Flashcards in Heart Failure Deck (39):
Definition of heart failure
Structural or functional cardiac disorder that impairs the ability of ventricles to eject blood (forward failure) or fill with blood (backward failure) or both.
What three things affect SV?
Preload, afterload, contractility.
How to calculate stroke volume?
End diastolic volume - end systolic volume
Stroke volume / end diastolic volume
Effect of increasing preload on PV loop
ESV stays pretty much the same, but EDV moves to the right along the EDPVR. So, stroke volume increases.
Effect of increasing contractility on the PV loop?
ESPVR curve rotates up. So while EDV remains the same, ESV decreases and SV increases.
Effect of increasing afterload on the PV loop?
ESV moves up along the ESPVR curve, so ESV increases and stroke volume decreases. EDV remains the same.
Systolic heart failure, and symptoms
Decreased cardiac output, decreased ejection fraction.
<50%. Dizziness, fatigue.
What counts as reduced ejection fraction?
Diastolic heart failure
Elevated LV and RV end-diastolic pressures.
Usually normal EF.
Etiology of systolic heart failure
Impaired contractility from:
Chronic volume overload from mitral regurg, aortic regurg.
Increased afterload from:
Etiology of diastolic dysfunction
Preserved EF but impaired diastolic filling from:
Basically, an alteration of structural properties.
Effect of systolic heart failure on PV loop
Decrease in contractility rotates ESPVR to the right. So ESV increases. Heart dilates to maintain SV (EDV increases in a process called remodeling). When remodeling occurs, filling pressure needs to increase, so signs of congestion occur down the line.
Heart dilation in systolic heart failure to compensate for decrease in SV from decrease in contractility. EDV increases as a result.
Effect of diastolic heart failure on the PV loop
Shift of the entire EDPVR up AND decrease of the EDV. This occurs as a result of the higher filling pressures. EF decreases somewhat due to the decrease in myocardial compliance.
Frank-Starling Compensation Mechanism
In heart failure, the entire stroke volume vs EDP/EDV graph shifts down. Thus, SV decreases.
To increase SV, the heart increases filling pressures. This can cause congestion.
This is the remodeling discussed above.
What happens to the ventricles in heart failure?
Increase in thickness to decrease wall stress.
Wall stress equation
Wall stress = Pressure X radius / Thickness
Increased thickness decreases wall stress.
Occurs as a result of pressure overload, new sarcomeres add in parallel with old. Narrow the lumen of the ventricle.
Occurs due to volume overload. New sarcomeres add in series with old. Increase volume of lumen, basically add to outside.
How does the neurohormonal system compensate for heart failure?
Sympathetic nervous system increases contractility and HR, also causes vasoconstriction. All these things increase CO and maintain BP.
RAAS causes vasoconstriction and increases blood volume by increasing retention of Na in kidney.
ADH also increases blood volume by promoting absorption of water in kidney.
Symptoms of left sided heart failure
Dyspnea, orthopnea, PND, cough, fatigue
Symptoms of right sided heart failure
Edema (peripheral and ascites)
Signs of left sided heart failure
Tachycardia, tachypnea, rales, pleural effusion, loud P2, S3, S4
Why does left sided heart failure have loud P2?
Due to pulmonary arterial hypertension. More blood is filling right side and therefore the pulmonary valve needs to close after the aortic valve.
Why does left sided heart failure have loud S3 and S4?
Loud S3 because there is elevated filling pressure of the ventricle. (This is what happens in diastolic HF to overcome the fact that blood isn't getting out or ventricle isn't stretching).
Loud S4 because atrial kick causes gush of blood again.
These are not valve sounds, so they are low pitched.
Signs of right sided heart failure
JVD, hepatomegaly, peripheral edema.
Why does S2 vary with respiration
Inspiration causes more filling, therefore more time to fill pulmonary arteries and PV closes later than AV.
What causes S1?
Mitral/tricuspid valve closure
What causes S2?
1) No limitation of physical activity
2) Slight limitation of activity. Dyspnea with moderate activity.
3) Marked limitation of activity. Dyspnea with minimal activity.
4) Severe limitation of activity. Symptomatic at rest.
Stages of chronic HF
Stage A: high risk of HF, without structural heart disease or symptoms.
Stage B: Heart disease with asymptomatic LV dysfunction
Stage C: Prior or current symptoms of HF with structural heart disease
Stage D: Advanced heart disease and severely symptomatic or refractory HF.
Labs to do with suspected HF
CBC (for anemia)
Electrolytes and creatinine (before diuretics)
Fasting Glucose (rule out DM)
Thyroid function (Rule out thyrotoxicosis/hypothyroidism)
Iron studies (hereditary hemochromatosis)
Antinuclear activity (rule out SLE)
Viral Studies (rule out viral myocarditis)
BNP (usually >400 in HF)
Chest x-ray in HF
Cardiac Testing for suspected HF?
EKG - look for ischemia, AV block, LBBB, amyloidosis
Echo: Look at LVEF, structural/valvular abnormalities
How to manage symptoms of HF?
Diuretics to decrease pulmonary and systemic congestion.
Vasodilators and ionotropic drugs to increase CO.
ACE inhibitors and angiotensin receptor blockers to decrease Na retention.
Lifestyle factors to treat chronic systolic HF
Lower salt intake, alcohol cessation (can cause dilated cardiomyopathy), medication compliance.