Heart Failure I: Pathophysiology Flashcards Preview

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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?

~40 billion

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
-pericardial issues


What three key mediators affect blood flow?



According to the Frank-Starling Law, what increases stroke volume?

Diastolic filling


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)
=>increases SV


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?

-decreased filling
-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
-lung disease
-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
>Increased HR


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)


Okay, so besides compensating for low CO by increasing HR and fluid retention, what else can you do?

Increase contractility