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Phase 2a Peer Teaching > Cardiology Peer Teaching > Flashcards

Cardiology Peer Teaching Flashcards

1
Q

what sort of thing can a bicuspid aortic valve predispose to

A
  • go undetected initially but later leads to:
    • aortic stenosis
    • aortic regurgitation
  • predisposes to
    • IE
    • aortic dissection
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2
Q

what would the treatment be for a bicuspid aortic valve be

A

surgical valve replacement

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3
Q

what are the differences between the two types of ASD

A
  • Primum: presents earlier and may involve the AV valves
  • Secundum: asymptomatic until adulthood - affects higher in the septum
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4
Q

what happens in an ASD and what can this lead to?

A
  • there becomes a L–>R shunt
  • as heart compliance falls with age the shunt increases
  • pulmonary hypertension ensues
  • heart failure and SoB by 40
  • can lead to Eisenmenger’s complex where the shunt is reversed due to the PHTN
  • this leads to cyanosis and organ damage
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5
Q

what happens in a VSD

A

there’s a L–>R shunt

there’s no cyanosis as LVP is still greater than RVP

larger holes can cause problems during infancy while smaller ones may be asymptomatic

both increase IE risk

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6
Q

what condition would you see a boot shaped heart on x ray

A

teratology of fallot

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7
Q

what is coarctation of th aorta

A

it is a narrowing at the site of the ductus arteriosus

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8
Q

what happens in mild and severe coarctation of the aorta

A
  • severe:
    • blocks aorta, patient may collapse with heart failure
  • mild
    • raised BP and systolic murmur
      • murmur best heard over left scapula ‘scapula bruit’
  • both cause a radio-femoral delay
    • i.e. BP higher in right arm than left
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9
Q

how would you treat mild and severe coarctation of the aorta

A

both need repair: surgically or with a stent

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10
Q

which is most common ASD primum or secundum

A

secundom

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11
Q

what is eisenmenger’s complex

A

it is a complication of VSD or ASD

reversal of the L–>R shunt due to pulmonary HTN and right sided hypertrophy

causes marked cyanosis, clubbing, heart failure, syncope and polycythaemia

there is very poor prognosis and it can only be cured with a transplant

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12
Q

how would VSD present in an infant

A

SOB

poor feeding

failure to thrive

needs fixing before eisenmenger’s syndrom arises

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13
Q

name two conditions associated with coarctation of the aorta

A

bicuspid aortic valve and Turner’s syndrome

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14
Q

Mother comes to see you. Her two year old has been having episodes where he gets restless and cries for no reason, however as soon as he is allowed to squat down the crying stops. He is a bit underweight for his age and on examination you notice a bit of clubbing.

diagnosis?

A

Teratology of Fallot

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15
Q

what are the 4 features of teratology of fallot

A

VSD

Pulmonary stenosis

RV hypertrophy

overriding aorta

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16
Q

why do toddlers squat in teratology of fallot

A

it increases TPR so helps to alleviate some of the R->L shunt

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17
Q

what happens in teratology of fallot

A

they have the 4 deformities

these cause R->L shunt

then after the DA closes they’ll become progressively more cyanotic as there’s less and less flow to the lungs

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18
Q

mortality of teratology of fallot

A

without surgery it’s 95%

with surgery it’s 5-10%

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19
Q

what number of live births have teratology of fallot

A

3-6/100,000 live births

commonest cyanotic cardiac disorder

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20
Q

how long shoult the PR interval be

A

120-200ms

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21
Q

how wide should the QRS be

A

110ms

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22
Q

in which leads will the QRS be upright in

A

I and II

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23
Q

in which leads will QRS and T waves have the same direction

A

I, II and III

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24
Q

what proportion of men and women die from IHD in the UK

A

one in 7 men and one in 11 women

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25
Q

what number of deaths does IHD cause in the UK every year

A

70,000

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26
Q

three broad causes of IHD

A
  1. inhibited blood flow
  2. increased distal resistance
  3. reduced O2 carrying capacity (anaemia) or availability (hypoxia)
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27
Q

4 modifiable risk factors for IHD

A
  • smoking
  • obesity
  • exercise
  • diet
  • cocaine use
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28
Q

4 clinical risk factors for IHD

A

depression

hypertension

diabetes

hyperlipidaemia

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29
Q

three non-modifiable risk factors for IHD

A

age

genetics

gender M>F

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30
Q

psychosocial risk factors for IHD

A

high demand, low control jobs

low social interaction/support

low social class

low income

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31
Q

9 things included in the QRISK2

A

BP

Age

Ethnicity

Smoking

Cholesterol

RA

DM

Anti-hypertensives

BMI

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32
Q

what is the gold standard investigation for angina pectoris

A

Angiogram – Gold standard, shows luminal narrowing

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33
Q

what does qrisk tell us

A

the risk of CV event in the next ten years

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34
Q

presentation of angina pectoris

A

chest pain brought on by exertion but rapidly resolves with rest

may radiate to arms, jaw and neck

pain can be exacerbated by emotion

May also get some dyspnoea, palpitations or syncope

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35
Q

what is the most common manifestation of stable IHD

A

angina pectoris

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36
Q

what is the prevalence of angina pectoris

A

5% among men, 4% among women

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37
Q

ECG in angina pectoris

A

usually normal, may show ST depression and T wave inversion

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38
Q

what is the lifestyle advice for angina pectoris

A

eat less

move more

stop smoking

control diabetes better

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39
Q

what investigations would you do on a patient with angina pectoris

A

ECG

Bloods: looking for anaemia

CXR - check heart size and pulmonary vessels

Angiogram - this is gold standard and will show luminal narrowing of coronary arteries

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40
Q

what is the medical treatment of angina pectoris

A
  • control hypertension and diabetes
  • beta blockers
    • atenolol
  • CCB if beta blockers contraindicated e.g. asthma
    • amlodipine
  • statin
    • simvastatin
  • aspirin
  • ACE inhibitor
    • ramipril
  • if severe try ARB
    • candesartan
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41
Q

surgical treatment of angina pectoris

A
  • PCI (percutaneous coronary intervention)
    • stenting or ballooning the narrowing
    • risk of restenosis or thrombosis
    • less invasive
  • CABG (coronary artery bypass graft)
    • good prognosis but longer recovery
    • not for the frail
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42
Q

ACS includes

A

unstable angina

NSTEMI

STEMI

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43
Q

rare causes of ACS

A

emboli

coronary spasm

vasculitis

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44
Q

how would ischaemis show on an ECG

A

ST depression and T wave flattening

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45
Q

Ix for ACS

A
  • ECG
  • Bloods:
    • FBC
    • U&E
    • glucose
    • lipids
  • Cardiac enzymes:
    • Troponin T
    • CK-MB
    • myoglobin
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46
Q

Acute changes seen on ECG following ACS

A

Tall T waves, ST elevation, new LBBB

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47
Q
  • draw the differentiating ACS diagram with the timeframes:
    • admission
    • working diagnosis
    • ECG
    • Biochemistry
    • Diagnosis
A
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48
Q

what is the definition of unstable angina

A

acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage

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49
Q

what is the outlook for patients with unstable angina

A

50% will have an MI within 30 days if left untreated

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50
Q

Ix for unstable angina §

A
  • FBC = anaemia aggravates it
  • Cardiac enzymes = excludes infarction
  • ECG = when in pain shows ST depression
  • Coronary angiography
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51
Q

symptoms of MI

A

acute central chest pain radiating to jaw or shoulder and lasting >20 mins, with nausea, SOB and palpitations

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52
Q

pulse and BP in MI

A

can be up or down

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53
Q

signs of MI

A
  • clammy and pale
  • 4th heart sound
  • pansystolic murmur
  • may later develop peripheral oedema
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54
Q

who are silent MIs most commonly seen in

A

the elderly or diabetics

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55
Q

Acute management of a STEMI

A
  • ABCDE
    • C- secure IV access
  • MONA
    • morphine
    • oxygen (only if sats <94%)
    • nitrates
    • aspirin (chew)
  • Refer for PCI immediately
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56
Q

actue management of NSTEMI

A
  • MONA
  • anti-coagulation with fondaprinux (Xa inhibitor)
  • double up with a second anti-platelet like clopidogrel
  • give IV nitrate if the pain then continues
    • glyceryl trinitrate (GTN)
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57
Q

Advice points for patient following ACS

A

1 month no sex

drivers, airline pilots must not return to work

diet: high in oily fish, fruit and veg, low in sat fats

increase exercise

stop smoking

improve management of diabetes

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58
Q

what is the most common cause of pericarditis

A

cocksackie B virus

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59
Q

what 4 drugs for post MI management

A

aspirin

B blocker (CCB like verapamil if CI)

ACEi like ramipril

statin like simvastatin

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60
Q

differential diagnoses of chest pain

A
  • Cardiac: ACS, aortic dissection, pericarditis, myocarditis
  • Respiratory: PE, pneumonia, PT, pleurisy, ca. lung
  • Musculoskeletal: rib fracture, chest trauma
  • Costochondritis
  • GORD
  • Oesophageal spasm
  • Anxiety/panic attack
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61
Q

signs and symptoms of peripheral vascular arterial disease

A
  • 6 Ps of limb ischaemia
    • pain (cramping relieved by rest)
    • pallor
    • pulselessness
    • paresthesis
    • paralysis
    • perishing cold
  • may cause ‘punched out’ ulcers
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62
Q

test for peripheral arterial disease

A
  • Buerger’s test
    • postural colour change
    • 45 degree elevation of legs when lying down –> observable colour change
    • colour returns when hung over bed
    • one leg at a time to compare
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63
Q

Ix for peripheral arterial disease

A
  • exclude:
    • DM
    • arteritis
    • anaemia
  • ABPI
    • normal is 1-1.2
    • PAD is 0.5-0.9
  • colour duplex USS
  • MR/CT angiography
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64
Q

management of peripheral arterial disease

A
  • risk factor modification
    • quit smoking
    • treat HTN
    • lower cholesterol
    • improve DM control
    • lower fat diet
    • exercise improves blood flow
  • medicatons
    • clopidogrel as 1st line
  • PTA if severely stenosed
    • percutaneous transluminal angioplasty
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65
Q

when is PAD critical limb ischaemia

A

triad of ischaemic rest pain, gangrene and arterial insufficiency ulcers

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66
Q

how would the limb appear in critical limb ischaemia

A

‘dusky’

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67
Q

management of critical limb ischaemia

A

surgical embolectomy

local thrombolysis

if not revascularised in 4-6hrs they’ll lose the limb

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68
Q

what are the two subdivisions of low output heart failure

A
  • systolic failure
    • low CO due to insufficient ventricular contraction
    • EF<40%
  • diastolic failure
    • inability of the ventricle to relax and fill normally leads to increased filling pressures
    • EF >50% (heart failure with preserved EF: HFpEF)
    • caused by restrictive pericarditis, tamponade, ventricular hypertrophy, restricted cardiomyopathy etc
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69
Q

what’s the socrates for pericarditis

A

–S = central, retrosternal

–O = 3 days ago

–C = sharp

–R = left shoulder

–A = SOB, cough, hiccups fever

–T = constant

–E = made worse on inspiration, relieved by leaning forwards

–S = 7/10

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70
Q

causes of pericarditis

A
  • mostly viral
    • cocksackie B
    • EBV
    • mumps
  • bacterial
    • staph/strep
    • pneumonia
  • Post MI - dressler syndrome
  • autoimmune
    • SLE
    • RA
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71
Q

signs of pericarditis

A
  • tachypnoea
  • tachycardia
  • fever
  • SOB
  • auscultation –> pericardial friction rub
  • pericardial effusion may be visible on X-ray
72
Q

7 Ix for pericarditis

A
  • ECG
  • FBC
  • CRP
  • Cardiac enzymes (^ Trop)
  • Echo
  • CXR
  • Pericardial tap / biopsy - for rarer causes
73
Q

what would ECG of pericarditis show

A

PR depression on all leads

74
Q

management of pericarditis

A

–Treat the cause!

–NSAIDs – to manage pain and inflammation

–Corticosteroids – for symptomatic relief

–Manage complications

75
Q

what is the clinical definition of heart failure

A

A state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues

76
Q

equation for CO

A

–CO = HR x SV

77
Q

what is the difference between high output and low output HF

A
  • high output: blood requirements of the body are too high
    • anaemia
    • pregnancy
  • Low output: heart is not functioning efficienty
    • IHD
78
Q

causes of systolic heart failure

A

IHD

MI

cardiomyopathy

79
Q

causes of diastolic heart failure

A

constrictive pericarditis

cardiac tamponade

restrictive cardiomyopathy

80
Q

causes of high output heart failure

A

anaemia

pregnancy

hyperthyroidism

81
Q

pathophysiology of heart failure

A
  • compensatory changes made in response to the beginning of heart failure themselves become pathological
    • RAAS
    • Sympathetic stimulation
    • Cardiac changes
82
Q

how does sympathetic stimulation change in HF

A
  • peripheral vasoconstriction
    • meant to increase perfusion of organs by increasing BP
    • but actually increases afterload in heart causing increased hypertrophy and failure
83
Q

how does RAAS change in HF

A
  • RAAS is increased in order to increase perfusion of organs
    • increased volume and vasoconstriction leads to:
      • salt and water retention
      • increases afterload and preload
84
Q

cardiac changes in HF

A
  • –Ventricular dilatation
  • –Myocyte hypertrophy
  • both are meant to increase CO
  • but actually they both reduce EF
85
Q

what happens with pre-load in heart failure

A
  • Increased preload:
    • Failure of the heart muscle means more blood is left behind in the ventricles after systole
    • This results in increased preload
    • This stretches myocardium à which maintains cardiac output up to a point
86
Q

why is there salt and water retention in HF

A
  • Reduced cardiac output leads to diminished renal perfusion, activating RAAS by secretion of renin from the kidney
  • this increases BP which increases afterload
87
Q

why is there myocyte remodelling in HF

A
  • In response to ischaemia, myocyte damage, etc.
  • Hypertrophy, loss of myocytes and increased interstitial fibrosis
88
Q

draw the HF diagram

89
Q

Left sided heart failure symptoms

A

Exertional dyspnoea

Fatigue

Paroxysmal nocturnal dyspnoea

nocturnal cough (pink frothy sputum)

90
Q

left sided heart failure signs (8)

A

–Cardiomegaly (displaced apex beat)

–3rd and 4th heart sounds

–Crepitations in lung bases

–Weight loss

–Reduced BP

–Tachycardia

–Cool peripheries

–Heart murmur

91
Q

symptoms of right sided heart failure

A

–Peripheral oedema

–Ascites

–Nausea

–Anorexia

92
Q

signs of right sided heart failure

A

–Raised JVP

–Hepatomegaly

–Pitting oedema

–Ascites

–Weight gain (fluid)

93
Q

causes of right sided heart failure

A

LVF

pulmonary stenosis

lung disease (cor pulmonale)

94
Q

Ix for heart failure

A
  • Bloods:
    • B-type Natriuretic Peptide
      • also raised in PE
    • FBC, LFTs, U&Es, BNP, TFTs
  • Cardiac enzymes:
    • troponin I, troponin T
  • CXR
  • ECG
  • Echo (TTE)
95
Q

what would you see on an HF x ray

A
  • ABCDE
    • Alveolar oedema (bats wings)
    • Kerley B lines (interstitial oedema)
    • Cardiomegaly
    • Dilated prominent upper lobe vessels
    • Pleural Effusion
96
Q

heart failure management

A
  • Lifestyle advice
  • symptomatic control
    • loop diuretic - furosemide
  • disease altering
    • ACEi - Ramipril
    • ARB if cough with ACEi - candesartan
    • BB - atenolol, propanolol, bisoprolol
      • not in asthma
    • aldosterone antagonist - spironolactone
97
Q

chronic heart failure treatment

A
  • ABCDE
    • •ACE inhibitors (ramapril) / ARB (candesartan, valsartan)
  • B-blockers (atenolol)
  • CCB and other vasodilators (amlodipine, hydralazine)
  • Diuretics and digoxin (furosemide - loop diuretic, spironolactone - aldosterone antagonist)
98
Q

what is supraventricular tachycardia

A

any tachycardia which arises from the atria or atrioventricular junction

99
Q

what is bradycardia

100
Q

what is tachycardia

101
Q

what are some pathological conditions where sinus tachycardia occurs

A

–Anaemia

–Fever

–Heart failure

–Acute PE

–Hypovolaemia

102
Q

what are the 3 types of supraventricular tachycardia

A

–Atrial fibrillation

–Atrial flutter

–Atrioventricular nodal re-entry tachycardia (AVNRT)

103
Q

what is the management of sinus tachycardia

A

–Correction of the cause

–Beta blockers to slow sinus rate (e.g. atenolol)

104
Q

what is Atrioventricular nodal re-entry tachycardia (AVNRT)

A

this is where there’s an accessory pathwat from the AV node to the SA node that restarts the cycle before ventricular contraction

most common type is wolf parkinson white where the accessory pathway is called the bundle of kent

can lead to up to 200bpm

105
Q

what is CHADS2VASc used to calculate

A

risk of stroke in AF

106
Q

what is the most common arrhythmia

A

atrial fibrillation

107
Q

what happens in AF

A

there are many smaller, disorganised contractions in the atria rather than one bigger coordinated contraction

this is mechanically ineffective

the AVN will conduct a proportion of these impulses with irregular ventricular response

108
Q

what does the pulse feel like in AF

A

irregularly irregular

109
Q

causes of AF

A
  • any condition that leads to raised atrial pressure
    • heart failure
    • hypertension
    • rheumatic heart disease
110
Q

what is the pathophysiology of atrial fibrillation

A
  • atrial activation 300-600/min
  • only a proportion of these conducted by AVN
  • HR 120-180
111
Q

What are the symptoms of atrial fibrillation

A

–Asymptomatic

–Palpitations

–Fatigue

–Heart failure

112
Q

how is the risk of stroke affected with AF

A

•5 x risk of stroke (embolism due to thrombus formed in atrium)

113
Q

what are the three principles of AF management and give an example of each

A

•Rate control:

–Beta blockers (atenolol) or CCB (verapamil, diltiazem) or Digoxin

•Rhythm control:

–Electrical DC cardioversion

–Amiodarone

•Anticoagulation with Warfarin:

–Target INR is 2-3

114
Q

how does amiodarone work

A

prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability

115
Q

how does AF look on an ECG

A
  • ’Irregularly irregular’
  • F waves
  • No clear P waves
  • QRS is rapid and irregular
116
Q

whats on chadsvasc and what does the scoring mean

A

●0 = No anticoagulation

●1 = consider oral anticoagulation or aspirin

●2 = oral anticoagulation (warfarin, rivaroxaban)

117
Q

what would you see on an ECG of atrial flutter

A

sawtooth flutter waves

118
Q

what is atrial flutter and what is the tretment

A

often associated with af

regularly irregular

atrial rate is ~300bpm and you’ll have a 2:1 or 3:1 ratio with ventricular rate

so here ventricular rate would be 150bpm

(based on how it conducts it’s a 2:1 if at 300 but don’t worry about why)

Rx is radiofrequency catheter ablation

119
Q

extrinsic causes of bradycardia

A

–Drug therapy - BB, digoxin

–Hypothyroidism

–Hypothermia

–Raised intracranial pressure

120
Q

intrinsic causes of bradycardia

A

– Acute ischaemia

– Infarction of SAN

– Sick sinus syndrome

121
Q

treatment for intrinsic causes of bradycardia

A

treat with atropine

122
Q

how does atropine work

A

competitive, reversible antagonist of the muscarinic acetylcholine receptors so it counters rest and digest

123
Q

what is sick sinus syndrome

A

sinoatrial block leads to intermittent failure of SAN depolarisation

ECG will have severe sinus bradycardia or intermittent long pauses between consecutive p waves

if symptomatic needs pacemaker insertion

124
Q

what are teh two places there can be heart block

A
  1. block in AVN or bundle of His = AV block
  2. block in lower conduction system = RBBB or LBBB
125
Q

what is the PR interval normally

A

0.12-0.2 seconds

126
Q

what is the length of the QRS complex normally

A

0.08-0.1 seconds

127
Q

what is the normal timing of the QT interval

A

0.4-0.43 seconds

128
Q

what is the RR interval normally

A

0.6-1.0 seconds

129
Q

what are the causes of heart block

A

coronary artery disease

cardiomyopathy

fibrosis of the conducting tissues (in elderly people)

130
Q

what is first degree heart block

A

delayed AV conduction leads to PR interval being prolonged more than 0.2 seconds

its asymptomatic so no treatment

131
Q

what are the two types of seconds degree heart block

A

Mobits typ I (wenckebach)

Mobitz type II

132
Q

describe Mobitz type I

A

–Progressive PR interval prolongation, until a P wave fails to conduct and a QRS is dropped —> then the cycle repeats itself

–Light headedness, dizziness, syncope

133
Q

describe mobitz type II

A

same as Mobitz type I except you don’t have the progressive lengthening of the PR and the QRS is dropped quite randomly

they may have fatigue, chest pain, SOB, syncope and postural hypotension

134
Q

causes of third degree heart block

A

CHD, infection, HTN

135
Q

Describe third degree heart block

A

all atrial activity fails to conduct to the ventricles - there is no association between atrial and ventricular activity

ventricular contractions are maintained by spontaneous escape rhythm

136
Q

what would the ECG show on 3rd degree heart block

A

P waves and QRS are totally independent of each other

p waves are said to march through

137
Q

treatment for 3rd degree heart block

A

atropine or permanent pacemaker

138
Q

how will a RBBB appear on ECG

A

M shape in V1 and W shape in V6

139
Q

causes of right bundle branch block

A

PE

IHD

ASD

VSD

140
Q

what are the causes of LBBB

A

IHD

Aortic valve disease

141
Q

what would the ECG look like in LBBB

A

W shape in V1 and M shape in V6

142
Q

equation for blood pressure

A

CO x peripheral resistance = blood pressure

143
Q

who should you suspect HTN in in clinic and how would you confirm this

A

>140/90 in clinic confirm with 24hr ambulatory BP monitor

144
Q

three things you need to Ix in HTN and how to do it

A
  • Eye problems
    • fundoscopy looking for:
      • papilloedema
      • bilateral retinal haemorrhages
  • Overall CVD risk
    • QRISK
    • fasting glucose
    • cholesterol
  • End organ damage
    • urine analysis (looking for proteinuria/haematuria)
    • 12 lead ECG (looking for past MI/LV hypertrophy)
145
Q

what is essential HTN and how common is it

A

it’s if the HTN has a primary cause

this is 95% of HTN

146
Q

name 4 secondary causes of HTN

A
  • Renal
    • CKD
  • Endocrine
    • Conn’s
  • Other
    • Coarctation of aorta
    • Pregnancy
147
Q

lifestyle advice for HTN

A
  • Stop smoking
  • Low-fat diet
  • Reduce alcohol and salt intake
  • Increase exercise
  • Reduce weight if obese
148
Q

what is the management for HTN

149
Q

name the 4 important types of valvular disease

A
  • Aortic Stenosis
  • Mitral Regurgitation
  • Aortic Regurgitation
  • Mitral Stenosis
150
Q

3 causes of aortic stenosis

A

congenital bicuspid valve

degenerative calcificaton

rheumatic heart disease

151
Q

3 types of aortic stenosis

A

Supravalvular, Subvalvular, Valvular

152
Q

when do symptoms occur in aortic stenosis

A

when valve area is about 1/4 of normal

153
Q

presentation of Aortic stenosis

A

exertional syncope

angina

dyspnoea

heart failure

154
Q

what is the gold standard for diagnosis of aortic stenosis

A

echocardiography

155
Q

can you remember the poem for types of heart block

156
Q

management of aortic stenosis

A

good dental hygeine and IE prophylaxis in dental procedures

surgical valve replacement or Transcatheter Aortic Valve Implantation (TAVI)

157
Q

management for mitral valve regurgitation

A
  • vasodilator
    • ACEi: ramipril
  • rate control: BB, CCB, Digoxin
  • diuretics to control symptoms
  • surgery if deteriorating symptoms
158
Q

causes of valve regurge

A

bicuspid aortic valve

infective endocarditis

159
Q

signs of aortic regurgitation

A

  • Collapsing (water hammer) pulse
  • Wide pulse pressure
  • Displaced hyperdynamic apex beat
  • Early diastolic murmur
160
Q

what is Mitral stenosis

A

•Obstruction of LV inflow that prevents proper filling during diastole

it’s common with AF

161
Q

management of aortic regurge

A

surgery to replace valve before LV dysfunction

162
Q

Name 3 causes of mitral stenosis

A

infective endocarditis

RA

IE

163
Q

Presentation of mitral valve stenosis

A
  • Dyspnoea
  • Fatigue
  • Palpitations
  • Chest pain…
164
Q

signs of mitral valve stenosis

A
  • Malar flush on cheeks
  • Low volume pulse
  • Tapping, non displaced apex beat
  • Rumbling mid-diastolic murmur
  • Loud opening S1
165
Q

what is shock

A

•Circulatory failure resulting in inadequate organ perfusion

Low BP below <90mmHg

166
Q

name 4 types of shock

A

septic

anaphylactic

neurogenic

hypovolaemic

167
Q

Management of mitral stenosis

A

anticoagulate with warfarin

percutaneous mitral balloon valvotomy

168
Q

describe septic shock

A

•infection with any organism –> acute vasodilation from inflammatory cytokines

169
Q

describe anaphylactic shock

A

•Type-I IgE-mediated hypersensitivity, release of histamine

170
Q

describe neurogenic shock

A

distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury

171
Q

what causes hypovolaemic shock

A

•Bleeding, trauma, ruptured aortic aneurysm, GI bleed

172
Q

investigation and management of sepsis

A
  • Sepsis 6 (bufalo) should be achieved in first hr
    • Blood cultures
    • Urine output measured
    • Fluid given
    • Antibiotics given
    • Lactate measured
      • Serum lactate >2mmol/l is indicative of tissue hypoperfusion and severe sepsis
    • Oxygen given if sats low
173
Q

what should your first approach to management of shock be

A
  • ABCDE
    • secure airway
    • assess breathing
    • assess circulation (BP and capillary refil time) and establish IV access
    • Disability
    • Environment
174
Q

what is the ECG of pericarditis

A

widespread concave ST elevation and PR depression

175
Q

55yo Caucasian Man with HTN develops renal impairment. Which of the following medications should be stopped

a. Ramipril
b. Verapamil
c. Losartan
d. Spironolactone
e. Amlodipine

176
Q

example of thiazide like diuretic

A

indapamide

Phase 2a Peer Teaching (10 decks)

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