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Flashcards in Management of Heart Failure Deck (62):
1

Why would you do a CORNOARY ANGIOGRAM study in a newly diagnosed HF patient?


• You could also do CTA, stress test, MRI
• Looking for ischemia and scarring

2

Why would you do a IRON study in a newly diagnosed HF patient?

• Hemocrhomatosis
• Iron deficiency

3

What are the three general goals for any treatment in medicine?



• Improve quantity of life
• Improve quality of life
• Decrease financial and resource burden of disease

4

What 9 studies should be done in the situation of a new HF diagnosis?

• Vitals (BP and HR)
• ECG
• CMP and CBC (basic labs)
• CXR
• BNP
• Echo
• Coronary angiogram
• Thyroid
• Iron

5

What are the five general goals in HF management in particular?

• Correction of underlying cause of HF
• Elimination of precipitating factors
• Reduction of congestion
• Improve flow
• Modulate neurohormonal activation

6

Why would you do a VITALS study in a newly diagnosed HF patient?



• Hypertension is you main concern here

7

Why would you do an echocardiogram study in a newly diagnosed HF patient?

• Dilation,
• LV function
• Wall motion
• PHTN
• prognosis

8

Why would you do a BNP/NOT-proBNP study in a newly diagnosed HF patient?

• Also can do troponins
• Looking for underlying heart damage
• Marker of severity and prognosis

9

Why would you do a CXR study in a newly diagnosed HF patient?

• Coexistant lung disease
• Baseline for future comparison

10

Why would you pull BASIC LABS in a newly diagnosed HF patient?

• Renal failure
• Liver dysfunction
• Anemia
• Infection
• Diabetes Mellitus

11

Why would you do a ECG tudy in a newly diagnosed HF patient?

• Tachyarrhythmia
• Atrial fibrilation
• PVCs

12

What do Diuretics do (general)?

• HF management by way of Reverse sodium and fluid retention

13

Using the idea of Frank-Starling curves, why does diuretic treatment not mess with stroke volume?

• Works at far end of Frank-Starling curve typically
• Significant decreases in pressure produce MINIMAL changes in stroke volume and CO
• Symptoms of congestion can be reduced without major effects on blood flow

14

What conditions might require the use of IV diuretics?

• Congested intestine may not absorb diruetic well PO
• Worsening renal function may require a higher dose

15

When are diuretics used?

• Part of treatment of HF
• Can be used acutely or chronically (PO or IV)

16

What are the two main classes of diuretics used?

• Loop diuretics (preferred b/c of potency)
• Thiazide diuretic (can augment the use of loop diuretic)

17

What is the use of Diuretics treating?

• They increase salt and water excretion
• Decreasing intravascular fluid volume
• Decreasing venous congestion
• Decreasing dyspnea and edema
○ Far right of frank-Starling curve, so decreasing the ventricular end diastolic pressure by decreasing volume/filling does not drastically reduce stroke volume

18

What is meant by the cycle of neurohormonal activation?




• Initially, low LV filling will lead to low CO
• Low CO is sensed by the baroreceptors (producting baroreceptor reflex) and the juxtaglomerular apparatus in the kidney (initiating RAAS activation)
• RAAS and adrenergic activation are the results of the two pathways
• Increased sodium retention, heart rate, and vasoconstriction are the end products, all trying to increase the volume of the blood and increase LV filling to fix the low CO
• This CHRONICALLY results in lower LV squeeze (systolic HF) AND/OR increased stiffness (diastolic HF)
• It also CHRONICALLY results in supranormal filling pressures (compensating for stiffened heart and overall higher pressures)

19

When blood pressure falls what does the kidney release and what does that accomplish?

• Renin, and this cleaves angiotensinogen to angiotensin I
• Angiotensin I is cleaved by ACE to Angiotensin II
• Angiotensin II induces the adrenal gland to release aldosterone which influences salt retention and water retention

20

What are the side effects of ACE inhibitors?

• Hypotension
• Worsening renal function (afferent vasocontraction)
• Hyperkalemia
• Cough (kinin potentiation)
• Angioedema

21

What are the effects of ACE inhibitors?

• Direct vasodilation
• Decreased aldosterone activation

22

What are the three drugs we talked about that are ACE inhibitors?

• "blank_pril"
• Lisinopril
• Enalapril
• Benazepril
○ Block ATI to ATII conversion

23

What are the unfortunate chronic results of the neurohormonal activation cycle?

• This CHRONICALLY results in lower LV squeeze (systolic HF) AND/OR increased stiffness (diastolic HF)
• It also CHRONICALLY results in supranormal filling pressures (compensating for stiffened heart and overall higher pressures)

24

What are the three angiotensin receptor blockers we discussed in class?




• "blank_sartans"
• Valsartan, candesartan, losartan
○ Block the receptor for angiotensin II in the adrenal gland
○ Blocks the increased salt and water retention of RAAS activation
"blank_sartans" in a drug name means what?
• They are angiotensin receptor blockers
• Block RAAS activation

25

What are the side effects of angiotensin receptor blockers?

• ARBs do not produce kinin potentiation
○ No cough - PLUS!
• ARBs have similar side effects to ACE inhibitors
○ Hypotension
○ Worsening renal function (afferent vasocontraction)
○ Hyperkalemia
○ Angioedema

26

What are some notes for clinical use of angiotensin receptor blockers?

• They are equivalent to ACE inhibitors in function
• Controversial whether use in combo with ACE inhibitors is providing an added benefit
• Generally used when patients develop cough because of ACE inhibitor use

27

What are the two aldosterone receptor blockers we discussed?



• Spironolactone and eplerenone
• Block effect of aldosterone on the kidney
• It's also an antifibrotic
• Main side effect = hyperkalemia

28

Why would you use an aldosterone receptor blocker and not an ACE inhibitor or ARB?

• ACEi and ARB use are not complete
• Aldosterone receptor blocking is more powerful and results in the most salt excretion

29

What is the main side effect of aldosterone receptor blocker use?

• Main side effect = hyperkalemia

30

What are the three Beta-Blockers we discussed?




• "blank_olols"
• Metoprolol
• Carvedilol
• Bisoprolol
○ Antagonize effect of sympathetic system
○ Negative chronotrope
○ Negative inotrope

31

What are the side effects of beta-blockers?

• Negative inotrope - short term loss for long term gain
○ Fluid retention
○ Hypotension
○ Decreased CO, even cardiogenic shock
• bronchoconstriction

32

What happens in an Alpha1 blockade?

• Vasodilation (counteracts the sympathetic nervous system mediated vasoconstriction)

33

What happens in a Beta1 adrenergic blockade?

• Negative chronotropy
• Negative inotropy

34

What is meant by Beta-Blockers having a negative inotrope effect?

• Decreased inotropy = decreased contractility
• Sympathetic nervous system usually increases inotropy so these will stop that increase

35

What is meant by Beta-Blockers having a negative chronotrope effect?

• Negative chronotropy = decreased heart rate
• Sympathetic nervous system and adrenergic activation usually increases heart rate

36

When is the combo of ACE inhibitor and beta-blocker recommended?


• HF patients with EF less than 40%
• Reduces rist of HF hospitalization and premature death

37

What is meant by MRA?

• Somehow that means aldosterone receptor blockers
○ Eplerenone
○ Spironolactone
• Indicated in patients with persisting symptoms and EF of less than 35%, even with treatment with ACE inhibitors or ARB and beta-blocker

38

What is the alternative to ACE inhibitor if the patient can't tolerate it?

• ARB, angtiotensin receptor blocker

39

When is digoxin use recommended?

• EF less than 45%
• Unable to tolerate beta-blocker
• Should be used in combo with ACE inhibitor or ARB and MRA
○ diuretics

40

What are the three general effects of vasodilators?




• Arterial vasodilation
• Venous vasodilation
• Pulmonary arterial vasodilation

41

What does Arterial vasodilation result in?

• Decrease in LV afterload
• Reduced cardiac work
• Less mitral regurgitation

42

What does Venous vasodilation result in?

• Decrease in preload

43

What does Pulmonary arterial vasodilation result in?

• Decrease in RV afterload

44

What are the electrical therapies for HFrEF?



• Implanted cardioverter defibrillators
• Cardia resynchronization therapy (biventricular pacemakers (CRT or BiV)

45

When should you use Cardia resynchronization therapy (biventricular pacemakers (CRT or BiV) and what does it do?

• Left ventricular lead placed from RA through coronary sinus over epicardium of LV
○ 3 leads = RA, RV, cor sinus/LV
• For pts with QRS duration over 120msec (bundle branch block)
• Cuases the LV lateral wall and septal wall to contract together
○ More efficient contraction to increase SV
○ Improve mitral valve function to decrease regurgitation
• Usually placed with ICD

46

What does Implanted cardioverter defibrillators treatment do?

• Pateints with LVEF less than 35% or prior dangerous heart rhythms
• Abort sudden cardiac death from ventricular tachycardia/fibrillation

47

In ACUTE therapy (decompensating pt) what are the HF treatment changes?

• IV diuretics
• IV vasodilators
• IV inotropes for shock
• Positive pressure ventilation (CPAP/BiPAP, intubation) for hypoxia
○ May also reduce preload
• May need to cut back on beta-blockers (only in

48

What is the clinical use of the inotropic agents?

• IV agents used short term in ICU to reverse shock
○ Long term they worsen remodeling and increase mortality
• Digoxin has no effect on mortality but may reduce symptoms and hospitalization
○ Some decrease in heart rate in Atrial fibrillation is to be expected
○ In high doses causes digoxin toxicity which mostly manifests as arrhythmias
○ Completely renally cleared so needs dose adjustment with renal dysfunction

49

severe cases)
What are the 3 inotropic agents we discussed?

• Digoxin (PO)
○ K/Na exchanger
• Dobutamine (IV)
○ Beta agonist (opposite of beta blocker)
• Milrinon (IV)
○ Phosphodiesterase inhibitor
○ Similar effect to dobutamine, prolongs cAMP signal

50

What are the aggressive advanced therapies for heart failure?



• Remember this is a progressive disease, usually seen in older patients, and the end is nigh (5 year median survival)
• Cardiac transplantation
• Mechanical circulatory support/ ventricular assist devices
○ Bridge to transplant OR the final therapy

51

In the summary slides what treatments were listed for prolonging survival of pts with HFrEF?

• They all reduce remodeling
○ ACE inhibitors - lisinopril
○ Angiotensin Receptor blockers - valsartan
○ Beta blockers - carvedilol, meoprolol
○ Aldosterone Antagonists - spironolactone, eplerenone
○ Vasodilators - nitrates and hydralazine
○ Cardiac resynchronization therapy - biventricular pacing
○ Implantable cardioverter defibrillator (ICD)
§ Prevents death but doesn't help symptoms

52

In the summary slides, what treatments were listed for improving symptoms of heart failure?

• Diuretics
○ Furosemide in particular
• Inotropes (HFrEF)
○ Digitalis PO
○ If acute HF with shock, dobutamine and milronone

53

What is meant by HF stage A?


• At high risk (has pre-factors) but not showing disease or symptoms

54

What is the treatment for HFpEF?

• Therapy consits of treating underlying disorder
○ Hypertension, diabetes, kidney dysfunction, aortic stenosis
• Diruetics are used to keep volume normal
• Vasodilators are used to maintain normal blood pressure

55

Do the therapies for HFrEF work for HFpEF?

• Nope. ACEI, ARB, spironolactone do not show success in HFpEF patients
• Neither are ICD/CRT indicated
• Therapy consits of treating underlying disorder
○ Hypertension, diabetes, kidney dysfunction, aortic stenosis
• Diruetics are used to keep volume normal
• Vasodilators are used to maintain normal blood pressure

56

What are the therapy goals for Stage D HF?

• End of life care
• AGGRESSIVE - transplant, chronic inotropes, permanent mechanical support, experimental surgery

57

What are the therapy goals for Stage C HF?

• Dietary salt restriction and getting rid of underlying cuase
• ALL - Diruetics, ACEI, beta blockers
• SELECT - Aldosterone antagonist, ARB, digitalis, hydralazine/nitrates
• DEVICES - BiV, ICD

58

What are the therapy goals for Stage B HF?

• Same as A (get rid of underlying cause)
• ACEI or ARB
• Beta blockers
• Implantable defibrilators

59

What are the therapy goals for treating HF stage A?

• Treat hypertension
• Encourage smokin cessation
• Treat lipid disorders
• Discourage alcohol intake
• ACE inhibitors or ARB in appropriate patients for vascular disease or diabetes

60

What is meant by HF stage D?

• Refractory HF requiring specialized interventions

61

What is meant by HF stage B?

• Structural heart disease but no symptoms YET

62

What is meant by HF stage C?

• Structural heart disease with prior or current symptoms
• A spectrum, and usually oscillatory