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Exam study Flashcards

1
Q

What clinical features (on Hx) are highly suggestive of AMI?

A
  • Acute central chest pain, lasting >20mins, often a/w nausea, sweating and SOB.
  • Pain is non or only partially relieved by GTN
  • There is often a history of IHD or previous MI
  • Presence of multiple cardiovascular risk factors
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2
Q

What clinical features (on exam) are highly suggestive of AMI?

A

• Patient may be distressed, pale, anxious, and mildly feverish
• Signs of heart failure often present, these include
1. Elevated JVP
2. Basal crepitations
3. Left ventricular S3
4. +/- new onset murmurs

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3
Q

To diagnose AMI… and what are you looking for?

A

• Order a 12 lead ECG monitor, looking for
1. Acute ST and T wave changes
2. Abnormal Q waves
3. Past evidence of LVH or previous MI
• Cardiac enzymes looking for elevated troponin levels. Note that
1. Troponin T peak at 12-24 hr and elevated for >1wk.
2. So early CK-Mb rise diagnose an MI, & normal levels at 20hr rule it out.

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4
Q

What tests do you order to assess severity of AMI?

A
  • CXR, looking for signs of pulmonary congestions and cardiomegaly
  • FBE – anaemia aggravates angina; leukocytosis indicates infarction
  • U&E to assess electrolytes disturbances and BSL to exclude hypoglycemia
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5
Q

The ECG shows ST elevation of 2mm in V2-4. What is the likely diagnosis?

A
  • Anterior infarct
  • Antero-septal infarct (left anterior descending)
  • Possibility of vasospasm
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6
Q

Briefly explain the role of troponins in the diagnosis of AMI?

A
  • Troponins are myocardial regulatory proteins that are released into the blood following myocardial damage or infarction
  • 2 Types of troponins are currently measured – Troponin I and T
  • Troponin I are highly specific for myocardial injury (better than troponin T or CK-MB)
  • Troponin T is also useful because it has a large diagnostic window, as it is increased from 12hours to 10 days following AMI
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7
Q

What are the treatment options for AMI?

A

• If initial ECG is normal, then repeat after 30mins
• If STEMI or new LBBB (i.e. we are sure it’s infarction), then treatment includes
1. Aspirin
2. Emergency reperfusion therapy with either angioplasty (PTCA) or thrombolysis
• If Non-STEMI (i.e. we are not sure if it’s infarction), then treatment includes
1. Antiplatelet therapy, e.g. LD aspirin, clopedigrel
2. Antithrombotic therapy, e.g. clexane
3. Followed by angiograph, preferably within 24-48hrs

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8
Q

Discuss the principles of management of STEMI

A

• When a patient p/w AMI – try to get them to cath lab asap, provided the ECG criteria are met, i.e.
1. ST segment elevation of >1mm in > 2 contiguous limb leads or
2. ST segment elevation of >2mm in > 2 contiguous precordial leads or
3. New LBBB
• If primary PTCA is not an option, e.g. in country hospital, then patient should be thrombolysed
• All patients should have
1. Oral or iv beta-blockers (as guided by PR and BP) and aspirin
2. Oral, topical or iv nitrates and/or morphine (esp. if patient has angina)
3. An ACEi within the first 24hrs of infarction (if BP permits)
4. Anticoagulants with unfractionated or fractionated heparin

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9
Q

What is your long term management of AMI?

A

• Modifying risk factors, e.g. stop smoking, exercise, lose weight, control HT, DM, lipids (stabilise plaque)
• Unless contraindicated, both STEMI and NSTEMI patients should be treated long term with
1. Aspirin – low dose 75-150mg/day (reduces mortality by 34%)
2. Beta-blockers – e.g. atenolol 50-100mg/day PO (if contraindicated, give Ca channel blockers)
3. ACEi – also esp. useful if patient’s EF

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10
Q

What signs indicate re-perfusion?

A
  • Relief of chest pain
  • Resolution of ST elevation
  • Early peak of cardiac enzymes
  • New onset arrhythmias (esp. runs of VT)
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11
Q

What are the indications for thrombolysis?

A
  • Ischaemic chest pain >1/2 hour in duration
  • ST elevation of 2mm or more in 2 consecutive chest leads (i.e. V leads)
  • ST elevation of 1mm or more in 2 consecutive limb leads (i.e. II, III, aVF)
  • New onset acute LBBB
  • Evidence of acute posterior MI
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12
Q

What determines the prognostic factors following MI?

A

• 2 main prognostic factors following MI are
1. The LV function
2. Degree of underlying CAD
• Worse prognosis if
1. Patient is elderly
2. Infarct is large or anterior
3. History of hypertension prior to infarct
4. Presence of any of the complications of AMI

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13
Q

Main causes of bradyarrhythmias

A
  1. Primary SA node dysfunction

2. AV conduction problems (of which there are first degree, second degree and complete heart block)

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14
Q

What are the causes of sinus node dysfunction?

A
  • Idiopathic SA node degeneration
  • Increasing age (reducing blood flow to SA node, senile amyloidosis)
  • Hypothyroidism
  • Medications (e.g. beta blockers)
  • Less common causes e.g. CLD, hypothermia, vasovagal syncope, severe hypoxia, hypercapnia, acidemia, etc…
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15
Q

If a patient has sinus node dysfunction, what is the typical clinical presentation?

A
  • Sinus rate 3s)

* Sick sinus syndrome (combination of dizziness, fatigue, syncope, CCF)

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16
Q

What is your management of sinus node dysfunction?

A
  • Diagnosis is made on clinical presentations and ECG holter monitor
  • No Rx if asymptomatic
  • If symptomatic - IV atropine 0.5mg IV rapidly until PR 60-100bpm
  • PPM if chronically symptomatic
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17
Q

What is first degree AV block?

A

Delayed conduction from atrium to ventricle, characterised by prolonged PR (>0.22s), but all impulses are conducted

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18
Q

What is second degree AV block?

A

intermittent complete failure of conduction of atrial impulse to ventricle, with dropped (non-conducted) P waves on ECG. There are 3 main types of second degree block
• Mobitz type I (Wenkebach) – increase PR interval until a beat is dropped (AV nodal dx)
• Mobitz type II – Sudden dropped QRS with no preceding change in PR interval (infranodal dx)
• 2:1 or 3:1 block –every 2nd or 3rd P wave is followed by a QRS complex

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19
Q

What are the causes of AV conduction disturbances?

A
  • Idiopathic fibrosis – increasing frequency with age
  • IHD, esp. AMI
  • Calcific aortic stenosis – involvement of ring close to AV node
  • Drug toxicity – many antiarrhythmic agents, including digoxin
  • Post-operative – esp. aortic valve replacement
  • Congenital complete heart block
  • Infection – aortic valve endocarditis with root abscess, diphtheria, Lyme disease, rheumatic fever
  • Multisystem disease – sarcoidosis, amyloidosis, ankylosing spondylitis, Reiter’s syndrome, rheumatoid arthritis, scleroderma, SLE
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20
Q

Discuss the clinical presentation of various degree heart block

A

• First degree and Mobitz type I – patients are usually asymptomatic, but may progress to higher grade AV block
• Mobitz type II and complete heart block
1. Syncope (Stokes-Adams attack) – loss of consciousness is abrupt, without warning, and the patient appears pale; rare in Mobitz type II
2. Pre-syncope and dizzy spells, fatigue, dyspnoea, sudden death

21
Q

What signs are indicative of 1st degree HB?

A

no signs are manifest

22
Q

What signs are indicative of 2nd degree HB (Mobitz I and II and 2:1;3:1)?

A
  • Mobitz type I – irregular pulse with dropped beats•
  • Mobitz type II – occasional dropped beats (irregular pulse)
  • 2:1 or 3:1 block – bradycardia, oedema, raised venous pressure
23
Q

What signs are indicative of complete HB?

A
  1. Bradycardia
  2. Large-volume pulse
  3. Raised JVP with occasional cannon waves
  4. Variable intensity of S1
  5. Peripheral oedema
24
Q

When is PPM indicated?

A

for second degree Mobitz type II block or complete heart block

25
Q

causes of atrial fibrillation in elderly?

A

If patient is old, think of the following
• Increasing age
• IHD
• Uncontrolled HT in the elderly
• CCF
• Valvular disease, esp. Mitral valve
• Medication, esp. digoxin (proarrhythmic), amiodarone

26
Q

causes of atrial fibrillation in young?

A
  • Thyrotoxicosis (note also that AF may be the only clinical feature in the elderly)
  • Acute alcohol intoxication
  • Illicit narcotic abuse (e.g. cocaine, amphetamines)
  • Constrictive pericarditis
27
Q

how do pts with AF present clinically?

A
  • Patient is asymptomatic, often found incidentally

* May c/o rapid and irregular palpitation, a/w dyspnoea, fatigue, dizziness or angina

28
Q

what signs are suggestive of AF?

A
  • Pulse is irregularly irregular

* ECG shows absent P waves, rapid and irregular QRS

29
Q

What conditions other than an AF may cause an irregularly irregular rhythm?

A
  • Multiple ventricular premature beats
  • Multiple atrial premature beats
  • Atrial flutter with variable block
  • Multifocal atrial tachycardia
30
Q

Name some common sites of systemic embolization

A

• Brain, leg, kidney, superior mesenteric artery, coronary artery and spleen

31
Q

Why do people get atrial flutter?

A
  • Idiopathic (no underlying heart disease or other reasons)
  • Coronary artery heart disease
  • HT heart disease
  • Risk factors, e.g. cardiomyopathy, hypoxia, COAD, thyrotoxicosis, phaechromocytoma, alcohol, etc…
32
Q

What are the typical presentations of atrial flutter?

A
  • Patient often p/w palpitation +/- fatigue, dyspnea and chest pain
  • Symptoms are usually not as well tolerated as AF because the ventricular response is poor
  • Acute atrial flutter can cause hypotension, angina or CCF
33
Q

O/e for atrial flutter, what are you looking for?

A
  • Assess vital signs – does the patient need to be resuscitated?
  • Pulse may be rapid, or absent (if too fast)
  • Atrial rate 300bpm, a/w organic heart dx, ventricular rate often 150bpm 2:1 block
  • Inferior leads – ‘flutter waves’ or ‘saw tooth’ baseline
  • Carotid sinus pressure decreases ventricular rate
34
Q

What is WPW syndrome?

A
  • WPW syndrome occurs when a congenital accessory conduction pathway exist b/n atria and ventricles, thereby bypassing the normal cardiac conduction system
  • WPW syndrome is not inherited. During early cardiac development, direct physical continuity exists b/n ventricular and atrial myocardium
  • In growth of AV sulcus, tissue at a later stage in cardiac development interrupts this, but defects may persist into neonatal and subsequently adult life
  • Term infants have frequently been found to have these connections, but they are presumed to be non-functional in most
  • Accessory connections appear microscopically to be normal myocardial muscle bundles bridging atrial and ventricular myocardium; they may have subepicardial or subendocardial locations; they are multiple in ~10% of patients with the condition
  • Ebstein’s anomaly is a/w their presence, and multiple pathways are more common in these patients
  • If conduction occurs in sinus rhythm, pre-excitation is apparent on the ECG
  • Complications of WPW syndrome include AF and Sudden cardiac death (rare)
35
Q

What are the typical presentations of WPW syndrome?

A
  • Most patients are asymptomatic – the only feature is presence of pre-excitation on ECG
  • Palpitation – due to re-entry tachycardia (sudden onset and termination, regular, rapid, often >200bpm); may also be caused by paroxysmal AF (in ~5% of patients)
  • Chest pain – during tachycardia; pain or discomfort similar to angina, rarely indicates CAD
  • Impaired consciousness – dizziness or faintness common; syncope less frequent (5%) and usually follows vasodilatation occurring as a secondary response to tachycardia
  • Polyuria – accompanying sustained episodes of tachycardia
36
Q

O/e for WPW, what you looking for?

A

• If patient is in sinus rhythm – no clinical signs
• During tachycardia, clinical signs a/w impaired circulation may be found, e.g.
1. Rapid pulse
2. Hypotension
3. Alteration in venous pulse wave form

37
Q

If you suspect WPW syndrome, what investigations would you do?

A

• Resting ECG – looking for
1. Short PR interval
2. Widened QRS complex
3. Delta wave
• ECG during tachycardia
1. Usually (90%) narrow complex tachycardia
2. Retrograde atrial activation may be seen as P waves of altered configuration inscribed in ST segment
3. Rate-related bundle branch block or antidromic tachycardia results in broad QRS complex tachycardia

38
Q

Discuss the principles of management of WPW syndrome

A

• Conservatively – in patients with frequent symptoms, lifestyle is restricted by occurrence of palpitations (often related to stress or exertion) or by side effects of drug treatment
• Pharmacological treatment
1. Acutely – adenosine
2. Recurrent – sotalol, flecainide, amiodarone
3. Avoid digoxin, verapamil, and B-blockers (all may shorten the refractory period of the accessory pathway)Drugs are now considered second-line treatment for WPW syndrome
• Non-pharmacological treatment
1. Catheter ablation of congenital pathway
2. Surgery

39
Q

What are ventricular ectopic?

A

• In this condition, what happens is that a certain region in the ventricles develop it’s own pacemaker signal, and completely ignores the conduction sent from the SA node.

• VE is characterised by
1. Widen QRS complexes with bizarre appearance (not patient’s normal beat)
2. No P wave preceding these QRS complexes
3. A full compensatory pause usually follows
• Exercise generally abolishes premature beats in normal hearts, and the rhythm becomes regular
• VE are commonly seen in post-MI patients, but it can also be seen in normal healthy people

40
Q

Briefly discuss the principles of management of ventricular ectopic

A
  • If no underlying cardiac disease, and patient has intermittent ventricular ectopic – no treatment is needed; just observe
  • If frequent – need to exclude hypo or hyperkalemia, hypomagnesemia, hyperthyroidism, and organic heart disease.
  • If patient is symptomatic (e.g. dizziness, syncope, SOB), treat with beta-blockers
41
Q

What is ventricular tachycardia?

A
  • In this condition, the ventricle is beating fast (160-240bpm) paroxysmally, irrespective of SA node signals
  • The rate is moderately regular, with 3 or more consecutive ventricular premature beats
  • The hallmark of the problem is presence of AV dissociation, which causes the ventricular arrhythmias to proceed independently of the normal atrial rhythm
  • VT is either sustained (lasting >30s) or non-sustained (
42
Q

How do patients typically present if they had ventricular tachycardia?

A
  • Most patients are asymptomatic
  • Rapid and regular palpitations a/w dizziness, syncope or near syncope, esp. PHX of IHD
  • Sudden SOB
  • Cardiac arrest or sudden death
43
Q

What are the causes of ventricular tachycardia?

A
  • Acute ischaemia – coronary obstruction by thrombus
  • Large scar old infarction – previous surgery, dysplasias
  • Microscopic scar infiltration – fibrosis
  • No clinical disease, e.g. RV outflow tachycardia, RV dysplasia
  • Functional disease, ‘fasicular’ tachycardia
  • Tumours, malformations, other causes (rare)
44
Q

What investigations would you perform to test for VT?

A

• ECG
1. Initially to confirm the diagnosis; then after treatment, to compare the sinus rhythm
2. Reveals tachycardia with QRS complexes 140ms duration
3. Evidence of AV dissociation (independent P waves, fusion beats, capture beats, 2nd degree ventriculo-atrial block)
4. Marked LAD and RAD during tachycardia
5. Absence of RS complexes in chest leads during tachycardia
• Adenosine test
1. Initially to distinguish from junctional or atrial tachycardia
2. If patient is stable, but tachycardic, and ECG is not helpful, then give incremental boluses of adenosines – this should terminates almost all junctional tachycardia, slows most atrial tachycardia, but affects almost no ventricular tachycardia except those arising in the RV outflow tract
• Cardiac enzymes – after treatment, if history suggests infarction
• Exercise test – under supervision to look for coronary disease, to provoke arrhythmia, and to assess drug efficacy
• 24hr ECG recording – to quantify frequency of ventricular arrhythmia and associated arrhythmias (e.g. ventricular premature beat)
• Echo – to assess LV and RV function

45
Q

Discuss the principles of management of ventricular tachycardia

A

• Conservative – avoid strenuous exercise; normal diet unless evidence of coronary disease
• Immediate treatment (if emergency)
1. CPR is necessary
2. Lignocaine iv or procainamide in stable patients
3. DC converts in severe or unstable patients. Note that do not give verapamil as it may cause profound collapse and even death
• Long-term treatment
1. Maintenance therapy – sotalol (if good LV function) or amiodarone (if poor LV function)
2. Consider implantation of automatic defibrillator device to terminate tachycardia
3. Ablation of localised focus or circuit causing tachycardia – using radiofrequency energy and low-energy direct current

46
Q

What is VF?

A
  • This condition is similar in concept to AF, except the pathology is in the ventricles.
  • So what happens is that multiple areas in the ventricle send out signals in an uncoordinate manner, rendering the ventricular contraction fast and irregular
  • This affects cardiac output (i.e. severely reduced or no CO at all), and can lead to death if not treated immediately
  • Patient is pulseless, become rapidly unconscious and respiratory arrest
47
Q

What are the causes of VF?

A
  • Patients with IHD
  • Following administration of antiarrhythmic drugs (esp. those that induce prolonged QT intervals and torsade de pointes)
  • Patients with severe hypoxia or ischaemia
  • Patients with WPW who develop AF with an extremely rapid ventricular response
48
Q

What is your immediate action if you recognise VF?

A

• Immediate DC conversion. Must sedate px first with midazolam or diazepam

MD2 (12 decks)

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