CVS L1: Heart Failure Flashcards
1
Q
LVF Sx
A
- 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
2
Q
LVF Etiology
A
- 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
3
Q
Pathophysiologic changes associated with heart failure:
A
- Hemodynamic changes
- Neurohumoral changes
- Cellular changes
4
Q
Causes of Systolic Dysfunction
A
- Coronary artery disease
- Valvular heart disease
- Hypertension
- Aging
- Dilated cardiomyopathy
5
Q
Normal Left ventricular pressure-volume loop
A
- 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
6
Q
Changes in left ventricular P-V loop in Systolic Dysfunction:
A
- 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
7
Q
Hemodynamic Changes in Systolic dysfunction
A
- 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
8
Q
Compensated LV failure
A
SV is partially restored due to increased preload (EDV) shown by the PV loop C:
9
Q
Diastolic dysfunction
(aka HF with preserved systolic function or HF with preserved EF)
A
- Causes: Any disease that produces
- Decreased relaxation (Eg:constrictive pericarditis)
- Increased stiffness of ventricle (Eg:hypertrophic cardiomyopathies)
10
Q
Hemodynamic Changes in Diastolic dysfunction
A
- 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
11
Q
Ejection Fraction (EF)
A
- 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
12
Q
Neurohumoral Changes in Heart Failure:
A
- Increased sympathetic activity
- Activation of Renin-Angiotensin-
- Aldosterone System (RAAS)
- Increased release of ADH (vasopressin)
- Release of cytokines and peptides
13
Q
Neurohumoral Changes (continued): Increased sympathetic activity:
A
- 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
14
Q
Neurohumoral Changes (Continued): Activation of RAAS
A
- 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)
15
Q
Neurohumoral Changes (Continued): Other cytokines/peptides in heart failure
A
- 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
22
Q
Third Heart Sound (S3) pfizz basis
A
- 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
24
Q
Causes of RVF
A
- 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
30
Q
Elevated Jugular Venous Pressure
A
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
32
Q
P-V loop in progressive LVF
A
- 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
