Cardiology Flashcards

1
Q

What are the clinical features of Myocarditis?

A

Usually young patient with acute history (recent flu like illness)

  • Preceeding Viral Syndromefever, myalgia, URTI symptoms around 2-3 weeks before initial presentation
  • Chest Pain → indicates perimyocarditis
  • Cardiac Arrhythmiaspalpitations
  • Dyspnoea
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2
Q

What are the investigations for Myocarditis?

A
  • Endomyocardial Biopsy- Gold standard
  • 12-Lead ECG → ordered immediately in anyone with chest pain or cardiac symptoms. May see ST elevation and T wave inversion.
  • Bloods → increased cardiac enzymes (CK, CK-MB, Troponin), increased ESR, increased BNP
  • CXR → cardiac enlargement, pleural effusions, bilateral pulmonary infiltrates (pulmonary oedema)
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3
Q

What is Myocarditis?

A

Inflammation of the myocardium in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease

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4
Q

What is Chronic Pericarditis?

A

Lasts >3 months. Leads to constrictive pericarditis (raised JVP)

Constrictive Pericarditis ⇒ dyspnoea, right heart failure (peripheral oedema), raised JVP

Positive Kussmaul’s sign (paradoxical rise in JVP on inspiration)

pulsus paradoxus (large drop in BP during inspiration - sign of tamponade).

CXR may show pericardial calcification.

Kussmaul’s Sign = differentiates constrictive pericarditis and cardiac tamponade.

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5
Q

What is Dressler’s Syndrome ?

A

pericarditis several weeks after an MI

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6
Q

What are the clinical features of Pericarditis?

A

Clinical Features:

Chest Painacute in onset, sharp & pleuritic. -
- May be stabbing or aching.
- Relieved when sitting up or leaning forwards (hence also worse when lying down).
- Can radiate to neck and shoulders (typically left side)

Pericardial Rub → occurs in 1/3 of cases.
-Superficial scratchy or squeaking sound
-best heard with the diaphragm of the stethoscope over the left sternal border.
-Heard best at the left sternal edge with the patient leaning forward at end-expiration.

May also have fever & myalgia

Cardiac TamponadeBeck’s Triad = raised JVP, decreased BP, muffled heart sounds
- Pulsus Paradoxus → abnormally large drop in BP during inspiration

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7
Q

What constitutes under Beck’s Triad and what is this indicative of?

A

raised JVP, decreased BP, muffled heart sounds

cardiac tamponade

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8
Q

What is the ECG finding of Pericarditis?

A

saddle shaped ST elevation (IN ALL LEADS) + PR depression

Widespread ST elevation (as oppose to STEMI, which will only cause ST elevation in leads corresponding to territory)

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9
Q

What are the investigations for Pericarditis?

A
  • Transthoracic Echocardiographypericardial effusion (cardiac tamponade) may be present
  • CXR → pericardial effusion
  • Troponin → elevation indicates myopericarditis or other aetiologies such as ACS
  • U&Es → elevated urea suggests a uraemic cause
  • Blood Culture → positive if infective cause
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10
Q

What is the management for Pericarditis?

A
  • Often self-limitingNSAIDs (Can also give PPI prophylaxis to protect against effects of high doses of NSAIDs)
  • If the patient has idiopathic or viral pericarditis, add Colchicine and continue it for 3 months.
    • Main side effect is diarrhoea
  • Surgical:
    • If TamponadePericardiocentesis
    • If Recurrent → Pericardiectomy (complete removal of the pericardium)
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11
Q

What is the management for Vasovagal Syncope?

A

Patient education + avoiding triggers

Volume expansion → increased dietary salt and electrolyte-rich sports drinks

Fludrocortisone

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12
Q

What 4 specific cardiac arrhythmias can cause cardiac arrest?

A

ventricular fibrillation (VF), pulseless ventricular tachycardia (VT), pulseless electrical activity (PEA), and asystole

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13
Q

Which out of the 4 specific cardiac arrhythmias can cause cardiac arrest are shockable and non shockable?

A

shockable rhythm (VT/VF)
non-shockable rhythm (asystole/PEA)

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14
Q

What is the management plan for Shockable Rhythms (Pulseless VT or VF)?

A

CPR (30:2 ratio) and Defibrillation + Adrenaline.

May also use anti-arrhythmic such as amiodarone.

If due to Torsade de Pointes, give magnesium.

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15
Q

What is the management plan for Non-Shockable Rhythms (PEA or Asystole)?

A

CPR and Adrenaline. No defibrillation.
Atropine (once) if rate <60bpm

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16
Q

What is Cardiac Arrest?

A

Sudden state of circulatory failure due to a loss of cardiac systolic function

17
Q

What is the Secondary Prevention of MI (long-term management) ?

A

Dual Antiplatelet Therapy (aspirin + ticagrelor/clopidogrel)
ACEi (ramipril), Beta Blocker (bisoprolol)
Statin (atorvastatin 80mg - secondary prevention dose)

18
Q

What is the initial management for Acute ACS?

A

MOAN

  • Morphine (patients with severe pain)
  • Oxygen (only if sats <94%)
  • Aspirin (300mg)
  • Nitrates (contraindicated if hypotensive, <90mmHg)
19
Q

What is the management for STEMI?

A
  • Aspirin 300mg and continue indefinitely
  • Symptoms <12h and PCI possible in 2hAngiography + PCI
    • Also give Prasugrel
  • Symptoms <12h and PCI not possible in 2hThrombolysis (alteplase + antithrombin)

If present >12h after symptoms, manage pharmacologically.

20
Q

What is Supra-Ventricular Tachycardia?

A

A regular, narrow-complex tachycardia with no P waves and a supraventricular origin. (regular = distinguishing feature from AF which is irregular)

21
Q

How does Wolf-Parkinson-White Syndrome present on an ECG?

A

Delta waves (slurred upstroke in QRS) after SVT termination

22
Q

What is the management for Supra-Ventricular Tachycardia?

A

Haemodynamically Stable

- 1st Line → **Vagal Manouveres** (eg. carotid sinus massage or valsalva manoeuvre - exhalation against closed airway/blowing into syringe)

- 2nd Line (chemical cardioversion) → **IV Adenosine** (6mg then 12mg then 12mg) (Adenosine is contraindicated in asthma patients ⇒ use **Verapamil**)

    - MOA ⇒ causes transient heart block in the AV node (makes patient feel like they’re about to die). Short acting (half life <10secs).

    - Side Effects of Adenosine ⇒ chest pain (brief + intense), bronchospasm, flushing
  • If Haemodynamically Unstable (Systolic BP <90mmHg)DC Cardioversion
23
Q

What is the management for AF and when is rhythm control preferred over rate control?

A

Rate Control → 1st line = beta-blocker (propanolol) or rate-limiting CCB (diltiazem** or verapamil).

-2nd line = **digoxin** (**if patients sedentary** or other drugs unsuitable, eg. avoid propanolol in asthmatics)

- Don’t use beta blocker and verapamil together ⇒ can lead to heart block
  • Rhythm Control (1st line over rate control if clear reversible cause for AF) **→ DC cardioversion (give LMWH prior) **or Amiodarone/Flecainide
24
Q

What is VT and how does it present on an ECG

A

A regular broad-complex tachycardia originating from a ventricular ectopic focus. The rate is usually >120 bpm.

ECGrate >100bpm, broad QRS complexes, no P waves, AV dissociation

SVT = QRS <120ms (narrow-complex). VT = QRS >120ms (broad-complex).

25
Q

How does Torsades de Pointes present on an ECG

A

Polymorphic VT - VT with varying amplitude → associated with long QT interval. Corkscrew appearance

May deteriorate into VF and cause sudden death.

26
Q

What is the management for Ventricular Tachycardia?

A

ABC approach, check whether patient has pulse or not (if in cardiac arrest may require defibrillation).

Stable VT (Haemodynamically Stable) → IV Amiodarone 300mg (chemical conversion)
- Verapamil is contraindicated in VT
- Amiodarone ⇒ can cause hypo or hyperthyroidism

If Haemodynamically Unstable (ie. tachycardic and hypotensive - systolic BP <90mmHg) → DC Cardioversion

Torsades de PointesIV magnesium sulfate (if stable, if unstable DC cardiovert)

27
Q

How does an VF ECG present?

A

Not Regular (as opposed to VT)

VT = Very Tidy. VF = Very Funny.

Irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death

28
Q

What is the management for Ventricular Fibrillation?

A

Check if patient has a pulse → Initiate ALS

Urgent Defibrillation and Cardioversion (and CPR)
Survivors will need an Implantable Cardioverter Defibrillator (ICD)

29
Q

What are the ECG presentations for the different types of Heart Block

A

First Degree → fixed prolonged PR interval (>0.2s/200ms = 1 large square)

    - Normal variant in athlete (asymptomatic), hence doesn’t require tx in that case (as is mobitz I)

Mobitz Type I → progressively prolonged PR interval, then eventually dropped beat

Mobitz Type II → intermittently a P wave is not followed by a QRS (PR interval is constant)

Complete Heart Block → no relationship between P waves and QRS complexes (complete AV dissociation)

30
Q

What is the management for Heart block?

A

Chronic Block (definitive management) → permanent pacemaker

Acute Block → IV atropine (may need temporary (transcutaneous) pacing if this does not work)

- Atropine = used for bradycardias to speed up heart
31
Q
A