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Chapter 2 - Cardiovascular system > 1. Arrhythmias > Flashcards

1. Arrhythmias Flashcards

1
Q

What are arrhythmia?

A

An abnormal heart rhythm caused by abnormal electrical activity

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2
Q

Types of arrhythmias

A

Arrhythmias are classified in accordance to where they start in the heart

Supraventricular - start above the ventricles in the atria
* Atrial fibrillation
* Atrial flutter
* Paroxysmal superventriclar tachycardia

Ventricular - start in the ventricles and more deadly type of arrythmias
* Ventricular tachycardia
* Ventricular fibrillation
* Torsade de pointes

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3
Q

Atrial fibrillation

A

Most common type of arrhythmia. A fast and irregular heart rhythym that orginates in the atria

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4
Q

Atrial fibrillation types

A

Paroxysmal - episodes last < 7 days
Persistent - episodes last > 7 days
Permanent - Present all the time

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5
Q

Atrial fibrillation symptoms

A
  • Palpitations
  • Dyspnoea
  • Dizziness, Tiredness
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6
Q

Atrial fibrillation complications

A
  • heart failure; as bloood is being pumped inefficiently around the body
  • stroke; as an irregular heart rhythm causes blood to pool in the atrium, causing a clot, which can be expelled from the heart, to the brain and lead to a stroke
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7
Q

Arrhythmia treatment determining factors

A

Two types:

  1. Rate control aims to reduce the ventricular rate
    Usually first line, UNLESS:
    * new onset atrial fibrillation with symptoms < 48 hrs and NO haemodynamic instability
    * reversible cause
    * atrial flutter suitable for ablation
  2. Rhythym control aims to restore sinus rhythm
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8
Q

Rate control treatment

A
  • Beta blocker (not SOTALOL)
  • Rate-limiting CCB (diltiazem, verapamil) - not to be used in heart failure
  • Digoxin (ONLY FOR sedentary patients and non-paroxysmal)

If monotherapy does not work,
2nd line: combination therapy bUT cannot combined VERAPAMIL and DIGOXIN together = interaction

If dual therapy is infeffective, rhythym control should be considered

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9
Q

Stroke prevention assesment

A

CHA(2)DVAS(2)S

C - chronic heart failure or left ventricular systolic dysfunction [1]
H - Hypertension [1]
A(2) - AGE 75+ [2]
D - diabetes mellitus [1]
S(2) - Stroke/TIA/VTE [2]
V - vascular disease [1]
A - 65-74 years [1]
S - sex i.e female 1[1]

2 points or more = high risk = Anticoagulant

Warfarin or DOAC (only for patients who do not have issues with their heart valves)

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10
Q

Rhythm control tretament

A

Through the use of anti-arrhythmic drugs:
* Amiodarone
* Flecainide and Propafenone - avoid in ischaemic heart disease, e.g angina

For paroxysmal atrial fibrillation <48 hrs:
Pill-in-pocket approach can be used

For patients post-cardioversion: standard beta-blocker NOT sotaolol

Atrial flutter: managed in a similar way HOWEVER these patients respond better to catheter ablation

Beta blockers aree used as they reduce sympathomomimetic activity which

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11
Q

Risk of bleeding

A

O - older 75+ [1]
R - reduced haemoglobin, haematocrit, anaemia [2]
B - bleeding history [2]
I - insufficient kidney function [1]
T - treatment with antiplatelet [1]

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12
Q

Paroxysmal supraventricular tachycardia

A

When the heart rate beats super fast in a short while, short circuit in the atrium causes the atrium to contract over and over agin

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13
Q

Paroxysmal supraventricular tachycardia treatment treatment

A

Usually stops spontaenously, can also be managed with:

  1. Vagal nerve stimulation - when the parasympathetic nervous system is activated to reduce the heart rate
    e.g face in cold water, valsalva manoevure
  2. IV adenosine, Verapamil

If the episodes are recurring:
catheter ablation OR anti-arrhythmic drugs

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14
Q

Ventricular arrhythmias

A

Includes ventricular tachycardia and ventricular fibrillation.
Ventricualr arrthymias are the worst type, as the ventricles pump blood directly out of the body and to lungs, so has a greater impact on bodily function when changes occur in their rhythym

Ventricular tachycardia - ventricles contract very quickly over again. This can also lead to ventricular fibrillation

Ventricular fibrillation - when the heart beats so fast, it stops working and goes into cardiac arrest = MEDICAL EMERGNECY = DEFRIBRILLATOR

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15
Q

Ventricular arrhythmias management

A

Ventricular fibrillation - cardiopulmonary resuscitation and defribrilator

Most patients at risk of a cardiac arrest are fitted with a defribillator implant

Patients whom are haemodynamically unstable:
* Require diect current
* Stable and sustained: IV anti-arrhythmic drug

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16
Q

Torsade de pointes

A

Life-threatening type of ventricular tachycardia with a long QT interval

Hypokalaemia is a risk factor for a prolonged QT interval = torsade de pointes

17
Q

Torsade de pointes symptoms and treatment

A

Symptoms
* Fainting
* Seizures
* Palpitations
* Dyspnoea

Treatment:

IV magnesium sulphate

18
Q

Classes of anti-arrhythmic drugs

A

Class I:
Na+ channel blockers
(membraine stabilising drugs)
* Lidocaine
* Flecainide
* Propafenone
* Disopyramide

Class IV
Rate-limiting Ca2+ channel blockers
* Diltiazem
* Verapamil

Class III
K+ Channel blockers
* Amiodarone
* Sotalol
* Dronedarone

Class II:
* Beta-blockers

Other:
* Adenosine (CI Asthma/COPD)
* Digoxin (Sedentary patients with non-paroxysmal atrial fibrillation and heart failure)

19
Q

Amiodarone mechanism of action

A

Blocks K+ channels that repolarise the heart during phase 3 of the cardiac action potential

20
Q

Amiodarone uses

A

Treats most types of arrhythmias and used during CPR to revive a patient with pulsless ventricular tachycardia or ventricular fibrillation

21
Q

Amiodarone oral loading dose

A

200mg TDS for 1 week, then BD for 1 week, then OD as maintenance

22
Q

Amiodarone key counselling

A

Patients should on amiodarone should be provided an alert card

23
Q

Amiodarone side effects

A

P -pulmonary toxicity, prolonged QT interval
H - hyper/hypothyroidism, hepatotoxicity
O - optic neuritis
N - neuropathy in limbs
E - eyes corneal micordeposits
S - slate-grey skin, sensitive to light

24
Q

Amiodarone side effects

A

As amiodarone has a long half life, the dangerous effects can persist for a month or more after stopping treatment

Corneal micro-deposits
Can affect driving at night as the lights can cause dazzling

Grey skin, phototoxicity
Patients should use high SPF sunscreen and protect skin

Optic neuropathy
Amiodarone can damage the topic nerve, patients should report impaired vision

Peripheral neuropathy
Can present as pins and needles, numbness, tremors

Thyroid dysunfction resulting in high or levels of thyroid levels
monitor: TFT, TSH, T3, T4

Hepatotoxicity
Patients should report signs of liver toxicity - abdominal pain, dark urine, jaundice, persistent vomiting
Monitor: LFT’s
STOP: if 3x increase in AST and ALT

Pulmonary toxicity
Patients should report shortness of breath or cough

QT prolongation:
Monitoring: Potassium
Patients should report signs of an erratic, irregular or slow heartbeat

Bradycardia

25
Q

Amiodarone drug interactions

A
  • Amiodarone is metabolised by cytochrome P450 enzymes, interacts with drugs that inhibit this: Grapefruit juice, Cimetidine
  • Amiodarone is an enzyme inhibitor, therefore increasing blood vessels of some drugs: important to consider with NTI drugs;
    Digoxin (half-dose), phenytoin, Warfarin, ciclosporin, Tacrolimus
  • Interacts with drugs that also cause bradycardia:
    beta-blocker, digoxin, rate-limiting CCB (diltiazem and verapamil) cardio-depression
  • Interacts with statins as they also cause rhabdomyolysis
    Dose adjustments must occur
  • Interacts with drugs that also prolong the QT interval:
  • antipsychotics, anti-arrhythmic drugs, citalopram, escitalopram (SSRI’s), Clomipramine (TCA), Clarithromycin, Erythromycin (macrolides), domperidone, hydroxyzine, Lithium, Methadone, Quinolone, 5-HT3 antagonist e.g ondansetron

Hypokalaemic drugs and drugs that prolong the QT interval, increase the risk of torsade de pointes
Hypokalaemic drugs: B2 agonist salbutamol, corticosteroid, loop and thiazide diuretics, theophylline

  • Interacts with drugs that also cause peripheral neuropathy
    cisplatin, isoniazid, metronidazole, nitrofurantoin, phenytoin, vinca alkaloid
26
Q

Digoxin mechanism of action

A

Digoxin increases the force of contraction of the heart by inhibiting Na+/K+ ATPase in myocardium. Also reduces heart rate and depresses electrical impulses

27
Q

Digoxin uses

A

Patients with non-paroxysmal atrial fibrillaton AND heart failure

28
Q

Digoxin therepeutic drug monitoring

A

0.8 - 2mcg/L
Treat patients and not level

Therapeutic drug monitoring:
Measure plasma levels 6 hours after dose
No regular monitoring required UNLESS toxicity or renal impairement as digoxin is renally cleared so it can accumulate and cause toxicity in renal imapirement

29
Q

Digoxin dose

A

Lower doses are given in renal imapirement and in the elderly.
Loading doses are usually given for rapid treatment like to restore sinus rhythm as quickly as possible

Maintenance doses are given orally once daily
* Non-paroxysmal atrial fibrillation in sedentary patients: 125-250mcg
* Worsening or severe heart failure: 62.5-125mcg

Tablet digoxin and oral solution digoxin have a different bioavailibility
Switching from IV to oral, dose needs to increased by 20% - 33%

30
Q

Digoxin toxicity signs

A

G - gastro-intestinal: N/V, abdominal pain
R - rash (skin reactions)
A - arrhythmias e.g bradycardia, heart block
C - CNS: confusion, delerium, hallucinations
E - eyes: blurred vision, blind spot, yellow halos

31
Q

Factors that increase the risk of digoxin toxicity

A

Hypokalaemia predisposes to digoxin toxicity, as digoxin works on the same sites as potassium on the N/K+ ATPase, so when K+ levels are low digoxin can bind more easily, increasing its effects

Renal impairement also increases the risk of digoxin toxcity

32
Q

Digoxin interactions

A
  • Interacts with hypokalamaemic drugs as this increases the risk of digoxin toxicity:
    Corticosteroids, B2 agonist, diuretics (loop and thiazide) theophylline

P-glycoproetin an efflux transporter protein and kicks drugs outside of cells
* If this is inhibited by a drug, digoxin levels increase: = toxcity
inhibitors - amiodarone, rate-limiting CCB’s, clarithromycin, erythromcyin, itraconazole/ketoconazole

  • If this is induced by a drug, digoxin levels will decrease = therapeutic failure
    inducers - phenytoin, rifampicin, St John’s Wort

Interacts with drugs that reduce renal excretion = digoxin toxicity as digoxin is renally cleared
ACE inhibitor/ARBS, NSAIDs

**Interacts with drugs that also cause bradycardia **
Beta-blocker, Rate-limiting CCBS (diltiazem and verapamil)

  • High blood calcium predisposes to digoxin toxicty, so digoxin interacts with:
    Vitamin D supplements, e.g colecalciferol, calcium supplements

Chapter 2 - Cardiovascular system (10 decks)

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