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Finals Studying - Condensed > Cardio > Flashcards

Cardio Flashcards

1
Q

eqn for CO

A

CO = HR x SV

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2
Q

eqn for MAP

A

MAP = CO x TPR

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3
Q

normal MAP

A

70-150mmHg

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4
Q

what is MAP

A

the average arterial BP in one cardiac cycle

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5
Q

cause of 1st HS

A

closure of AV valves

mitral and tricuspid

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6
Q

what does 1st HS signify

A

start of systole

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7
Q

cause of 2nd HS

A

closure of aortic and pulmonary valves

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8
Q

what does 2nd HS signify

A

start of diastole

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9
Q

3rd HS

A

early diastolic sound

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10
Q

4th HS

A

late diastolic sound

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11
Q

normal calibration of ECG

A

25 mm/sec

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12
Q

PR interval

A

AV nodal delay

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13
Q

normal PR interval length

A

0.12-0.20 secs

3-5 small squares

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14
Q

Lead I

A

LA - RA

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15
Q

Lead II

A

RA - LL

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16
Q

Lead III

A

LA - LL

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17
Q

1 large sq on ECG - length of time?

A

0.2secs

5 large sq = 1 sec

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18
Q

QRS complex

A

ventricular depolarisation

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19
Q

normal length of QRS complex

A

< 0.12 sec

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20
Q

QT interval

A

start of the QRS to the end of the T wave

ventricular depolarization + ventricular repolarization

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21
Q

assessing axis deviation

A

left hand = lead 1
right hand = aVF

both hands up = normal
left up = LAD
right up = RAD

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22
Q

sinus tachy HR

A

> 100 bpm

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23
Q

sinus brady HR

A

< 60 bpm

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24
Q

Mx sinus brady

A

atropine 500 mcg

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25
Q

mode of action of atropine

A

non selective muscarinic antagonist -

reduces parasympathetic drive to the heart by blocking the vagus nerve

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26
Q

bradys at risk of asystole

A

recent asystole
Mobitz type II
complete heart block with broad QRS
ventricular pauses >3s

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27
Q

pathology of AF

A

fibrillating atria -
impulses don’t travel co-ordinated from the SA node to the AV node, leading to multiple wavelets of re-entry in the atria.

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28
Q

classifications of AF

A

lone
paroxysmal - self terminating. last <7d
persistent - not self-terminating. last >7d
permanent - continuous AF that cannot be cardioverted

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29
Q

sinus arrhythmia

A

physiological - beat to beat variation in the P-P interval

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30
Q

ECG in AF

A

absent P waves

irregularly irregular rhythm

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31
Q

Mx of AF if presenting acutely

A

DC cardioversion

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32
Q

which is 1st line in AF Mx: rate or rhythm control

A

rate, EXCEPT if:

  • co existent HF
  • first onset AF
  • obvious reversible cause
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33
Q

rate control Mx of AF

A 
b-blocker
rate limiting CCB (e.g. diltiazem) 
digoxin (if sedentary lifestyle) 
- any as monotherapy
- then offer dual therapy
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34
Q

criteria for attempting rhythm control on AF pts

A
  • must meet the conditions for rhythm control as 1st line
  • had symptoms for <48h
  • been anticoagulated for 4w beforehand
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35
Q

electrical rhythm control Mx of AF

A

Trans-oesophageal echo or anti-coagulation for 3/4w

then DC cardioversion

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36
Q

pharmacological rhythm control Mx of AF if no HD

A

flecanide

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37
Q

pharmacological rhythm control Mx of AF if Hx of HD

A

amiodarone

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38
Q

method for assessing anticoagulation in AF

A

CHADS2 VAS score

0 = no Tx
1 = consider (males ), no Tx (female)
2 or more = offer Tx

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39
Q

anticoagulation in AF

A

warfarin or NOAC

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40
Q

CHADS2 VAS score

A 
C = congestive HF
H = HTN 
A = age >75 = 2 
D = diabetes
S = previous stroke or TIA 
V = vascular disease
A = age 65-74 = 1
S = sex female
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41
Q

ECG in atrial flutter

A

saw tooth baseline

flutter waves

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42
Q

Mx atrial flutter

A
  1. radiofrequency ablation of tricuspid valve (curative)
  2. rate control
  3. rhythm control (pharmacological or electrical)

+ anticoagulation

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43
Q

what is AV re-entry tachycardia (AVRT)

A

a SVT

there is an accessory pathway allowing conduction re-entry between the atria and the ventricles.

i.e. AV conduction + accessory pathway

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44
Q

direction of the accessory pathway in AVRT

A

either direction - anterograde or retrograde or both

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45
Q

example of AVRT

A

wolff Parkinson white syndrome (WPW)

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46
Q

pre-excitation definition

A

when the ventricles are excited quicker via the accessory pathway as there is no AV node in this pathway to slow down conduction

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47
Q

WPW on ECG

A

regular narrow complex tachy

slurred upstroke (delta wave)

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48
Q

Mx AVRT

A

(regular narrow complex tachy Mx)

  1. vagal manoeuvres
  2. adenosine 6mg IV
  • if no effect give 12mg
  • if no effect give further 12mg
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49
Q

Mx SVT- in asthmatics

A

DONT GIVE ADENOSINE

- verapamil

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50
Q

what is AV nodal re-entry tachycardia (AVNRT)

A

a SVT

there is an entire re-entry circuit in the AV node

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51
Q

causes of AVNRT

A

caffeine
spontaneous
alcohol
beta agonists

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52
Q

AVNRT on ECG

A

regular narrow complex tachy

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53
Q

MX AVNRT

A

(regular narrow complex tachy Mx)

  1. vagal manoeuvres
  2. adenosine 6mg IV
  • if no effect give 12mg
  • if no effect give further 12mg
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54
Q

mode of action of adenosine

A

blocks the AV node

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55
Q

causes of a broad complex tachy of Supraventricular origin

A

regular:
- SVT with BBB

irregular:

  • AF with BBB
  • pre-excited AF (i.e. AF with WPW)
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56
Q

Mx of SVT with BBB

A

same as for regular narrow complex Mx

  1. vagal manoeuvres
  2. adenosine 6mg IV
  • if no effect give 12mg
  • if no effect give further 12mg
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57
Q

Mx AF with BBB

A

Tx as for irregular narrow complex Mx

  1. rate control with b blocker or diltiazem
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58
Q

Mx of pre-excited AF

A

consider amiodarone

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59
Q

what medicine should not be given in pre-excited AF

A

adenosine!!
this blocks the AV node and increases conduction down the aberrant pathway, and if they’re in AF this will make them more likely to go into VT or VF.

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60
Q

supraventricular ectopics

  • what are they
  • ECG appearance
A

ectopic beat from the atria

ECG: premature P wave in the ST seg of sinus beat previously

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61
Q

what is a junctional rhythm

A

origin of the electrical impulse at the AV node, so electrical impulses travel up to atria and down to ventricles simultaneously.

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62
Q

cause of a junctional rhythm

A

digoxin toxicity

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63
Q

junctional rhythm ECG

A

inverted P wave after the QRS complex, in the ST segment

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64
Q

bigeminy ventricular premature complex

A

1 sinus beat - 1 ventricular premature complex

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65
Q

trigeminy ventricular premature complex

A

2 sinus beats - 1 ventricular premature complex

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66
Q

how to distinguish between VT and SVT with aberrancy

A

give adenosine - blocks AV node

no response = increase likelihood of VT

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67
Q

monomorphic VT Mx

A

IV amiodarone

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68
Q

most common cause of VT

A

MI

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69
Q

most common cause of polymorphic VT

A

prolongation of the QT interval (many causes)

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70
Q

polymorphic VT = ?

A

torsades de pointes

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71
Q

Mx polymorphic VT

A

IV magnesium sulphate 2g over 5min

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72
Q

ECG VF

A

no clear discernable waveforms

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73
Q

Mx VF

A

ALS Mx

150J DC shock
amiodarone 300mg IV after 3 shocks

74
Q

1st degree heart block

A

prolongation of PR

stable

75
Q

Mobitz type 1 heart block

A

type of 2nd degree HB

progressive PR lengthening
then eventual missed ventricular beat

76
Q

Mobitz Type II heart block

A

type of 2nd degree HB

constant PR interval, with eventual missed beat

77
Q

types of 2nd degree heart block

A

Mobitz type I

Mobitz type II

78
Q

3rd degree heart block

A

no relationship between P wave and QRS complexes

79
Q

Mx 3rd degree heart block

A

bradycardia algorithm

IV atropine 500mcg + isoprenaline

Transvenous pacing insertion

80
Q

LBBB

A

WilliaM

V1 = W
V6 = M
81
Q

RBBB

A

MorroW

V1 = M 
V6 = W
82
Q

3 features of typical anginal pain

A
  1. substernal chest discomfort
  2. pain brought on by exertion
  3. pain is relieved by rest or GTN
83
Q

criteria for a pt to have ‘atypical’ angina pain

A

2 of the features of typical angina

84
Q

Mx stable angina

A

(all get: lifestyle changes + aspirin + statin + GTN)

  1. B-blocker or CCB
    - rate limiting CCB (verapamil or diltiazem)
  2. Dual therapy
    - (CCB must be switched to nifedipine - cant co-prescribe b blocker and verapamil!)
  3. if not tolerating addition of dual therapy, give either:
    - long acting nitrate
    - ivabradine
    - nicorandil
    - ranolazine
  4. PCI or CABG - if max therapy unsuccessful
85
Q

cause of angina

A

atherosclerotic plaque forms physical blockage in the lumen of the coronary artery.

86
Q

cause of MI

A

rupture of atherosclerotic plaque, causing complete blockage of the coronary artery.

87
Q

unstable angina presentation

A
  • new ST depression or T wave inversion in the presence of ischaemic sympt
  • prolonged angina at rest
  • NO increase in cardiac biomarkers @ 12h
88
Q

NSTEMI presentation

A
  • new ST depression or T wave inversion in the presence of ischemic sympt
  • INCREASE in cardiac biomarkers @12h
89
Q

STEMI presentation n

A
  • new ST elevation or new LBBB in the presence of ischemic symptoms
  • INCREASE in cardiac biomarkers @12h
90
Q

Initial Mx of ACS

A

‘MONA + T’

M = morphine 10mg in 10ml slow IV
O = oxygen if sats <94-98%
N = sublingual GTN
A = aspirin 300mg PO (then 75mg OD) 
T = ticagrelor 180mg PO (then 90m OD )
91
Q

timeframe for PCI in STEMI

A

<2h

if >2h, thrombolyse

92
Q

timescale for PCI in NSTEMI or UA

A

if haemodynamically unstable - immediately

if intermediate GRACE score - within 3 d

if low risk GRACE score - as out pt

93
Q

long term Mx ACS

A

CVS risk reduction:

  • aspirin (lifelong)
  • ticagrelor (12m)
  • BP control

B-blocker
ACEi
GTN

94
Q

Mx heart failure

A
  1. ACEi + Beta-Blocker
    • Spironolactone
    • Ivabradine
    • Digoxin or Hydralazine/Isosorbide mononitrate

(Loop Diuretic - furosemide for symptom relief)

95
Q

Ix for HF

A
  1. Basic bloods, incl BNP level or NT-proBNP level, urinalysis, ECG, CXR
  2. Echo
96
Q

ECG findings in HF

A

non-specific:

  • pathological Q waves
  • left bundle branch block
  • left ventricular hypertrophy (LVH)
  • atrial fibrillation
  • non-specific ST and/or T-wave changes
97
Q

Mx acute HF

A

‘PODMAN’

P = position
O = oxygen (high flow)
D = diuretic (IV furosemide 40mg stat) 
M = morphine 
A = anti-emetic 
N = nitrates
98
Q

pathology of left HF

A

low CO from left heart.

blood backs up into L atrium - pulmonary veins - lungs.

99
Q

presentation left HF

A 
pulmonary oedema 
orthopneoa 
paroxysmal nocturnal dyspnea 
cough (pink frothy sputum) 
3rd HS
100
Q

orthopnoea

A

SOB when lying flat

101
Q

CXR appearance in HF

A

‘ABCDE’

A = alveolar oedema 'bats wings'
B = kerley B lines
C = cardiomegaly 
D = dilated prominent upper lobe vessels
E = pleural effusion
102
Q

pathology of right HF

A

low CO from right heart.

blood flows back up into R atrium - SVC - peripheral.

103
Q

presentation right HF

A 
peripheral oedema
elevated JVP
hepatomegaly 
ascites
normal CXR
104
Q

pt has clinic BP reading >140/90 mmHg - whats the next step

A

ABP< (24h monitoring) or HBPM

105
Q

pt has ABPM of <135/85mmHg - what happens next

A

monitor - not HTN.

106
Q

pt has ABPM of >135/85mmHg - what happens next

A

they have stage 1 HTN

only get Tx if <80y and any of:

  • target organ damage
  • CVS disease
  • renal failure
  • diabetes
  • 10y CVS risk >20%
107
Q

pt has ABPM of >150/95mmHg - what happens next

A

they have stage 2 HTN

  • start drug Tx for HTN
108
Q

Drug Mx HTN

A
  1. < 55 - ACEi
    > 55 or Afro-Caribbean - CCB
  2. A + C
  3. A + C + D
    • spironolactone (if K <4.5)
      + thiazide like diuretic (if K >4.5)
    • alpha blocker or beta-blocker
109
Q

primary prevention statin dose

A

atorvastatin 20mg

110
Q

secondary prevention statin dose

A

atorvastatin 80mg

111
Q

what are statins also called

A

HMG-CoA reductase inhibitors

112
Q

why should simvastatin be taken at night

A

have short half life - most cholesterol is synthesized at night when dietary intake is low

113
Q

ECG lead changes - inferior MI

A

II, III, aVF

114
Q

coronary artery affected - inferior MI

A

right coronary artery

115
Q

ECG lead changes - anterior MI

116
Q

coronary artery affected - anterior MI

A

left anterior descending artery

117
Q

ECG lead changes - posterior MI

A

reciprocal changes in V1-V2

118
Q

ECG lead changes - lateral MI

A

I, aVL, V5-V6

119
Q

coronary artery affected - lateral MI

A

left circumflex artery

120
Q

PAILS mnemonic

A 
P = posterior 
A = anterior 
I = inferior 
L = lateral 
S = septal

ST elevation in these leads commonly causes reciprocal ST depressions in the corresponding leads in the next letter

121
Q

rheumatic fever

A

autoimmune disease that can occur following Group A strep infection

122
Q

presentation rheumatic fever

A 
fever
joint pains
chest pain 
SOB 
swollen joints
123
Q

common heart murmur in rheumatic fever

A

mitral regurg

124
Q

Mx rheumatic fever

A

IM benzathine benzylpenicillin

125
Q

cause of acute native valve endocarditis

126
Q

causes of subacute native valve endocarditis

A

strep viridans

enterococcus

127
Q

valve usually affected by IVDU endocarditis

128
Q

cause of prosthetic valve endocarditis

A

coagulase negative staph

129
Q

acute endocarditis

  • how quickly does it present
  • presentation
A

days - weeks

spiking fevers, tachy, fatigue

130
Q

subacute endocarditis

  • how quickly does it present
  • presentation
A

weeks - months

constitutional symptoms

131
Q

janeway lesions

A

painless macular plaques on palms and soles

- endocarditis sign

132
Q

osler nodes

A

small painful nodules on fingers and toes

- endocarditis sign

133
Q

roth spots

A

oval pale retinal lesions

- endocarditis sign

134
Q

Mx native valve subacute endocarditis

A

amox + gent

135
Q

Mx native valve acute endocarditis

136
Q

Mx prosthetic valve endocarditis or MRSA

A

vanc + gent

137
Q

systolic murmurs

138
Q

diastolic murmurs

A

need to be accentuated

139
Q

MRS ASS

A

mitral regurg + aortic stenosis

  • both systolic
140
Q

mitral valve location

A

between lt atria and lt ventricle

141
Q

tricuspid valve location

A

between rt atria and rt ventricle

142
Q

mitral stenosis

A
  • mitral valve is hardened
  • diastolic murmur
  • low rumbling mid diastolic murmur with opening snap
  • loud S1
  • malar flush
  • tapping apex
143
Q

where is mitral stenosis best heard

A
  • at the apex in the left lateral position during expiration
144
Q

mitral regurgitation

A
  • mitral valve is leaky
  • systolic murmur
  • pansystolic murmur
  • radiates to the axilla
145
Q

aortic stenosis

A
  • aortic valve is hardened, and struggles to open
  • systolic murmur
  • ejection systolic murmur
  • radiates to the carotids
146
Q

pulse in aortic stenosis

A

slow rising

147
Q

pulse in aortic regurg

A

collapsing

148
Q

aortic regurgitation

A
  • aortic valve is leaky

- diastolic murmur

149
Q

where is aortic regurg heard best

A

left sternal edge sitting forwards

150
Q

corrigans sign

A

visible carotid pulsation

  • aortic regurg
  • sign of backflow
151
Q

quinkes sign

A

red coloured pulsation in nails

  • aortic regurg
  • sign of backflow
152
Q

de mussets sign

A

head bobbing

  • aortic regurg
  • sign of backflow
153
Q

causes of acute myocarditis

A 
idiopathic 
viral (flu, HIV, hepatitis) 
bacterial 
drugs 
toxins
154
Q

presentation myocarditis

A

acute Hx

young person, chest pain, SOB, tachycardia

155
Q

typical HS in myocarditis

A

soft S1, S4 gallop

156
Q

Mx myocarditis

A

supportive

157
Q

causes of dilated cardiomyopathy

A

alcohol
HTN
viral infections

158
Q

presentation dilated cardiomyopathy

A

mitral regurg

HF sympt

159
Q

Mx dilated cardiomyopathy

A

same as for HF

160
Q

inheritance of hypertrophic cardiomyopathy

A

autosomal dominant

161
Q

typical pulse in hypertrophic cardiomyopathy

A

double apical ‘jerky’ pulse

double carotid pulsation

162
Q

ECG in hypertrophic cardiomyopathy

A

deep Q waves
LVH
non specific ST seg and T wave changes
+/- AF

163
Q

Ix used for family screening in hypertrophic cardiomyopathy

164
Q

dressler’s syndrome

A

pericarditis post-MI

165
Q

pericarditis presentation

A

acute central chest pain
worse on lying down
relieved by sitting forwards

166
Q

ECG pericarditis

A

saddle shaped ST elevation n

PR depression

167
Q

Mx pericarditis

A

NSAIDS + PPI

168
Q

what is pericardial effusion

A

accumulation of fluid within the pericardial sac, has potential to progress to tamponade

169
Q

most common cause of constrictive pericarditis

170
Q

constrictive pericarditis

A

heart is encased in a rigid thickened and fibrotic pericardium.

171
Q

beck’s triad

A

muffled HS
raised JVP
falling BP

172
Q

what is becks triad seen in

A

cardiac tamponade

173
Q

pulsus paradoxus

A

reduced BP on inspiration (cardiac tamponade)

174
Q

ECG in hypokalaemia

A 
increased amplitude of PR 
PR prolongation 
T wave flattening + inversion n
ST depression 
U waves
175
Q

ECG in hyperkalaemia

A

tall tented T waves
flattening of P wave
QRS prolongation
arrhythmia

176
Q

postural hypotension definition

A

fall in systolic BP of <20mmHg on standing

177
Q

driving own car after PCI

A

don’t need to tell DVLA

start driving aft 4 w

178
Q

driving bus or lorry after PCI

A

need to tell DVLA

not drive for 6 w, then DVLA reassesses

179
Q

J wave on ECG

A

hypothermia (small hump at end of QRS)

180
Q

half life of adenosine

181
Q

adverse effects of adenosine

A

chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

Finals Studying - Condensed (22 decks)

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