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Cardiology Flashcards

1
Q

ECG findings of digoxin effect

A

Down-sloping “sagging” appearance of ST depression (reverse tick)
Flattened, inverted or biphasic T waves
Shortened QT interval

Dijoxin effect - DALI (salvador dali’s moustache)

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2
Q

Cardiovascular drugs which can cause gynaecomastia

A 
Anti-hypertensives:
- Spironolactone
- Methyldopa
- Calcium channel blockers
Atrial fibrillation treatment:
- Digoxin
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3
Q

Congenital long QT syndrome predisposes to what complications

A

Polymorphic ventricular tachycardia

  • syncope
  • cardiac arrest
  • sudden death
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4
Q

Syndromes which cause congenital long QT syndrome

A

Romano-Ward Syndrome:
- autosomal dominant

Jervell and Lang-Nielsen Syndrome

  • autosomal recessive
  • also causes deafness
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5
Q

Role of cadioversion when in AF or atrial flutter

A

Prevents deterioration into VT

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6
Q

Management of angina

A

Non-pharmacological (smoking cessation, diet modification, exercise, weight reduction, salt reduction, stress reduction)
Pharmacological:
- appropriate management of risk factors (anti-hypertensives/diabetics, statins, smoking cessation aids as indicated)
- Antiplatelet therapy (aspirin)
- Symptom control - GTN, beta-blockers, Ca channel blockers, isosorbide mono-/d-nitrate)
Surgical:
- revascularisation if angina refractory or progressing (PCI, CABG)

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7
Q

Clinical features of inferior MI

A

Raised JVP without pulmonary crepitations
Bradycardia (AV node dys-syncrhony)
Hypotension (reduced RV output)
MAY have Kussmaul JVP in acute setting

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8
Q

Cardiac biomarkers

A

Elevated in myocardial infarction, normal in unstable angina
CK-MB - peaks early and returns to normal after 36-72 hours (useful for determining reinfarction)
Troponins - repeat 6-12h after admission if negative at first

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9
Q

Initial management of acute coronary syndrome

A

Aspirin
GTN + IV morphine as required
12-lead ECG in transit
O2 as required

In inferior MI with hypotension: DO NOT GIVE GTN, increase preload with fluids

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10
Q

Risk stratification in acute coronary syndrome

A

TIMI (thrombolysis in MI prediction score)

  1. Age over 65
  2. More than 3 CAD risk factors
  3. Known CAD
  4. Aspirin use in last 7 days
  5. Severe angina (2+ episodes of rest pain in 24h)
  6. ST deviation on ECG
  7. Elevated CK-MB or troponin

Each risk factor = 1 point

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11
Q

TIMI score values

A 
1-2 = low-risk
3-4 = moderate risk
5+ = high risk
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12
Q

Management of NSTEMI or unstable angina

A

Low-moderate risk:

  • aspirin
  • nil anticoagulants or invasive management indicated
  • optimise therapy + lifestyle for risk factors
  • Long-term SAAB
  • Symptomatic relief (GTN etc)

High-risk:

  • aspirin AND clopidogrel
  • unfractionated heparin or SC enoxaparin
  • IV tirofiban or eptifibatide
  • beta-blocker
  • Coronary angiography and revascularisation within 48 hours unless contraindicated
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13
Q

Treatment of STEMI

A

Symptom onset less than 1hr prior to presentation:
If PCI available within 1h PCI, if not = fibirnolysis

Symptom onset 1-3h before presentation
PCI if available within 90min or fibrinoysis

Symptom onset 3-12h before presentation:
PCI if available within 90m (or 2h incl. transport offsite), otherwise fibrinolysis

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14
Q

Indications for CABG

A

Suitable anatomy
Contraindications to fibrinolysis or PCI
Cardiogenic shock

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15
Q

Drug eluding stent v bare metal stent

A

DES: generally small vessel disease (reduced risk of restenosis and scarring)

BMS: generally used in large arteries at risk of restenosis from scarring, but due to large diameter blood flow should not be significantly reduced
Must be replaced in 10y time so are not used in vessels that are difficult to reach

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16
Q

Anti-thrombin therapy indications

A

Should be used in PCI +/- Gp IIa/III inhibitor

Should be used in fibrinolysis with fibrin-specific agents

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17
Q

Fibrinolytic agents

A

Streptokinase - lower rate of intracranial haemorrhage
Fibrin-specific agents (reduced mortality v streptokinase)
- Alteplase

Agents of choice (second generation):

  • Reteplase
  • Tenecteplase (lower rate of bleeding than alteplase)
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18
Q

Timeline of gross pathology following AMI

A

4-24h: gradual development of pale centre, peripheral dark mottling, oedematous
3-7d: pale/yellow rubbery centre, haemorrhagic border
1-3w: infarcted area is pale, thin with red/grey border, loss of tissue mass (granulation tissue)
3-6w(permanent): silver scar becoming tough and white (replacement of granulation tissue with dense fibrosis)

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19
Q

Complications of acute myocardial infarction

A

Acutely:
Mechanical
- rupture of left ventricular free wall
- rupture of interventricular septum (d3-5)
- papillary muscle rupture (MV prolapse)
Electrical:
- Inferior MI (transient sinus bradycardia, 1st degree AV block, complete heart block)
- Anterior MI (2nd or 3rd degree AV block, bifascicular or trifascicular block)
Other:
- peri-infarction pericarditis, pericardial effusion

Chronic:

  • mitral regurg (LV dilatation)
  • Dressler’s syndrome
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20
Q

Pathophysiology of Dressler’s syndrome

A

Myocardial injury - release of cardiac antigens - antibodies formed - immune complexes deposited onto pericardium - inflammatory response

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21
Q

Management of Dressler’s syndrome

A

Resolves with NSAIDs in most cases

If refractory - steroids (may delay myocardial healing)

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22
Q

Precipitants of acute pulmonary oedema

A

Cardiogenic: acute MI, arrhythmia, pericarditis, acute valvular dysfunction, endocarditis
Fluid overload
Drugs (NSAIDs, Ca channel blockers)
Noncompliance (with fluid restriction or meds)
Pulmonary embolus
Acute renal failure
High output states (septic, anaemia, thryotoxicosis)

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23
Q

Clinical features of acute pulmonary oedema

A 
Severe dyspnoea
Distress
Pallor 
Sweating
Tachycardia
Poor peripheral perfusion
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24
Q

Management of acute pulmonary oedema

A 
O2 via non rebreather mask
IV access
continuous ECG
S/L GTN every 5 minutes for 3 doses (reduce preload)
CPAP or BiPAP (reduce alveolar oedema)
Frusemide to red. fluid overload
Morphine (red. distress and WOB)

If in rapid AF - digoxin
Fluid overload not responding to frusemide - spironolactone

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25
Q

Definition of congestive heart failure

A

A condition in which an abnormality of cardiac function results in failure of the heart to circulate blood at the rate required by the tissues at normal filling pressures.

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26
Q

2 main pathological causes for congestive heart failure

A
  1. Loss of myocytes (MI, myocarditis, cardiomyopathy, infiltration, toxins etc.)
  2. Abnormal myocyte stress (HTN, valvular disease, persistent tachycardia)
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27
Q

Systolic v diastolic heart failure

A

Systolic:

  • poor contraction in systole, impaired LV contractility
  • causes ventricular dilatation
  • poor prognosis

Diastolic:

  • preserved LV contractility, preserved ejection fraction
  • normal heart size
  • impaired relaxation (stiff ventricle) - higher pressure needed to fill same volume
  • good prognosis
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28
Q

Causes of diastolic heart failure

A

Severe concentric hypertrophy (HTN, aortic stenosis, HCM)
Restrictive cardiomyopathy (e.g. amyloid)
MI
transient ischaemia (relaxation of myocardium requires ATP)

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29
Q

NYHA class for grading heart failure severity

A

I: no symptoms, even during exercise
II: reduced physical capacity during medium exercise
III: Severely reduced physical capacity during slight exercise, asymptomatic at rest
IV: symptomatic at rest

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30
Q

Management of systolic congestive heart failure

A 
Treat underlying cause
Manage risk factors (incl Na and H2O restriction)
Pharmacological:
- ACE-i, ARB
- Diuretics (symptom relief)
- Digoxin/inotropes
- Beta-blockers
- Spironolactone

Devices: +/- cardiac resynchronisation therapy or automatic implantable cardiac defibrillator

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31
Q

Management of diastolic heart failure

A

Treat underlying cause
Beta-blockers
Negative inotropic calcium antagonists (verapamil, diltiazem)
Dual chamber pacing

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32
Q

Beta blockers especially indicated in congestive heart failure

A

bisoprolol

Metoprolol

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33
Q

Causes of acute pericarditis

A

Infection

  • viral (echovirus, Coxsackie B_
  • secondary TB
  • Pyogenic bacteria (rare but fulminant)

Non-infectious:

  • Post-MI (early or Dressler’s)
  • Uraaemia (CKD)
  • Neoplastic disease
  • Radiation
  • Rheumatic disease (SLE, RA, systemic sclerosis)
  • Drug induced (procainamide, hydralazine, phenytoin)

Idiopathic

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34
Q

ECG in acute pericarditis

A

Widespread ST elevation

PR depression in all leads except AvR where elevated (indicates atrial injury)

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35
Q

Indications for pericardiocentesis

A

Cardiac tamponade
Moderate to large effusions refractory to medical therapy with severe symptoms
Suspected bacterial or neoplastic pericarditis

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36
Q

Indications for pericardial biopsy and pericardioscopy

A

Relapsing cardiac tamponade
Suspected bacterial or neoplastic pericarditis
Worsening pericarditis despite appropriate treatment without a specific diagnosis

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37
Q

Indications for hospitalisation in pericarditis

A

Haemodynamic compromise
Fever
Immunosuppression
Failure to respond to NSAIDs

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38
Q

Management of acute pericarditis

A

Treat underlying cause (e.g. dialysis - uraemia, antibiotics)

Pain relief via NSAIDs (naproxen, ibuprofen)
Colchicine
+/- corticosteroids

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39
Q

Indications for corticosteroids in pericarditis

A

Significant effusion +/- tamponade
Failure to respond to NSAIDs alone
Autoimmune or uraemic aetiology

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40
Q

Prognosis in acute pericarditis

A

Purulent: poor prognosis, high mortality
Uraemia: good prognosis following dialysis
Neoplastic: poor, treament mainly palliative as indicates widely metastatic cancer

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41
Q

Definition of cardiac tamponade

A

Accumulation of pericardial fluid under high pressure, compressing the cardiac chambers and limiting filling of the heart leading to reduced stroke volume, cardiac output and blood pressure

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42
Q

Causes of cardiac tamponade

A

Any cause of acute pericarditis can progress to tamponade, most commonly:

  • neoplastic
  • post-viral
  • uraemic

Acute haemorrhage into pericardium (blunt or penetrating chest trauma, rupture of LV free wall, complication of type A dissecting aortic aneurysm)

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43
Q

Clinical features of cardiac tamponade

A 
Distended JVP
Hypotension
Muffled heart sounds
Sinus tachycardia
Pulsus paradoxus
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44
Q

Definition of pulsus paradoxus

A

BP dropping over 10mmHg on inspiration

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45
Q

ECG findings in cardiac tamponade

A

electrical alternans (consecutive normally conducted QRS complexes alter in amplitude)

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46
Q

Definition of paroxysmal atrial fibrillation

A

AF which self-resolves within 7 days, even if only for periods of minutes/less

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47
Q

Indications for rate control in atrial fibrillation

A 
Pulse deficit (difference between heart rate and peripheral pulse rate)
Heart failure

Beta-blocker, Ca-channel antagonist (verapamil, diltiazem), digoxin, cardiac ablation

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48
Q

Cause of atrial fibrillation

A

Inflammatory reaction in atria

Re-entrant pathways around the entrance of the pulmonary veins into the left atrium

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49
Q

Danger of Wolf-Parkinson-White syndrome with atrial fibrillation

A

Accessory pathway by-passing the AV node which slows the ventricular rate below that of the atria, if skips AV node, HR can by up to 300bpm

50
Q

Management of atrial fibrillation in Wolff-Parkinson-White syndrome

A

DO NOT USE AV NODAL BLOCKING DRUGS (adenosine, Ca blockers, b-blockers)

Immediate cardioversion (risk of very fast tachycardia) - DC prefrered followed by radiofrequency ablation

If stable, option of medical treatment - procainamide or ibutilide

51
Q

Cardioverting patients with AF

A

Ensure that unlikely to return to AF post-cardioversion by prescribing amiodarone (req. loading dose then maintenance doses)

52
Q

Amiodarone: mechanism, pharmacology, side effects

A

K+ channel inhibitor - reduce K efflux from cells
Half-life 60d (hence needs loading then maint. doses)
S/E; photosensitivity, thyroid disease (6mthly TFT), pulmonary fibrosis (check annually)

53
Q

Definition of atrial flutter

A

A type of supraventricular tachycardia caused by a re-entry circuit within the RIGHT atrium

54
Q

Features of atrial flutter on ECG

A 
Narrow complex tachycardia
Regular atrial activity at 300bpm
"saw tooth" pattern of flutter waves
Flutter waves may resemble P waves in V1
Loss of isoelectric baseline
Fixed AV block (3:1) OR variable AV block (irregular QRS complexes)
55
Q

Management of atrial flutter

A

Anticoagulation as with AF (though is less thrombogenic)
High rate of success with ablation (smaller re-entry circuit therefore easier than AF, and less prone to recurrence than AF)

56
Q

AV nodal re-entry tachycardia

A

Often wrongly used synonymously with supraventricular tachycardia.

A tachycardia originating from a FUNCTIONAL re-entry pathway within the AV node

57
Q

Definition of supraventricular tachycardia

A

Any tachyarrhythmia arising from above the level of the Bundle of His

58
Q

Causes of AVNRT

A 
Typically paroxysmal
May occur spontaneously or upon provocation with:
- exertion
- caffeine
- alcohol
- beta-agonists
- sympathomimetics (amphetamines)
59
Q

Clinical presentation of AV nodal re-entry tachycardia

A 
Sudden onset rapid, regular palpitations
\+/- presyncope/syncope
If existing CAD, may cause angina pain
SOB
Anxiety
Polyuria (raised atrial pressure - increased ANP)
\+/- brief drop in BP
60
Q

ECG features of AV nodal re-entry pathway

A
  • Regular tachycardia 140-280
  • NARROW QRS complexes
  • +/- ST depression
  • QRS alternans (minor)
  • P wave may be buried in QRS complex or visible after QRS
61
Q

Management of SVT

A 
May cease spontaneously or continue indefinitely until medically treated
Vagal manoeuvres:
- Valsalva manoeuvre
- eyeball pressure
- carotid sinus massage
Adenosine!
62
Q

Definition of Wolf-Parkinson-White syndrome

A

A pre-excitation syndrome which is a combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia

63
Q

Pathophysiology of WPW

A

Pre-excitation = early activation of ventricles due to impulses bypassing AV node via an accessory pathway (abnormal conduction pathway formed during cardiac development)

As there is direct conduction from atria to ventricles bypassing the AV node, AF or a flutter can lead to a very high ventricular rate which may degenerate to VT or VF

64
Q

What is the WPW accessory pathway known as

A

Bundle of Kent or AV bypass tract

65
Q

ECG features in WPW

A 
Reduced PR interval (no AV nodal delay)
Broad QRS
Delta wave (slurring slow rise of initial part of QRS)
66
Q

Definition of ventricular tachycardia

A

A series of three or more consecutive ventricular complexes occurring at a rate of 100-250 bpm

67
Q

Common causes of VT

A
  • MI (within first 72h)
  • Non-ischaemic cardiomyopathy
  • Infiltrative disease (sarcoidosis, amyloidosis)
  • Infectious disease (myocarditis, Lyme disease)
  • Inflammatory diseases (SLE, RA etc.)
  • Mitral valve prolapse
  • Digoxin toxicity - bidirectional ventricular tachycardia
  • K and Mg abnormalities
  • blunt chest trauma
68
Q

Screening for VT

A

Based on family history: annual ECG:
- hypertrophic cardiomyopathy
- arrhythmogenic right ventricular cardiomyopathy
- Brugada
Patients with previous MI and reduced LVEF

69
Q

Prevention of VT

A 
Lifestyle modification (including appr. alcohol to reduce cardiomyopathy)
Implantable cardioverter-defibrillator (ICD)
70
Q

Clinical presentation of VT

A 
Palpitations, light-headedness
Dyspnoea
Chest pain
Syncope
Anxiety
\+/- red. BP
\+/- inc. RR
\+/- inc. JVP
\+/- signs of reduced perfusion
71
Q

ECG features of ventricular tachycardia

A

Wide-complex tachycardia

72
Q

Specific forms of VT

A

Monomorphic VT: NOT Torsade de pointes

Polymorphic VT AKA Torsade de points:
- gradual change in amplitude and twisting of QRS complezes around isoelectric line

73
Q

Causes of torsade de pointes

A

Associated with prolonged Qt interval
hypoK
HypoMg
K-channel blockers (e.g. sotalol)

74
Q

Treatment of polymorphic VT (torsade de pointes)

A

usually terminates spontaneously
Frequently recurs and may degenerate into VF

Magnesium sulfate! - reduced amplitude of early after-depolarisations due to reduce calcium influx

If refractory: isoproterenol

75
Q

Management of VT

A

IV amiodarone
(may use lidocaine)
Defib if haemodynamic collapse
ICD often required - especially if onset after MI
If ICD contraindicated (too old, frail etc.) regular amiodarone is an option

76
Q

Causes of ventricular fibrillation

A 
MI
Electrolyte abnormalities
Cardiomyopathy
Long QT syndrome
Brugada syndrome
Drugs
Environmental
PE
Cardiac tamponade
77
Q

ECG findings in VF

A

Chaotic irregular deflection or varying amplitude
No identifiable P waves, QRS complexes or T waves
Rate 150-500bpm
Amplitude reduces with duration (coarse VF-fine VF - degenerates into asystole due to depletion of myocardial energy stores)

78
Q

Management of VF

A

Defibrillation every time!

ALS algorithm

79
Q

Definition ofBrugada syndrome

A

An inherited non-structural arrhythmic disorder that can cause life-threatening arrhythmias in young, healthy people without prior warning

80
Q

Epidemiology of Brugada syndrome

A

Most common inherited arrhythmic disorders causing sudden death in young healthy patients
Autosomal dominant
Undiagnosed = estimated mortality 10%

81
Q

ECG features of Brugada syndrome

A

Prominent ST elevation (2mm) in more than 1 of leads V1-3 followed by an inverted T wave (Brugada sign)

  • may be chronic or intermittent
  • can be unmasked/augmented if intermittent by:
  • antiarrhythmic drugs
  • fever
  • ischaemia
  • cocaine/alcohol
  • hypothermia
  • hypoK
  • post DC cardioversion
82
Q

Management of Brugada syndrome

A

ICD insertion

83
Q

Definition of long QT syndrome

A

A congenital or acquired condition in which QT interval on ECG is more than 2 large squares (i.e. prolonged ventricular repolarisation) predisposing to malignant ventricular arrhythmias

84
Q

Types of genetic long QT syndrome

A

Type 1: red. outward K current (impairs repolarisation) - AD or AR
Type 2: red. outward K current (impaired repolarisation) AD
Type 3: inc. inward Na current (enhance depolarisation) AD

85
Q

Acquired causes of long QT syndrome

A 
Drugs:
- amiodarone
- TCAs
- fluconazole
- erythromycin
- metoclopramide
- methadone
- SSRIs
Myocardial disease (MI, ARF, CHB, cardiomyopathy)
Electrolytes (hypoCa, HypoK, hypoMg)
86
Q

What does a wide, inverted P wave in V1 indicated

A

Left atrial dilatation

e.g. from mitral stenosis

87
Q

What does a peaked P wave indicated

A

Right atrial enlargement

88
Q

ECG findings of L BBB

A

Broad QRS
Deep S waves in precordial leads (W pattern in V1-3)
Broad monophasic R waves in lateral leads (M pattern)
L axis deviation

89
Q

ECG findings of RBBB

A 
Broad QRS
RSR' (M pattern) in V1-3
W pattern in lateral leads
ST depression and T wave inversion in R precordial leads
Normal axis
90
Q

First degree AV block

A

Increased PR interval (more than 5 small squares)

Causes: mitral valve surgery, hypoK

91
Q

Second degree AV block Mobitz I (Wenckebach)

A

Progressive prolongation of PR interval - non-conducted P wave
P-P relatively constant, R-R progressively shortens
Causes: inf MI, athletes, cardiac surgery, drugs (b-blockers, Ca-blockers, digoxin, amiodarone)

If symptomatic, respond to atropine
No treatment required if asymptomatic

92
Q

Second degree AV block Mobitz II

A

intermittent non-conducted P waves (2:1 or 3:1)
Constant PR interval in conducted beats
Due to failure of conduction at His-Purkinje system below AV node
Causes: ant MI, hyperK, idiopathic fibrosis, septal surgery, inflammatory conditions, autoimmune, infiltrative, drugs

More associated with haemodynamic compromise, bradycardia and progression to CHB than Wenckebach
35% risk of asystole
Requires ultimate insertion of permanent pacemaker

93
Q

Third degree (complete) AV block

A

Absence of AV conductin
P and QRS not in synch (each going at own rates) - junctional or ventricular escape rhythms
Atrial rate = 100bpm, vent = 20

Likely to resbond to atropine if secondary to Mobitz I progression
Manage with permanent pacemaker

Complications: ventricular standstill, sudden cardiac death

94
Q

Trifascicular block

A

Conduction disease in all three fascicles:

  • R BBB
  • L anterior fascicle block (LA deviation)
  • L posterior fascicle

Causes: IHD, HTN, AS, congenital heart disease, hyperK, digoxin toxicity

If complete (incl. third degree heart block) OR symptomatic - treat with PPM

95
Q

ECG features of hyperkalaemia

A
  1. 5-6.5: tall tented T waves
  2. 5-7.5: loss of P wave
  3. 5-8.5: widening of QRS
  4. 5+: further widening of QRS - sine wave
96
Q

ECG features of hypokalaemia

A 
Intially (once less than 2.7):
- T wave flattening and inversion
- ST depression
- Prominent U waves
- Long QU interval
- inc. amplitude and length of P
- prolonged PR
With worsening:
- frequent ectopics
- supraventricular tachyarrhythmias
97
Q

ECG features of hypercalacaemia

A 
Shortened QT interval
J waves (when over 3.4) - notching of terminal QRS, best seen in V1
98
Q

ECG features of hypocalcaemia

A

Prolonged QT interval

T wave normal

99
Q

Junctional escape

A 
Occur when rate of supraventricular impulses arising at AV node are less than the intrinsic rate (40-60)
- narrow QRS
- rate 40-60
- no relationship between QRS and any atrial activity
- P wave inverted in lead II if visible
Causes:
- severe sinus bradycardia
- sinus arrest
- complete AV block
- hyperK
- drugs (b-blocker, ca-blocker, digoxin)
100
Q

Ventricular escape

A

Occur when rate of supraventricular impulses arriving at ventricle are less than the intrinsic rate (20-40)

  • Broad QRS +/- L/R BBB morphology
  • rate 20-40
101
Q

Causes of secondary hypertension

A

Vascular (arteritis, coarctation of aorta)
Endocrine (phaeochromocytoma, Cushing’s, renin producing tumour, primary hyperaldosteronism/Conn’s)
Renal (RAS, fibromuscular hyperplasia of renal artery- young women, GN, chronic pyelonephritis, polycystic kidneys)
Iatrogenic (steroids, OCP)

102
Q

Non-pharmacological management of HTN

A 
Dietary salt restriction
Weight loss (1mmHg for every 1% weight loss)
Diet
Exercise
Alcohol restriction
Vitamin D if low
Patient education
Smoking cessation (reduced overall CVS risk, not BP)
103
Q

Management of hypertensive emergency

A 
Antiemetic
IV fluid
Analgesia (pain will exacerbate HTN)
NO IV ACE-I in Aus:
- Pick short-acting ACE-i (captopril - can absorb through buccal mucosa)
OR Ca-channel blockers (Nifedipine)
Prazosin (alpha blocker)

Nitrates have little effect in severe HTN

104
Q

Definition of hypertrophic cardiomyopathy

A

An autosomal dominant myocardial disorder of sarcomeres characterised by disorganised myocyte architecture and marked hypertrophy or the LV wall, without dilatation, that is not explained by another cardiac or systemic disorder

105
Q

Clinical features of hypertrophic cardiomyopathy

A

Mostly asymptomatic

  • SOBOE
  • fatigue
  • atypical or angina chest pain
  • presyncope/syncope (esp. during exertion)
  • palpitations
  • mid-systolic murmur, maximal at apex and LLSB, INCREASES ON VALSALVA
  • S4
  • LV tilt
106
Q

Diagnosis of hypertrophic cardiomyopathy

A

Transthoracic echocardiogram

- maximal LV wall thickness over 15mm

107
Q

Complications of hypertrophic cardiomyopathy

A

Ventricular tachyarrhythmias - sudden cardiac death
Heart failure with SOBOE +/- chest pain
AF - thromboembolisation

108
Q

Management of asymptomatic hypertrophic cardiomyopathy

A

Modification of risk factors for CAD (DM, lipids, HTN, smoking, weight)
Minimisation of exacerbations
- low-intensity aerobic exercise
- adequate hydration
- avoid situations leading to vasodilation

109
Q

Management of symptomatic hypertrophic cardiomyopathy

A 
Lifestyle+
For angina/SOB:
- b-blockers
- verapamil
Acute hypotension
- avoid positive inotropes
Invasive therapies
- septal reduction therapy (transaortic septal myectomy or alcohol ablation)
- implantable devices (dual chamber pacemaker)
110
Q

Definition of dilated cardiomyopathy

A

A group of diseases involving the myocardium and characterised by myocardial dysfunction, coronary atherosclerosis, valvular dysfunction or structural heart disease resulting in dilation of the whole heart and impaired systolic function

111
Q

Causes of dilated cardiomyopathy

A

Idiopathic
Infection (adenovirus, parvoviurs, HIV, mycobacterial, toxoplasmosis)
Alcoholism
Uncontrolled tachyarrhythmia
Peripartum (last trimester - 6m post)
Chemotherapy (especially anthracycline/doxorubicin)
Substance abuse (cocaine, heroin)

112
Q

Diagnosis of dilated caridomyopathy

A 
CXR:
- enlarged cardiac silhouette
- pulm vasc. congestion
- pleural effusion (R side)
ECG: 
- nonspecific +/- arrhythmias +/- LBBB
Echo:
- red. ejection fraction
- global hypokinesis
- four-chamber enlargement (especially LV)
- mitral or tricuspid regurgitation
113
Q

Management of dilated cardiomyopathy

A

Treatment of underlying disease
Dietary Na restriction
Cardiac rehab

Pharmacological:

  • diuretics if sx of heart failure and evidence of fluid overload
  • ACE-i: all patients with reduced LVEF
  • B-blockers: start following resolution of acute exacerbation
  • Aldosterone antagonists: in symptomatic HF (mortality benefit)
114
Q

Classifications of infective endocarditis

A

Acute v subacute
Native v prosthetic valve
R v L sided

115
Q

Organisms in infective endocarditis

A 
Acute:
- s. aureus
- s. pneumoniae
- strep species
- haemophilus influenzae
Subacute:
- Strep viridans
- strep bovis
- enterococci
- s. epidermidis (prosthetic valves)
HACEK:
- haemophilus parainfluenzae
- actinobacilus
- cardiobacterium hominis
- Eikenella corrodens
- kingella kingae
IVDU associated:
- s. aureus
- p. aeruginosa
- candida
- brucella
116
Q

Areas of heart affected by infective endocarditis

A

Areas of high mechanical stress/turbulence:

  • mural endocardium
  • valves
  • prosthetic components
  • shunts
  • septal defects
  • sites of jet streams
117
Q

Diagnostic criteria for infective endocarditis

A

DUKES CRITERIA
2 major criteria OR 1 major + 3 minor OR 5 minor
Bacterial Endocarditis FIVE PM
Major:
B: blood cultures of typical IE organisms more than 12 hours apart
E: Endocardial involvement (new regurg or echo)

Fever
Immunological (GN, Roth’s spots, Osler’s nodes, RF)
Vascular (janeway’s lesions, arterial emboli, ICH, aneurysms)
Echo findings not meeting above
Predisposition (heart condition or IVDU)
Microbiological evidence not meeting above

118
Q

Management of infective endocarditis

A 
Prolonged ABx:
- parenteral
- guided by susceptibility testing
Non-pharm
- surgical intervention if m medical insufficient - indicated if HF, uncontrolled infection, prevention of embolic events)
General measures:
- management of CHF
- O2
- haemodialysis if renal failure
119
Q

Complications of infective endocarditis

A

Heart failure
Perivalvular (annular) abscess
Inflammatory response
Pericarditis
Intracardiac fistula
Septic embolisation (stroke, paralysis, blindness, ischaemic extremities, splenic or renal infarct, PE, acute MI)
Neuro complications (abscess, meningitis, encephalopathy, haemorrhage, seizures)
Renal (infarct, abscess, GN, acute interstitial nephritis, AKI)
MSK (vertebral osteomyelitis, septic arthritis)

120
Q

infective endocarditis most at risk of septic embolisation

A

L-sided vegetation
Large vegetation
Atrial fibrillation
S. aureus or S. bovis

121
Q

Most common cause of mitral stenosis

A

rheumatic heart disease (pretty much the only causes)

122
Q

Aetiological types of myocardial infarction

A

I: spontaneous (ruptured plaque/thrombus formation)
II: Secondary to ischaemic imbalance (e.g. hypotension, spasm)
III: Death (unable to get biomarkers to confirm)
IV: a = during PCI, b - in-stent thrombosis
V: associated with CABG

Medicine (12 decks)

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