AssessmentsHeart failure: Clinical practice
USMLE® Step 1 style questions USMLE
USMLE® Step 2 style questions USMLE
A 74-year-old caucasian man comes to the clinic for a planned review. His past medical history is significant for New York Heart Association (NYHA) Stage II heart failure. His current medications include lisinopril 20 mg, furosemide 20 mg, potassium chloride 10 mg twice daily, rosuvastatin 10 mg, and low dose aspirin. He also supplements his medications with fish oil several days a week. Given his class of heart failure, which of the following medications could be added to his heart failure treatment to optimize mortality benefits?
Content Reviewers:Rishi Desai, MD, MPH
This can happen in two ways, either the heart’s ventricles can’t pump blood hard enough during systole, called systolic heart failure, or not enough blood fills into the ventricles during diastole, called diastolic heart failure.
In both cases, blood backs up, causing congestion or fluid buildup, which is why it’s also often called congestive heart failure.
All right, so the heart needs to squeeze out a certain volume of blood each minute, called cardiac output, which is the heart rate - or the number of beats in a minute - multiplied by the stroke volume – or the volume of blood squeezed out with each heartbeat.
The ejection fraction is normally around 50 to 70%, between 40 to 50% is borderline, and anything below 40% is systolic heart failure or heart failure with reduced ejection fraction.
There’s also diastolic heart failure, or heart failure with preserved ejection fraction.
That’s where the heart has very thick ventricular walls so that the chamber doesn’t get an adequate load of blood, so the heart is squeezing hard enough but not filling up enough.
In this case, the stroke volume is low, but the ejection fraction is normal.
All right, so heart failure can affect the right ventricle, the left ventricle, or both ventricles, so biventricular heart failure, which defines where the failure is happening - and then there’s systolic or diastolic failure, which defines why the failure is happening.
Because of differences in diffusion rates, all the extra fluid makes oxygenation harder, but ventilation of carbon dioxide still works pretty well.
Patients often have dyspnea, as well as orthopnea or difficulty breathing when lying down flat. That’s because lying flat allows more venous blood to flow back to the heart and into the pulmonary circulation -worsening the congestion.
All this extra fluid in the lungs causes crackles or rales on auscultation.
A sign of severe left ventricular systolic failure is pulsus alternans, which is when there’s alternating strong and weak peripheral pulses.
This occurs because the ejection fraction is significantly decreased, which in turn causes a reduction in stroke volume, so more blood will remain in the ventricle.
As a result, during the next systole, the myocardial muscle will be stretched more than usual, leading to an increase in myocardial contraction and a stronger systolic pulse.
That can cause jugular venous distention, which can be seen with the patient sitting at 45 degrees as the jugular vein having a fluid wave that represents the filling level.
Normally it should be less than 3 centimetres vertical height above the sternal angle, but in heart failure it goes higher than that.
Blood can also back up into the liver and the spleen, and both can get enlarged.
That’s where applying pressure with a finger leaves a pit in the tissue for a few moments.
This mostly affects the legs, because gravity causes most of the fluid to “pool” there.
Now, since the ventricles work in series, left sided heart failure can also cause right-sided heart failure, and more rarely, right sided heart failure will cause left sided heart failure as well, since the backing up of blood in the venous system will affect the arterial system over time. So patients often develop signs of both right and left sided heart failure.
Now, if the ventricles are stiffened or dilated, eventually the atria will also undergo remodeling to adapt to the higher filling pressures.
For this reason, in heart failure, there’s often a third heart sound or S3 heard on auscultation, which occurs after S1 and S2.
Finally, in advanced heart failure, there’s decreased tissue perfusion leading to a resting sinus tachycardia, cool, pale, sometimes cyanotic extremities, and diaphoresis or excessive sweating due to hypotension, as well as narrow pulse pressure due to the drop in ventricular stroke volume.
On an ECG, there might be clues about the underlying cause of heart failure like an arrhythmia or evidence of coronary artery disease.
In a patient with any type of congestive heart failure, the key lab value is the brain natriuretic peptide or BNP.
A BNP level above 400 pg/ml is typical in heart failure, between 100 and 400 pg/ml is borderline, so further testing needs to be done, and below 100 pg/ml is unlikely to be heart failure.
BNP levels can also be used to monitor a response to treatment as well.
Echocardiography is then done to confirm the diagnosis of heart failure.
It can estimate the ejection fraction, as well as measure ventricular wall and chamber size which helps distinguish systolic versus diastolic heart failure.
Finally, a cardiac catheterization is the insertion of a catheter into a chamber, valve, or vessel of the heart.
This can be done to measure the pressure in the chambers, study valvular function, and can be used to inject contrast media into the ventricles to perform ventriculography, which measures the ejection fraction.
In addition, a coronary angiogram can be done to assess the coronary circulation to look for evidence of myocardial ischemia.
After diagnosing heart failure, it should be classified.