Congestive Heart Failure

Question 1

Left sided CHF causes

Answer 1

• Ischemia
• Hypertension (concentric left ventricular hypertrophy that is more difficult to oxygenate with blood and also greater area to perfuse leading to ischemic damage)
• Dilated cardiomyopathy (not able to contract as well)
• Myocardial infarction
• Restrictive cardiomyopathy (disorder when heart cannot be filled properly)

Question 2

Left sided HF symptom

Answer 2

Pulmonary congestion- increasing hydrostatic pressure in blood vessels causing

1- Pulmonary edema with dyspnea
2- Proxismal nocturnal dyspnea (laying flat for hours)
3- Orthopnea (laying flat for minutes)
4- Crackles (interstitial space filled with fluid)
5- hemosiderin laden macrophages: heart failure cells in the alveoli

(Rupture of engorged blood vessels will cause leakage of blood into the alveoli causing macrophages to consume iron rich blood, turning brown ish on histo)

6- decreased forward perfusion

(causing activation of renin angiotensin system, releasing aldosterone increasing the total peripheral resistance and total blood volume)
give ace inhibitor for this
7- crackles it rales on auscultation (bibasilar inspiratory crackles)
8- S3 heart sound right after S2 ( rapid ventricular filling due to overly compliant ventricles) also called ventricular gallop

Question 3

Right sided CHF MCC?

Answer 3

Left sided failure

Question 4

Right sided CHF other causes

Answer 4

• left-to-right shunt
• chronic lung disease (cor pulmonale)
  This will cause hypoxia that makes blood vessels in the lungs will constrict, the right heart will have to pump against this constriction leading to right sided hypertrophy and then failure

Question 5

Clinical features of RHF

Answer 5

Blood backs up to body leading to congestion in veins of systemic circulation leading to:

• JVD- jugular venous distension

• congestive hepatopathy
Painful HSM (hepatosplenomegaly) , may lead to cardiac cirrhosis due to long standing congestion in the liver
nutmeg liver

• Dependent pitting edema due to increased hydrostatic pressure in the lower extremities as it is also draining into the right heart.

Question 6

What’s ARNI

Answer 6

ARNI, or an angiotensin receptor/neprilysin inhibitor, is made up of two drugs put together to treat heart failure. It contains an ARB (angiotensin II receptor blocker) and a neprilysin inhibitor.
Sacubitril/valsartan hypertensive drugs

Question 7

Which 2 drugs form ARNI?

Answer 7

Sacubitril and valsartan

Question 8

MOA of ARNI

Answer 8

Valsartan blocks the action of a hormone from the kidney called angiotensin II, which can be harmful in patients with heart failure, by blocking the receptors to which angiotensin I normally attaches. This effect stops the hormone’s harmful effects on the heart, and it allows blood vessels to dilate or widen.

Sacubitril blocks the breakdown of natriuretic peptides produced in the body. Natriuretic peptides cause sodium and water to pass into the urine. This effect reduces the work on the heart and reduces blood pressure. The combined effect of the two medicines reduces the strain of the failing heart.

Question 9

ARNI used for?

Answer 9

Heart failure with reduced ejection fraction

Question 10

Contraindications for ARNI

Answer 10

Sacubitril/valsartan should NOT be started until 36 hours after discontinuing an ACE-inhibitor.
Sacubitril/valsartan must not be taken in addition to an ACE-inhibitor or an ARB.
It must not be taken by patients who have had cough or have suffered an allergic reaction with ACE-inhibitors or by patients who have had angioedema by any cause in the past. The most common side effects with sacubitril/valsartan (which may affect more than 1 in 10 people) are low blood pressure, high blood potassium levels (hyperkalemia) or mild impairment of kidney function.

Question 11

left sided HF

Answer 11

• most common type of heart failure.
• It is a “forward failure” because the left-side of heart cannot eject blood into
  aorta.
• This decreased left ventricular output results in increased left atrial pressure & pulmonary venous pressure, which causes: Pulmonary congestion and Pulmonary edema

Question 12

Pitting edema in LHF

Answer 12

Low cardiac output—
Less blood to organs—
Causing fatigue and activation of RAAS—
RAAS increases Na and water absorption
Fluid retention—
Increase in blood volume—
Increase in End Diastolic volume—
Increase in contractility —
Long term of this causes pulmonary edema—
= Prepheral edema

Low cardiac out put also activated the sympathetic nervous system that increases left ventricular contractility further causing edema

Question 13

Low cardiac output causes what?

Answer 13

Low cardiac output also activates the sympathetic nervous system that increases left ventricular contractility further causing edema

Also low organ perfusion leads to activation of RAAS -(prev slide)

Question 14

Rx decreasing mortality

Answer 14

1- ACE inhibitors
Captopril, enalpril, lisinopril

2- ARBs aldosterone receptor blockers
Losartan, candesartan, valsartan

3- Aldosterone receptor antagonists
Spironolactone

4- Beta blockers
Carvedilol, bisprolol, metoprolol

5- Neprilysin inhibitors <ARNI></ARNI>

Question 15

Don’t give Beta blocker in?

Answer 15

Decompenaated HF AS IT decreases heart rate and force of contraction

Question 16

Rx symptomatic relief

Answer 16

Thiazide diuretics furosemide
or
loop diuretics hydrochlorothiazide

Question 17

Rx decrease symptom + mortality

Answer 17

Hydralazine and nitrates
Arterial and venous dilators that decrease pre and after load

Question 18

Ivabradine given why?

Answer 18

Is acts on inward current of SA node
reduces heart rate
Decreased oxygen demand
Reduces mortality
Ineffective in A FIB

Question 19

Which Ionotropic agent is given?

Answer 19

Digoxin

Positive ionotrop
Increases contractility
Used in CHF and Afib
Does not affect mortality.

Question 20

Types of HF

Answer 20

Systolic and Diastolic

Question 21

Systolic HF

Answer 21

• due to decreased contractility of LV Leading to decreased cardiac output due to decreased stroke volume resulting in a decreased EF.

• There is a high EDV end diastolic volume/ pressure as there more blood left after each heartbeat.

• There’s also high EDP Pressure in ventricle is also high at the end of diastole

• Normal is 50-70%
• Ischemic heart disease, especially MI - most common cause
• Hypertension(resulting in cardiomyopathy)
• Valvular Heart Disease
• Dilated cardiomyopathy
• Myocarditis

Question 22

Diastolic HF

Answer 22

• Sufficient contractility but not enough blood returning to ventricles
• low stroke vol but EF Normal
As total vol is also low
• EDP is elevated
• EDV is normal
as atria capable of squeezing blood into the ventricle

Causes:
•Hypertension leading to myocardial hypertrophy.

• Valvular Heart Diseases
• Hypertrophic cardiomyopathy
• Restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis)
• Constrictive pericarditis
• Cardiac tamponade

Question 23

Bi ventricular HF

Answer 23

Both right and left HF

Question 24

BNP

Answer 24

Brain Natriuretic Peptide (BNP):

BNP is a cardiac neuro-hormone produced by ventricular myocardium
BNP helps distinguish CHIF from other causes of dyspnea such as pulmonary embolus, asthma, and pneumonia.
BNP is increased in CHF.
If BNP level is normal it excludes CHE BNP is elevated in conditions associated with left ventricular systolic dysfunction.

The higher the BNP, the higher the cardiovascular and all-cause
mortality.

Question 25

BNP levels

Answer 25

HEART FAILURE >400 pg/mL

BORDERLINE 100-400 pg/mL

UNLIKELY <100 pg/mL

Answer 26

Do:
1- chest X-ray
2- Ecg
3- Echo- EF, ventricular wall and chamber size(sys or di), valve and arterial pressure (causes and effect)
4- Catheterisation of chamber, valve or vessel. To check pressure valve function and inject contrast media into ventricles for EF.
5- Coronary angiogram for myocardial ischemia