic dysfunction
- 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
Compensated LV failure
SV is partially restored due to increased preload (EDV) shown by the PV loop C:
Diastolic dysfunction
(aka HF with preserved systolic function or HF with preserved EF)
- Causes: Any disease that produces
- Decreased relaxation (Eg:constrictive pericarditis)
- Increased stiffness of ventricle (Eg:hypertrophic cardiomyopathies)
Hemodynamic Changes in Diastolic dysfunction
- 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
Ejection Fraction (EF)
- 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
Neurohumoral Changes in Heart Failure:
- Increased sympathetic activity
- Activation of Renin-Angiotensin-
- Aldosterone System (RAAS)
- Increased release of ADH (vasopressin)
- Release of cytokines and peptides
Neurohumoral Changes (continued): Increased sympathetic activity:
- 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
Neurohumoral Changes (Continued): Activation of RAAS
- 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)
Neurohumoral Changes (Continued): Other cytokines/peptides in heart failure
- 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
BNP
- 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
Cellular Changes
- 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
Basis for dyspnea in patient with CHF due to LVF
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
Basis for orthopnea
From erect to recumbent position
↓
Blood pooling in the pulmonary circulation coming from the extremities and abdomen
↓
Marked elevation in LV pressure
↓
Orthopnea
Basis for PND
- 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)
Physical examination findings in CHF due to LVF & pathophysiological basis:
- 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
Third Heart Sound (S3) pfizz basis
- 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
Fourth Heart Sound (S4) pfizz basis
- 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)
Causes of RVF
- 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
reversed Bernheim effect
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.
Clinical Presentation of RVF:
- Shortness of breath
- Pedal edema (pitting type)
- Abdominal pain
Basis for shortness of breath in RVF:
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)
Basis for Pedal Edema, Anasarca, Ascites
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)
Physical examination in RVF:
- 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)
Elevated Jugular Venous Pressure
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
Hepatojugular reflux:
- 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
P-V loop in progressive LVF
- 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
