Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 Cardiovascular > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

What is an arrythmia?

A

Problem with RATE or RHYTHM.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is atrial fibrillation?

A

A supraventricular tachyarrhythmia characterised by rapid, chaotic, ineffective atrial electrical conduction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the aetiology of atrial fibrillation? (x3)

A
  • Systemic causes: thyrotoxicosis, hypertension, pneumonia and alcohol
  • Heart: mitral valve disease, ischaemic heart disease, rheumatic heart disease, cardiomyopathy, pericarditis, sick sinus syndrome, atrial myxoma
  • Lung: bronchial carcinoma, PE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is sick sinus syndrome?

A

Caused by ischaemia, infarction or fibrosis of the sinus node, presenting with bradycardia (from intermitted failure of sinus node depolarisation) and intermitted tachycardia (caused by increased ectopic pacemaker activity).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathophysiology of atrial fibrillation? (x2)

A

Dilation of the atria with fibrosis and inflammation causes a difference in refractory periods within the atrial tissue and promotes electrical re-entry that results in AF. CVS entities such as hypertension, congestive heart failure, and coronary disease, through mechanisms such as myocardial stretch and fibrosis with disruption in cell-to-cell coupling, can also lead to triggers and electrical remodelling that may promote AF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the different types of atrial fibrillation? (x4)

A
  • Paroxysmal: recurrent AF that terminates spontaneously within 7 days
  • Persistent: sustained AF for more than 7 days, or less than 7 days but necessitates pharmacological or electrical cardioversion
  • Permanent: refractory to cardioversion or accepted as final rhythm.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the epidemiology of atrial fibrillation?

A

Very common in the elderly (around 5% of over 65years).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the symptoms of AF?

A

Often asymptomatic. Some patients may experience palpitations or syncope.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the signs of AF? (x3)

A

Irregularly irregular pulse, difference in apical beat and radial pulse, tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does an ECG show in AF? (x2)

A

Uneven baseline (fibrillations) with absent P waves, irregular QRS complexes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the investigations for AF? (x2 (x3))

A
  • BLOODS: TFT to assess cause, U&Es (to assess renal function as this will impact on management), K+, Mg2+, Ca2+ (hypokalaemia, hypomagnesaemia or hypercalcaemia increases risk of digoxin toxicity)
  • ECHOCARDIOGRAM: assess for cause such as mitral valve disease, left atrial dilation, left ventricular dysfunction or structural abnormalities.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an echocardiogram?

A

Cardiac USS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is meant by haemodynamically stable?

A

Normal and stable BP and HR, which may be associated with syncope, MI, shock.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is atrial fibrillation managed acutely? (x2)

A
  • HAEMODYNAMICALLY UNSTABLE: RHYTHM CONTROL – electrical cardioversion with pre-cardioversion anticoagulation using LMWH such as enoxaparin or heparin.
  • HAEMODYNAMICALLY STABLE or OVER 65 (UNSTABLE): RATE CONTROL – with AVN-blocking drugs, usually beta-blocker such as BISOPROLOL and oral anticoagulant. Failure of treatment, consider combination therapy, adding diltiazem (calcium-channel blocker), and digoxin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is atrial fibrillation managed chronically? (x2)

A
  • ANTICOAGULATE: DOAC or warfarin and aim for INR between 2.5 and 3.0.
  • RATE CONTROL for all patients: beta blocker, and digoxin as second-line
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What decides whether to anticoagulate patients with chronic AF?

A

CHA2DS2-VASc score to predict risk of stroke: 2 points assigned to age over 74, 1 for 65/74, HTN, DM, recent cardiac failure and vascular disease. Men with score over 0 and women over 1 are anticoagulated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the complications of atrial fibrillation? (x3)

A

Thromboembolism, bradycardia (from effect of AF on AVN), congestive heart failure (from responsive rapid ventricular rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is atrial flutter?

A

Characterised by atrial rate of 300 per min and ventricular rate of 150 per min (2:1 heart block as AV node conducts every second beat).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the aetiology of atrial flutter? (x7)

A

Atrial dilation, congenital heart disease, fibrosis, toxic condition such as thyrotoxicosis, alcoholism, or pericarditis. AF may also convert to atrial flutter on anti-arrhythmics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the pathophysiology of atrial flutter?

A

Reentrant waveforms travel up the interatrial septum and down the right atrial free wall (typical form) or vice versa (reverse typical form).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does an ECG show with atrial flutter?

A

Saw-tooth baseline with rate of around 300 per min.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the nomenclature of atrial flutter?

A

You say ‘x:1 block’ based on the number of ‘flutters’ for each QRS complex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does atrial flutter look like on ECG?

A

In the typical anti-clockwise form, there are negatively directed saw-tooth atrial deflections in leads II, III, and aVF, and positive deflections in V1. In the reverse typical form, the pattern is inverted. Photo shows typical form.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does atypical atrial flutter present on an ECG?

A

Continuous undulation (moving smoothly up and down) of the atrial complex with atrial rates above 240 bpm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is atrial flutter treated?

A

Same as AF. Though conservative techniques to reverse it such as vagal manoeuvres may work (vagal manoeuvres slow the HR by stimulating the vagus nerve).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is supraventricular tachycardia?

A

Rapid regular rhythm arising from a discrete area within the atria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the aetiology of supraventricular tachycardia? (x6)

A
  • Digoxin toxicity
  • Cardiomyopathies
  • IHD
  • Previous cardiac surgery
  • Thyrotoxicosis
  • Exogenous stimulants such as amphetamines, cocaine and acute alcohol intoxication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the types of supraventricular tachycardia?

A
  • Atrial fibrillation
  • Atrial flutter
  • Wolff-Parkinson-White syndrome
  • Focal atrial tachycardia
  • AV node re-entry tachycardia
  • Multi-focal atrial tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is focal atrial tachycardia? ECG?

A

Recurrent, regular tachycardia with a fixed heart rate between 100-250 bpm. P waves are visible BEFORE EVERY QRS and are uniform i.e., there is just simple increased beats-per-minute in the atrium and normal PQRST waveforms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the most common presentation of digoxin toxicity (in relation to the types of supraventricular tachycardias)?

A

Focal atrial tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is AV node re-entry tachycardia? ECG?

A

Regular tachycardia with a fixed heart rate between 140-280 bpm. P waves may be visible, but usually occur AFTER the QRS complex with a short R-P interval.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is multi-focal atrial tachycardia? ECG?

A

Irregular tachycardia at a rate between 120-200 bpm. P waves occur before every QRS and there are at least three different P-wave morphologies when looking at a single lead.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the symptoms and signs of supraventricular tachycardia? (x2)

A
  • Palpitations from high heart rate
  • Fatigue or syncope from poor CO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How are vagal manoeuvres used to investigate supraventricular tachycardias? What else can be used?

A

Vagal manoeuvres stimulate the vagus nerve which decreases HR. IV adenosine can do the same thing. This is helpful in differentiating atrial tachycardias (focal and multifocal atrial tachycardias) from other causes of supraventricular tachycardia such as AF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How are focal atrial tachycardias treated? (x4)

A
  • Adenosine causes AV node blockade
  • Beta-blocker or calcium-channel blocker to control ventricular response rate or breaking the tachycardia.
  • Ibutilide or amiodarone can also be used if the above are contraindicated or haven’t worked.
  • When the cause is digoxin toxicity, treatment is instead aimed at supportive care and withholding digoxin (NB: digoxin is used to treat AF and atrial flutter).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the complications of supraventricular tachycardias? (x2)

A

Congestive heart failure from poorly effective heart beating and low CO, and cardiomyopathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is Wolff-Parkinson-White syndrome?

A

Disorder of electrical conductivity in the heart. Someone has WPW syndrome when they are symptomatic. Asymptomatic patients are said to have a WPW pattern.

38
Q

What is the pathophysiology of Wolff-Parkinson-White syndrome?

A
  • Occurs when one or more strands of myocardial fibres capable of conducting electrical impulses (known as accessory pathways and often referred to as Bundle of Kent) connect the atrium to the ipsilateral (same side) ventricle across the mitral or tricuspid valves. This pre-excites part of the ventricle, as accessory pathways (unlike the AVN) have no conduction delay.
  • In other words, there is a defect in the atrioventricular electrical insulation at the AV groove. This defect is the accessory pathway that permits premature excitation of the ventricle.
  • WPW predisposes patients to supraventricular arrythmias from retrograde impulse conduction through the accessory pathway (or conduction via accessory pathway and retrograde through the His-Purkinje system) – this is called atrioventricular re-entrant tachycardia (AVRT).
  • Atrial fibrillation, flutter and tachycardia may also occur
39
Q

What is the aetiology/risk factors of WPW? (x7)

A
  • Congenital defect – most commonly Ebstein’s anomaly where leaflets of the tricuspid valve (septal and posterior leaflets) adhere to the underlying myocardium.
  • Genetic mutation/family history
  • Hypokalemic periodic paralysis (weakness/paralysis from drop in potassium)
  • Hypertrophic cardiomyopathy
  • Mitral valve prolapse
  • Atrial/ventricular septal defect
  • Transposition of the great vessels
40
Q

What is the epidemiology of Wolff-Parkinson-White syndrome: Prevalence? Gender? Age?

A

Presence of WPW pattern ECG in general population is 0.1% - 0.3%. Male to female ratio is 2:1. Present from birth (likely attributable to congenital being most common cause).

41
Q

What are the signs and symptoms of WPW?

A

Palpitations, syncope, SOB and chest pain from arrythmias.

42
Q

What does an ECG show in WPW?

A

Delta wave on ECG (slurred QRS upstroke). Short PR interval and widening of the QRS complexes with secondary ST-T wave changes.

43
Q

What are the other investigations for WPW? (x2)

A
  • Echocardiogram to identify associated hypertrophic cardiomyopathy, Ebstein’s anomaly etc.
  • Electrophysiology: invasive programmed electrical stimulation and monitoring to locate and understand the physiology of the accessory pathway(s) involved
44
Q

What is heart block?

A

Impairment of the AVN impulse conduction.

45
Q

What is first degree heart block?

A

Prolonged conduction through the AVN.

46
Q

What are the two types of second degree heart block?

A

Mobitz Type 1 (Wenckebach) and Mobitz Type 2 (Hay).

47
Q

What is Mobitz Type 1 second degree heart block?

A

Progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AVN. The cycle then begins again.

48
Q

What is Mobitz Type 2 second degree heart block?

A

Intermittent or regular failure of conduction through the AVN. Defined by the number of normal conductions per failed or abnormal one.

49
Q

What is third degree heart block?

A

AKA Complete heart block. No relationship between atrial and ventricular contraction through failure of conduction through the AVN, and ventricular contraction generated by a focus of depolarisation within the ventricle (ventricular escape – where excitation comes from an accessory pacemaker).

50
Q

What is the aetiology of heart block? (x6)

A
  • Most common: MI or STEMI
  • Infection such as rheumatic fever, infective endocarditis, myocarditis, Lyme disease
  • Drugs such as digoxin, beta-blockers, calcium-channel blockers (these are AV blocking agents)
  • Metabolic such as hyperkalaemia (increases depolarisation and slows conduction), cholestatic jaundice and hypothermia
  • Infiltration of conducting system such as sarcoidosis, cardiac neoplasms and amyloidosis
  • Degeneration of conducting system
51
Q

What is the epidemiology of heart block: Age? Clinical cases?

A

More common at age 50 and increases with advancing age. Majority of 250 000 pacemakers implanted annually are for heart block.

52
Q

What are the symptoms of each heart block type?

A
  • FIRST: asymptomatic
  • MOBITZ I: asymptomatic
  • MOBITZ II: may cause Stokes-Adams attacks (syncope caused by ventricular asystole), dizziness, palpitations, chest pain and heart failure.
  • THIRD: may cause Stokes-Adams attacks (syncope caused by ventricular asystole), dizziness, palpitations, chest pain and heart failure.
53
Q

What are the signs of each heart block type?

A
  • Often normal. Examine for signs of the cause.
  • MOBITZ II: (not common) signs of reduced CO such as hypotension when bpm is less than ~40.
  • THIRD-DEGREE: slow large volume pulse (high SBP and wide PP), JVP may show ‘cannon A waves’ (occurs when right atrium contracts against closed tricuspid valve causing refluxive pulsation in jugular vein; indicates complete AV dissociation), and less commonly signs of reduced CO.
54
Q

What does first-degree heart block look like on ECG?

A

Prolonged PR interval (over 0.2 seconds):

55
Q

What does Mobitz I heart block look like on ECG?

A

Progressively prolonged PR interval, culminating in a P wave that is not followed by a QRS:

56
Q

What does Mobitz II heart block look like on ECG?

A

Intermittently, a P wave is not followed by a QRS. May be a regular pattern:

57
Q

What does third-degree heart block look like on ECG? Differentiating QRS complexes?

A

No relationship between P waves and QRS complexes. QRS complexes initiated by focus in the bundle of His are narrow; QRS complexes initiated more distally are wide and slow rate:

58
Q

What are the other investigations for heart block? (x3)

A

Look for other signs of cause: CXR (cardiac enlargement, pulmonary oedema), bloods (TFT, digoxin level, cardiac enzymes, troponin), echocardiogram (wall motion abnormalities, aortic valve disease, vegetations).

59
Q

How is first-degree or Mobitz I heart block managed?

A
  • If patients are asymptomatic, then patient should just be monitored as they are low risk.
  • If symptomatic, (i) discontinue AV blocking medications such as beta-blockers, and (ii) infrequently, a dual-chamber (RA and RV) permanent pacemaker.
60
Q

How is Mobitz II and third-degree heart block managed?

A
  • Asymptomatic/mildly symptomatic: (i) discontinue AV-node blocking drugs, (ii) permanent pacemaker
  • Severely symptomatic: (i) temporary (external) pacemaker and IV atropine in patients with acute block, (ii) permanent pacemaker
61
Q

What are the complications of heart block? (x2)

A

Cardiac arrest, heart failure.

62
Q

What is bundle branch block?

A

A form of heart block associated with a defect in the bundle branches (offshoots of the bundle of His).

63
Q

What is the anatomy of the bundle branches?

A

Bundle of His divides into the right and left bundle branches. The right bundle branch contains one fascicle (meaning bundle). The left bundle branch contains two fascicles – left anterior and left posterior fascicles.

64
Q

How does RBBB present on an ECG? (x4)

A
  • Prolongation of last part of the QRS
  • rsR’ ‘bunny ear’ pattern in the anterior precordial leads (V1-V3) i.e., a terminal R wave (meaning the last deflection in the complex is an R wave).
  • Slurred S wave in lead I, aVL and often V5&6.
  • Right axis deviation.
  • NB: ST segment depression are normal in leads V1-3.
65
Q

How does LBBB present on an ECG? (x5)

A
  • Widens the entire QRS
  • An rS complex in V1
  • Broad monophasic R waves in lateral leads (I, aVL, V5-6)
  • Absence of Q waves in lateral leads
  • Commonly left axis deviation.
66
Q

What is an easy way of remembering LBBB and RBBB interpretation on ECG?

A

LBBB – WiLLiaM (V1 QRS looks like W and V6 looks like M). RBBB – MaRRoW (V1 QRS looks like M and V6 looks like W).

67
Q

What is characteristic of T waves in bundle branch block?

A

T wave will be deflected opposite to the terminal deflection of the QRS complex.

68
Q

What is ventricular tachycardia?

A

Defined as presence of a wide complex QRS (>120 milliseconds) at a rate of >100bpm, that originates in the ventricles and is not due to aberrant conduction (e.g., bundle branch block). It is a CARDIAC ARREST RHYTHM.

69
Q

What is the aetiology of ventricular tachycardia? (x6)

A
  • IHD
  • Cardiomyopathy
  • Channelopathies: congenital or acquired abnormalities in cardiac sodium channels (long QT syndrome, Brugada syndrome), potassium channels (long QT syndrome, show QT syndrome), and calcium channels (catecholaminergic polymorphic VT).
  • Electrolyte imbalances
  • Infectious such as Chagas disease
  • Some patients may also be idiopathic and have no evidence of structural heart disease – called idiopathic VT
70
Q

What is the epidemiology of ventricular tachycardia: Common cause?

A

Most common cause is ischaemia, especially in Western world.

71
Q

What are the types of ventricular tachycardia?

A
  • Sustained: lasts at least 30 seconds or requiring termination due to haemodynamic instability
  • Non-sustained: lasts for at least three consecutive beats but terminating spontaneously in less than 30 seconds and not resulting in haemodynamic instability
  • Polymorphic: different wide QRS complex morphologies
  • Monomorphic: organised, single-morphology QRS complexes
72
Q

What is meant by haemodynamically unstable?

A

Associated with hypotension, signs of diminished cerebral perfusion (syncope, confusion, dizziness), or signs of coronary perfusion (angina, dyspnoea).

73
Q

What is Torsades de pointes?

A

Form of polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation.

74
Q

What is the aetiology of Torsades de pointes?

A

Hypomagnesemia, hypokalaemia, and congenital and acquired long QT syndrome.

75
Q

What is the pathophysiology of ventricular tachycardia? (x3 mechanisms)

A

Depends on aetiology: (1) in patients with IHD, prior MI or cardiomyopathy, areas adjacent to damaged myocardium are susceptible to re-entrant arrhythmias because these areas are hypoxic which can be hyperirritable; or (2) VT arises from EADs (leading to Torsades de pointes); or (3) VT arises from DADs (leading to idiopathic and other polymorphic VTs).

76
Q

What are EADs and DADs?

A

Early after-depolarisations (EADs) are depolarisations that occur during phase 2 or 3, before normal repolarisation is complete. Delayed after-depolarisations (DADs) occur during phase 4 after repolarisation is complete but before a normal action potential would occur.

77
Q

What are the symptoms and signs of ventricular tachycardia? (x5)

A

Tachycardia, hypotension (reduced CO), weak pulse, signs of cerebral hypoperfusion (syncope, dizziness), signs of coronary hypoperfusion (angina, dyspnoea).

78
Q

What are the findings on an ECG of VT? (x4)

A
  • QRS over 120 milliseconds at a rate of 100 bpm or greater.
  • May show AV dissociation
  • May show previous MI
  • QRS over 140 milliseconds in RBBB or 160 milliseconds in LBBB (because these pathologies already result in wider QRS complexes).
79
Q

What other investigations are there for VT? (x3)

A
  • Electrolytes: imbalance suggestive of aetiology
  • Troponin/creatinine kinase-MB elevated in MI (suggestive of aetiology)
  • Echocardiogram: depressed left ventricular function and evidence of cardiomyopathy
80
Q

How is VT managed: Haemodynamically unstable? Haemodynamically stable? TdP? Ongoing?

A
  • Haemodynamically unstable: synchronized cardioversion (same as defibrillation but on a patient that still has a pulse), then anti-arrhythmic medication such as IV amiodarone or lidocaine.
  • Haemodynamically stable: anti-arrhythmic medication, then synchronised cardioversion if failure
  • Torsades de pointes: IV magnesium sulphate for hypomagnesaemia (common aetiology), isoprenaline infusion (non-selective beta adrenoceptor agonist), and temporary/permanent pacing
  • Ongoing VT: ICD (implantable cardioverter defibrillator), then anti-arrhythmic therapy and catheter ablation (identify site of arrythmia and ablation of affected tissue)
81
Q

What are the complications of VT? (x2)

A

VF, sudden cardiac death (cardiac arrest).

82
Q

What is ventricular fibrillation?

A

When the ventricles of the heart quiver and pump inefficiently. It is a CARDIAC ARREST RHYTHM.

83
Q

What is the aetiology of cardiac arrest? (x7)

A
  • Very similar to VT:
  • IHD (including MI)
  • Cardiomyopathy
  • Channelopathies: congenital or acquired abnormalities in cardiac sodium channels (long QT syndrome, Brugada syndrome), potassium channels (long QT syndrome, show QT syndrome), and calcium channels (catecholaminergic polymorphic VT).
  • Electrolyte imbalances
  • Myocarditis
  • Near drowning or major trauma
  • 1% of patients may also be idiopathic
84
Q

What is the pathophysiology of VF?

A

Same as VT. Only there is virtually no CO.

85
Q

What are the signs and symptoms of VF?

A

Similar to VT: Tachycardia, hypotension (virtually no CO), NO pulse, signs of cerebral hypoperfusion (syncope, dizziness), signs of coronary hypoperfusion (angina, dyspnoea).

86
Q

How does VF look like on an ECG? How does this differ from VT?

A

Ventricular rate exceeds 400. Unlike VT, VF looks completely disorganised and there are no discernible P waves, QRS complexes or T waves.

87
Q

How is VF managed?

A

Look at cardiac arrest notes; VF is treated as cardiac arrest: Defibrillation and CPR, epinephrine, anti-arrhythmic and magnesium. People who survive are often also considered for an implantable cardioverter-defibrillator (ICD).

88
Q

What are the complications of VF?

A

Cardiac arrest (sudden cardiac death).

89
Q

What is the prognosis of VF?

A

The prognosis of cardiac arrest is 2%; the prognosis of VF is therefore also 2%.

90
Q

How does hyperkalaemia result in reduced conduction?

A
  • In normal physiology, depolarisation occurs from intracellular movement of sodium, intracellular movement of calcium maintains the depolarisation, and repolarisation occurs from extracellular movement of potassium.
  • In hyperkaliaemic states (when extracellular concentration of potassium is high), the action potential duration shortens due to faster repolarisation
  • Moderate increases in potassium result in faster conduction velocities as potassium affects myocardial excitability. However, when potassium levels rise further still, sodium channels become inactive, and conduction velocity decreases and refractory periods increase, thereby resulting in bradycardia.
91
Q

What does hyperkalaemia look like on an ECG?

A
  • K+ over 5.5 mmol/L: tall, tented T waves
  • K+ over 6.5 mmol/L: P wave widens and flattens, long PR
  • K+ over 7.0 mmol/L: bradycardia, prolonged QRS, sine (mathematical) wave appearance
  • K+ over 9.0 mmol/L: cardiac arrest – asystole, VF, PEA
92
Q

How is hyperkalaemia managed?

A
  • 10 10 50 50 10
  • 10ml of 10% IV calcium gluconate – protects myocardium
  • 50ml of 50% dextrose
  • 10 units of insulin – drives potassium into cells

Year 3 Cardiovascular (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions