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Integrative > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Give some examples of causes of heart failure.

A

ISCHAEMIC HEART DISEASE (systolic heart failure)

Hypertension

Dilated cardiomyopathy

  • infection
  • toxins e.g. alcohol, drugs, poisons
  • pregnancy (peri-partum and post-partum)
  • idiopathic

Diabetes

(Congenital) valvular heart disease

Restrictive cardiomyopathy e.g. amyloidosis

Hypertrophic cardiomyopathy

Pericardial disease e.g. constrictive pericarditis

High-output heart failure (increased O2 requirement by body)

  • anaemia
  • pregnancy
  • hyperthyroidism
  • arteriovenous fistula

Arrhythmias

  • AF
  • heart block

Infection

  • rheumatic fever —> calcification of valves
  • Chagas’ disease
  • HIV
  • viral myocarditis
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2
Q

How does heart failure progress? What scale is used?

A

New York Heart Association

Class 1 = no symptomatic limitation of physical activity

Class 2 =

  • slight limitation of physical activity
  • ordinary physical activity results in symptoms
  • no symptoms at rest

Class 3 =

  • marked limitation of physical activity
  • less than ordinary physical activity results in symptoms
  • no symptoms at rest

Class 4 (very poor prognosis) =

  • inability to carry out any physical activity without symptoms
  • may have symptoms at rest
  • discomfort increases with any degree of physical activity
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3
Q

What are the factors affecting cardiac output? How may these be affected in disease states?

A

Heart rate
e.g. chronic AF —> tachycardia; bradycardia

Venous capacity (LV preload) 
e.g. dehydration, fluid overload

Myocardial contractility
e.g. metabolic disturbances (hypo/hyperkalaemia, hypocalcaemia)

Aortic and peripheral impedance (afterload)

e. g. hypertension
e. g. hypertension

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4
Q

Describe the structural changes in the heart that occur in systolic heart failure. How can these inform about the cause of the heart failure?

A

Increased LV capacity but reduced LV output (less blood pumped put during systole)

  • thinning of myocardial wall due to fibrosis and necrosis (e.g. MI) weakens heart muscle (cannot pump as well)
  • dilatation pulls valve leaflets apart —> mitral valve regurgitation

Structural changes cause arrhythmias

Neuro-hormonal changes

Scar present = heart failure caused by MI
No scar present = heart failure caused by something other than MI

note: early revascularisation in MI will prevent/reduce extent of heart failure
note: heart can remodel around areas of fibrosis/necrosis to avoid rupture

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5
Q

Outline how sympathetic activation following myocardial damage contributes to heart failure.

A

Myocardial damage stimulates baroreceptors which cause sympathetic activation (initially improve cardiac output)

—> RAAS activation —> fluid retention —> increases wall stress —-> increased myocardial oxygen demand AND myocardial hypertrophy

—> Vasoconstriction —> increases wall stress —> increased myocardial oxygen demand AND myocardial hypertrophy

—> increased heart rate and contractility —> increased myocardial oxygen demand

—> direct cardiotoxicity —> myocyte damage

Increased myocardial oxygen demand —> decreased contractility

+ down-regulation/uncoupling of beta-receptors
+ NA induces cardiac hypertrophy, myocyte apoptosis, mycocyte necrosis
+ NA up-regulates RAAS
+ reduction in heart rate variability (reduced parasympathetic activity and increased sympathetic activity)

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6
Q

What hormones are activated in heart failure?

A
  • RAAS
  • natriuretic hormone
  • ADH
  • endothelin
  • prostaglandins/nitric oxide
  • kallikrein system (proteases)
  • TNF-alpha
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7
Q

Reminder: outline the renin-angtiotension-aldosterone system

A

renin ACE
Angiotensinogen ——-> Angiotensin I ——> Angiotensin II

Angiotensin II

  • –> AT1R (vasoconstriction)
  • –> AT2R —> increased nitric oxide (vasodilatation)

Bradykinin —> BK2R —> increased nitric oxide (vasodilatation)

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8
Q

What are the effects of angiotensin II?

A
  • vasoconstriction (AT1R)
  • LV hypertrophy and mycocyte dysfunction
  • aldosterone release —> sodium and water retention —> volume overload —> hypertension
  • ?stimulates thirst by central action
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9
Q

How can heart failure lead to renal failure?

A

Initially reduced renal blood flow activates RAAS (macula densa) to raise the blood pressure and maintain GFR

When this mechanism fails GFR falls, causing a raise in [urea]serum and [creatinine]serum

Exacerbated by ACE inhibitors and angiotensin receptor blockers (cause a 10%+ reduction in renal blood flow in normal individuals)

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10
Q

Describe the structural changes in the heart that occur in diastolic heart failure.

A

Reduced LV compliance impairing myocardial relaxation (stiff, thickened muscle cannot relax)
—> reduced diastolic LV filling —> reduced cardiac output AND increased pressure in left atrium —> increased pressure in pulmonary arteries

Neurohormonal activation

Concentric left ventricle hypertrophy

note: unable to compensate by increasing LV end-diastolic pressure
note: normal ejection fraction (50%-60%)

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11
Q

What is the aetiology of diastolic heart failure?

A
  • frequently elderly females
  • SYSTOLIC HEART FAILURE
  • hypertension
  • diabetes
  • obesity (poor diastolic relaxation of the heart)
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12
Q

What is the aetiology of systolic heart failure?

A
  • ISCHAEMIA
  • dilated cardiomyopathy (idiopathic, viral, peri-partum, hypertension)
  • valvular
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13
Q

What are the causes of right-sided heart failure?

A

Heart:

  • LEFT-SIDED HEART FAILURE
  • pulmonary/tricuspid valve disease
  • left to right shunts
  • isolated right ventricular cardiomyopathy

Lung:

  • cor pulmonale
  • chronic lung disease
  • PE
  • pulmonary hypertension

reminder: it is uncommon for one side of the heart to fail in isolation; usually have biventricular (congestive) heart failure

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14
Q

What are the symptoms of left-sided heart failure?

A
  • fatigue
  • exertional dyspnoea (severe heart failure: dyspnoea at rest)
  • orthopnoea
  • paroxysmal nocturnal dyspnoea (opening windows, sitting on the edge of the bed)
  • ankle swelling (fluid retention)
  • chest pain (due to cardiac ischaemia; increases resp. rate)
  • anorexia (due to breathlessness whilst eating)
  • dizziness
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15
Q

What are the signs of left-sided heart failure?

A
  • overt breathlessness
  • ?anaemia
  • tachycardia
  • blood pressure depends on aetiology
  • cardiomegaly (displaced apex beat)
  • gallop rhythm (3rd + 4th heart sounds)
  • mitral regurgitation murmur
  • basal pulmonary crackles (fluid overload)
  • peripheral oedema (fluid overload)
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16
Q

What are the signs and symptoms of “pure” right-sided heart failure?

A

Distension and fluid accumulation in areas drained by systemic veins

  • fatigue
  • dyspnoea
  • anorexia
  • nausea
  • raised JVP
  • tender, smooth hepatic enlargement
  • dependent pitting oedema
  • ascites
  • pleural effusion
17
Q

What are the investigations for heart failure?

A

FBC

  • ?anaemia exacerbating heart failure
  • ?anaemia causing breathlessness mimicking heart failure

Renal function & electrolytes

  • ?heart failure affecting GFR
  • ?concomitant renal problems

Glucose & lipids

  • ?diabetes
  • ?hyperlipidaemia exacerbating heart failure

B-type natriuretic peptide

  • increased in heart failure but not in COPD
  • level indicates severity of heart failure (level falls when heart failure improves)

ECG

  • ?MI
  • ?signs suggestive of cardiomyopathy e.g. left bundle branch block

CXR

  • ?cardiomyopathy
  • ?fluid overload —> pulmonary oedema

Echocardiography

  • compare left and right ventricles
  • visualise valves

Chest CT

  • ?evidence of lung disease
  • ?cor pulmonale
18
Q

What are Kerley B lines? What are they caused by?

A

Thickened subpleural interlobular septa (usually at lung bases)

Causes:

  • pulmonary oedema
  • lymphangitis carcinomatosis (lymphatic spread of cancer)
  • pulmonary lymphoma
  • pneumonia (viral, mycoplasma, PCP)
  • interstitial pulmonary fibrosis
  • pneumoconiosis
  • sarcoidosis
19
Q

Outline the management of heart failure.

A

LIFESTYLE

  • reduce salt intake
  • reduce alcohol intake
  • increase aerobic exercise
  • reduce BP

PHARMACOLOGICAL

  1. ACE inhibitors (or angiotensin receptor blockers if not tolerated e.g. cough or nitrates if angiotensin receptor blockers not tolerated)
  2. Beta-blockers
  3. Spironolactone

+ loop diuretics (reduce fluid retention —> symptomatic relief)
+ antiarrhythmics (if req.)

Acute heart failure (heart failure causing cardiogenic shock)

  • inotropes
  • phosphodiesterase inhibitors
  • digoxin/beta-blockers

CARDIAC SURGERY

  • heart transplant (in suitable young patients with poor prognosis)
  • mechanical assist devices (external pump)
  • treat underlying cause e.g. valve surgery, revascularisation

IMPLANTABLE PACEMAKERS = biventricular pacing (left bundle branch block causes asynchronous contraction)

IMPLANTABLE DEFIBRILLATORS = if heart failure puts at risk of VT or VF

20
Q

Reminder: define heart failure.

A

State in which the heart fails to maintain adequate circulation for the needs of the body despite an adequate filling pressure

21
Q

Define the term systolic heart failure.

A

LV pump failure due to reduced cardiac contractility or fluid overload, although filling pressure is adequate.

22
Q

Define the term diastolic heart failure.

A

Normal LV function but failure to adequately perfuse heart due to concentric LV hypertrophy (impaired relaxation)

23
Q

Reminder: define contractility.

A

Extent to which a given increase in venous pressure leads to an increase in stroke volume at a given fibre length.

24
Q

Reminder: define preload and afterload.

A

PRELOAD = end-diastolic filling pressure (stretch applied to single cardiac myocyte prior to contraction)

AFTERLOAD = pressure heart must work against to eject blood during systole (systolic pressure)

25
Q

What compensatory mechanisms help support the cardiac output in heart failure?

A

Baroreceptor activation —> increased sympathetic stimulation —> tachycardia —> increased cardiac output

Reduced renal perfusion —> reduced GFR —> RAAS activation ——> vasoconstriction and venoconstriction —> increased total peripheral resistance —> increased BP

26
Q

What are the main aims of the treatment of heart failure?

A

Reduce fluid overload (symptom management)

  • diuretics (reduce Na+ and water retention)
  • ACE-inhibitors/angiotensin II receptor blockers (reduce RAAS activation)

Increase inotropy

Reduce oxygen demand of the heart
- beta-blockers

27
Q

How is central venous pressure estimated?

A

Estimate JVP (compare height of internal jugular vein to sternum at 45 degrees)

Cannulate internal jugular vein (central line)

Cannulate subclavian vein

28
Q

What are crackles/crepitations? What can they be caused by?

A

Short interrupted breath sounds due to fluid build-up in the lungs

  • fine crackles = high frequency, short duration
  • coarse crackles = low frequency, long duration

Caused by abnormally closed airway opening during inspiration (INSPIRATORY)

OR abnormally closed airway closing during expiration (EXPIRATORY)

OR air bubbles moving through fluid

OR rapid equalisation of gas pressures —> pressure wave

  • increased elastic recoil pressure
  • inflammation/oedema in lungs —> narrows airways
29
Q

Contrast the different timing of crackles and their different causes.

A

Early-mid inspiratory crackles (coarse) = large central airways affected

  • e.g. bronchitis (early), bronchiectasis (mid)
  • gravity independent (does not resolve with posture)
  • associated with obstructive pathology
  • resolve with coughing

Late inspiratory crackles (fine) = peripheral airways affected

  • e.g. pneumonia
  • gravity dependent (resolves with posture)
  • associated with restrictive pathology
  • does not resolve with coughing
30
Q

What are the signs found in the respiratory exam in heart failure.

A

Late inspiratory fine crackles in posterior lung bases

Reduced breath sounds (pleural effusions)

+/- dullness to percussion

Integrative (10 decks)

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