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NSCC 7320 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is “systolic HF” referred to as now?

A

HF with reduced EF

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2
Q

What is “diastolic HF” referred to as now?

A

HF with preserved EF

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3
Q

What are some features of systolic HF? What is the EF? At what point would an ICD be considered for this patient?

A

LV contractility issues leading to decreased CO and EF (<40%). Ventricle is large, dilated, overloaded. Preload is increased, afterload is increased. S3 gallop present. EF <40% ICD considered.

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4
Q

What are some features of diastolic HF? What is the EF?

A

Stiff, non-compliant ventricle unable to relax during diastole leading to increased pressure in L.A. and pulmonary vasculature. EF is normal (preload:SV). CO decreased, S4 gallop present.

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5
Q

What are the differences between Class I, II, III, IV HF?

A

Class I: no symptoms, can perform activities without limitations
Class II: mild symptoms, somewhat limited in ability, but no symptoms at rest
Class III: Noticeable limitations in ability, comfortable only at rest.
Class IV: Unable to do any physical activity, symptoms present at rest.

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6
Q

What are some causes of HF?

A

HTN, ischemic heart disease, valvulat heart disease

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7
Q

What are some characteristics of acute HF?

A

Sudden onset of symptoms with a marked imbalance between O2 supply and demand. Hemodynamic deterioration, can include acute deterioration of chronic HF (ADHF) from MI, acute myocarditis

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8
Q

What are some characteristics of chronic HF?

A

Still experiencing symptoms but not rapidly changing. Adequately treated with appropriate techniques and therapies

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9
Q

What is De Novo HF?

A

New diagnosis of HF

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10
Q

What are clinical benefits of Beta Blockers in relation to HF?

A

Delay/reverse remodelling of ventricles and improve LV systolic function.

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11
Q

What are important self management strategies to teach patients?

A

Daily weights (report if gain of 2.5 kg over a week or 2 kg in 24 hours), restrict Na and sometimes fluids, exercise regularly

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12
Q

When would a patient want to report symptoms of HF on an outpt basis?

A

Weight gain, chest pain, increasing fatigue, increasing SOB, inability to lie flat in bed, waking at night with SOB, increased swelling/tight fitting clothes or shoes

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13
Q

What is ventricular remodelling?

A

Hypertrophy of cardiac muscle cells which cannot contract properly. Increased ventricular muscle mass, changes in ventricular shape and impaired contractility.

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14
Q

In relation to SNS stimulation and RAAS stimulation in response to decreased CO from HF, what compounds are released that are of no benefit to HF patient? Why?

A

RAAS: aldosterone, angiotensin 2, ADH/vasopressin, endothelin
SNS: norepi
Angiotensin 2, vasopressin, norepi, endothelin all cause vasoconstriction (increases preload and increases afterload resulting in more work for the heart to manage)
ADH, aldosterone result in Na and H2O absorption (increases circulating volume therefore increasing preload)

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15
Q

What neurohormonal system occurs in HF that is beneficial to the patient?

A

ANP, BNP production in response to stretch and dilation which causes diuresis and vasodilation (decreases preload, decreases afterload, decreases workload of heart).

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16
Q

What is the main lab test when we are trying to confirm presence of HF VS COPD?

A

BNP in HF will be very high, BNP in COPD will be very low.

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17
Q

What are some characteristics of left sided HF? What type of MI might this person have had if HF is related to ischemia? What types of issues will we see occur with ventilation and oxygenation?

A

LV fails to pump blood forward, resulting in backup of blood in LA and pulmonary vasculature resulting in pulmonary edema, SOB, coughing, frothy sputum (pink tinged). Anterior MI. Ventilation - dec lung compliance, increased WOB. Oxygenation - V/Q mismatch dead space-like and shunt-like, dec SA.

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18
Q

What are some characteristics of right sided HF? What type of MI might this person have had if HF is related to ischemia? What mnfts might we see?

A

RV fails to pump blood fully into pulmonary vasculature and to left side of heart resulting in reduced flow to left ventricle and a backup of blood in RA. Inferior MI. + JVD, ascites/cyanosis, liver enlargement (poss liver function issues), bilateral leg/pedal edema, fatigue

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19
Q

What manifestations would we see in biventricular HF?

A

Mnfts of both right and left sided HF (lung and full body issues).

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20
Q

What is the process of septic cardiomyopathy? What is the outcome?

A

Endotoxins (from an inflammatory response) result in reduced myofibril response to Ca, mitochondrial dysfunction and down regulation of Beta adrenergic receptors resulting in cardiomyopathy. Outcome is decreased CO and O2 delivery.

21
Q

What is the main focus of medical management for HF?

A

Block neuroendocrine response and promote O2 supply and demand balance, prevent/reverse ventricular remodelling.

22
Q

What is the “triple therapy” drug regime for HF?

A

ACE I/ARB (if patient cannot take ACEI), MRA, B blocker

23
Q

Provide examples of ACE I. What is the short-term action in HF? Long-term action? What is their affect on O2 supply and demand?

A

Ramipril, enalapril, captopril.
Short-term: vasodilation
Long-term: block neurohormonal effects Reverse ventricular remodelling. Decrease afterload, increase CO, decrease myocardial O2 demand.

24
Q

Provide examples of B blockers. Short term effects? Long term? Affect on O2 S and D?

A

Metoprolol bisoprolol, carvedilol.
Short term: dec contractility and HR
Long term: block negative effects of excessive SNS on myocardial cells, reverse ventricular remodelling
Dec HR, dec myocardial O2 demand, increased filling time (myocardial perfusion), decreased contractility (decrease myocardial workload and demand).

25
Q

Provide examples of ARBs. Short term and long term effects? Effects on O2 S and D? When would ARBs be used?

A

Candesartan, valsartan. Short term: vasodilate
Long term: reverse ventricular remodelling, block neurohormonal effects
Decreased afterload increase CO, decrease myocardial O2 demand. Used when patient cannot tolerate ACE I due to intractable cough or angioedema.

26
Q

Provide examples of mineralocorticoid agonists? What are their longterm effects? Effect on O2 S and D?

A

Spironolactone, metalazone. Block aldosterone receptors, block neurohormonal effects of aldosterone. Dec preload resulting in improved contractility and CO, thereby increasing O2 supply

27
Q

What is the goal for management of acute HF? How would you achieve this?

A

Restore O2 supply. Manage excessive preload (increased preload is leading to decreased contractility and increased afterload which decreases SV and CO). Also want to support contractility and ventilation/oxygenation and decrease O2 demand.

28
Q

What are some options to manage excessive preload in HF?

A

Diuretics - IV lasix #1 choice, vasodilators (Nitro) if patient’s BP is satisfactory, or patient is experiencing hypertensive HF.

29
Q

For ongoing hemodynamic instability, once preload has been addressed, what is a drug that can support this?

A

Inotrope like dobutamine or milrinone.

30
Q

How does dobutamine work? What is its effect on O2 supply and demand? When would we want to have extreme caution when using this drug?

A

Synthetic catecholamine that works on B1 and some B2 receptors. Increases contractility, has some vasodilation, has little effect on HR. Use with extreme caution in LVOT obstruction (like in hypertrophic cardiomyopathy, SAM)

31
Q

How does Milrinone work? What is it’s effect on O2 supply and demand? When would we want to have extreme caution when using this drug?

A

Phosphodiesterase 3 inhibitor increases levels of cyclic adenosine monophosphate in myocardium and smooth muscle cells resulting in increased Ca+. Increases contractility, vasodilation (of pulmonary vasculature and in periphery, decreases afterload. It is an “inotrope and vasodilator”. Use with caution in LVOT obstruction (cardiomyopathy and SAM)

32
Q

What are the most common arrhythmias in patients with HF?

A

A fib, VT, VF

33
Q

What are some commonly used antiarrythmics? What would we want to caution when administering amiodarone?

A

Amiodarone, B blocker, digoxin. Amiodarone can cause cardioversion, would want to use with caution when patient has been in irregular rhythm for unknown amount of time (clots).

34
Q

For a patient with ventricular dysrhythmias and HF what is a common treatment? What does their EF need to be under?

A

ICD. <40%.

35
Q

Beyond regular medical therapy for HF, what are some short term management options?

A

IABP, Impella, ECMO

36
Q

What is LVOT obstruction?

A

Hypertrophied heart results in narrowing outflow track (i.e. track from LV out into aorta). Using medications like + inotropes need to be used with caution as they may further narrow the LVOT and patient will have a massive reduced BP

37
Q

What is the main function of intra-aortic balloon pump? How long would this treatment be used for?

A

Pushes blood into coronary arteries during diastole. Increases coronary artery perfusion and decreases afterload. No longer than 5 days (usually 3)

38
Q

What is the main function of an impella?

A

Off load LV by pulling blood from LV and ejecting it into aorta

39
Q

What is the main function of ECMO?

A

VV ECMO - bypassing lungs only VA ECMO - bypass lungs and heart

40
Q

What are some longterm management strategies for HF?

A

Automatic internal defibrillator (AICD), cardiac resynchronization therapy, cardiac surgery, CABG, valve repaire/replacement, ventricular remodelling/removal of LV aneurysms, LVAD, heart transplant

41
Q

When would an AICD be placed? What can it do? What can happen to patients with this?

A

EF <40% and/or history of sudden cardiac arrest. Can pace dual chambers, overdrive pacing, cardioversion and defibrillation. PTSD from ++ shocks.

42
Q

What is cardiac resynchronization therapy? When is it considered?

A

Biventricular pacing, helps ventricles beat in synchronized fashion. Considered when QRS >120 ms

43
Q

What is the main focus of CABG in relation to long term therapy for HF?

A

Recruit dormant tissue with reperfusion

44
Q

What is a LVAD? When is this often used?

A

Left ventricle assist device, often used as a bridge to transplant or long-term therapy.

45
Q

What are some complications of HF?

A

Rejection, long term immunosuppressant therapy, more prone to CA, increased kidney injury, increased gastric issues.

46
Q

What is an issue with long-term use of ‘old school’ inotropes like digoxin and dobutamine?

A

Increase O2 consumption of myocardium, increased risks for arrythmias due to increased Ca intracellularly, accelerate myocardiac remodelling, apoptosis, and overall worse prognosis in middle-long term

47
Q

What is the focus of palliative care for someone with HF?

A

Manage symptoms and optimize QOL

48
Q

What are some things that will have to be managed in palliative HF patient?

A

SOB, fatigue, N/V, edema, pain, cachexia/anorexia, ICD deactivation

NSCC 7320 (7 decks)

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