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Phase 4 - GR > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How to work out rate in ECG

A

300/ Number of squares in R-R interval

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2
Q

how long should p wave be?

A

120-200ms

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3
Q

Prolonged PR interval indicates

A

AV block

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4
Q

Shortened PR interval indicates ? What other feature of this condition do you often see on ecg

A

atrial impulse to ventricles quicker i.e. accessory pathway

associated with delta wave (slurred QRS upstroke) in Wolff Parkinson White

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5
Q

QRS normal length ?

A

80-120ms

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6
Q

Where is the j point

A

where S waves meets ST segment

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7
Q

When is ST elevation significant?

A

> 1mm in 2 or more limb leads

or >2mm in 2 or more chest leads

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8
Q

What is the t wave?

A

ventricular repolarisation

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9
Q

When is a t wave “tall” what could this mean?

A

> 5mm in limb AND >10mm in chest

associated hyperacute STEMI and hyperkalaemia

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10
Q

Inverted T wave is normal where?

A

V1 and lead III

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11
Q

Inverted t waves association?

A

ischaemia, PE, BBB

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12
Q

What is sinus bradycardia

A

<60bpm

every P wave is followed by a QRS

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13
Q

Physiological causes of sinus bradycardia?

Pathological?

A

Physiological: athletes, young due to *high resting vagal tone (vagal activity is continuous)
Pathological: acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP

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14
Q

When do you treat bradycardia

A

<40bpm / symptomatic

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15
Q

Mx of symptomatic bradycardia

A

IV atropine - anticholinergic, i.e. muscarinic antagonist, reduces vagal tone

Temporary pacing wire

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16
Q

What is sick sinus syndrome? Causes ?

A

Result of dysfunction of SA node with impairment of ability to generate impulse

Normally idiopathic fibrosis of node

ischaemia
digoxin toxicity

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17
Q

Causes of AV block

A

MI/ischemia (inferior)
SLE
myocarditis

(lyme disease endocarditis, degeneration of HIS-PURKINJE, drugs (digoxin, BB, CCB))

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18
Q

1st degree heart block is?

A

PR > 0.2s, PR constant, every P followed by QRS

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19
Q

2nd degree heart block?

A

Intermittent failure of conduction from atria to ventricles. Some P are not followed by QRS

Mobitz type I (Wenckebach) failure at level of AV node.
PR interval progressively lengthens and is then blocked.

Mobitz type II intermittent failure of P wave conduction.
PR interval is constant + prolonged. Fixed PR interval, dropped QRS waves2:1 block or 3:1 block

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20
Q

What is 3rd degree heart block? Usual cause?

A

Complete failure conduction atria to ventricles

myocardial fibrosis

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21
Q

Name 3 causes of RBBB

A

Rheumatic heart disease
RVH
IHD, myocarditis, cardiomyopathy, degenerative disease conduction system

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22
Q

Name 2 changes on ECG of RBBB

A

MarroW
QRS > 0.12s

Secondary R wave in V1, V2 - RSR’ [Seconary R in RBBB]

Deep, wide slurred S wave in I, V5, V6

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23
Q

LBBB associated conditions. Name 2

A

Coronary artery disease, hypertensive heart disease, dilated cardiomyopathy, anterior infarction

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24
Q

Name 2 ECG changes in LBBB

A

WilliaM

Wide QRS > 0.12s

Absent Q in V5, V6

Broad R in I, V5, V6

Deep S in V1, V2 [Long S in LBBB]

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25
Q

Ix in brady?

A

12 lead ECG

electrolyte imbalance
UE, glucose, Ca, Mg, TFT, toxicology

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26
Q

Mx of brady

A

Treat cause - correct electrolytes / stop negative chronotropes

IV atropine 0.5mg (may repeat up to 3mg)

Poor response - transcutaneous pacing

\9May also try glycopyrrolate (antimuscarinic), glucagon (if due to BB or CCB))

Temporary or permanent pacing (esp @heart block, sick sinus)

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27
Q

What Sx do you get with sinus tachy and why?

A

In diastole coronary blood flow increases. As HR increases diastole shortens.

Decreased flow to heart with increased ventricular rate = angina type symptoms, chest pain, faintness, SOB

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28
Q

Definition and Some causes of sinus tachy

A

Every P followed by QRS, rate over 100

Physiological: exertion, anxiety, pain

Pathological: fever, anaemia, hypovolaemia

Endocrine: thyrotoxicosis, phaeo

Pharmacological: sympathomimetic, adrenaline, alcohol, caffeine, salbutamol

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29
Q

Ix in sinus tachy

A

12 lead ECG, cardiac enzymes, FBC (anaemia), TFT

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30
Q

Mx acute regular sinus tachy

Mx ongoing sinus tachy

A

Vagal manoeuvres: carotid massage (young pt due to stroke risk),

*vasalva manoeuvre (forceful exhalation against closed airway with nose pinched),

facial immersion in cold water

Ongoing:
BB
or non-dihydropyridine CCB (diltiazem, verapamil)

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31
Q

Eg of some SVTs

A

AF / fibrilation
Sinus tachy
AV re-entry tachy ….

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32
Q

What is the most common cause of paroxsysmal narrow complex tachy cardia (SVT) ? Usual onset?

A

AV nodal re entry tachy

late teens / 20s

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33
Q

ECG of SVT? Name 2 things

A

Regular rhythm, narrow QRS, rate 130-250

Retrograde atrial conduction: inverted P waves in II, III, AVF (inferior)

Atrial and ventricular depolarisation together - P waves buried in QRS

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34
Q

Mx of AVNRT (its an SVT)
1/2nd line?
prophylaxis?
curative?

A

First line: Vagal maneuvers may stop as transiently block AV node

Second line: *Adenosine (for junctional) can acutely stop as transiently blocks AV node. Feel like death.

Prophylaxis: one of the above or a BB

Curative: radiofrequency ablation

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35
Q

What is the delta wave seen in WPW ?

A

Slurred upstroke of the QRS

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36
Q

Mx of WPW
Acute?
Prophylaxis?
Currative?

A

Vagal maneuvres ± adenosine

Prophylaxis: drug for AV node and accessory: flecainide (1c) or sotalol (3)

Curative: radiofrequency ablation

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37
Q

Main complications of narrow complex SVT?

A

MI

HF

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38
Q

Mx of complications of Narrow SVT

If BP<90, chest pain (MI), heart failure, heart rate >200

A

DC cardioversion with general anaesthetic

± IV amiodarone (150mg IV over 10 mins)

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39
Q

Rhythm in AF

A

Irregularly irregular ventricular rhythm

Paroxysmal = spontaneous termination within 7 days
Persistent = 7 days to one year
Permanent = over a year

Risk factors:

  • old age
  • family history
  • male
  • obesity

Causes:

  • Ischaemia - MI
  • infection - myocarditis, endocarditis
  • structural - mitral stenosis or any valvular disorder
  • hyperthyroid
  • hyper K

Symtptoms:

  • palpitations
  • syncope
  • dizziness
  • chest pain
  • fatigue
  • SOB

Signs:

  • hypotension
  • irregularly irregular pulse
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40
Q

Main complications of AF

A

Rapid chaotic atrial firing causes stagnation of blood in atria leads to thrombus formation and risk of embolism leading to increased risk of stroke

Reduction of cardiac output (esp in ex) may lead to heart failure

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41
Q

Mx of AF

A

Rate control:
First line: standard BB or rate limiting CCB (diltiazem, verapamil)
Dual therapy add digoxin or two of above (**ONLY DILTIAZEM)

Rhythm control
Persist over 48 hours offer electrical cardioversion (DC) (transoesophageal)
Consider amiodarone for 4W before + 12M after

Anticoagulate

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42
Q

When can you not use fleicanide for AF?

A

Ischemic / structual cause

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43
Q

What to do if drug Mx fails in AF?

A

left atrial catheter ablation (if paroxysmal) or pace and ablate (if permanent) (AV node)

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44
Q

What is meant by pharmacological cardioversion

A

IV amiodarone

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45
Q

ECG of atrial flutter

A

Atrial rate 300 - no p waves *F waves

Undulating saw-tooth Flutter waves

Regular ventricular rhythm 150bpm (2:1 and 4:1 common)

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46
Q

Causes of Atrial flutter

Name 2

A

CAD, HTN, hyperthyroid, obesity, alcohol, COPD

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47
Q

Ix in atrial flutter

A

TFT, FBC (anaemia precipitates HF), UE (potassium), renal func, LFT/coag for warfarin
Imaging: echo for underlying cardiac function

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48
Q

Mx of atrial flutter

A

Rhythm control: cardioversion or medications

  • DC cardioversion (if >48hours ensure adequate anticoag)
  • Or IV amiodarone, sotalol, fleicanide
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49
Q

Mx of recurrence of atrilal flutter

A

radiofrequency catheter ablation

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50
Q

Management of broad complex tachy?

what to monitor?

If unstable?

A

Support ABC, O2 and venous access

Monitor ECG, BP, sats

Identify and treat reversible cause e.g. electrolyte abnormalities potassium

Unstable:
DC schock
Or AMIODARONE 300mg IV over 10-20 mins

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51
Q

What should you consider long term and why for VT

A

It is usually due to damage so requires maintenance anti-arrhythmics (BB/CCB)
or consider ICD implantable cardioversion defibrillator

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52
Q

What does torsades de points look like on ECG?

A

Like a sound wave

(In sinus:
Prolonged QT and prominent U wave
In tachycardia:
Varied axis and varied amplitude QRS)

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53
Q

What may happen to torsades if untreated?

A

Deteriorate to VF

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54
Q

Mx torsades?

A

IV magnesium sulphate

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55
Q

What does VF look like on ECG?

A

Chaotic (varying amplitudes)
No identifiable P, QRS, T
Rate 150-500

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56
Q

Mx of VF acute? long term?

A

Defibrillation

Long term:
BB and ICD (implantable cardioverter defibrillators)

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57
Q

Mx of brugada?

A

ICD implantable cardioverter defibrillator

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58
Q

What is the brugada sign?

A

Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T

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59
Q

ECG finding in PE

A

*Sinus tachycardia - main finding

S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10%

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60
Q

ECG of hypothermia

A

brady

```
J wave
Late delta wave, positive deflection at junction of QRS and ST segment
~~~

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61
Q

What is amiodarone used for?

A

For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work

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62
Q

Some adverse affects of amiodarone? name 2

A

Hypotension during IV infusion.

Chronic use 
lungs (pneumonitis), 
heart (AV block), 
liver (hepatitis), 
skin (grey discolouration),
thyroid (long half life - hypothyroidism / thyroid crisis)
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63
Q

Adenosine use?

A

First line diagnostic and therapeutic in SVT (inc junc)

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64
Q

What is important thing about adenosine

A

Pt feels like they gonna die for a bit

Blocks SA and AV node - causes bradycardia and asystole - doom feeling
May induce bronchospasm in asthma or COPD

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65
Q

What to do when giving adenosine

A

must always monitor with continuous ECG

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66
Q

Digoxin uses?

A

Reduce ventricular rate (AF, AFl) - after CCB or BB

Severe heart failure - 3rd line

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67
Q

Important to remeber with digoxin

A

low theraputic index

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68
Q

which drugs have bad interactions with digoxin

A

Loop + thiazide diuretics cause hypokalaemia - toxicity

Amiodarone, CCB, spironolactone all increase plasma digoxin - toxicity

SAC those drugs if you’re gonna use them with digoxin you must be LOOPY

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69
Q

How do you monitor for digoxin toxicity?

What target level in blood?

A

Monitor symptoms (or vent rate) + ECG + renal dysfunction + hypokalaemia

(Sx - Nausea, vomiting, diarrhoea, dyspnoea, confusion, dizziness, headache, blurred vision)

Target blood conc
Target 1.0-1.5nmol/l
Above 2.0nmol/l suggests toxicity

ST-segment depression - reverse tick sign

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70
Q

CCBs uses

A

Rate control in SVT inc AF +AFl

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71
Q

Why should you not give CCB with BB

A

both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole

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72
Q

When ar BBS used 1st line?

A

IHD reduce angina
CHF improve prognosis
AF reduce rate and maintain sinus rhythm
SVT to restore sinus rhythm

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73
Q

SE of BBs

A

Fatigue, cold extremities, headache, impotence

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74
Q

When are BBs CI ? how to mitigate?

A

Asthma - B2 blockade causes bronchospasm, usually safe in COPD

Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol)

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75
Q

Where to listen for heart valves

A

Mitral area - apex midclavicular, 5th IC

Tricuspid - inferior right sternal (4th IC)

Pulmonary - left 2nd IC next to sternum

Aortic - right 2nd IC next to sternum

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76
Q

What position are mitral murmurs best heard?

A

@apex + radiate to axilla, heard best in left lateral position

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77
Q

MR murmur

A

pansystolic

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78
Q

MS murmur?

A

Loud opening snap S1 and mid-diastolic murmur

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79
Q

How to differentiate between MR / TR

A

Both pansystolic but TR does not radiate to axilla

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80
Q

PS murmur ? Interesting fact?

A

Crescendo-decrescendo systolic (louder then softer).

disappear on inspiration

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81
Q

PR murmur

A

early diasolic

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82
Q

When are aortic murmurs best heard?

A

holding breath

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83
Q

AS murmur?

A

Crescendo-decrescendo systolic

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84
Q

Aortic regurge best heard?

A

Early diastolic best heard leaning forward on breath hold (pulmonary diappears)

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85
Q

Usual cause of AS

A

Senile calcification

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86
Q

triad of SX in AS

A

chest pain (predisposes to chest pain),

heart failure (obstruction -> LV hypertrophy -> LV failure),

syncope (insufficient blood)

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87
Q

o/e AS?

A

Slow rising pulse

Narrow pulse pressure (diff between syst and dia)

LV hypertrophy -> apex thrill

Crescendo-decrescendo early systolic murmur heard at R2IS transmitted to carotids

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88
Q

What Ix confirms Dx of AS? other Ixs?

A

Echo

ECG
CXR

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89
Q

Mx of AS ? what if not fit for sugery?

A

Avoid heavy exertion, modify RF for CAD

If symptomatic - prompt valve replacement - first line

If not fit for surgery
Second line - balloon valvuloplasty - risk of re-stenosis
TAVI - transcatheter aortic valve replacement

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90
Q

Complications of mechanical heart valves

A

Predisposition to infective endocarditis

Small emboli

Decompensation - increased pressure in pulmonary - CHF

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91
Q

How to prevent IE with new heart vlaves

A

ABX prophylaxis

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92
Q

Target INR in valve replacement

A

Anticoagulate mechanical heart valves

Target INR 2.5-3.5 for aortic

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93
Q

Causes of AR

A 
Bicuspid 
rheumatic fever 
IE 
collagen 
Marfans / ehler danlos / turners
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94
Q

How does AR present?

A

SOBOE/non specific or symptoms of left heart failure (orth, paroxysmal nocturnal dyspnoea)

95
Q

Seen o/e AR?

A

Early diastolic murmur as R2IS sitting forward in expiration not well transmitted to carotids

Collapsing water hammer pulse

Wide pulse pressure

96
Q

What might be seen on CXR of AR?

A

signs of hf due to volume overload

97
Q

AR is monitored regularly. What is the drug mx of AR. If HTN/HF? Marfans?

A

With HF or HTN - ACE-I or A2RB

With Marfan’s - BB to slow aortic root dilatation

98
Q

Mx if SX in AR / deterioration of LV function

A

valve replacement

99
Q

Normal size of mitral? when is MS servre?

A

4-6cm2, severe if 1cm2

100
Q

What sx can present due to a large LA in MS

A

hoarseness

dysphagia

101
Q

O/E of MS

A 
Malar flush (CO2 retention), raised JVP, RVH - 
laterally displaced apex/RV heave (4th intercostal tricusp), 
signs of RHF (hepatomegaly, ascites, peripheral oedema)

Mid-late diastolic murmur best heard in left lateral
Loud S1 with opening snap

102
Q

Seen on CXR of MS if progressing to RHF

A

LA enlargement, interstitial oedema (Kerley A/B lines), prominent pulmonary vessels

103
Q

MR Mx if signs of LV dysfunction / AF?

A

Surgery

104
Q

how often do you monitor MR

A

6/12

105
Q

whatt causes rheumatic fever

A

Group A beta haemolytic streptococci (pyogenes)

106
Q

When does rheumatic fever occur? and what is affected?

A

2-4 weeks post streptococcal pharyngitis or skin infection

Joints, skin, heart, nervous system

107
Q

What blood test can provide evidence of strep infection

A

antistreptolysin O titre

or DNase B titre

108
Q

Which criteria used for rheumatic fever

A

jones

109
Q

Ix rheumatic fever

A

Evidence of streptococcal: throat culture, antistreptococcal antibodies (ASO, *anti-DNase B) rise during first month. Check 2 weeks apart for a rise

ECG: PR, ST elevation (saddle shape) suggests pericarditis

CXR - ?heart failure

FBC (WCC), ESR, CRP

Doppler echo for carditis

110
Q 
Mx of rheumatic fever.
how to eradicate strep? 
If HF? 
supress inflammation? 
if they have chorea?
A

Enforce bed rest till inflam markers normal

Eradicate strep - single IV benzylpenicillin + oral penicillin

Treat HF: diuretics, ACEI and digoxin

Suppress inflammation: NSAIDs

For chorea: self-limiting, may suppress with haloperidol (beware EPSE)

111
Q

Fever + new murmur is what

A

= endocarditis until proven otherwise

112
Q

IE RFs

A

Valve: disease, replacement

Congenital structural heart

Previous IE

Hypertrophic cardiomyopathy

IVDU

113
Q

Most common pres of IE? Name 3 signs

A

*Majority are fever + chills + poor appetite + wt loss

FROM JANE
Fever > 38 + tachycardia

Roth’s spots - eyes, retinal haemorrhage with pale centre

Osler’s nodes - painful red blisters @ terminal phalanges and toes

Murmur - Tricuspid with s.aureus

Janeway lesions - painless red maculae on thenar eminence

Anaemia/Arthritis: subacute = asymmetic > 3 jts, acute = septic monoarticular

Nail haemorrhage - splinter - red and linear

Embolic phenomena e.g. stroke

114
Q

Which bug is most common for IE? and which murmur is classic from it?

A

s aureus
tricuspid

[strep viridans is next most]

115
Q

Main complications of IE

A

MI / pericarditis
glomerulonephritis
stroke / embolic

116
Q

Ix in IE

A

FBC (WCC, anaemia), ESR/CRP, RF

Transthoracic echo within 24 hours

Blood cultures (subacute or chronic = 3 sets from peripheral sites with 6hrs between them, acute = start ABX then take 2 within 1 hour)

CXR

ECG

117
Q

How long are you gonna give IV ABx for IE? which for staph / strep?
MRSA?

A

4 weeks
staph - fluclox
srep - benpen

MRSA - vanc

118
Q

General Ix for cardiomyopathy

A

Bloods: FBC, ESR, U+E, LFT, cardiac enzyme, TFT

CXR

ECG: usually abnormal

Transthoracic doppler echocardiography: can confirm Dx of hypertrophy and exclude valvular

MRI: to distinguish constrictive and restrictive disease

119
Q

HF CXR features

A

ABCDE (alveolar oedema - bat wing, kerley B - interstitial, cardiomegaly, dilated upper lobe vessels, pleural effusion

120
Q

what is the Most common cause of sudden cardiac death in young people and athletes and what kills them?

A

hypertrophic cardiomyopathy

arrythmia / LV outflow tract obstruction

121
Q

what usually causes myocarditis

A

coxackie virus

122
Q

Ix for myoocarditis.

A

FBC - leukocytosis, ESR or CRP (75%), Cardiac enzymes: CK, TrI, TrT

+ve Viral serology

*Gold standard - endomyocardial biopsy

ECG: ST elev/dep + T wave inversion

CXR: normal cardiac silhouette but other signs of heart failure

123
Q

typical sx of HF

A

breathless, fatigue, ankle swelling

124
Q

typical signs of HF

A

tachycardia, tachypnoea, pulmonary rales, pleural effusion, raised JVP, peripheral oedema, hepatomegaly

125
Q

What EF is usual cut off for HF

A

<40%

126
Q

differenece between LHF / RHF in presentation

A

RHF: peripheral oedema, abdo distension (ascites), facial engorgement, pulsing in neck and face (tricuspid regurg)

LHF: dyspnoea, fatigue, cold peripheries, muscle wasting, orthopnoea, PND, nocturnal cough - pink frothy sputum

127
Q

If previous MI and new HF what Ix and when?

A

2 week wait for specialist and doppler echo

LV func, diastolic func, LV thickness, valvular disease

128
Q

General Ix for HF

A

BNP - if high -> 2 week wait for echo

ECG

FBC, UE, Cr, LFT, glucose, fasting lipids, TFT, consider cardiac enzymes

CXR

ejection fraction

129
Q

Acute Mx of HF ?
when stable?
Monitor what?
when to follow up?

A

A-E

Oxygen + IV diuretics (furosemide) [F for failure, O is a heart]
± NIV (only if severe dyspnoea + acidaemia) or IV (if resp failure or reduced conc)

Monitor ECG and ABG, catheterise them!!!

When stable: BB (bisoprolol or metoprolol) + ACEI (or ARB) + aldosterone antagonist (spironolactone)

*monitor renal function, electrolytes, HR and BP for diuretics and BB

Follow up in 2 weeks

130
Q

Chronic HF mx (no LV dysfucntion)

A

Lifestyle (ex, smoking, alc, diet), patient education, depression

Annual influenza vaccination, pneumococcal vaccination (once only) - prophylactic

Inform DVLA, air travel likely ok

Manage comorbities: HTN, prevention MI, diabetes

Anticoagulants + statins

131
Q

Mx LV dysfunction in HF 1/2/3 line?

If Hx of ventricular arrhythmia?

A

ACEI + BB (start low and increase dose)

Add Aldosterone antagonist (spironolactone), ARB or hydralazine with nitrate - monitor K+

Third line: digoxin or ivabradine

Implantable cardioverter defibrillator [if previous ventricular arrhythmia]

132
Q

4 stages of atherosclerosis

A

1 fatty streak
2 intimal hyperplasia
3 fibrous cap
4 plaque formation

133
Q

How do statins work?

A

hmg-coa refuctase inhibitors

134
Q

when might you prescibe statins

A

QRISK2 > 10% (10 year risk) - primary prevention if <84
History of CVD
Familial hypercholesterolaemia
Anyone over 85

135
Q

statin SEs

A

myalgia (stiff, weakness, cramps)

136
Q

What should you monitor with statins

A

LFTS

137
Q

2 modifiable and 2 unmodifiable RFs for HTN

A

Modifiable: smoking, weight, alcohol, stress, exercise, dietary salt

Non-modifiable: old, fam Hx, ethnicity, gender

138
Q

name 3 secondary causes of HTN

A

Renal disease: intrinsic (75%) i.e. glomerulonephritis, polyarteritis nodosa, systemic sclerosis, PCKD, or renovascular renal artery stenosis -> increased renin by decreased perfusion

Endocrine: cushings, conns, thyroid, phaeo, acromegaly, hyperparathyroid

Coarctation aorta

Pre-eclampsia and pregnancy

Drugs - decongestants, COCP, steroids

139
Q

how to calculate BP

A

CO X TPR

140
Q

Some end organ damage in HTN . NAME 3

A

Brain - Encephalopathy: seizure, vomiting, nausea

Dissection - delayed/weak femoral pulses

Pulmonary oedema - heart failure

Nephropathy - proteinuria ± loin bruit

Eclampsia

Papilledema

Retinopathy (hypertensive)

141
Q

what might be seen on retinopathy of HTN

A

Grade 1: tortuous retinal arteries + silver wiring

Grade 2: AV nipping

Grade 3: flame haemorrhages and cotton wool spots

Grade 4: papilloedema

142
Q

Htn general Ix

A

Urine dipstick (protein + blood), serum Cr and electrolytes (K+ low = Conn’s, Ca+ high = hPTH) , renal USS

12 lead ECG (LVH or heart failure) + echo

Fundoscopy

Lipids and FBG

143
Q

What Ix in HTN for 2ndary cause

Neuroendocrine tumors?

Coarcation

Thyroid

Cushing

Hypokalaemia

Renal artery stenosis

Phaeo

A

24 hr VMA -Vanillylmandelic Acid (for neuroendocrine tumors)

MRI / echo - coarcatation

TSH

Urinary free cortisol and dexamethasone suppression test - cushing

Renin/aldosterone levels - hypoK

MRI renal arteries

24hr mepinephrines

144
Q

HTN pharmacological mx

A

<55 - ACEi /ARB
>55 CCB (amlodipine)
Dual therapy

add indapamide (thiazide like diuretic)

resistant 
add spironolactone (if low potassium) or increase TLD (if high potassium
145
Q

common se of amlodipine

A

ankle swelling

146
Q

Target BP in HTN

A

<140/90

147
Q

Ischemia and arteries / leads on ECG

A

Anterior leads
v3/v4 - LAD

Lateral leads
1 V5, V6 - circumflex

Inferior leads
II, III, aVF - RCA

Septal leads
V1,V2 LAD

148
Q

What should you do with all new angina ?

A

Refer to Rapid Access Chest Pain Clinic for confirmation of Dx and severity assessmentUrgently - within 2 weeks

149
Q

DDx angina

A

Pain over 5 mins - MI

Acute pericarditis - worse on inspiration, lying flat, swallowing

MSK - worse on mvmt

GORD

Pleuritic pain - sharp pain on deep inspiration, ?pneumonia or PE

150
Q

Ix in anginaa

A

ecg - can see ischemic changes with excercise stress test
-ST flattening / inversion

FBC (anaemia),

FBG (diabetes),

FBChol/triglycerides,
LFT (baseline before statin)
\U+E (renal func),

TFT (increased work, hypo assoc cholesterol)

151
Q

key non pharmacological mx of stable angina

A

modify Rfs

patient education

152
Q

pharmacotherapy of stable angina

A

GTN

1st
BB or CCB

2nd combine - only amlodipine as CCB

3rd Add ivabradine

Reduce caridac RFs

  • aspririn / clopidogrel
  • could give statin
153
Q

What if angina cant be controlled by pharmacology

A

CABG / PCI

154
Q

Ix in ACS
ECG - What does ST elevation / depression suggest?
Pre existing CAD?

Name 2 cardiac enzymes?
When are they most sensitive - how long do they last?

2 other Ix?

A

12 lead ECG
ST elevation - transient = angina, fixed = acute infarction
ST depression or T wave inversion = unstable angina or NSTEMI
Pre-existing CAD = LVH, Q waves

T wave inversion = previous MI,
Pathological Q waves = ongoing or old MI

Cardiac enzymes: troponin T, troponin I, CK-MB (creatinine kinase), AST, LDH, CK

troponins most sensitive (3-6 hours post infarct - max at 12-24 hours, persist 14 days) *test troponins at 6 and 12 hours
[CK-MB is cardiac specific, troponins are a marker for cardiac necrosis but also marker for skeletal muscle injury]

Bloods: FBC (anaemia and baseline for anticoagulants), blood glucose (hyperglycaemia is common = poor prog), renal function, electrolytes, lipids, TFT

Imaging: CXR (complications of ischaemia i.e. pulmonary oedema etc. , or PE, pneumothorax, TAA), TTE wall motion abnormalities

155
Q

mx for all ACS

A

Resuscitation: ABCDE (IV fluids)

Pain: GTN + intravenous opioid with antiemetic (morphine + metoclopramide)

Dual antiplatelet: loading dose *300mg aspirin + ticagrelor 180mg

Assess O2 sats: give high flow O2 if <94%

Monitor with 12 lead ECG

—-> PCI if within 120 mins vs fibrinolysis

156
Q

What scale is used to assess 6 month mortality post acs? what to do if risk is over 1.5%?
Over 3% ?
surgical option?

A

GRACE

<1.5%
loading dose 300mg clopidogrel and continue for 1year

<3%
coronary angiography

PCI / CABG

157
Q

Mx of STEMI

A

MONA
Morphine, Oxygen, Nitroglycerin and Aspirin

ECG

GRACE

Reperfusion - either PCI [if within 120mins] / fibronolysis

158
Q

Eg of drug used for fibronolysis

A

altepase

streptokinase

159
Q

key non pharma changes forpost acs

A

Discuss secondary prevention, lifestyle changes, smoking cessation

160
Q

Whats given post MI ? what do you monitor?

A

ABSeeD

ACEI,

BB,

statin,

dual antiplatelet (aspirin + clopidogrel),

monitor BP, monitor renal function, assessment of LV function

Aspirin action = inhibits COX irreversibly

161
Q

Driving post ACS?

A

4 weeks off driving,

1 week if treated by angioplasty

162
Q

What is dresslers syndrome?

A

Post ACS

late pericarditis, inflammatory reaction in response to necrotic tissue

occurs at *2-8 weeks - severe chest pain, worse supine, *left ventricular thrombosis in 20% post infarct and 60% if large anterior

163
Q

name 3 coplications post MI

A

DEPARTS + fails

Death, dresslers
Electrical: tachy + bradyarrhythmias
Pericarditis (acute), papillary muscle rupture
Aneurysm -> persistent ST elevation
Re-MI / rupture - tamponade
Thrombus - stroke
Shock - cardiogenic
VSD
Heart failure - pulmonary oedema
164
Q

Unresponsive cardiac arrest

A

999
A+B (if breathing turn to recovery)
C - CPR 30:2, when airway secured = uninterrupted compressions and ventilate at 10/min
D defibrillator: AED automated external defibrillator
Complete 2 minutes of CPR between debif attempts
After 3rd shock give adrenaline + amiodarone
2 minutes CPR
Adrenaline
2 minutes CPR
Adrenaline

165
Q

Name 2 causes of pericarditits

A 
Viral: *coxsackie, EBV + staphylococcal/haemophilus... 
Rheum: *SLE, sarcoid + ….
Post MI: *Dressler’s 24-72 hours
Drugs: hydralazine
Other: *uraemia
166
Q

What causes granulomatous pericarditis

A

TB, sarcoid, fungal, RA

167
Q

What things aggrevate pain in pericarditis? relieve?

A
  • Aggravated by inspiration, cough, swallow, lying flat

* Relieved by sitting up and lying forward

168
Q

O/E acute pericarditis

A

pericardial friction rub

Tachypnoea, tachycardia, fever

If tamponade -> becks triad 
3xD
Decreased heart sounds (muffled)
Distended jugular veins
Decreased arterial blood pressure
169
Q

what is becks triad ?

A

Hypotension, elevated systemic venous pressure (JVP), muffled heart sounds

170
Q

Ix in pericarditis

A

serial ECGs

CXR
(globular heart if >250ml)

FBC (WCC), ESR/CRP (raised) U+E (uraemia?) cardiac enzymes (if MI)

Echo - if suspect effusion or tamponade

171
Q

mx stable pericarditis

A

Stable: rest + treat cause + NSAIDs (naproxen) ± PPI, (if uraemic consider dialysis)

172
Q

When to admit pericarditis

A

if fever, evidence tamponade, a large effusion (echo free space > 20mm), on warfarin, trauma, fail to respond NSAIDs

173
Q

Pericarditis with falling blood pressure what should you suspect ? Mx?

A

suspect cardiac tamponade - immediate peircardiocentesis with echo

174
Q

Mx of reccurent pericarditis

A

colchicine in addition to NSAIDs

175
Q

What is cardiac tamponade

A

Collection of blood/fluid/pus/gas in the pericardial space. A large volume will result in reduced ventricular filling leading to haemodynamic compromise

176
Q

mx of tamponade

A

O2 + volume expansion + increase venous return (legs up) + inotrope (dobutamine) + pericardiocentesis

177
Q

presentation of peripheral arterial disease

A

Intermittent claudication
Cramping pain in calf, thigh, buttock on walking. Symptoms worse uphill. Relieved by rest. Rest time, claudication distance.

Ischaemic rest pain
Severe unremitting pain in foot, stops from sleeping, relieved by dangling or foot on cold floor

178
Q

o/e lower limb ischemia

A

absent reduced femoral pulse

trophic changes - pale,cold, hairless, skin change

ulcers

Buerger’s angle 20 degrees = angle to which leg must be raised before it becomes pale

cap fill prolonged

179
Q

Name 2 DDx of lower limb ischemia

A

Sciatica, spinal stenosis, DVT, entrapment

180
Q

Ix for lower limb ischemia

A

BP, FBC (amaemia aggravates), ESR (giant cell arteritis), thrombophilia screen, FBG, lipids, ECG (CAD), renal function, urine dip

Doppler ultrasonography (dublex) to calculate ABPI

181
Q

What ABPI for mild/mod/severe PAD

A

<0.9 = mild PAD, <0.8 = mod, <05 = ischaemic rest pain

1 is normal

182
Q

6 ps of acute limb ischemia

A

: pale, pulseless, pain, perishingly cold, parasthesia, paralysed

183
Q

mx of acute lower limb ischemia

A

Requires re-vasc in 4-6 hours with *immediate heparinisation

184
Q

Complications of PAD

A

Acute limb ischemia
infection
poor healing
gangrene

185
Q

General Mx of PAD

A

Modify Rfs
Smoking, exercise, weight

Statins

ACEI

Manage Diabetes / HTN

Antiplatelet - clopidogrel

manage pain

186
Q

What imaging if you are considering revascularisation of PAD ?

A

Duplex USS ± CT angiography

187
Q

What is aortic dissection

A

Intimal tearing lead to disruption of media provoked by intramural bleeding. This leads to separation of the layers and formation of a false lumen

188
Q

What simple Ix in aortic dissection for a key sign

A

BP may be different in both arms

189
Q

What do you need to differentiate aortic dissection from and why?

A

Differentiate from MI as thrombolysis will be fatal with dissection

190
Q

Imaging for aortic dissection/?

A

CXR - widened mediastinum, cannot exclude dissection

TTUS - site and extent of dissection

MRI for diagnosis and identification of other vessels

191
Q

Aortic dissection complications

A

Rupture + multi-organ failure + cardiac tamponade + hypotension

192
Q

Mx aortic dissection

A

Analgesia (morphine) and oxygen

ICU

Manage HTN aggressively - aim 100-120SBP
IV beta blockers (labetalol) to reduce ventricular contraction
IV nitroprusside (emergency vasodilator

Surgical repair

193
Q

Sx of thoracic aortic aneurysm ?

A

Symptoms due to local compression: hoarseness, cough, stridor, dyspnoea, SVC obstruction, dysphagia

194
Q

Sx if TAA ruptures

A

SHIT GON HIT THE FAN - Dude who binned it in ICE

acute pain + collapse/shock + aneurysm erosion into local structure: haematemesis (aorto-oesophageal fistula), haemoptysis (aorto-bronchial), haemothorax, cardiac tamponade

195
Q

Ix in TAA acute?

chronic?

A

Acute: FBC, clotting, renal/liver, cross-match,
ECG,
CT contrast,
MR angiography

Chronic: 
FBC, ESR/CRP, LFT/amylase, 
ECG, 
LuFT, 
USS, 
*TTE, 
*AUS (for AAA) 
CT angiography, 
MR angiography (for cause, infective, inflammatory, pancreas (DDx))
196
Q

Mx of TAA ? In who?

A

Surgery: *graft insertion or TEVAR (thoracic endovascular aneurysm repair)

if symptomatic *regardless of size
or Marfans
Ascending > 5.5cm, descending >6cm

197
Q

What would you do for pt with marfans and TAA

A

lifelong BB, regular imaging of aorta and restriction physical activity

198
Q

Ix AAA? What sign could indicate imminent rupture?

A

FBC, clotting, renal, liver, crossmatch, ESR/CRP
ECG, CXR
*USS for initial assessment
CT for more anatomical detail, evidence of mural thrombus - *crescent sign - indicates blood within thrombus - imminent rupture
MRI angiography

199
Q

Mx of AAA

A

Regular USS monitoring

smoking, HTN, statin, antipt, low dose aspirin

Inform DVLA at *over 6cm

Elective surgical repair if >5.5cm or rapid expansion >1cm/year or symptomatic

  • Open Or
  • EVAR
200
Q

Triad of features in AAA rupture

A

flank/back pain, hypotension, pulsatile abdominal mass

201
Q

Ix of AAA rupture

A

FBC (Hb will be normal, high WCC), group and save/crossmatch, baseline U+E

USS / FAST scan

[CXR, AXR (75% are calcified)]

ECG for MI

202
Q

Mx AAA rupture

A

Large bore IV access

Group and crossmatch, order 4-6 units blood, FFP, Pt

Immediate theatre

Secure proximal aortic control

Prosthetic graft repair and stem bleeding - EVAR

(they probs gonna die tho)

203
Q

Types of shock

A

Hypovolaemic - loss of blood/fluid - decreases CO
-Blood loss - haemorrhage, fluid loss - dehydration/burns/pancreatitis

Cardiogenic - heart unable to pump enough blood for body - decreases CO

Distributive

 - Septic - decreases systemic vascular resistance, decrease SVR
 - Anaphylactic - intense allergic reaction leading to massive release of histamine and other vasoactive mediators - decrease SVR
 - Neurogenic - spinal cord injury, epidural, spinal anaesthesia causes decreased SVR
204
Q

What kills patients in shock?

A

coagulopathy, hypothermia, metabolic acidosis

205
Q

Which organs are specifically at risk in sepsis?

A

Kidney (acute tubular necrosis),

lung (ARDS),

heart (MI),

brain (confusion, irritability coma)

206
Q

Ix in hypovolaemic shock?

A

Hb, UE, LFT, group and crossmatch, ABG + lactate, monitor urine

207
Q

What is meant by compensated hypovolaemic shock?

A

baroreceptors result in increased myocardial contractility, tachycardia and vasoconstriction.
->Maintain BP. Release vasopressin, aldosterone, renin

208
Q

Mx of hypovolaemic shock

A

Raise legs

ABCDE

Crossmatch + blood for Ix as previous + catheter + ABG

Airway + high flow O2 + 2 large bore IV cannula

Fluid resus saline or Hartmann’s 500ml over 15 mins *may give 2l total then escalate

If haemorrhagic shock give blood as soon as possible O-ve

Pain relief - pain increases metabolic rate and increases ischaemia IV opiates

Surgery to stem blood loss: e.g. REBOA after resus

209
Q

Usual cause of cardiogenic shock

A

acute MI

210
Q

What things do you need to monitor in cardiogenic shock

A

cardiac monitoring,
BP - art line,
venous pressure - CVC,
urinary catheter

211
Q

Mx cardiogenic shock

A

ABCDE
fluids
O2

Pain relief *IV morphine

cardiac inotropes *dopamine or dobutamine
Revascularisation

212
Q

Anaphylaxtic shock mx

A

ABCDE
Lie flat
high flow O2 [/Intubate]

IM adrenaline
IV fluid challenge (500ml in 5 mins)
IV chlorphenamine (antihistamine) + hydrocortisone

Bronchodilators: salbutamol IV or nebulized,
ipratropium inhaled, aminophylline IV

213
Q

3 key signs of septic shock

A

SOFA score (2 or more is not good)

HAT
Hypotension - < 100mmHg
Altered metal state - GCS < 15
Tachypnoea - >=22

214
Q

Mx of sepsis

A 
Blood cultures + septic screen, U+E
Urine output - monitor hourly
Fluid resuscitation
Antibiotics - tazocin? gent? according to local guidelines
Lactate, ABG/VBG
Oxygen to correct hypoxia
215
Q

Bar buffalo what other Ix might you do in sepsis

A

FBC, UE, urine dip, LFT, glucose, *clotting inc D-dimer and fibrinogen for DIC, CXR, AUSS - find the infection

216
Q

Complications of spesis

A

DIC, renal failure, cardiorespiratory failure

217
Q

amiodarone side effects

A

prolong QT

pseudohypothyroidism

218
Q

hyperK Mx

A

calcium gluconate
Actrapid [insulin] with dextrose
salbutamol nebs
calcium resonium - for long term

219
Q

3 ECG hyperK

A

tall tented T
broad QRS
flat P
[prolonged QT]

220
Q

2nd Heart block mx

A

Unstable
atropine
-trancutaneous pacing if doesnt work

Stable
Treat cause -eg hypothyroid / pericarditis
Pacing if needed

221
Q

3rd degree mx

A

Pacing

unstable = transcutaneous / venos pacing

stable - dual chamber pacing

222
Q

ST elevation in all leads cause?

A

pericarditis

SAH

223
Q

Short term vs long term PE

A 
Short 
LMWH 
D dimer 
Wells 
CTPA , V/Q scan

Warfarin / NOAC 3-6months

224
Q

Further Ix after cute Mx of PE

A

1-3 Day ECG

Abdo pelvis thorax CT - Rule out malignancy

225
Q

What is an NSTEMI

A

Elevated troponin, inverted / depressed T waves

226
Q

What Ix post management of ACS

A

Echo

[could also check HbA1c for diabetes]

227
Q

Acute HF mneumonic

A 
LM[N]OP 
Loop diuretic Eg furosemide 
Morphine 
[Nitrates] - No longer 
Oxygen 
Posture

CPAP

228
Q

How does furosemide work

A

works on the ascending loop of henle to competitively inhibit the Na-K-2CL cotransporter

229
Q

PCI vs fibrinolysis

A

PCI = has to be within 120 minutes of the time that fibrinolysis could be given in.

230
Q

Risks of angiograms

A

bleeding, infection, trauma to structures, failure, heart attack

231
Q

Reasons for raised troponin

A

MI, unstable angina, trauma to heart, any of the iris’s around the heart, CKD, sepsis

232
Q

Capture beat

A

normal beat within VT

233
Q

What are the 8 shockable rhythms

How often do you give adrenaline in

A

Pulseless VT, VF,

1/10,000 by IV injection repeated every 3-5 minutes

234
Q

What are the reversible causes of cardiac arrest

A

tension penumothorax
tamponade
thormbosis
toxins

haemorrhage
hypothermia
hypokalaemia/hyperkalaemia
hypoxia

Phase 4 - GR (22 decks)

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