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CardioResp > Cardio > Flashcards

Cardio Flashcards

1
Q

Summary of stable angina?

A

Typically symptomatic when >70% coronary stenosis

<20 mins, subsides after rest/GTN
Exertion

Stress test: ST depression/elevation, T wave inversion

Angio: coronary a stenosis

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2
Q

Treatment of stable angina?

A

GTN

1st: Ca channel blocker or β blocker
2nd: add other
3rd: long acting nitrate, ivabradine, nicorandil or ranolazine

ACEi/ARB, aspirin/clopi, statin

CABG/PCI

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3
Q

Summary of unstable angina?

A

Sx at rest

ECG: ST depression, T wave inversion
Serial trop

300mg aspirin 
Nitrates
Morphine 
O2 if <94%
Fondaparinux if no immediate PCI
PCI: immediate if unstable, within 72 hrs if GRACE score >3%, give heparin 
Aspirin + prasugrel or ticagrelor if high risk bleeding
Aspirin + clopi if low risk bleeding

if GRACE score <3% - conservative management, give aspirin + ticagrelor if not high risk of bleeding, or aspiring + clopidogrel if high risk

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4
Q

What does GRACE score take into account?

A 
age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels
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5
Q

Summary of vasospastic angina?

A

Coronary artery vasospasms

Triggers: cold weather, stress, hyperventilation, smoking, cocaine use, alcohol, allergic reactions, drugs that tighten BVs

Can occur any time

ECG - Transient ST elevation

Tx: 
Ca channel blockers 
Nitrates 
Aspirin can aggravate ischaemic attack
β blockers can ↑vasospasm.
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6
Q

Complications of MI?

A

DARTH VADER

Death 
Arrthymia
Rupture
Tamponade
Heart Failure
Valve disease
Aneurysm
Dressler syndrome
Embolism
Recurrence regurgitation
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7
Q

Investigations for MI?

A

Trop

CKMB

STEMI: ST↑, new onset LBBB, reciprocal ST depression

NSTEMI: ST depression, loss of R wave, T wave inversion

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8
Q

Management of MI?

A 
Aspirin 300mg 
Morphine, metoclopramide
O2 <94%
GTN, IV nitrates 
Dual anti-plt 
Statins 
Cardiac rehab

STEMI
Thrombolysis: Tenecteplase, alteplase
If presents within 12 hrs > PCI within 120 mins. Heparin with bailout glycoprotein IIb/IIa

NSTEMI

Fondaparinux if not having angiography
PCI if unstable, >3% GRACE score. Heparin

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9
Q

Inferior leads?

A

II, III, aVF

RCA

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10
Q

Anteroseptal leads?

A

V1-V4

LAD

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11
Q

Anterolateral leads?

A

V4-6, I, aVL

LAD or L circumflex

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12
Q

Lateral leads?

A

I, aVL +/- V5-6

L circumflex

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13
Q

Posterior leads?

A

Changes in V1-V3

Reciprocal changes of STEMI are typically seen:
horizontal ST depression
tall, broad R waves
upright T waves
dominant R wave in V2

Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)

Usually L circumflex, also R coronary

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14
Q

Causes of bradycardia?

A

Intrinsic causes: congenital abnormalities, fibrosis, post MI, IE, infections, iatrogenic, amyloid, sarcoid, SLE, hypothyroidism.

Extrinsic: toxins, drugs (digoxin, β blockers, CCBs), hyperkalaemia, hypothyroid, adrenal insuff, hypoxia, hypothermia, Cushing’s triad, AN.

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15
Q

Management of bradycardia?

A

Unstable

Atropine 500mcg, repeat every 3 mins, up to max 3mcg
Adrenaline, dopamine, isopremaline
Transcut/transvenous pacing

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16
Q

Causes of heart block?

A 
Infiltrative/ dilated cardiomyopathies eg myocarditis, amyloidosis, sarcoidosis, lymphoma. 
Muscular dystrophy
Lyme disease/ acute rheumatic fever. 
Myocardial ischaemia
Congenital heart disease + congenital 3rd degree AV block. 
Hyperkalaemia
High vagal tone
Cardiac surgery/ trauma 
Meds: BB, CCB, digoxin
CO, cyanide 
Lev’s disease
17
Q

Summary of 1st degree heart block?

A

PR interval > 0.2 seconds, every P wave followed by normal QRS

Signal delayed, continues to ventricles

Usually asymptomatic

R away from P = first degree

No Tx, if Sx can get pacemaker fo transact pacing

18
Q

Summary of T1 2nd degree heart block?

A

Morbitz 1/Wenckebach

Usually asymptomatic
Light-headedness, dizziness, syncope

Longer, longer, longer, drop = Wenkebach

PR interval lengthens each beat until blocked (dropped beat/no QRS)
Constant PP interval
Following omission, PR interval reset + cycle repeats
Narrow irregular QRS

No treatment if asymptomatic
If Sx can get pacemaker of transscut pacing

19
Q

Summary of T2 2nd degree heart block?

A

Morbitz II

Block commonly bundle of His

Intermittent dropped beats, no progressive lengthening of PR interval

Often regular conduction intervals eg 2:1

Fatigue, dyspnoea, chest pain, syncope

PR interval is constant but the P wave is often not followed by a QRS complex
Prolonged PR interval >200ms
Regular QRS complexes with occasional dropped QRS
PR interval constant

Pacemaker
Transcut pacing

Some P’s don’t get through, then Mobitz II

20
Q

Summary of 3rd degree AV block?

A

Signal blocked every time, no association between atrial + ventricle activity.
Ventricles contract at lower rates than atria, ventricular pacemaker cells set rate

Syncope, confusion, dyspnoea, severe chest pain, risk of dying

No association between P + QRS
Regular PP + RR intervals

ICU, CCU
Epinephrine
Pacing

If Ps and Qs don’t agree, then you have third degree

21
Q

Summary of LBBB?

A

Electrical signal for contraction of L ventricle completely blocked/delayed along 1 bundle branch.
Retrograde depolarisation from R>L via purkinje fibres

Asymptomatic
Reversed splitting on auscultation

New LBBB is always pathological. Causes of LBBB include:
> myocardial infarction - diagnosing a myocardial infarction for patients with existing LBBB is difficult, Sgarbossa criteria can help with this
> hypertension
> aortic stenosis
> cardiomyopathy
> rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

WilliaM

  • W in V1
  • M in V6

QRS complex > 120Ms
Neg V1, pos V6
V1: QS or ‘little r’ rS, no R wave, deep S wave W shape
V6: large, notched R wave, M shape

22
Q

Summary of RBBB?

A

Electrical signal for contraction of R ventricle completely blocked/delayed along 1 bundle branch.

Asymptomatic
Wide splitting on auscultation

Causes of RBBB
> normal variant - more common with increasing age
> right ventricular hypertrophy
> chronically increased right ventricular pressure - e.g. cor pulmonale
> pulmonary embolism
> myocardial infarction
> atrial septal defect (ostium secundum)
> cardiomyopathy or myocarditis

in RBBB there is a ‘M’ in V1 and a ‘W’ in V6

QRS complex > 120Ms
T wave inversion
QRS double peaked.
M shape in V1 tall R waves, W-shape in V6 from wide slurred S shape
ST depression + T wave inversion in leads V1-V3.

23
Q

Summary of sick sinus syndrome?

A

a disease in which the SAN becomes damaged and is no longer able to generate normal heartbeats at the normal rate.

Abnormal heart rhythms caused by malfunction of SAN

Brady, tachy, tachy-brady, long pauses

Sarcoidosis, amyloidosis, haemochromatosis, chagas disease, cardiomyopathies

Meds: CCB, BB, digoxin

Complications:
Sinus arrest
AT, AF
VTE

ECG
Tilt table testing
Holter monitor
Exercise/ atropine stress test: inadequate ↑HR

Management
Pacemaker
Treat tachy with meds > BB

24
Q

Management of narrow-complex tachycardia?

A

Regular
> vagal manoeuvres, carotid sinus massage, Valsalva manoeuvre
> followed by IV adenosine 6mg, then 12mg, then 18mg. CI in asthmatics
> if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. beta-blockers)
> electrical cardioversion
> probable SVT

Irregular
> probable atrial fibrillation
> if onset < 48 hr consider electrical or chemical cardioversion
> rate control: beta-blockers are usually first-line unless there is a contraindication, then diltiazem
> if HF - digoxin or Amiodarone

25
Q

Management of broad-complex tachycardia?

A

Regular
> assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
> loading dose of Amiodarone 300mg over 20-60 mins, then followed by 900mg 24 hour infusion
> if SVT with BBB - treat for regular narrow complex tachy

Irregular
> seek expert help.
> Possibilities include:
atrial fibrillation with bundle branch block - the most likely cause in a stable patient - treat as narrow complex
> atrial fibrillation with ventricular pre-excitation > give Amiodarone
> torsade de pointes

26
Q

Summary of sinus tachycardia?

A

Narrow complex QRS, regular ventricular rhythm. P before every QRS. Rhythm originates in SAN.

Causes = Physical deconditioning, hypoxia, PE, hypovolaemia, hyperthyroid, anaemia, caffeine, alcohol, nicotine, cocaine, amphetamines, aminophylline, atropine, clozapine, catecholamines.

Inappropriate: persistent ↑HR, unrelated to/out of proportion to cause

27
Q

What is focal atrial tachy?

A 
SVT, atrial focus outside SAN. 
Mostly idiopathic 
HTN, heart disease, cardiomyopathy
MI, infection, alcohol poisoning 
Congenital heart disease 
Catecholamine excess
Drug toxicity: cocaine, digoxin, theophylline

ECG:
Morphology of P waves depends on site origin but remains constant
Regular rhythm

Management:
Vagal manoeuvres 
If persists: IV adenosine, CCB (verapamil, diltiazem), BB blockers
Catheter ablation 
Pacemaker
28
Q

What is multifocal atrial tachy?

A

Multifocal origin of pacemaker activity

Causes = COPD, theophylline, isoproterenol, ↓K, Mg, hypoxia, hypercapnia, acidosis, RA enlargement
Typically in seriously ill patients with respiratory failure. Tends to resolve following Tx of underlying disorder.

ECG:
HR > 100bpm 
Irregularly irregular
P waves 3+ varying morphologies 
Narrow QRS 
SVT 
Management:
Beta blockers
CCB eg verapamil 
IV Mg
Correct reversible causes
29
Q

What is junctional tachycardia?

A

Abnormal automaticity or myocytes in AVN or proximal bundle of His

a form of supraventricular tachycardia

Narrow complex
Regular
P wave inverted in lead 2, can be hidden within QRS or immediately before QRS
Short PR interval

Prevention
BB eg metoprolol
CCB > verapamil
Catheter ablation

Acute management
vagal manoeuvres:
> Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
> carotid sinus massage
intravenous adenosine
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
contraindicated in asthmatics - verapamil is a preferable option
> electrical cardioversion

30
Q

Summary of atrial fibrillation?

A

first detected, recurrent, paroxysmal, persistent, permanent (cannot be cardioverted or deemed inappropriate)

Palpitations, dyspnoea, chest pain

Irregularly irregular pulse

Rate/rhythm control
- rate control except in coexistent HF, first onset AF or where obvious reversible cause

Rate - BB or rate-limiting CCB (diltiazem). Can have combination of 2 of BB, diltiazem or digoxin if mono therapy doesn’t control rate

Rhythm - short duration of Sx (<48 hours) or anticoagulation prior

31
Q

Summary of CHA2DS2-VASc score?

A

C - congestive HF - 1
H - hypertension (or treated HTN) - 1
A2 - age >75 = 2, age 65-74 = 1
D - diabetes - 1
S2 - prior stroke, TIA to thromboembolism = 2
V - vascular disease (including IHD, and PAD) = 1
S - sex (female) = 1

0 - no treatment
1 - males - consider anticoagulation, females- no Tx
2 - offer anticoagulation

Choice of anticoagulation - warfarin and NOACs

32
Q

Summary of atrial flutter?

A

a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.

ECG findings
> ‘sawtooth’ appearance
> as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min
> flutter waves may be visible following carotid sinus massage or adenosine

Management
> is similar to that of atrial fibrillation although medication may be less effective
> atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
> radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

33
Q

What is AV re-entrant tachycardia?

A

Accessory pathway between atria + ventricles.

Allows signal to move backwards. More than 1 ventricular contraction can be stimulated from 1 impulse from SAN.

Orthodromic: through AVN, ventricles contract, up through accessory pathway, atria contract, back down AVN etc.

Antidromic: signal down through accessory pathway, ventricles contract, up through AVN atria contract, back down accessory.

Features:
Palpitations 
Chest discomfort 
SOB
Light-headed
Syncope

Orthodromic: regular, narrow QRS tachy, p waves retrograde (after QRS)
Antidromic: regular, wide QRS tachy. P waves often not visible, delta waves, short PR interval.

Acute termination: vagal manoeuvre, carotid sinus massage, adenosine, electrical cardioversion.
Chronic prevention: amiodarone, procainamide, sotalol, flecainide, radiofrequency catheter ablation.

34
Q

What is WPW syndrome?

A

Congenital accessory pathway (Bundle of Kent) conducts signal between A+V. Ventricles start to contract a bit early, pre-excitation.

As accessory pathway does not slow conduction AF can degenerate rapidly to VF

Signal takes longer through AVN, combines with single from BoK to contract ventricle.

Set up re-entry loop, BoK propagate signals both ways. Come down AVN, go back up BoK, causing atria contraction + AVRT.

Tachyarrhythmias
Palpitations 
Chest discomfort
SOB
Light headed 
Syncope 
Find physical activity exhausting

Short PR interval
Delta wave: slurred upstroke of QRS
Widening of QRS complex due to ventricular pe-excitation
AF or flutter, very high >200-250

Differentiating between type A and type B**
type A (left-sided pathway): dominant R wave in V1 
type B (right-sided pathway): no dominant R wave in V1 (in exams mostly type B with LAD)
Associations of WPW
HOCM
mitral valve prolapse
Ebstein's anomaly
thyrotoxicosis
secundum ASD

Management
definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol***, amiodarone, flecainide

*** sotalol avoided if coexistent AF > can deteriorate to VF

35
Q

Summary of atrioventricular nodal re-entry tachycardia (AVNRT)?

A

Supraventricular tachycardia

Accessory pathway within AVN. 2 pathways, form loop

Slow-fast: typical, signal depolarisation down both pathways, reaches end of β path (fast) 1st. signal splits, travels. To ventricles (contraction), + travels up α path, meets slow signal, cancel each other out. Both go into refractory. α refractory shorter, ready 1st, signal from α exits to ventricles. Also travels up β, by time all way round, α out of refractory, re-entrant loop.

Fast slow: atypical, anterograde conduction via fast pathway, retrograde via slow.

RF: F>M, stress, alcohol, caffeine hyperthyroid, exercise, electrolyte disturbance

ECG
SVT 140-280bpm
Absent p waves, signal getting through atria + ventricles almost same time
p waves immediately before/ after QRS complex. P waves inverted/ retrograde
R waves (small secondary R waves)
Narrow QRS complexes

Management:
Adenosine
Ca channel blockers eg verapamil, diltiazem
Slow AVN: vagal manoeuvre (carotid sinus massage/ valsalva manoeuvre) > activates vagus nerve, blocks AVN temporarily.
Electrical cardioversion

Prevention
Beta blockers eg metoprolol
Radiofrequency catheter ablation: ablation of slow alpha pathway

36
Q

Summary of VT?

A

broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

monomorphic VT: most commonly caused by myocardial infarction
polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval

Non re-entrant/focal
Abnormal automaticity of specific area of ventricle. Ventricular pacemaker cells fire at high rate, preventing SAN firing.

Re-entrant VT
More common
Cardiomyocytes altered when stressed by stimuli eg drugs, changing conduction speed + refractory period

Non-sustained: at least 3 beats, resolve spontaneously in <30s.

Sustained: >30s, or requiring termination earlier due to haemodynamic instability.

Adverse signs (SBP < 90, chest pain, HF) then immediate cardioversion. If not, then antiarrhytmics. if these fail, then electrical cardioversion may be needed.

Drug therapy
> amiodarone: ideally administered through a central line
> lidocaine: use with caution in severe left ventricular impairment
> procainamide

If drug therapy fails
> electrophysiological study (EPS)
> implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function

Electrical cardioversion: pulse delivered to heart on R wave, if delivered on T wave could induce VF

37
Q

Causes of long QT interval?

A

Congenital:
> Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
> Romano-Ward syndrome (no deafness)

Drugs:
> amiodarone, sotalol, class 1a antiarrhythmic drugs
> tricyclic antidepressants, fluoxetine
> chloroquine
> terfenadine
> erythromycin

electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia

acute myocardial infarction

myocarditis

hypothermia

subarachnoid haemorrhage

CardioResp (3 decks)

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