2.01 - Heart Flashcards

(32 cards)

1
Q

What is the difference between STEMI, NSTEMI, and UA

A

STEMI -
ST elevation
New onset LBBB
Raised troponin

NSTEMI -
No ST elevation or LBBB
Raised troponin

UA -
No ST elevation or LBBB, normal troponin

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2
Q

What is the most common cause of ACS

A

Artery narrowing or blockage secondary to IHD or atherosclerosis

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3
Q

What are the causes of coronary artery occlusion

A

Vasculits (Kawasaki disease)
Coronary vasospasm (cocaine)
Coronary dissection

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4
Q

What are some causes of changes of oxygen demand leading to ACS

A

Anaemia
Hyperthyroidism
Severe sepsis

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5
Q

What are the modifiable risk factors for ACS

A

High cholesterol
HTN
Smoking
Diabetes
Obesity

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6
Q

What are the non-modifiable risk factors for ACS

A

Agę
Family history
Male sex
Premature menopause

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7
Q

what is the frank starling law

A

the ability of the heart to respond to increased venous return by increasing stroke volume

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8
Q

how does the frank starling law work normally

A

increased venous pressure ->
raised EDV ->
increased preload (due to stretch) ->
more forceful contraction ->
increase in stroke volume

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9
Q

how does heart failure break down the frank starling law

A

over stretching of cardiomyocytes -> impaired contractlity -> stroke volume cannot increase to match EDV
-> oedema in lungs and ankles

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10
Q

what are the vascular causes of heart failure

A

ischaemic heart disease
hypertension

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11
Q

what are the muscular causes of heart failure (3)

A

dilated cardiomyopathy
hypertrophic cardiomyopathy
congenital heart disease

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12
Q

what are the valvular causes of heart failure (2)

A

stenosic valves
regurgitant valves

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13
Q

what is an electrical cause of heart failure

A

arrhythmia

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14
Q

what are the causes of high output heart failure (SALT)

A

Septicaemia
Anaemia
Liver failure
Thyrotoxicosis

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15
Q

what compensatory mechanisms are involved in the pathophysiology of heart failure (4)

A

increasing preload
increasing heart rate
RAAS activation
SNS activation

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16
Q

how does increasing preload contribute to heart failure

A

increase EDV to compensate for reduced ejection fraction -> maintain cardiac output
large increase in EDV can lead to pulmonary oedema, ascites, peripheral oedema

17
Q

how does increasing heart rate contribute to pathogenesis of heart failure

A

cardiac output = stroke vol * heart rate
unable to increase stroke vol so increase heart rate instead
sustained tachycardia leads to cardiomyocyte death and remodelling -> cardiomegaly

18
Q

how does RAAS activation contribute to pathogenesis of heart failure

A

renal hypoperfusion due to reduced CO -> RAAS
-> vasoconstriction and water retention
-> increased mean arterial pressure (BP)
-> oedema

19
Q

How does SNS activation contribute to pathogenesis of heart failure

A

increases myocardial contractility and heart rate
can trigger cardiomyocyte death when chronicall activated
causes a positive feedback loop and increases RAAS activation

20
Q

what are the clinical features of left sided heart failure (7)

A

paroxysmal nocturnal dyspnoea
orthopnoea
cyanosis
fatigue
SOB on exertion
tachycardia
Sx of pulmonary congestion

21
Q

what are the clinical features of right sided heart failure (7)

A

raised JVP
fatigue
peripheral oedema
ascites
anorexia, nausea, vomiting
weight gain
Hx of chronic pulmonary problems

22
Q

What are the diagnostic investigations for heart failure

A

B Natiuretic Peptide (BNP)
Transthoracic Echocardiography (TTE)

23
Q

what (other than heart failure) can cause a raised BNP

A

sepsis
diabetes
old age
hypoxia
CKD
liver cirrhosis

24
Q

what are the three positive (yes heart failure) results of a TTE

A

HFrEF - LVEF <40%
HFmrEF - LVEF 40-49%
HFpEF - LVEF >50%

25
what are the requirements for each class of heart failure (new york classification)
1) no limitation to activity, no symptoms 2) slight limitation, symptomatic on exertion 3) marked limitation, symptomatic on light activity 4) physical activity impossible without discomfort, symptomatic at rest
26
what further blood tests (other than BNP) are done when investigating heart failure
FBC - anaemia, infection U&E - renal failure as cause of oedema LFT - liver failure as cause of oedema Cholesterol and HbA1c - risk stratification TFT - exclude thyroid disease
27
what imaging (other than TTE) is done to investigate heart failure
chest x ray cardiac mri
28
what can be seen on a chest x ray of a heart failure patient (5)
cardiomegaly alveolar oedema kerley B lines pleural effusion upper love diversion
29
what is cardiac mri used for when investigating heart failure
follow up if TTE was non diagnostic determine aetiology of heart failure
30
what is the conservative management of heart failure
lifestyle modification patient education annual flu vax smoking cessation alcohol support travel and driving advice
31
what is the medical management in HFrEF and HFmrEF
ACE inhibitors Beta blockers Mineralocorticoid Receptor Antagonists (MRAs) Loop diuretic
32
What is the medical management in HFpEF
loop diuretic (furosemide) if symptomatic of fluid overload specialist referral comorbidity management