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Finals > Cardio > Flashcards

Cardio Flashcards

1
Q

Acute LVF + Pulmonary Oedema

how does acute left ventricular failure occur?

A

when the L ventricle is unable to adequately move blood through the L side of the heart and out into the body

this causes a backlog of blood that increases the amount of blood stuck in the L atrium, pulmonary veins + lungs

as the vessels in these areas are engorged with blood due to the increased volume + pressure they leak fluid and are unable to reabsorb fluid from surrounding tissue

this causes pulmonary oedema

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2
Q

Acute LVF + Pulmonary Oedema

what is pulmonary oedema

A

where the lung tissues and alveoli become full of interstitial fluid

this interferes w/ the normal gas exchange in the lungs, causing SOB, O2 desats + other signs + symptoms

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3
Q

Acute LVF + Pulmonary Oedema

triggers

A
  • Iatrogenic (eg aggressive fluids in frail elderly pt with impaired ventricular function)
  • sepsis
  • MI
  • arrhythmias
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4
Q

Acute LVF + Pulmonary Oedema

presentation

A
  • rapid onset breathlessness
  • exacerbated by lying flat + improves on sitting up
  • T1 resp failure (low O2, normal CO2)
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5
Q

Acute LVF + Pulmonary Oedema

symptoms

A
  • SOB
  • looking + feeling unwell
  • cough (frothy white/pink sputum)
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6
Q

Acute LVF + Pulmonary Oedema

examination findings

A
  • increased RR
  • reduced O2 sats
  • tachycardia
  • 3rd heart sound
  • bilateral basal crackles ‘wet’ on auscultation
  • hypotension in severe cases (cardiogenic shock)

may also be signs + symptoms related to underlying cause eg

  • chest pain in ACS
  • fever in sepsis
  • palpitations in arrhythmias
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7
Q

Acute LVF + Pulmonary Oedema

right sided heart failure examination findings

A
  • raised JVP (backlog on the R side of the heart leading to an engorged jugular vein in the neck
  • peripheral oedema (ankles, legs, sacrum)
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8
Q

Acute LVF + Pulmonary Oedema

work up

A
  • hx
  • clinical examination
  • ECG: ischaemia + arrhythmias
  • ABG
  • CXR
  • Bloods: BNP + trop if suspecting MI
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9
Q

Acute LVF + Pulmonary Oedema

inx

A

diagnosis confirmed by BNP or echo

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10
Q

Acute LVF + Pulmonary Oedema

what is BNP

A

B-type Natriuretic Peptide is a hormone released from the heart ventricles when the myocardium is stretched beyond the normal range

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11
Q

Acute LVF + Pulmonary Oedema

what does a high BNP indicate?

A

the heart is overloaded w/ blood beyond its normal capacity to pump effectively

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12
Q

Acute LVF + Pulmonary Oedema

what is the action of BNP

A

to relax the smooth muscle in blood vessels

this reduces the systemic vascular resistance making it easier for the heart to pump blood through the system

Also acts on kidneys as a diuretic to promote the excretion of more water in the urine

this reduces the circulating volume helping to improve the function of the heart

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13
Q

Acute LVF + Pulmonary Oedema

disadvantage of testing for BNP

A

sensitive but not specific

-ve –> rule out heart failure
+ve –> can have other causes

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14
Q

Acute LVF + Pulmonary Oedema

other causes of a raised BNP

A
  • tachycardia
  • sepsis
  • PE
  • renal impairment
  • COPD
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15
Q

Acute LVF + Pulmonary Oedema

what is an echo useful in assessing?

A

the function of the LV and any structural abnormalities in the heart

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16
Q

Acute LVF + Pulmonary Oedema

what is the main measure of LV function

A

ejection fraction

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17
Q

Acute LVF + Pulmonary Oedema

what is the ejection fraction

A

the % of the blood in the LV squeezed out with each ventricular contraction

and ejection fraction above 50% is considered normal

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18
Q

Acute LVF + Pulmonary Oedema

CXR findings

A

ABCDE

Alveolar oedema (Bat’s wings)

Kerley B lines

Cardiomegaly: cardiothoracic ratio of >0.5

upper lobe venous Diversion: prominent upper lobe vessels

bilateral pleural Effusion

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19
Q

Acute LVF + Pulmonary Oedema

why is there prominent upper lobe vessels on CXR

A

usually when standing erect, the lower lobe veins contain more blood and the upper lobe veins remain relatively small

In LVF, there is such a back-pressure that the upper lobe veins also fill will blood and become engorged

referred to as upper lobe diversion. This is visible as increased prominence and diameter of the upper lobe vessels on a CXR

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20
Q

Acute LVF + Pulmonary Oedema

mnx

A

Pour SOD

Pour away (stop) their IV fluids

Sit up

Oxygen

Diuretics eg IV furosemide

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21
Q

Acute LVF + Pulmonary Oedema

mnx of severe acute pulmonary oedema or cardiogenic shock

A
  • IV opiates
  • NIV: CPAP or if not, may need full intubation and ventilation
  • inotropes eg noradrenalin to strength force of heart contraction
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22
Q

Chronic Heart Failure

causes (2)

A
  1. systolic heart failure: impaired left ventricular contractions
  2. diastolic: left ventricular relaxation

this impaired LV function results in chronic back-pressure of blood trying to flow into and through the left side of the heart

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23
Q

Chronic Heart Failure

presentation

A
  • breathlessness worsened by exertion
  • cough: frothy white/pink sputum
  • orthopnoea: how many pillows?
  • Paroxysmal Nocturnal Dyspnoea
  • peripheral oedema
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24
Q

Chronic Heart Failure

what causes paroxysmal nocturnal dyspnoea

A
  1. fluid settling across a large SA of their lungs as they sleep lying flat. If standing up, fluid sinks to lung bases and upper lungs clear to be used more efficiently for gas exchange
  2. during sleep, the resp centre in the brain becomes less responsive so RR and effort does not increase in response to reduced O2 sats. More pulmonary congestion and hypoxia before waking up and feeling very unwell
  3. less adrenalin during sleep so myocardium is more relaxed which reduced CO
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25
Q

Chronic Heart Failure

dx

A
  • clinical presentation
  • N-terminal pro-B-type natriuretic peptide (NT-proBNP)
  • Echo
  • ECG
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26
Q

Chronic Heart Failure

causes (4)

A
  1. IHD
  2. valvular heart disease (commonly aortic stenosis)
  3. HTN
  4. Arrhythmias (commonly AF)
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27
Q

Chronic Heart Failure

first line medical treatment (4)

A

ABAL

ACE inhibitor: Ramipril

BB: bisoprolol

Aldosterone antagonist if not controlled with A + B: spironolactone or eplerenone

Loop diuretics improves symptoms: furosemide

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28
Q

Chronic Heart Failure

guidelines before implementing medical trx

A
  • refer to specialist
  • discussion + explanation of condition
  • surgical trx in severe aortic stenosis or mitral regurg
  • HF specialist nurse input

additional

  • yearly flu + pneumococcal
  • stop smoking
  • optimise trx of co-morbidities
  • exercise as tolerated
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29
Q

Chronic Heart Failure

what to use instead of an ACEi if they’re not tolerated

A

Angiotensin Receptor Blocker (ARB)

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30
Q

Chronic Heart Failure

what medicine to avoid in patients with valvular heart disease

A

ACEi

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31
Q

Cor pulmonale

what is it

A

right sided heart failure caused by respiratory disease

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32
Q

Cor pulmonale

pathophysiology

A

the increased pressure + resistance in the pulmonary arteries (pulmonary HTN)

results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries

this leads to back pressure of blood in the RA, vena cava and systemic venous system

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33
Q

Cor pulmonale

respiratory causes

A
  • COPD (most common)
  • PE
  • interstitial lung disease
  • CF
  • primary pulmonary HTN
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34
Q

Cor pulmonale

presentation

A
  • SOB
  • peripheral oedema
  • increased breathlessness on exertion
  • syncope (dizziness + fainting)
  • chest pain
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35
Q

Cor pulmonale

signs

A
  • hypoxia
  • cyanosis
  • raised JVP (due to back log of blood in jugular veins)
  • peripheral oedema
  • 3rd heart sound
  • murmur: pan-systolic in tricuspid regurg)
  • hepatomegaly
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36
Q

Cor pulmonale

why is there hepatomegaly

A

due to back pressure in the hepatic vein (pulsatile in tricuspid regurg)

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37
Q

Cor pulmonale

mnx

A

treat underlying cause and symptoms

long term o2 therapy is often used

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38
Q

Cor pulmonale

prognosis

A

poor prognosis unless there’s a reversible underlying cause

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39
Q

Hypertension

what BP would suggest a dx

A

> 140/90 in clinic

or >135/85 with ambulatory or home readings

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40
Q

Hypertension

what is primary hypertension

A

essential hypertension (accounts for 95%)

HTN has developed on its own and does not have a secondary cause

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41
Q

Hypertension

secondary causes of HTN

A

ROPE

Renal disease (most common secondary cause)

Obesity

Pregnancy induced HTN/ pre-eclampsia

Endocrine: Conn’s syndrome

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42
Q

Hypertension

If BP is very high or does no respond to trx, what condition should you consider

A

renal artery stenosis

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43
Q

Hypertension

complications (5)

A
  • IHD
  • cerebrovascular accident (stroke or haemorrhage)
  • hypertensive retinopathy
  • hypertensive nephropathy
  • HF
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44
Q

Hypertension

how often to NICE recommend measuring BP to screen for HTN

A

every 5years but more often in patients on the borderline for dx

every year in pts with T2DM

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45
Q

Hypertension

define white coat effect

A

> 20/10mmHg difference in BP between clinic + ambulatory or home readings

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46
Q

Hypertension

which reading do you use if the difference in of each arm is >15?

A

the higher pressure

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47
Q

Hypertension

stage 1

A

clinic: >140/90
home: >135/85

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48
Q

Hypertension

stage 2

A

clinic: >160/100
home: >150/95

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49
Q

Hypertension

stage 3

A

clinic: >180/120

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50
Q

Hypertension

what inx should all patients with a new dx have

A
  • urine albumin:creatinine ratio for proteinuria
  • dipstick for microscopic haematuria for kidney damage
  • Bloods: HbA1c, renal function and lipids
  • fundus examination for hypertensive retinopathy
  • ECG for cardiac abnormalities
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51
Q

Hypertension

medical mnx: stage 1 aged <55 and non-black

A

A

ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)

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52
Q

Hypertension

medical mnx: step 1 aged >55 and black

A

C

Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)

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53
Q

Hypertension

medical mnx: step 2 non black

A

A+C

alternatively A+D or C+D

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54
Q

Hypertension

medical mnx: step 2 black

A

ARB + C

Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily)

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55
Q

Hypertension

medical mnx: step 3

A

A+C+D

Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)

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56
Q

Hypertension

medical mnx: step 4

A

A + C + D + additional

if serum K ≤ 4.5mmol/l –> K sparing diuretic such as spironolactone

if serum K > 4.5 –> alpha blocker (doxazosin) or BB (atenolol)

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57
Q

Hypertension

how does spironolactone work

A

a potassium sparing diuretic

blocks the action of aldosterone in the kidneys

sodium excretion + potassium reabsorption

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58
Q

Hypertension

when can potassium sparing diuretics be helpful

A

when thiazide diuretics are causing hypokalaemia

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59
Q

Hypertension

which meds can cause hyperkalaemia

A
  • spironolactone

- ACEi

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60
Q

Hypertension

trx targets for <80years

A

<140 / <90

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61
Q

Hypertension

trx targets for >80years

A

<150 / <90

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62
Q

Murmurs

what is the first heart sound (S1) caused by

A

the closing of the AV valves (tricuspid + mitral valves)

at the start of the systolic contraction of the ventricles

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63
Q

Murmurs

what is the second hear sound (S2) caused by?

A

the closing of the semilunar valves (pulmonary + aortic valves)

once the systolic contraction is complete

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64
Q

Murmurs

what is a 3rd heart sound (S3) caused by?

A

rapid ventricular filling causing the chordae tendineae to pull their full length and twang

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65
Q

Murmurs

why can a 3rd heart sound be normal in a young healthy person

A

because the heart functions so well that the ventricles easily allow rapid filling

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66
Q

Murmurs

what can a 3rd heart sound indicate in older patients

A

HF because their ventricles and chordae are stiff and weak so they reach their limit much faster than normal

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67
Q

Murmurs

what does a 4th heart sound indicate

A

rare and always abnormal

stiff or hypertrophic ventricles

caused by turbulent flow from an atria contracting against a non-compliant ventricle

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68
Q

Murmurs

where is the pulmonary valve anatomically

A

2nd ICS left sternal border

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69
Q

Murmurs

where is the aortic valve anatomically

A

2nd ICS right sternal border

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70
Q

Murmurs

where is the tricuspid valve anatomically

A

5th ICS left sternal border left sternal border

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71
Q

Murmurs

where is the mitral valve anatomically

A

5th ICS mid clavicular line (apex area)

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72
Q

Murmurs

where is Erb’s point

A

3rd ICS on the left sternal border

the best area for listening to heart sounds S1 and S2

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73
Q

Murmurs

what special manoeuvre can emphasise mitral stenosis

A

patient on their left hand side

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74
Q

Murmurs

what special manoeuvre can emphasise aortic regurgitation

A

patient sat up leaning forward and holding exhalation

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75
Q

Murmurs

how to assess a murmur (SCRIPT)

A

Site: where is it loudest

Character: soft/blowing/ crescendo/decrescendo

Radiation

Intensity: what grade?

Pitch: high/low/grumbling

Timing: systolic/diastolic

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76
Q

Murmurs

what is murmur grade 1

A

difficult to hear

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77
Q

Murmurs

what is murmur grade 2

A

quiet

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78
Q

Murmurs

what is murmur grade 3

A

easy to hear

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79
Q

Murmurs

what is murmur grade 4

A

easy to hear with a palpable thrill

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80
Q

Murmurs

what is murmur grade 5

A

can hear with stethoscope barely touching chest

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81
Q

Murmurs

what is murmur grade 6

A

can hear with stethoscope off the chest

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82
Q

Murmurs

where does mitral stenosis cause hypertrophy

A

left atrial hypertrophy

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83
Q

Murmurs

where does aortic stenosis cause hypertrophy

A

left ventricular hypertrophy

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84
Q

Murmurs

where does mitral regurg cause dilatation

A

left atrial dilatation

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85
Q

Murmurs

where does aortic regurg cause dilatation

A

left ventricular dilation

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86
Q

Murmurs

what is mitral stenosis caused by

A
  • RHD

- Infective endocarditis

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87
Q

Murmurs

describe a mitral stenosis murmur

A

mid-diastolic

low pitched ‘rumbling’ murmur

loud S1

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88
Q

Murmurs

why is there a loud S1 in mitral stenosis

A

due to thick valves requiring a large systolic force to shut, then shutting suddenly

can palpate a tapping apex beat due to loud S1

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89
Q

Murmurs

what is mitral stenosis associated with

A

malar flush

AF

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90
Q

Murmurs

why is malar flush associated with mitral stenosis

A

back-pressure of blood into the pulmonary system causing a rise in CO2 and vasodilation

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91
Q

Murmurs

why is mitral stenosis associated with AF

A

LA struggling to push blood through the stenotic valve causing strain, electrical disruption and resulting fibrillation

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92
Q

Murmurs

what condition does mitral regurgitation cause

A

congestive cardiac failure because the leaking valve causes a reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart

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93
Q

Murmurs

describe the murmur in mitral regurgitation

A

pan-systolic

high pitched ‘whistling’ murmur

radiates to L axilla

may hear 3rd heart sound

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94
Q

Murmurs

causes of mitral regurgitation

A
  • idiopathic weakening of the valve with age
  • ischaemic heart disease
  • Infective endocarditis
  • RHD
  • connective tissue disorders
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95
Q

Murmurs

what is the most common

A

aortic stenosis

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96
Q

Murmurs

describe an aortic stenosis murmur

A

ejection-systolic

high pitched murmur

crescendo-decrescendo

radiates to the carotid

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97
Q

Murmurs

signs of a pt with an aortic stenosis

A
  • murmur radiates to the carotids as the turbulence continues up into the neck
  • Slow rising pulse and narrow pulse pressure
  • exertional syncope due to difficulty maintaining good flow of blood to the brain
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98
Q

Murmurs

causes of aortic stenosis (2)

A
  • idiopathic age related calcification

- RHD

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99
Q

Murmurs

describe an aortic regurgitation murmur

A

early diastolic

soft

associated with Corrigan’s pulse

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100
Q

Murmurs

aortic regurg: what is Corrigan’s pulse

A

aka collapsing pulse

rapidly appearing and disappearing pulse at carotid as the blood it pumped out by ventricles and then immediately flows back through the aortic valve back into the ventricles

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101
Q

Murmurs

why does aortic regurgitation result in heart failure

A

due to back pressure of blood waiting to get through the left side of the heart

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102
Q

Murmurs

aortic regurg: what is an Austin-Flint murmur

A

early diastolic ‘rumbling’ murmur

heard at the apex

caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate

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103
Q

Murmurs

causes of aortic regurg (2)

A
  • idiopathic age related weakness

- connective tissue disorders

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104
Q

Atrial Fibrillation

pathophysiology

A

disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node

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105
Q

Atrial Fibrillation

presenting sx (4)

A
  • palpitations
  • SOB
  • syncope
  • assc conditions: stroke, sepsis, thyrotoxicosis
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106
Q

what are the 2 Ddx for an irregularly irregular pulse?

A
  1. Atrial Fibrillation

2. Ventricular ectopics

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107
Q

how to tell the difference between AF and ventricular ectopics

A

ventricular ectopics disappear when the HR gets over a certain threshold

a regular heart rate during exercise suggests ventricular ectopics

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108
Q

Atrial Fibrillation

ECG (3)

A
  • absent P waves
  • narrow QRS tachycardia
  • irregularly irregular ventricular rhythm
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109
Q

Atrial Fibrillation

what is valvular AF

A

pts with AF who also have moderate or severe mitral stenosis or a mechanical heart valve

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110
Q

Atrial Fibrillation

what are the most common causes of AF

A

SMITH

Sepsis

Mitral valve pathology (stenosis or regurg)

Ischaemic Heart Disease

Thyrotoxicosis

Hypertension

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111
Q

Atrial Fibrillation

what are the 2 principles to treating AF

A
  1. rate or rhythm control

2. anticoagulation to prevent stroke

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112
Q

Atrial Fibrillation

what is the 1st line trx

A

rate control

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113
Q

Atrial Fibrillation

when would rate control not be 1st line trx (4)

A
  1. reversible cause of AF
  2. within last 48hrs
  3. causing HF
  4. remain symptomatic despite rate controlled
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114
Q

Atrial Fibrillation

what are the options for rate control (3)

A

1st line: BB e.g. atenolol 50-100mg once daily

  1. CCB e.g. diltiazem
  2. digoxin
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115
Q

Atrial Fibrillation

rate control: when should you not use CCB (diltiazmem)

A

in HF

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116
Q

Atrial Fibrillation

rate control: when is digoxin used

A

only in sedentary people, needs monitoring and risk of toxicity

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117
Q

Atrial Fibrillation

when is rhythm control offered (4)

A
  1. reversible cause
  2. new onset <48hrs
  3. AF is causing HF
  4. remain symptomatic despite being rate controlled
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118
Q

Atrial Fibrillation

options for rhythm control

A
  1. single cardioversion event

2. long term medical rhythm control

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119
Q

Atrial Fibrillation

rhythm control: when should immediate cardioversion be done?

A

<48hrs

or severely haemodynamically unstable

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120
Q

Atrial Fibrillation

rhythm control: when should delayed cardioversion be done

A

> 48hrs and they are stable

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121
Q

Atrial Fibrillation

rhythm control: in delayed cardioversion, what should they have whilst waiting

A

anticoagulation for a minimum of 3w prior to cardioversion

and rate control

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122
Q

Atrial Fibrillation

rhythm control: what are the 2 options for cardioversion

A
  • pharmacological cardioversion

- electrical cardioversion

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123
Q

Atrial Fibrillation

rhythm control: what is the first line for pharmacological cardioversion

A
  • flecanide

- amiodarone (drug of choice in pts with structural heart disease)

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124
Q

Atrial Fibrillation

rhythm control: what does electrical cardioversion involve

A

sedation or GA + a cardiac defibrillator to deliver controlled shocks to restore sinus rhythm

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125
Q

Atrial Fibrillation

rhythm control: what drugs can be used for long term medical rhythm control

A

1st line: BB

2nd line: Dronedarone for when pts have had successful cardioversion

Amiodarone: useful in pts with HF or L ventricular dysfunction

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126
Q

Atrial Fibrillation

what is paroxysmal AF

A

when the AF comes and goes in episodes

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127
Q

Atrial Fibrillation

mnx for paroxysmal AF

A
  1. anticoagulation based on CHADSVASc

2. pill in the pocket: Flecanide

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128
Q

Atrial Fibrillation

paroxysmal AF: what criteria is needed to be able to use pill in the pocket approach

A
  • infrequent episodes without any underlying structural heart disease
  • able to identify when they are in AF
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129
Q

Atrial Fibrillation

when should you avoid flecanide

A

in atrial flutter as it can cause 1:1 AV conduction resulting in a significant tachycardia

130
Q

Atrial Fibrillation

how does AF cause an ischaemic stroke

A
  • uncontrolled movement of atria leads to blood stagnating in the LA, particularly the atrial appendage
  • stagnated blood leads to a thrombus
  • then mobilised (embolus) and trvels with the blood
  • atrial–> ventricle –> aorta –> carotid arteries –> brain
  • lodge in cerebral arteries
131
Q

Atrial Fibrillation

how much does anticoagulation reduce the risk of stroke

A

2/3

132
Q

Atrial Fibrillation

Anticoagulation: what is warfarin

A

a vitamin K antagonist

133
Q

Atrial Fibrillation

Anticoagulation: what does an INR of 2 indicate

A

the patient takes them twice as long to form a blood clot

134
Q

Atrial Fibrillation

Anticoagulation: what is the target INR if on warfarin

A

2-3

135
Q

Atrial Fibrillation

Anticoagulation: why does warfarin react with many drugs

A

because the cytochrome P450 system in the liver is involved in the metabolism of warfarin

136
Q

Atrial Fibrillation

Anticoagulation: what affects the INR

A

food containing vit K:
- leafy green veg

things that affect P450:

  • cranberry juice
  • alcohol
137
Q

Atrial Fibrillation

Anticoagulation: what can reverse the DOACS, apixaban and rivaroxaban

A

Andexanet alfa

138
Q

Atrial Fibrillation

Anticoagulation: what can reverse the DOAC, dabigatran

A

Idarucizumab

139
Q

Atrial Fibrillation

Anticoagulation: what are the advantages of DOACs

A
  • no monitoring required
  • no major interaction problems
  • equal or better than warfarin at preventing strokes in AF
  • equal or less risk of bleeding than warfarin
140
Q

Atrial Fibrillation

what tool is used for assessing whether a pt with AF should be started on anticoagulation

A

CHA2DS2-VASc

141
Q

Atrial Fibrillation

CHA2DS2-VASc

A 
C – Congestive heart failure
H – Hypertension                                      
A2 – Age >75 (Scores 2)
D – Diabetes
S2 – Stroke or TIA previously (Scores 2)
V – Vascular disease                                 
A – Age 65-74
S – Sex (female)
142
Q

Atrial Fibrillation

what assessment tool is used to establish a pt’s risk of major bleeding whilst on anticoagulation

A

HAS-BLED

143
Q

Atrial Fibrillation

HAS-BLED

A 
H – Hypertension
A – Abnormal renal and liver function
S – Stroke
B – Bleeding
L – Labile INRs (whilst on warfarin)
E – Elderly
D – Drugs or alcohol
144
Q

Atrial Fibrillation

what does a CHA2DS2-VASc of 0 mean

A

no anticoagulation

145
Q

Atrial Fibrillation

what does a CHA2DS2-VASc of 1 indicate

A

consider anticoagulation

146
Q

Atrial Fibrillation

what does a CHA2DS2-VASc score of >1 indicate

A

offer anticoagulation

147
Q

Atrial Fibrillation

CHA2DS2-VASc >1 and high HAS-BLED score

A

usually the risk of stroke significantly outweighs the risk of bleeding so should anticoagulate

148
Q

Arrhythmias

what can the 4 possible rhythms seen in a pulseless unresponsive pt be categorised into?

A

shockable rhythms: defibrillation may be effective

non-shockable: defibrillation will not be effective

149
Q

Arrhythmias

what are the 4 possible rhythms seen in a pulseless unresponsive pt

A

ventricular tachycardia

ventricular fibrillation

pulseless electrical activity

asystole

150
Q

Arrhythmias

what are the 2 shockable rhythms

A

ventricular tachycardia

ventricular fibrillation

151
Q

Arrhythmias

what are the 2 non-shockable rhythms

A

pulseless electrical activity: all electrical activity except VF/VT, including if you see sinus rhythm without a pulse

Asystole

152
Q

Arrhythmias

trx of tachycardia in an unstable pt

A
  • consider up to 3 synchronised shocks

- consider an amiodarone infusion

153
Q

Arrhythmias

3 narrow complex (QRS<0.12s) tachycardias

A
  • atrial fibrillation
  • atrial flutter
  • SVT
154
Q

Arrhythmias

3 broad complex (QRS>0.12s) tachycardias

A
  • VT
  • SVT w/ BBB
  • AF variation
155
Q

Arrhythmias

what is atrial flutter caused by

A

a re-entrant rhythm in either atrium

the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway

156
Q

Arrhythmias

Atrial flutter: atrial bpm and ventricular bpm

A

atrial contraction at 300bpm

ventricular contraction at 150bpm

157
Q

Arrhythmias

what does ECG show if pt has atrial flutter

A

sawtooth appearance

P wave after P wave

158
Q

Arrhythmias

what conditions are associated with atrial flutter

A
  • HTN
  • IHD
  • cardiomyopathy
  • thyrotoxicosis
159
Q

Arrhythmias

trx of atrial flutter

A

similar to AF:
- rate/rhythm control: BB or cardioversion

  • treat the reversible underlying condition
  • radiofrequency ablation of the re-entrant rhythm
  • anticoagulation based on CHA2DS2-VASc
160
Q

Arrhythmias

what is SVT caused by

A

the electrical signal re-entering the atria from the ventricles

self-perpetuating loop as once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction

161
Q

Arrhythmias

what does the ECG look like in SVT

A

narrow complex tachycardia (QRS<0.12)

QRS complex followed immediately by a T wave, QRS, T wave etc

162
Q

Arrhythmias

what is paroxysmal SVT

A

SVT reoccurs and remits in the same pt over time

163
Q

Arrhythmias

what are the 3 main types of SVT based on the source of the electrical signal

A
  1. Atrioventricular nodal re-entrant tachycardia
  2. Atrioventricular re-entrant tachycardia
  3. Atrial tachycardia
164
Q

Arrhythmias

SVT: what is atrioventricular nodal re-entrant tachycardia

A

when the re-entry point is back through the AV node

165
Q

Arrhythmias

SVT: what is atrioventricular re-entrant tachycardia

A

when the re-entry point is an accessory pathway (WPW)

166
Q

Arrhythmias

SVT: what is atrial tachycardia

A

where the electrical signal originates in the atria somewhere other than the sinoatrial node

not caused by a signal re-entering from the ventricles

but from abnormally generated electrical activity in the atria

this ectopic electrical activity causes an atrial rate of >100bpm

167
Q

Arrhythmias

SVT: acute mnx of stable pt with SVT stepwise approach

A

continuous ECG monitoring

  1. Valsalva manoeuvre
  2. carotid sinus massage
  3. adenosine
  4. or verapamil
  5. direct current cardioversion
168
Q

Arrhythmias

SVT: what is the valsalva manoeuvre

A

forced expiration against a closed glottis. e.g. blowing hard against resistance into a plastic syringe

169
Q

Arrhythmias

SVT: what is the modified valsalva manoeuvre (REVERT trial)

A
  1. Position pt in a semi-recumbent position (45º)
  2. blow into syringe for 15 seconds
  3. Lower pt flat and passively raise their legs to a 45º angle for 15 seconds
  4. Return the patient to a semi-recumbent position for an additional 45 seconds
170
Q

Arrhythmias

SVT: how does adenosine work

A

slows cardiac conduction primarily through the AV node

it interrupts the AV node/ accessory pathway during SVT and ‘resets’ it back to sinus rhythm

171
Q

Arrhythmias

SVT: whom should you avoid adenosine in

A

if pt has:

  • asthma
  • COPD
  • HF
  • heart block
  • severe hypotension
172
Q

Arrhythmias

SVT: what should you warn pts before giving adenosine

A

the scary feeling of dying/impending doom when injected

173
Q

Arrhythmias

SVT: how should adenosine be administered

A

fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)

followed by a 20 ml IV Normal Saline bolus

6mg –> 12mg –> 12mg

174
Q

Arrhythmias

what is the long term mnx of pts with paroxysmal SVT

A

medication:

  • BB
  • CBB
  • amiodarone

radiofrequency ablation

175
Q

Arrhythmias

what is Wolff-Parkinson White Syndrome caused by

A

an extra electrical pathway connecting the atria and ventricles

176
Q

Arrhythmias

WPW: what is the extra pathway called

A

the Bundle of Kent

177
Q

Arrhythmias

WPW: definitive trx

A

radiofrequency ablation of the accessory pathway

178
Q

Arrhythmias

WPW: ECG changes

A
  • delta wave: slurred upstroke on the QRS complex
  • Wide QRS complex (0.12s)
  • Short PR interval
179
Q

Arrhythmias

why are most antiarrhythmic meds (BB, CBB. adenosine) CI’d in pts with WPW that develop AF or flutter

A

they increase the risk of the chaotic atrial electrical activity to pass through the accessory pathway into the ventricles

causing a polymorphic wide complex tachycardia

because they reduce conduction through the AV node therefore promoting conduction through the accessory pathway

180
Q

Arrhythmias

where is radiofrequency ablation performed

A

in a electrophysiology lab aka ‘cath lab’

181
Q

Arrhythmias

what does radiofrequency ablation involve

A
  • catheter into femoral veins
  • feeding a wire through venous system under xray guidance to the heart
  • find location of abnormal electrical pathway
  • radiofrequency ablation (heat) applied to burn the abnormal area
182
Q

Arrhythmias

when can radiofrequency ablation be used

A
  • AF
  • atrial flutter
  • SVTs
  • WPW
183
Q

Arrhythmias

what is Torsades de pointes

A

‘twisting of the tips’

a type of polymorphic (multiple shape) ventricular tachycardia

184
Q

Arrhythmias

Torsades de pointes: whom does it occur in

A

pts with a prolonged QT interval

185
Q

Arrhythmias

Torsades de pointes: ECG changes

A

normal ventricular tachycardia

QRS complex twists around baseline

QRS height progressively gets smaller, then larger, then smaller etc

186
Q

Arrhythmias

Torsades de pointes: what is it

A

prolonged Qt = prolonged repolarisation of the muscle cells in the heart after contraction

resulting in spontaneous depolarisation in some areas of heart myocytes (afterdepolarisations)

they spread through the ventricle, leading to a ventricular contraction prior to proper repolarisation occurring

when this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation, it is called Torsades de pointes

187
Q

Arrhythmias

Torsades de pointes: what can it lead to

A
  1. terminate spontaneously and revert back to sinus rhythm

2. progress to ventricular tachycardia –>cardiac arrest

188
Q

Arrhythmias

Torsades de pointes: causes of prolonged QT (3)

A
  1. Long QT syndrome (inherited)
  2. meds: antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide abx
  3. electrolyte disturbance: hypokalaemia, hypomagnesaemia, hypocalcaemia
189
Q

Arrhythmias

Torsades de pointes: acute mnx

A
  • correct cause (electrolyte disturbance or medications)
  • Mg infusion (even if they have normal serum Mg)
  • Defibrillation if VT occurs
190
Q

Arrhythmias

Torsades de pointes: long term mnx of prolonged QT syndrome (inherited)

A
  • avoid meds that prolong the QT interval
  • correct electrolyte disturbances
  • BB (not sotalol)
  • pacemaker or implantable defibrillator
191
Q

Arrhythmias

what are ventricular ectopics

A

premature ventricular beats caused by random electrical discharges from outside the atria

192
Q

Arrhythmias

Ventricular ectopics: what do pts often complain of

A

random, brief palpitations ‘an abnormal beat’

193
Q

Arrhythmias

Ventricular ectopics: whom are they more common in

A

pts with pre-existing heart conditions e.g. IHD or HF

but relatively common at all ages

194
Q

Arrhythmias

Ventricular ectopics: ECG changes

A

individual random, abnormal, broad QRS complexes on a background of a normal ECG

195
Q

Arrhythmias

Ventricular ectopics: what is Bigeminy

A

where the ventricular ectopics are occurring so frequently that they happen after every sinus beat

196
Q

Arrhythmias

Ventricular ectopics: what does the ECG look like in Bigeminy

A

normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on

197
Q

Arrhythmias

Ventricular ectopics: mnx

A
  • check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
  • reassurance + no trx for otherwise healthy ppl
  • seek expert advice in pts with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, FH of sudden death)
198
Q

Arrhythmias

when does 1st degree heart block occur

A

when there is delayed AV conduction through the AV node

199
Q

Arrhythmias

1st degree heart block ECG changes

A
  • every p wave results in a QRS complex

- PR interval >0.2s (1 big square)

200
Q

Arrhythmias

what is 2nd degree heart block

A

where some of the atrial impulses do not make it through the AV node to the ventricles

some p waves do not lead to QRS complexes

201
Q

Arrhythmias

what are the different types of 2nd degree heart block

A
  • Wenckebach’s phenomenon (Mobitz Type 1)

- Mobitz Type 2

202
Q

Arrhythmias

2nd degree heart block: what is Wenckebach’s phenomenon (Mobitz Type 1)

A

the atrial impulses become gradually weaker until it does not pass through the AV node

after failing to stimulate a ventricular contraction, the atrial impulse returns to being strong

cycle repeats

203
Q

Arrhythmias

Wenckebach’s phenomenon (Mobitz Type 1) ECG changes

A
  • increasing PR interval until QRS complex is missed

- the cycle repeats

204
Q

Arrhythmias

2nd degree heart block: what is Mobitz type 2

A

where there is intermitted failure or interruption of AV conduction

205
Q

Arrhythmias

2nd degree heart block: Mobitz type 2 ECG changes

A
  • PR interval remains normal

- a set of P waves for each QRS complexes e.g. 3:1 block is 3 P waves to each QRS complex

206
Q

Arrhythmias

2nd degree heart block: what is there a risk of in Mobitz type 2

A

asystole

207
Q

Arrhythmias

2nd degree heart block: what is 2:1 block

A

2 P waves for each QRS complex

every 2nd p wave is not a strong enough atrial impulse to stimulate a QRS complex

difficult to tell if caused by Mobitz type 1 or 2

208
Q

Arrhythmias

what is 3rd degree heart block

A

aka complete heart block

no relationship between P waves and QRS complexes

209
Q

Arrhythmias

what is there a significant risk of in 3rd degree heart block

A

asystole

210
Q

Arrhythmias

trx for stable bradycardia or heart block

A

observe

211
Q

Arrhythmias

trx for unstable bradycardia or heart block or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole)

A

1st line: atropine 500mcg IV

no improvement:
- atropine 500mcg IV repeated (up to 6 doses for a total to 3mg)

  • other inotropes: noradrenalin
  • transcutaneous cardiac pacing (using a defibrillator)
212
Q

Arrhythmias

trx In patients with high risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole)

A
  • temporary transvenous cardiac pacing

- permanent implantable pacemaker

213
Q

Arrhythmias

what is temporary transvenous cardiac pacing

A

using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the RA or ventricle to stimulate them directly

trx for pts with high risk of asystole

214
Q

Arrhythmias

what is atropine

A

an antimuscarinic

inhibits the parasympathetic nervous system

215
Q

Arrhythmias

what are the side effects of atropine

A

antimuscarinic: inhibits the parasympathetic nervous system

so
pupil dilatation, urinary retention, dry eyes and constipation

216
Q

Stable Angina

pathophysiology

A

narrowing of the coronary arteries reduces blood flow to the myocardium

chest pain when there is insufficient supply of blood to meet demand

217
Q

Stable Angina

what is unstable angina

A

when the sx come on randomly whilst at rest

and this is considered as an Acute Coronary Syndrome

218
Q

Stable Angina

what is the gold standard diagnostic inx

A

CT Coronary Angiography

219
Q

Stable Angina

what is CT Coronary Angiography

A

injecting contrast and taking CT images timed with the heart beat

to give a detailed view of the coronary arteries, highlighting any narrowing

220
Q

Stable Angina

baseline inx

A
  • physical exam: heart sounds, BMI
  • ECG
  • FBC (anaemia)
  • U&Es
  • LFTs
  • Lipid profile
  • TFTs
  • HbA1c
221
Q

Stable Angina

why check U&Es

A

prior to ACEi and other meds

222
Q

Stable Angina

why check LFTs

A

prior to statins

223
Q

Stable Angina

what are the 4 principles to mnx

A

RAMP

Refer to cardiology (urgent if unstable)

Advise them about the dx, mnx and when to call an ambulance

Medical trx

Procedural or surgical interventions

224
Q

Stable Angina

immediate symptomatic relief medical mnx

A

take GTN, then repeat after 5 min

still pain after repeated dose? call ambulance

225
Q

Stable Angina

how does GTN work

A

it causes vasodilation and helps relieve the sx

226
Q

Stable Angina

long term symptomatic relief

A

BB (bisoprolol 5mg OD)
or/and
CBB (amlodipine 5mg OD)

227
Q

Stable Angina

long term symptomatic relief other options (not 1st line)

A
  • long acting nitrates (isosorbide mononitrate)
  • Ivabradine
  • Nicorandil
  • Ranolazine
228
Q

Stable Angina

secondary prevention of CVD

A
  • aspirin (75mg OD)
  • Atorvastatin (80mg) OD
  • ACEi
  • BB (already on for symptomatic relief)
229
Q

Stable Angina

if CT coronary angiography shows ‘proximal or extensive disease’, what is offered

A

PCI (Percutaneous Coronary Intervention) with coronary angioplasty

230
Q

Stable Angina

what is PCI with coronary angioplasty

A

put catheter into brachial or femoral artery

feed up to coronary arteries under xray guidance

inject contrast

dilate the blood vessel with a balloon and/or inserting a stent

231
Q

Stable Angina

what is offered to patients with severe stenosis

A

Coronary Artery Bypass Graft (CABG)

232
Q

Stable Angina

what does CABG involve

A

open chest along sternum

take a graft from great saphenous vein

sew it on the affected coronary artery to bypass the stenosis

233
Q

Stable Angina

what scars are present in someone who has had a CABG

A
  • midline sternotomy scar

- great saphenous vein harvesting

234
Q

Stable Angina

what scars are present in someone who has had a PCI

A
  • femoral artery access
    or
  • brachial artery access
235
Q

ACS

cause

A

thrombus from an atherosclerotic plaque blocking a coronary artery

236
Q

ACS

why are anti-platelet meds (aspirin, clopidogrel, ticagrelor) the mainstay of treatment

A

when a thrombus forms in a fast flowing artery, it is made up of mostly platelets

237
Q

ACS

what does the left coronary artery branch into

A

the circumflex and LAD

238
Q

ACS

what does the RCA supply

A
  • RA
  • RV
  • inferior aspect of LV
  • posterior septal area
239
Q

ACS

what does the circumflex artery supply

A
  • LA

- posterior aspect of LV

240
Q

ACS

what does the LAD supply

A
  • anterior aspect of the LV

- anterior aspect of septum

241
Q

ACS

what are the 3 types

A
  • unstable angina
  • STEMI
  • NSTEMI
242
Q

ACS

dx if there is ST elevation or new LBBB

A

STEMI

243
Q

ACS

next inx if there is no ST elevation

A

troponin blood test

244
Q

ACS

diagnosis of NSTEMI

A
  • raised trop
    and/or
  • other ECG changes (ST depression, T-wave inversion, pathological Q waves)
245
Q

ACS

diagnosis of unstable angina or MSK chest pain

A
  • normal trop

- no pathological changes on ECG

246
Q

ACS

sx

A

Central, constricting chest pain associated with:

  • N+V
  • Sweating + clamminess
  • Feeling of impending doom
  • SOB
  • Palpitations
  • Pain radiating to jaw or arms
247
Q

ACS

what is silent MI

A

Diabetic patients may not experience typical chest pain during an acute coronary syndrome

248
Q

ACS

ECG leads: I, aVL, V3-V6
heart area and artery?

A

anterolateral

LCA

249
Q

ACS

ECG leads: V1-V4
heart area and artery?

A

Anterior

LAD

250
Q

ACS

ECG leads: I, aVL, V5-6
heart area and artery?

A

Lateral

Circumflex

251
Q

ACS

ECG leads: II, III, aVF
heart area and artery?

A

Inferior

RCA

252
Q

ACS

when is troponin measured

A

at baseline and 6 or 12 hours after onset of sx

253
Q

ACS

what does a rise in troponin indicate

A

myocardial ischaemia as the proteins are released from the ischaemic muscle.

254
Q

ACS

other causes of a raise in trop

A
  • Chronic renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
255
Q

ACS

why perform CXR

A

other causes of chest pain and pulmonary oedema

256
Q

ACS

why perform an echo

A

to assess functional damage

257
Q

ACS

why perform a CT coronary angiogram

A

to assess coronary artery disease

258
Q

ACS

acute STEMI mnx

A

if within 2hr: PCI

if not available within 2hr: thrombolysis

259
Q

ACS

examples of thrombolytic agents

A

streptokinase, alteplase and tenecteplase.

260
Q

ACS

Acute NSTEMI trx

A

BATMAN

BB unless contraindicated

Aspirin 300mg stat dose

Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)

Morphine titrated to control pain

Anticoagulant: Fondaparinux (unless high bleeding risk)

Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

261
Q

ACS

what is the scoring system that gives a 6-month risk of death or repeat MI after having an NSTEMI

A

GRACE score

262
Q

ACS

if GRACE score is medium or high (>5%), what may be considered

A

early PCI (within 4d of admission) to treat underlying coronary artery disease

263
Q

ACS

complications of MI

A

DREAD

Death

Rupture of the heart septum or papillary muscles

“Edema” (Heart Failure)

Arrhythmia and Aneurysm

Dressler’s Syndrome

264
Q

ACS

what is Dressler’s syndrome

A

aka post-MI syndrome

occurs 2-3w after an MI.

localised immune response causes pericarditis

265
Q

ACS

Dressler’s syndrome presentation

A
  • pleuritic chest pain
  • low grade fever
  • pericardial rub on auscultation
  • pericardial effusion
  • rarely a pericardial tamponade (where the fluid constricts the heart and prevents function).
266
Q

ACS

Dressler’s syndrome dx

A

ECG: global ST elevation and T wave inversion

echo: pericardial effusion

CRP+ESR: raised

267
Q

ACS

Dressler’s syndrome mnx

A

NSAIDs (aspirin / ibuprofen)

severe cases: steroids (prednisolone)

may need pericardiocentesis to remove fluid from around the heart.

268
Q

ACS

Secondary Prevention Medical Management

A

6A’s

Aspirin 75mg OD

Another antiplatelet: clopidogrel/ticagrelor up to 1y

Atorvastatin 80mg OD

ACE inhibitors

Atenolol (or other beta blocker titrated as high as tolerated)

Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

269
Q

Type 1 MI

A

Traditional MI due to an acute coronary event

270
Q

Type 2 MI

A

Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

271
Q

Type 3 MI

A

Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

272
Q

Type 4 MI

A

MI associated with PCI / coronary stunting / CABG

273
Q

CXR: Water-bottle-shaped enlarged cardiac silhouette

A

pericarditis

274
Q

what is Fleischner sign

A

Prominent central pulmonary artery

Fleischner sign is found in 20% of patient’s presenting with a pulmonary embolism

275
Q

Cardiac Tamponade

what is it

A

accumulation of fluid, blood, purulent exudate or air in the pericardial space raises the intra pericardial pressure.

thus diastolic filling is reducing thereby reducing the cardiac output

276
Q

Cardiac Tamponade

signs (3)

A

Beck’s Triad

  1. hypotension
  2. quiet heart sounds
  3. raised JVP
277
Q

Cardiac Tamponade

sx

A
  • SOB
  • tachycardia
  • confusion
  • chest pain
  • abdo pain
278
Q

Cardiac Tamponade

what may ECG show

A

low voltage QRS complexes or electrical alternans

279
Q

Cardiac Tamponade

what may CXR show

A

large globular heart

280
Q

Cardiac Tamponade

what may echo demonstrate

A

the amount of fluid around the heart and quantify the level of ventricular compromise.

281
Q

Cardiac Tamponade

1st line mnx in patients that are haemodynamically unstable

A

Pericardiocentesis: sampling of the fluid to find the underlying cause and treat the immediate problem

282
Q

Cardiac Tamponade

1st line mnx in pts haemopericardium, associated malignancy, traumatic/purulent effusion

A

surgical drainage

283
Q

Cardiac Tamponade

complications of pericardiocentesis

A

pneumothorax

284
Q

Acute bradycardia

definition

A

<60bpm

285
Q

Acute bradycardia

causes (4)

A
  • Sinus/AV nodal disease
  • Drug induced: BB, CBB
  • Electrolyte abnormalities
  • Hypothyroidism
286
Q

Acute bradycardia

clinical features (3)

A
  • dizziness
  • syncope
  • tiredness
287
Q

Acute bradycardia

initial mnx if there are any adverse features (shock, syncope, myocardial ischemia or HF)

A

IV atropine 500 micrograms

Repeat boluses can be given up to 3mg

288
Q

Acute bradycardia

how does atropine work

A

blocks the vagus nerve activity on the heart, which increases the firing rate of the SA node.

289
Q

Acute bradycardia

If there is a risk of asystole, or if the patient is unstable and has failed to respond to atropine sulfate, what next?

A

adrenaline/epinephrine should be given by intravenous infusion, and the dose adjusted according to response ( 2-10 mcg per minute.

290
Q

Patients with occlusion of the left anterior descending artery are particularly at risk of?

A

rupture of the interventricular septum due to infarction of the septal area.

291
Q

what may be heard in rupture of the interventricular septum

A

harsh and holosystolic murmur

292
Q

how may a rupture of the interventricular septum present

A
  • haemodynamic instability
  • hypotension
  • biventricular failure (often largely right-sided)
293
Q

what is the most common cause of sudden cardiac death in the young

A

Hypertrophic obstructive cardiomyopathy

294
Q

signs of Hypertrophic obstructive cardiomyopathy

A

harsh ejection systolic murmur that decreases in intensity on squatting.

295
Q

what should be considered in all patients with reasonable quality of life and a poor left ventricular ejection fraction (LVEF) of < 35% despite optimum medical therapy

A

Implantable cardioverter-defibrillator (ICD)

296
Q

what do J waves indicate

A

hypothermia

297
Q

leads V1-2: a coved ST elevation >2mm with subsequent negative T waves.

what could this be

A

brugada syndrome

298
Q

How is the QT interval correctly defined

A

Start of Q-wave to the end of the T-wave

299
Q

pt presents with acute bradycardia. Doesn’t respond to atropine or adrenaline. What is the next step

A

Transcutaneous pacing

300
Q

single chamber right ventricular pacemaker ECG findings

A

Pacing spikes preceding the P waves. Broad QRS complexes with an RSR pattern in V5-6.

301
Q

When Adenosine is contraindicated (asthma, COPD, HF). what can be given

A

Verapamil 2.5 - 5mg

302
Q

fever and weight loss. audible tumour “plop”, nail clubbing, sx of mitral obstruction / stenosis (such as atrial fibrillilation

what could this be

A

cardiac myoma

303
Q

what is high output cardiac failure

A

cardiac output is normal, but there is an increase in peripheral metabolic demands which exceed those that can be met with maximal cardiac output

304
Q

Causes of high output cardiac failure

A 
AAPPTT:
Anaemia
Arteriovenous malformation
Paget's disease
Pregnancy
Thyrotoxicosis
Thiamine deficiency (wet Beri-Beri)
305
Q

mode of inheritance for hypertrophic cardiomyopathy

A

autosomal dominant

306
Q

57 year old lady has HTN and DM. What medication do you give

A

ACEi!

all diabetics no matter what age should be on this

307
Q

ECG shows widespread downsloping ST segments

what drug causes this

A

digoxin

308
Q

mnx of heart failure after optimum medication (ABAL)

A

Cardiac resynchronisation therapy (CRT)

309
Q

an implantable cardiac defibrillator is inserted due to VF.

How long must he wait until he can drive a car again?

A

6m

310
Q

definition of syncope

A

transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery

311
Q

classification of syncope (3)

A
  1. Reflex syncope (neurally mediated)
  2. Orthostatic syncope
  3. Cardiac syncope
312
Q

what is 1. Reflex syncope (neurally mediated)

A
  • vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
  • situational: cough, micturition, gastrointestinal
  • carotid sinus syncope
313
Q

what is . Orthostatic syncope

A
  • primary autonomic failure: Parkinson’s disease, Lewy body dementia
  • secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
  • drug-induced: diuretics, alcohol, vasodilators
  • volume depletion: haemorrhage, diarrhoea
314
Q

what is cardiac syncope

A
  • arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (SVT)
  • structural: valvular, MI, HOM
  • others: PE
315
Q

inc for syncope

A
  • CVS examination
  • postural BP
  • ECG
  • carotid sinus massage
  • tilt table test
  • 24 hour ECG
316
Q

mnx of pericarditis

A

Naproxen and advise bed rest

317
Q

mnx of digoxin poisoning

A

digiband

318
Q

which JVP waveform is expected to be seen in a patient with tricuspid regurg

A

Prominent A-wave (which signifies forceful atrial contraction)

319
Q

what is the only recommended trx for asystole

A

IV adrenaline

320
Q

Why do you give high dose, long term antibiotics for endocarditis

A

no vascular supply to the valves

Finals (47 decks)

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