Heart Failure Flashcards
What is the definition of Cardiac Output?
Cardiac output is the amount of blood pumped by left ventricle into the aorta per minute
What is the formula for Cardiac output?
CO = Stroke volume (SV) x Heart Rate (HR)
List 3 factors that can affect cardiac output
1) Preload (volume)
2) Afterload (resistance)
3) Heart function- contractility, heart rate
What is the definition of cardiac failure?
1) Failure of the heart to pump at sufficient rate to service the metabolic requirements of the tissues OR
2) The ability to do so only at elevated filling pressures (after compensation)
What is the threshold for HF with reduced ejection fraction (HFrEF)? And list 3 common causes for HFrEF.
Threshold: EF< 40%
Common causes:
1) AMI
2) Long-standing increase in afterload
3) Arrhythmias
4) Cardiac myopathies
What is the threshold for HF with preserved ejection fraction (HFpEF)? Explain how HF symptoms can still occur despite preserved ejection fraction.
EF > 50%
Diastolic dysfunction -> failure of heart to relax adequately -> reduced suction force that draws blood from the atria into the ventricles -> slower/inadequate filling at the expense of higher pressures in the pulmonary venous system (more pronounced during exercise as heart has to handle an increased preload) -> coupled with reduced diastolic time for filling -> inability to handle preload -> backpressure effect on the lungs -> increased pulmonary venous pressure -> breathlessness
Right HF leads to backpressure on (1), and leads to what symptoms (2)?
1) Systemic veins
2) Edema, peripheral venous congestion
Left HF leads to backpressure on (1)? and leads to what symptom? (2)
1) Lungs
2) breathlessness
What is Ejection Fraction (EF)?
EF is the fraction of end-diastolic volume pumped out during systole
Amount of blood pumped out of the ventricle/ total amount of blood in ventricle after diastole = EF
What is the normal range for ejection fraction (EF)?
55-70%/ 0.55-0.7
Ejection fraction of less than ? is indicative of heart failure?
0.4 / 40%
HFpEF is primarily a (?) dysfunction?
Diastolic dysfunction leading to backpressure effects
HFrEF is primarily a (?) dysfunction?
Systolic dysfunction leading to backpressure effects
How may a HF patient present with “forward” failure effects?
1) Low BO
2) Tire easily
CO insufficient to sustain metabolic requirements -> tire easily
CO low -> low BP (note: in pts with HTN, BP can still be high)
How may a HF patient present with symptoms as a result of backpressure effects? List down the symptoms respective to right and left heart.
Left heart:
1)Breathlessness due to pulmonary edema (backpressure on pulmonary venous system)
2) Orthopnea- breathlessness when patients lie down flat, as the heart cannot deal with increased volume of blood coming back -> increased backpressure
3) Paroxysmal nocturnal dyspnea: breathlessness does not occur immediately, happens suddenly and at night. This is due to loss of sympathetic compensation during sleep, hence heart is no longer beating harder and faster, leading to increased venous return -> backpressure effect
Right heart:
1) Peripheral edema (ankles, sacral area): usually starts at the ankles if patient is mobile; pitting ankle can also occur in left HF as kidneys are activated to increase fluid reabsorption
2) Enlarged liver and spleen
What are the effects of compensation (both acute and long-term)?
Acute: increased sympathetic activation -> increased HR, contractility, sweating (sweat glands innervated by SNS)
Long-term: RAAS activated to reabsorb fluid -> decreased urine output, congestion in the venous system and peripheral edema
List the 4 different New York Heart Association (NYHA) classification of HF and its corresponding symptoms
Class I: No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea
Class II: Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea
Class III: Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea
Class IV: Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases.
What are the 5 main classes of medications indicated for HFrEF?
1) ARNi/ARBs/ACE-i +
2) Beta blockers +
3) MRA (mineralocorticoid receptor antagonist) +
4) SGLT2 inhibitors
5) +/- loop diuretics
What are the 2 medications that can used as an alternative to RAASI for HFrEF if patient is renally impaired?
1) Hydralazine
2) Isosorbite Dinitrate (can be used as an add-on)
What are the 3 classes of medications that can be used for optimisation of doses of RAASI and pulse/heart rate in HFrEF pts?
1) Beta blockers: target pulse rate < 70 bpm
2) Ivabradine: BP neutral, used when someone cannot tolerate BB or cannot push BP lower any more, used as an adjunct to reduce HR further
3) Digoxin (if AF): ivabradine cannot be used in AF patients as there is controversy over new onset of AF; digoxin is used on top of BB in AF
What are the cornerstones of therapy in patients with HFpEF?
1) Manage root causes: e.g. heart valve, amyloidosis
2) Aggressive management of comorbidities: e.g. HTN, AF
3) Recent evidence with Empagliflozin and Sacubitril Valsartan
What is the MOA of Sacubitril/Valsartan?
Sacubitril: pro-drug, upon activation to sacubitrilat, acts as a neprilysin inhibitor, preventing the breakdown of natriuretic peptides, leading to prolonged duration of favourable effects of these peptides against the pathogenesis of HF. (Neprilysin also breaks down Ang II, hence inhibition of neprilysin leads to accumulation of Ang II)
Valsartan: ARB, blocks the RAAS system to block the effect of excess angiotensin II
Why cant sacubitril be used together with ACE-inhibitors? What is the washout period when switching ACE-I and sacubitril/valsartan and why is there a need for a washout period?
Neprilysin also breaks down bradykinin. Hence sacubitril inhibition on neprilysin leads to a build-up of bradykinin. Usage with ACE-inhibitors will lead to an increased risk of angioedema.
Washout period: 36 hours- to lower the risk of angioedema
What are the 2 main types of SGLT2 inhibitors that is used in HF?
1) Empagliflozin
2) Dapagliflozin
When should SGLT2 inhibitors be commenced for HF patients? (List down the 6 criteria)
1) Can be started right after decompensation/ when patient is stable (how to tell if patient is stable: refer to points 3-6)
2) No increase in diabetic ketoacidosis
3) No IV inotrope or IV vasodilators within 2 days
4) Must have discontinued IV diuretic and
5) Chronic oral loop diuretic prescribed and/or administered
6) SBP >/= 100mmHg
What are the 3 beta-blockers used for HF?
1) Bisoprolol
2) Carvedilol
3) Metoprolol XL
(ONLY these 3 can be used in HF)
For ACE-I use in HF patients, list down:
1) When to initiate?
2) Monitoring parameters?
3) Follow up
1) Probably during admission, when stable
2)Renal Panel/ SCr + K, BP, urea
3) 1w after initiation and after last adjustment; follow Q4-monthly; do not double dose at < 2 weekly intervals
For ARNi use in HF patients, list down:
1) When to initiate?
2) Monitoring parameters?
3) Follow up
1) Consider during admission when stable, but probably outpatient. Consider reducing diuretic dose; if on ACEi, wash out for 36h first
2) Renal Panel/ SCr + K, BP, urea
3) 1w after initiation and after last adjustment; follow Q4-monthly; do not double dose at <2 weekly intervals
For BB use in HF patients, list down:
1) When to initiate?
2) Monitoring parameters?
3) Follow up
1) During admission, when stable: use of BB can suppress CO and may precipitate fluid overload when used in unstable patients
2) BP, pulse rate, clinical status
3) Do not double dose at <2 weekly intervals; do not uptitrate if in overload; may add ivabradine if PR not at goal; add digoxin if concomitant AF
For MRA (e.g. spironolactone) use in HF patients, list down:
1) When to initiate?
2) Monitoring parameters?
3) Follow up
1) Post MI + EF < 40% + HF sx/DM, probably during admission
2) Renal panel / SCr + K, urea, BP, gynecomastia (spironolactone)
3) 1w after initiation, 4w after adjustment; up-titrate: 4-8 weeks, can be longer for stable patients
For loop diuretics use in HF patients, list down:
1) When to initiate?
2) Monitoring parameters?
3) Follow up
1) Anytime when congested
2) Renal panel/ SCr+K, BP, urea, input/output, body weight
3) After initiation and adjustment, can be given PRN, watch KCl replacement; follow-up appointment: 2-4 weeks; may add metolazone (sequential blockade effects, complementary effects)
For SGLT2i use in HF patients, list down:
1) When to initiate?
2) Monitoring parameters?
3) Follow up
1) Consider during admission when stable, but probably outpatient
2) Renal panel/ SCr, BP, Euglycemia ketoacidosis, genitourinary tract infections
3) Follow up after initiation and adjustment; follow-up appt:2-4 weeks, can be longer for stable patients
Why is there a need for close monitoring of RAASi agents when acutely diuresing HF patients?
When acutely diuresing patients, patients will end up with a lot of concentration of electrolytes in the body, serum creatinine can rise/precipitate AKI due to loss of great amount of fluid -> kidney appears to be injured acutely
With RAASi agents, it can reduce efferent arteriolar constriction, hence perfusion in glomerulus decreases and could worsen the stage of AKI
Hence, in state of very bad overload, when aggressively diuresing patients, sometimes RAASI agents are not started, though small doses may be started for vasodilation effect -> caution in renal function, monitor closely
List 2 laboratory markers that can increase due to dehydration
1) Serum creatinine
2) Urea
-> caution in AKI
What are some key advice that should be given to patients on beta-blockers for HF?
1) Explain expected benefits: Given to improve symptoms, prevent worsening of HF, and increased survival. Symptomatic improvement may develop slowly after starting treatment, sometimes taking 3-6 months or longer
2) Possibility of temporary adverse effects: temporary symptomatic deterioration may occur during initiation or up-titration phase; in the long-term beta blockers improve well being
3) Report deterioration: tiredness, fatigue, breathlessness; can usually be easily managed by adjustment of other medications; DO NOT stop beta blocker without consulting physician
4) Weigh: during initiation or uptitration phase to detect and treat deterioration early, patients should be encouraged to weigh themselves daily (after waking, before dressing, after voiding, before eating), and to increase their diuretic dose should their weight increase persistently (>2 days) by > 1.502kg/day; NOTE: not everyone is capable of self-titration
What are some considerations when using beta-blockers in HF patients?
1) Do not start/increase BB when in overt overload
2) If PR<50bpm, halve the dose of BB
3) If PR >70bpm, double the dose of BB
4) If patient experience symptomatic hypotension, consider “sacrificing” other agents instead e.g. nitrates, CCBs instead
What are some considerations when using ARNi for HF?
1) Note dizziness/lightheadedness following up-titration; often improves with time, patient shld be reassured
2) Cough: common in HF patients, exclude pulmonary edema when new worsening cough develops; when a troublesome cough develops and can be proved to be due to ARNi and ACEi, substitution of ARB is recommended
3) Rise in Cr and K threshold: an increase of K up to 5.5 is acceptable; if Cr/k/urea rise excessively, investigate causes e.g. K-rich food intake, nephrotoxin/NSAID use, dehydration (review urea as well)
When should ivabradine be initiated in HF patients?
1) if PR still > 70bpm
2) Unable to tolerate/optimise BB
When should digoxin be initiated in HF patients?
Pulse rate control when concomitant AF
When should hydralazine/ isosorbite dinitrate be initiated in HF patients?
- Vaso + venodilator
- Alternative to RASi
- Additional BP control
List 5 classes of medications that are associated with increased risk of adverse effects in patients with HF
1) Glucocorticoids: sodium retention
2) NSAIDs: sodium retention and peripheral vasoconstriction, blunted response to diuretics and ACE-inhibitors
3) CCBs (other than amlodipine and felodipine): negative inotropy, neurohumoral activation
4) beta-2 agonists: sympathetic agonist activity, hypokalemia, tachyarrhythmias
5) Trimethoprim-sulfamethoxazole: risk of hyperkalemia/ AKI when taken with ACE/ARBs, risk of hyperkalemia when taken with MRA
6) Itraconazole: negative inotropic effect; also increase serum digoxin conc
7) Na-containing preparations (e.g. fleet phospho soda)
8) Na load QT-prolonging drugs (e.g. haloperidol, erythromycin): proarrhythmia
9) Licorice: mineralocorticoid excess; sodium retention and hypokalemia
What are some counselling points for HF patients?
1) Disease modifying role of medicines, onset, ADR
2) Clear communication of how and when to follow up
3) >2kg increase overnight or over 2-3 days
4) Fluid restriction: 800ml-1L, 1.2L when stable
5) Sodium intake and salt substitution
