Flashcards in Heart Failure I: Pathophysiology Deck (28)
What's the prevalence of heart failure in the US? What's the incidence (how many new ones in a year)?
prevalence: 6 million in US have HF
incidence: 550,000 new cases each year
What are the direct medical costs from HF?
12 million clinic visits
1,200,000 hospital visits
#1 in Medicare billing
How many people die from it? (directly/ indirectly)
57,000 per year = primary HF
281,000 per year = any mention of HF
Give a definition of heart failure.... (include two types of failure)
HF= inability of heart to pump blood forward at a sufficient rate to meet demands of body (forward failure) or ability to do so only if cardiac filling pressures are abnormally high (backward failure)
**Disclaimer: its a blanket syndrome that covers a lot of stuff
T/F: Heart failure is either predominantly by poor forward flow or backward build up of pressure?
False: both are almost always present
-decreased flow (cardiac output) typically results in congestion (increased filling pressures)
List as many possible dysfunctions causing HF that you can
-failure to contract (systole) or relax (diastole)
-left side, right side, or both dysfunction
-slow, fast, or asynchronous electrical conduction
-regurgitation (backflow) or stenosis (resistance)
-coronary artery problems
What three key mediators affect blood flow?
According to the Frank-Starling Law, what increases stroke volume?
How does inotropy affect preload?
Trick question: it doesn't
-it increases stroke volume by squeezing harder (contractility)
-is effective at any level of end-diastolic preload
How does inotropy work?
adrenergic/ catecholaminergic stimulation increases the amount of Calcium making a stronger contraction
If I have fibrosis, or hypertrophy, or ischemia in my heart, what will be most compromised?
=inability to relax and decreased diastolic filling at a given pressure
On a PV loop diagram, how will increased preload or compliance manifest? (basic directional shift)
Extend horizontally to the right (increased diastolic filling)
On a PV loop diagram, how will increased inotropy manifest? (basic directional shift)
extends vertically AND wider (pump out more blood)
=>increases stroke volume
On a PV loop diagram, how will increased after load manifest? (basic directional shift)
extends vertically but thinner (higher pressure- less volume pumped out)
=>decreases stroke volume
Whats the difference between systolic and diastolic dysfunction?
Systolic = decreased squeeze
diastolic = decreased filling
What are the primary causes of systolic HF?
Direct destruction of heart muscle (ie. MI)
Overstressed heart (ie. tacky, meth)
Volume overloaded heart muscle (ie. regurg)
What happens with decreased lusitropy?
Lusitropy = ability to relax
-you get impaired filling
Whats the difference between HFpEF and HFrEF? Which one is hallmark of systolic HF?
HFpEF (preserved ejection fraction)
HFrEF (reduced ejection fraction)
=Seen in systolic HF
How does the PV loop change with diastolic HF (stiffening)?
The bottom line shifts vertically of the x axis
-because you need to increase the pressure (y axis) to achieve same volume
How would left ventricular hypertrophy affect your hearts activities?
-preserved systolic function
How does external compression (pericardial fibrosis, pericardial effusion) affect the heart?
Cause diastolic HF
Why does a high afterload (hypertension, aortic stenosis, dialysis) cause diastolic HF?
***While this might immediately affect systolic function, over time this leads to hypertrophic cardiomyopathy which decreases ability to fill left ventricle
Whats the normal pulmonary pressure on the right heart?
22/ 10 mmHg
What are the effects of right sided heart failure?
decreased circulating blood
increased venous pressure
What are the causes of right sided heart failure?
-left heart failure
-RV volume overload (tricuspid regurg., shunt)
-damage to RV (infarction, myocarditis)
How does the body usually respond to decreased CO?
-Renin-angiotensin-aldosterone (RAAS) activation
>increased Na retention >> increase fluid
-Autonomic nervous system/ adrenergic activation
Why is the neurohormonal (adrenergic/RAAS) response considered "short term gain for long term loss"?
You increase fluid filling pressures which temporarily helps but stresses the heart even more
(Compensation via Frank-Starling = increasing end-diastolic pressure to maintain SV)