Heart failure Flashcards

1
Q

What is the healthy cardiac output, heart rate and stroke volume?

A

HR = 70bpm
Cardiac output ~ 5 L/min
Stroke volume ~ 70 ml

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2
Q

What percentage of patients wit heart failure did within 5 years?

A

50%

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3
Q

What are the 2 groups of heart failure?

A
  • Pump failure- damage to the heart muscle = decrease in myocardial contractility
  • Overloading - Extra workload on the heart:
    decrease force and velocity of contraction and delayed relaxation
    excessive afterload
    excessive preload
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4
Q

What is after load?

A

The pressure that the chamber of the heart has to generate in order to eject blood out of the chamber (total peripheral resistance- effort to push blood out of heart)

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5
Q

What is preload?

A

The volume of blood present in the ventricles after passive filling and atrial contraction

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6
Q

What are possible causes of pump failure of the heart?

A

Pump failure = can’t contract (systolic failure)
- Most common cause is ischaemic heart disease e.g after MI
Also, IHD, MI, Cardiomyopathy, arrhythmia, virus, infection, inflammation, excessive alcohol, diffuse fibrosis

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7
Q

What are the possible causes of overloading the heart?

A

Overwork and overstretch of cardiac muscle = decreased force of contraction
Causes:
- Excessive afterload- pressure heart has to generate e.g. in hypertension, high pulmonary vascular resistance e.g. in pulmonary hypertension, secondary to chronic lung disease
- Excessive preload (volume of blood in ventricle after filling)- blood presented to heart e.g. in Fluid retention e.g. due to renal failure, Excessive IV fluid infusions, polycythaemia (overproduction of RBCs), drugs such as NSAIDs, steroids as they increase sodium an water retention and therefore increase blood volume
- Also excessive demand on the heart e.g. anaemia, hyperthyroidism, throtoxicosis
- bradycardia or tachycardia
- anything that increases MI workload e.g. pregnancy, obesity, arrhythmia, infective endocarditis, anaemia

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8
Q

What are the 2 classifications of heart failure?

A

acute
chronic

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9
Q

Describe acute heart failure

A

Is rapid e.g. following a MI
- contractility immediately drops due to damage to muscle and therefore cardiac output falls suddenly. This stimulates the cardiovascular system to compensate to maintain output and peripheral perfusion back to normal = ‘compensated heart failure’

  • If the MI is severe, due to the extensive damage, there is no cardiac reserve and the CVS can’t compensate = ‘Decompensated heart failure’
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10
Q

Describe chronic heart failure

A

Pathophysiology is the same as acute:
- contractility immediately drops due to damage to muscle and therefore cardiac output falls suddenly
BUT instead of there being a rapid fall, it is progressive = patients can remain in compensated failure for a long time/indefinitely. Any severe stress can drive the patients into decompensated heart failure e.g. infection, fluid overload, anaemia

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11
Q

What is the ‘compensation process’ following heart failure?

A

The heart adapts to respond to changes:
Cardiac enlargement
Arterial constriction
Increased sympathetic drive
Salt and fluid retention

These are all good initially, but they become detrimental

CARDIAC ENLARGEMENT:
Progressive enlargement of ventricular size, shape and function
- Cardiac muscle stretches due to increased residual volume after contraction, so the heart appears enlarged with extra muscle
- BUT this muscle is ineffectual and becomes responsible for significant impairment of the heart as a pump
- Left ventricular hypertrophy - enlargement and thickening f muscular wall of left ventricle

ARTERIAL CONSTRICTION:
- When he cardiac output is decreased in heart failure: arteries constrict to divert blood to essential organs away from non-essential organs e.g. the skin or GI tract
- BUT this can also cause increased systemic vascular resistance = increased after load of heart

INCREASED SYMPATHETIC DRIVE:
When the heart fails and there is a decrease in tissue perfusion, the Sympathetic NS is stimulated by baroreceptors (detect BP) in blood vessel walls = exposes heart to catecholamines
= have positive inotropic and chronotropic effects
I = Increased force of contraction
C = increased rate of contraction
= increase in noradrenaline, angiotensin, aldosterone, vasopressin
= promotes excessive stimulation of the heart and vasoconstriction = increases contractility

SALT AND WATER RETENTION:
- When decreased cardiac output = decreased renal perfusion (decreased blood supply to kidneys):
This activates the renin-angiotensin system;
releases renin
= angiotensin 1 and 2 = vasoconstriction
= increases aldosterone release which retains water and salt as the distal renal tubule = blood volume and preload (detrimental!)
- promotes release of atrial natriuretic peptide- vasodilator counteracts increase in preload

THESE ARE ALL COMPLIMENTARY IN THE SHORT-TERM, BUT BECOME COUNTERPRODUCTIVE LONG-TERM

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12
Q

What are the symptoms of heart failure?

A

3 classical symptoms:
- Exercise limitation - due to decreased cardiac output- impaired oxygenation and blood flow to exercising muscles
- SOB- back pressure from heart causes fluid to accumulate in lungs. Is worse on exercising or lying down, may also have cough
- Oedema- swelling in ankles or feet (1st as gravity) due to retention of water and salt

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13
Q

What is the difference in presentation when the left side of the heart fails and when the right side fails?

A

RIGHT-SIDED:
- Right side receives deoxygenated blood from body)
- Peripheral oedema- ankles
- Hepatomegaly- liver enlargment
- Raised jugular venous pressure
- peripheral cyanosis
- Fluid and electrolyte retention

LEFT-SIDED:
- Left side receives oxygenated blood from lungs
- More common and more serious
- if left side fails = back log to lungs =
pulmonary oedema:
SOB
orthopnoea- sob on lying down- due to redistribution of fluid to lungs from abdomen
Paroxysymal nocturnal dyspnoea- sleeping but then wakes up suddenly short of breath sue to gradual accumulation of fluid in lungs= attacks of coughing and gasping
- cough, where, tiredness

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14
Q

What are the New York classification of heart failure symptoms?

A

Class 1 = no limiatiaons
ordinary physical activity doesn’t cause fatigue, breathlessness or palpitation

Class 2 (mild) = slight limitation in physical activity
comfortable at rest
ordinary physical activity e.g. stairs cause fatigue, breathlessness or palpitation

Class 3 (moderate) = Marked limitation of physical activity
comfortable at rest
less than ordinary physical activity symptoms e.g. walking to toilet

Class 4 ( severe) = unable to carry out any physical activity without discomfort
symptoms present even at rest
physical activity increases discomfort

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15
Q

How is heart failure diagnosed?

A

Review signs and symptoms:
- Raised jugular vein- being running along side of neck (isn’t normally visible) becomes visible due to venous distension
- lung sounds using a stethoscope - crackles at base
- assess for swelling of ankles or legs- sings of peripheral oedema

Tests:
- Natriuretic peptides- secreted from ventricles in HF as part of the complementary process. can measure brain natriuretic peptides and n-terminal pro-brain natriuretic peptides
- MOST IMPORTANT: Measure ejection fraction via electrocardiography (assesses performance of heart as a pump)- usual ejection fraction is 50-60%
Ejection fraction = blood ejected from ventricles at systole

If EF = <40% = heart failure with reduced election fraction
if EF = >50% = HF with preserved ejection fraction
41-50% =Hf with mid range ejection fraction

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16
Q

What is the ejection fraction in a healthy Person?

A

> 50%

17
Q

What does ejection fraction measure?

A

The volume of blood in ventricles that is ejected when the heart contracts at systole

18
Q

What does the choice of HF treatment depend on?

A

The underling cause of the HF- should always be determined

19
Q

What is the treatment for hf?

A

1st line is ACE inhibitors
- decrease preload and afterload
- improve symptoms and aids survuival
- start low dose and uptitrtte to max dose
- If intolerant can use ARBs

Joint first line= Beta-blockers
Only- bisoprolol, carvedilol, nebivolol are licensed ( NOT ATENOLOL)
- Decrease pre and after load
- Start low then slowly up titrate=
“ Start low, go slow” - as can worsen symptoms initially

Also joint first line = aldosterone antagonists e.g. spironolactone
- block aldosterone, and some diuretic effect

REST ARE ADD ON THERAPIES:
- Ivabradine - decrease heart rate by inhibiting If channels in the SA node
- Entresto- sacubitril/valsartan- dual- patients must stop ACEi or ARB 36 hours before starting as can cause a severe reaction when taking ace and arb in combination r.g. angiodema
- Digoxin- improves symptoms, not mortality
- SGLT-2 inhibitors e.g. dapagliflozin

20
Q

What must happen before starting a patient on Entresto (Saccubitril + valsartan)?

A

Patients must stop taking their ACE inhibitors or ARBs 36 hours before starting treatment.
- As there is a severe reaction that can be caused by taking ACE or ARBs in combination e.g. angiodema (valsartan is an arb)

21
Q

How are beta blockers started in hf patients?

A

Start low, go slow

22
Q

What drug class is metolazone?

A

An atypical thiazide-like diuretic
- if effective in decreased renal function

23
Q

What diuretics are used in HF?

A

Diureutcs decrease preload and decrease pulmonary and peripheral oedema and their associated symptoms

  • Thiazide-like
    less potent- used for mild HF e.g. bendroflumethiazide 5mg OM (ONLY 2.5mg in HT)
    Not effective at all in renal impairment- of eGFR <20 ml/min
  • Loop
    MAIN group used
    potent - often initiate treatment with IV furosemide 20-50 mg
    e.g. Furosemide (can be iv), bumetanide
    can use high doses
  • Metolazone-
    A-typical thiazide like diuretic
    Is effective in decreased renal function
    Can be used in combo with loop diuretic in resistant HF
    STAT dose - 2.5-5mg can be enough
    or short-term use- 2.5-5mg OD for2/3 days
    Long-term in severe hf- 2.5-5mg 2-3 times a week (on top of daily loop)