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x1 - Cardiovascular > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Congestion

A

A relative excess of blood in the vessels of a tissue/organ

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2
Q

Congestive heart failure pathophysiology

A

Heart is unable to pump sufficient blood from the ventricles

↓ cardiac output
activates renin-angiotensin-aldosterone system
↑ Na+ and H2O retention
↑ amount of fluid in body = fluid overload in veins

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3
Q

Causes of vascular congestion

A

DVT,
Hepatic cirrhosis,
Congestive cardiac failure,

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4
Q

Exudate

A

Due to increased vascular permeability
(part of the inflammatory process),
Higher protein/albumin and cell content

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5
Q

Transudate

A

Due to altered haemodynamic forces acting across the capillary wall. (e.g. cardiac failure)
Low protein/albumin and cell content

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6
Q

Starling forces in capillaries

A

HYDROSTATIC PRESSURE: forces fluid out of the capillary (higher at the arterial side - filtration)

ONCOTIC PRESSURE: forces fluid into the capillaries (higher at the venous side - reabsorption)

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7
Q

Factors affecting net flux and filtration of fluid in the capillaries

A

Hydrostatic pressure
Oncotic pressure
Permeability and area of endothelium

*Disturbance of normal components = oedema

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8
Q

oedema

A

accumulation of abnormal amounts of fluid in the extravascular compartment (tissues and body cavities)

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9
Q

Disturbances in starling forces leading to oedema

A

LVF = ↑ left atrial pressure = ↑ pulmonary vascular pressure = ↑ hydrostatic pressure = ↑ filtration = pulmonary oedema

RVF = blood retained in systemic veins = ↑ hydrostatic pressure in systemic capillaries = ↑ filtration = peripheral oedema

Lymphatic obstruction = ↓ lymph drainage = ↑ vascular fluid volume = ↑ hydrostatic pressure = lymphoedema

Abnormal renal function = NaCl and H2O retention = ↑ vascular fluid volume = ↑ hydrostatic pressure = oedema

Hypoalbuminaemia = ↓ oncotic pressure = ↑ filtration = peripheral oedema

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10
Q

Permeability oedema

A

Damage to endothelial lining = fluid (+ proteins etc.) leak out = oedema

e.g. acute inflammation, burns

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11
Q

Aetiology of heart failure

A

Any structural heart disease:

*LV systolic dysfunction*
Valvular heart disease
Pericardial constriction/effusion
LV diastolic dysfunction
Cardiac arrhythmias
Myocardial ischaemia/infarction
Restrictive cardiomyopathy
RV failure
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12
Q

Causes of left ventricular systolic dysfunction

A

Myocardial ischaemia/infarction
Severe aortic valve disease
Severe mitral regurgitation
Dilated cardiomyopathy (DCM)

Inherited
Toxins
Infective
Systemic disease
Muscular dystrophies
Hypertension
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13
Q

Epidemiology of heart failure

A 
Affects 1-2% UK population
increasing in prevalence due to:
-aging population
-hypertension
-CHD
-diabetes
-obesity
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14
Q

Prognosis for heart failure

A

Worsens with increasing NYHA class (I - IV)

average = 30-40% mortality at 1 year

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15
Q

Symptoms of heart failure

A

Dyspnoea
Fatigue
Oedema
Reduced exercise capacity

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16
Q

Signs of heart failure

A 
Oedema
Tachycardia
Raised JVP
Chest crepitations or effusions
3rd heart sound
Displaced or abnormal apex beat
17
Q

Investigations for heart failure

to show evidence of cardiac dysfunction

A

Bloods: BNP elevated in HF
ECG: LVSD unlikely if ECG normal
Echo: Shows dysfunction, effusion/tamponade, hypertrophy, shunts, congenital defects etc.
Cardiac MRI: Possible causes e.g. inflammation/ infarction/ fibrosis. LVEF
CXR: Cardiomegaly, hypertrophy, effusion etc.
Radionucleotide imaging: To assess ventricular function if echo not available
- Left ventriculogram: LVEF
- MUGA: Accurately obtains LVEF

18
Q

Screening tests for heart failure

A

12 lead ECG (90-95% sensitive)

BNP (Brain natriuretic peptide) - elevated in HF

19
Q

Treatment for heart failure

due to LVSD

A

Symptomatic treatment:
Diuretics (Furosemide)

Inhibition of RAAS:
ACE Inhibitors
ARBs
Aldosterone antagonist (spironolactone)

Enhance natriuretic peptide system: 
Neprysilin inhibitor (or ARNI)

Enhance cardiac function/ reduce workload:
Positive inotropes (Digoxin)
Nitrovasodilators
β-blockers
Ivabradine

Anticoagulant:
Warfarin (dilated ventricle gives rise to thrombus formation)

20
Q

Strengths of loop diuretics therapy in the treatment of congestive heart failure

A

Loop diuretics = the main stay of treatment

Loop diuretics can be used with thiazide-like diuretics in diuretic resistant patients

21
Q

Loop diuretics ADRs

A 
Dehydration
Hypotension
Hypokalaemia
Hyponatraemia
Gout
22
Q

Strengths of ACE inhibitors in the treatment of heart failure

A

Improve symptoms AND survival
Also prevent onset of heart failure
More effective than ARBs

23
Q

ACEIs drug-drug interactions

A

NSAIDS: acute renal failure
Potassium supplements: hyperkalaemia
Potassium sparing diuretics: hyperkalaemia

24
Q

Strengths of beta blockers in the treatment of heart failure

A

Improves survival

25
Q

Weaknesses of beta blockers in the treatment of heart failure

A 
POTENTIALLY HAZARDOUS (may precipitate severe deterioration):
Only for stable, dry patients
Must start at a low dose

Must be used in combination with ACEI/ARB and diuretic

26
Q

Neprysilin inhibitor

A

inhibits nepryilin which breaks down ANP and PNP
Decreases blood pressure

Often combined with an ARB making “angiotensin receptor neprysilin inhibitor” (ARNI)

27
Q

Furosemide drug-drug interactions

A 
Lithium: renal toxicity
NSAIDs: renal toxicity
Vancomycin: renal toxicity
Aminoglycosides: aural + renal toxicity
Antihypertensives: profound hypotension
28
Q

Body’s response to heart failure + therapeutic intervention

A

↓ CO is perceived as a loss in circulatory volume
= sympathetic activation (vasoconstriction, myocyte hypertrophy etc) + RAAS

[↑ in circulatory volume dilates heart = further ↓ CO]

Drug therapy:

  1. inhibits RAAS
  2. inhibits sympathetic response (↓ cardiac workload)
  3. diuretics (↓ salt + water retention from RAAS)
  4. ehance natriuretic peptide system (↓ BP)

x1 - Cardiovascular (8 decks)

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