Cardiac Failure Flashcards
What are the four determinants of CO?
- Input from venous return PRELOAD
- HEART RATE
- Strenght CONTRACTILITY
- Resisitance AFTERLOAD
What is normal CO?
5L/min
How is right ventricular EDP (end diastolic pressure) measured?
Approximated by jugular venous pressure (JVP)
at the end of diastole, RA pressure = RV pressure = JVP = end diastolic ventricular P
How is left ventricular EDP (end-diastolic pressure) measured?
Pulmonary artery wedge pressure (PAWP)
at the end of diastole:
LA pressure = LV pressure = pulmonary artery wedge pressure = LVEDP
What does pulmonary arterial wedge pressure measure?
pulmonary venous pressure
the balloon occludes the artery such thant only venous and capillary pressure are present
this tells us the LA EDP which = LV EDP
Where is PAWP measured?
In the pulmonary artery:
What is preload?
end diastolic pressure
LV EDP is equivalent to:
L atrial P
Pulmonary venous P
PAWP
RV EDP is equivalent to:
RA P
JVP
LV EDP is equivalent to:
LA P
PV P
PAWP
RV EDP is equivalent to:
RA P
JVP
Hydrostatic Pressure
Pressure pushing fluid out of a capillary
Osmotic Pressure
Pressure exerted by proteins in blood plasma; draws fluid into the vessel
Oedema is caused by
increases in venous pressure pushing fluid out of vessels/capillaries
(remember that atrial pressure is knocked off by the arterioles)
This occurs in:
heart failure (+venous return, -CO, +venous P)
kidney failure (proteinuria causes -protein tf -osmotic pressure)
liver failure (-albumin/proteins in plasma)
blocked lymphatics (cancer)
increased capillary permeability (infection)
EDP is a measure of
(two things)
- ventricular filling
- venous pressure driving fluid out of capillaries
e.g. LVEDP = preload: LV function
and LVEDP = LAP = PVP: lung capillaries
e.g. RVEDP = preload: RV function
RVEDP = RAP = JVP: peripheral capillaries
Pulmonary congestion occurs when
LV EDP is greater than pulmonary venous pressure
–> fluid out of pulmonary capillaries into lungs
due to hydrostatic:oncotic imbalance
~20-30mmHg
n: ~5-10mmHg
Cardiac Failure
When CO is less than body needs
usually due to a systolic failure and decreased contractility
CO for a specific degree of filling is lower i.e. less CO for any given ventricular filling (see graph)
Contractility
Force of contraction for any given preload and afterload
What is the mechanism of compensation in cardiac failure?
+EDP to maintain CO
by retaining fluid to increase venous return
EDP >20-25+mmHg leads to congestion
leads to shortness of breath
What is the most common cause of cardiac failure in Australia?
Ischaemic heart disease
What are the causal mechanisms of cardiac failure?
Loss of mocardial muscle:
- ischaemic heart disease leading to MI (most common)
- cardiomyopathy (especially dilated form)
Pressure overload (causing hypertrophy):
- aortic stenosis
- hypertension
Volume overload:
- valve regurgitation
- shunts (e.g. septal defects)
What are the causes of cardiac failure?
- ischaemic heart disease –> MI
- valvular heart disease
- hypertensive heart disease
- congenital heart disease (shunts, rearranged anatomy)
- cardiomyopathy
- cor pulmonale (RHF due to lung disease e.g. long-term lung disease causing right heart hypertrophy)
- pericardial disease (thickening of or fluid in pericardium)
What are the clinical features of LEFT cardiac failure?
- Shortness of breath
- Fatigue
- Tachycardia
- Lung crepitus
What are the clinical features of RIGHT cardiac failure?
Peripheral oedema (mainly; swollen ankles)
What are the ‘inappropriate adaptations’ to cardiac failure?
essentially, do more harm than good:
- Na+ and H2O retention (tf K+ loss = hypokalemia)
- Vasoconstriction (shunt blood to organs) = increased afterload
- hyperactivity of SNS & renin-angiotensin-aldosterone systems
How does the renin-angiotensin-aldosterone system affect cardiac failure?
leads to fluid retention:
- -CO
- -renal BF
- +renin: ang I–>ang II
- +aldosterone
- +fluid retention, Na+ retention
- K+ loss
- vasoconstriction (angiotensin)
