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Week 4 - Heart Failure > Management of Heart Failure > Flashcards

Management of Heart Failure Flashcards

1
Q

What assessments are undertaken for someone with HF?

A

NT-proBNP blood test - cardiac marker for HF
Troponin blood test - test for MI
ECG
Echo

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2
Q

What will an ECG of someone with HF either show?

A

Left / right ventricular hypertrophy
Arrhytmias
Bundle branch block
Ischemia
MI
Tachycardia / bradycardia
QRS complex and duration
Left atrial enlargement

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3
Q

What are the aims of HF management?

A

Provide symptom relief
Improve prognosis for the patient
Improve exercise tolerance
Reduce the incidence of acute exacerbation

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4
Q

What is the management process for someone with HF?

A

RAMPS
Refer to cardiology
Advise on condition
Medical treatment
Procedural / surgical intervention if required
Specialist MDT

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5
Q

What is the medical treatment for HF?

A

ACE inhibitors
Beta blockers
Aldosterone antagonists
Loop diuretics
(digoxin)

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6
Q

What is used to relieve fluid overload?

A

Diuretics
Titrate to correct dose
Review and adjust as needed after introducing other drug

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7
Q

What is used to reduce morbidity and mortality?

A

ACE and beta blocker
ARB is ACE not tolerated
?SGLT 2
Introduce one drug at a time

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8
Q

What do ACE inhibitors do for someone with HF?

A

Improve heart function

Reduces levels of angiotensin II so you get vasodilation - reduces after load - less force to which the heart has to pump blood out of the arteries

Kidneys activate the RAAS which increases NA/fluid retention in those with HF- more blood volume and higher pressure in heart - ACE reduces aldosterone release which causes fluid build up - lower blood volume and decreases heart’s workload

Slows down / reverse remodelling by reducing stress on heart and preventing effects of angiotensin II and aldosterone

Lowers blood pressure

Helps alleviate symptoms

Long-term protection of kidneys

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9
Q

What are the side effects of ACE inhibitors?

A

Dry persistent cough - doesn’t breakdown bradykinin
Hyperkalemia
Hypotension
Kidney dysfunction
Angiodemia (rare)
Fatigue and weakness
Dizziness and lightheadedness

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10
Q

What do beta blockers do for someone with HF?

A

Chronotropic effect - reduce heart rate - block effects of adrenaline and norephirine that increase heart rate.
Reducing heart rate gives the heart more time to pump between beats.

Inotropic effect - reduce force of contraction, in the long run helps the heart to rest, heal, prevents excessive strain and damage.

Blocks effects of hormones released due to SNS - preventing further damage to the heart and reversing some of the structural changes.

Prevent arrhythmias by stabilising heart’s electrical activity.

Lowers the heart rate - lowers the force of contraction which decreases heart’s overall demand for oxygen.

Improves left ventricular ejection fraction - partially due to the beta blocker’s ability to reverse damage

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11
Q

What is the mechanism of beta blockers?

A

Respond to adrenaline and norepinephrine

Block beta-1 receptors - reduce influence of SNS and slow heart rate, reducing force of contraction

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12
Q

What are the different types of diuretics?

A

Loop
Thiazide
Aldosterone

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13
Q

What is the mechanism of loop diuretics?

A

Inhibit reabsorption from thick ascending limb in loops of Henle

Inhibit the potassium-chloride co-transporter in the thick ascending limb

Leads to diuresis (increased water loss) and nature’s (increased sodium loss)

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14
Q

What are the effects of loop diuretics?

A

Less reabsorption of Na / water - increased natriuresis and diuresis

Promoting water excretion reduces total blood volume, reduction in the workload on the heart with the smaller volume so there is a decrease in pre-load. A reduction in circulating volume can also reduce after-load - helping improve cardiac output

Venous dilation - immediate reduction in venous return to the help and helps reduces congestion

Sudden drop in LV can result in decreased cardiac output and hypotension

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15
Q

What are the side effects to loop diuretics?

A

Hypokalaemia
Hyponatremia
Hypomagnesemia
Hypocalcemia
Hypochloraemia
Hyponatremia
Hyperglycaemia - insulin sensitivity due to diuretics
Hyperuricimea - increase uric acid levels
Dehydration - excessive fluid loss
Decreased renal perfusion - reduced blood flow to the kidneys
Acute kidney injury - over use of diuretics
Ototoxicity - hearing damage
Hypotension
Metabolic alkalosis

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16
Q

What are the signs for each of the following:
Hypokalaemia
Hyponatremia
Hypomagnesemia
Hyponatremia

A

Hypokalaemia - muscle weakness, fatigue, constipation and sometimes cardiac arrhythmias
Hyponatremia - confusion, headache, nausea, seizures/comas
Hypomagnesemia - lost in urine - muscle craps, arrhythmias, neurological issues
Hyponatremia - confusion, muscle cramps, muscle weakness, dizziness, drowsiness and vomiting

17
Q

Who are contradicted from loop diuretics?

A

Hypovolaemia
Dehydration
Severe hypokalaemia and hypontraemia
Anuria
Addisons
Liver cirrosis (liver scarring) with (pre) comatose (loss of brain function when liver can’t remove toxins)
Arrhythmias
Porphyria

18
Q

What is the mechanism of thiazide diuretics?

A

Inhibit sodium-chloride transporter in distal convoluted tubule
Reduced Na+/Cl- reabsorption

Increased excretion of Na+/Cl- and water follows
Reduction in blood volume
Reduction in pre-load
Helps relieve symptoms of fluid overload

Overtime causes direct vasodilation (relaxation of blood vessels)
Reduced blood pressure and after-load

Less efficacious than loop diuretics in producing diuresis and natriuresis

19
Q

What is the effect of thiazide diuretics?

A

Diuresis and natures
Reduction blood volume
Reduction in pre-load
Helps with symptoms of fluid overload

Antihypertensive agents
Reduce blood volume
Lowers systemic resistance
Decreases after-loads
Reduced after-load allows heart to pump more efficiently

Helps control fluid retention with increased excretion
Helps with symptoms of SOB and fluid retention

Lowers blood pressure

Diuresis = reduction pre-load
Lowering blood pressure and increasing vasodilation = reduces after-load

20
Q

What are the side effects of thiazide diuretics?

A

Hypokalameia – low potassium
Hyponatremia – low sodium
Hypomagnesemia – low magnesium
Hypercalcemia – high calcium

Hypokalaemia – increased excretion of potassium – symptoms: muscle weakness, fatigure, cramps and sometimes arrhytmias

Hyponatremia – excessive sodium excretion – symptoms: headache, confusion, nausea, fatigue and sometimes seizures/comas

Hypomagnesemia – sometimes promote loss of magnesium – symptoms: muscle weakness, cramps and arrhythmias
Hypercalcemia – thiazide diuretics cause an increase in calcium reabsoprtion – symptoms: fatigue, bone pain, kidney stones or calcification of tissues

Dehydration – excessive fluid loss – symtpoms: dry mouth, thirst, decreased urine output

Hypovolemia – reduced blood bolume – can result in hypotension / orthostatic hypotension

Metabolic effects:
Hyperglycaemia – high blood sugar – can cause insulin sensitivity
Hyperuricemia – increase in uric acid levels in the blood – may lead to gout
Hyperlipidemia – cause an increase in blood cholestrol and triglyceride level – may be a concern for patients with high cardiovascular risk

Acute kidney injury – excessive fluid loss may cause a reduced blood flow to kidney

May trigger sulfa allergy

Potential photosensitivity

Hypotension – diuretic effect cause significant drop in blood pressure

Muscle cramps and weakness – due to electrolyte imbalance

Erectile dysfunction

Rare blood disorders – thrombocytopenia, leukopenia, hemolytic anemia

21
Q

What is the mechanism to aldosterone antagonists?

A

Block the activity of aldosterone (adrenal cortex hormone that causes sodium retention) in the distal convoluted tubule and collecting duct – reduces the reabsorption of sodium and water back into the blood

In normal conditions, aldosterone binds to these receptors, promoting reabsorption of sodium and water and promoting excretion in potassium.

22
Q

What are the effects of aldosterone antagonists?

A

Prevents reabsoprtion of sodium and water

Potassium-sparing diuretics – prevent excretion of potassium in the urine

Aldosterone normally stimulates the exchange for potassium, casuing sodium to be reabsorbed and potassium to be lost. When aldosterone is blocked – reduced potassium loss – helps prevent hypokalemia (low potassium levels)

Reduction of pre-load and afterload – reduction in sodium and water retention – preload and afterload lowered – improving efficiency of the heart in patinets with heart failure

Antifibrotic and antiinflammatory effects – alderstone promtoes cardiac and vascular fibrosis – blocking aldosterone limits these effects

Aldosterone plays a role in RAAS – overactiviation of RAAS leads to fluid retention, high blood pressure and worsening heart failure – blocking alodsterone helps moderate RAAS activity – reducing cardiac dagame and helping patients with reduced ejection fraction heart failure

Useful in heart failure following an MI

Recommended in moderate-to-severe heart failure

Recommended patients with:
NYHA class II to IV heart failure
LVEF of 35% or less, unless contraindicated

Decrease the morbitidy and mortality associated with symptomitic chronic heart failure

Spironolactone and eplereone can both cause hyperkalaemia

23
Q

What are the side effects of aldosterone antagonists?

A

Hyperkalemia – aldosterone antagonists are potassium-sparing, so will get elevated potassium in the blood – symptoms: muscle weakness, fatigue, numbness, maybe arrhythmias

Gynecomastia (enlargement of breast tissue in men) and breast tenderness (men and women) - blocks andogren receptor too

Menstrual irregularities and sexual dysfunction

Hypotension – dizziness, lightheadness, orthostatic hypotension

Renal impairment – due to hyperkaelmia or volume depletion – can worsen with pre-exisitng kidney disease

GI side effects – nausea. Vomiting, diarrhea

Fatigue and malaise

Metabolic acidosis – more common in patients with kidney disease

Allergic reaction

CNS effects – drowsiness, lethargy, confusion and headaches – mild

24
Q

What is the mechanism of digoxin?

A

Decreased Na+/K+ ATPase pump
Increase Ca2+
Increase force
Helps pump more blood with each beat
Improving cardiac output

25
Q

What is the effect of digoxin?

A

Vagal activity increase (parasympathetic)
Reduced AV conduction
Reduced heart rate
Reduce symptoms
Prevent hospitalisation
Control rhythm
Enhance exercise

Week 4 - Heart Failure (7 decks)

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