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Cardiovascular Nafisa > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What is arrhythmia?

A

A general term for any irregularity in the RHYTHM or RATE of the heartbeat

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2
Q

Can you name some specific types of arrhythmias?

A
  • Ectopic beats
  • Atrial fibrillation
  • Atrial flutter
  • Bradycardia
  • Tachycardia
  • Ventricular Tachycardia
  • Ventricular Fibrillation
  • Supraventricular Fibrillation
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3
Q

What are ectopic beats?

A
  • abnormal heartbeat
  • occurs outside the normal rhythm of the heart and
    DOES NOT ORIGINATE from the hearts NATURAL PACEMAKER (the sinoatrial node)
  • INSTEAD originates in other areas of the heart such as the ATRIA/ VENTRICILES
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4
Q

What is atrial fibrillation?

A

RAPID and IRREGULAR electrical impulses fired in the ATRIA (upper chambers of the heart)

Cause ATRIA to FIBRILLATE (quiver)

leading to an IRREGULAR and often RAPID heartbeat

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5
Q

What is bradycardia?

A

a SLOW heart rate (heart beats slower than normal)

Typically fewer than <60 beats/ min in ADULTS

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6
Q

What is atrial flutter?

A

Rapid contractions of atria

SIMILAR to atrial fibrillation

But occurs in a MORE ORGANIZED and MORE REGULAR PATTERN

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7
Q

What is ventricular tachycardia?

A

a type of tachycardia that ORIGINATES in VENTRICLES (lower chambers of the heart)

a FAST heart rate

CAN be LIFE- THREATENING and MAY REQUIRE immediate MEDICAL ATTENTION

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8
Q

What is ventricular fibrillation?

A

a MEDICAL EMERGENCY
can lead to CARDIAC ARREST

It is:

a chaotic and extremely rapid heartbeat in ventricles

results in ventricles quivering instead of contracting#

this means that the heart cannot pump blood effectively

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9
Q

What is supraventricular tachycardia?

A

A type of tachycardia that originates in a space ABOVE ventricles

This space is NOT the atria by the way!

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10
Q

What is one way to diagnose what arrhythmia a patient is presenting?

A

ECG

This records the electrical activity of the heart over a period of time

Different arrhythmia= different patterns on ECG

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11
Q

How can we treat spontaneous ectopic heart beats in a patient who otherwise has a normal heart rate?

A

In these cases, treatment is rarely required. Just reassure the patient

However, if they are troubling the patient:

BETA BLOCKERS

( sometimes effective +may be safer than other suppressant drugs)

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12
Q

What are SYMPTOMS of atrial fibrillation?

A

HEART PALPITATIONS (pounding/ fluttering)

also:
- dizziness
- shortness of breath
- tiredness

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13
Q

What are COMPLICATIONS of atrial fibrillation?

A

STROKE

HEART FAILURE

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14
Q

Why would we want to treat atrial fibrillation?

A

To REDUCE SYMPTOMS

To PREVENT complications (i.e. stroke & heart failure)

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15
Q

What are the 3 different types of atrial fibrillation?

A

PAROXYSMAL AF

PERSISTENT AF

PERMENANT AF

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16
Q

Define PAROXYSMAL AF

A

episodes STOP WITHIN 48 hours WITHOUT TREATMENT

smal= small worry

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17
Q

Define PERSISTENT AF

A

episodes LAST > 7 days

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18
Q

What is PERMENANT AF

A

AF is present ALL THE TIME

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19
Q

What are the two general ways we treat atrial fibrillation?

A

Either by

CONTROLLING THE RHYTHM
or

CONTROLLING THE RATE

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20
Q

How is RHYTHM CONTROL achieved?

A

By CARDIOVERSION

There are TWO types of cardioversion:
- electrical
- pharmacological

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21
Q

What is electrical cardioversion?

A

Electrodes are placed on the chest

They send electric signals to your heart

To restore and maintain the rhythm of your heart

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22
Q

What is pharmacological cardioversion

A

Anti- arrhythmic drugs are used to restore and maintain the rhythm of your heart

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23
Q

When can we NOT use cardioversion?

A
  • if symptoms > 48 hours as there is an INCREASED risk of stroke

(basically cause atrial fibrillation can cause blood to pool and clots to form- so longer patient has had symptoms- the higher the chances that a clot has formed)

  • if have to do cardioversion tho even tho symptoms > 48 hours, ELECTRICAl IS preferred
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24
Q

What type of therapy should a patient be on BEFORE any cardioversion therapy?

Should this therapy be continued after their cardioversion and if so, HOW LONG FOR AFTER?

A

ANTICOAGULATION THERAPY for 3 weeks BEFORE cardioversion

AND continue for 4 weeks AFTER

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25
Q

How should patients be anticoagulated before cardioversion therapy?

A

As arial fibrillation INCREASES the likelihood of clot formation

Therefore, must anticoagulated the patient to get rid of potential clots that may have formed AND also REDUCE risk of clots forming

If we do cardioversion straight away without anticoagulation
- patient may have a clot
- the cardioversion can dislodge this clot and cause it to travel to the brain causing a stroke

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26
Q

What is does ‘haemodynamically unstable’ mean?

A

A medical condition where the cardiovascular system PARTICULARLY the hearts ability to pump blood is compromised

to the extent that it cannot adequately meet the body’s demands for oxygen and nutritions

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27
Q

How do we treat a patient with ATRIAL FIBRILLATION who is HAEMODYNAMICALLY unstable?

A
  • we must first rule OUT left atrial thrombus (a blood clot forming within the left atrium of the heart)

if patient does not have LEFT ATRIAL THROMBUS

begin ELECTRICAL CARDIOVERSION
AND
PARENTERAL ANTICOAGULANT

(the reason we rule out left atrial thrombus is again so that there isn’t the risk of that clot dislodging during the cardioversion and moving to the brain)

depending on whether its life threatening or not, and also its been <48 hours >48 hours; treatment can vary. Cards coming up on this dw

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28
Q

IF a patients atrial fibrillation TREATMENT FAILS to CONTROL their symptoms OR SYMPTOMS reoccur AFTER CARDIOVERSION; what must be done?

A

Patient needs SPECIALISED MANAGEMENT

Refer within 4 WEEKS

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29
Q

What pharmacological therapies can we use to CONTROL the HEART RATE in ATRIAL FIBRILLATION?

A

Beta blockers (not sotalol)

Rate limiting CCB

Digoxin

(monotherapy- dual therapy- rhythm control)

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30
Q

How do rate limiting CBB help CONTROL HEART RATE?

A

Block calcium channels in the heart

Reduce electrical conduction through atrioventricular node

Slows down heart rate

(The AV node helps regulate heart rhythm)

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31
Q

How do BETA BLOCKERS help CONTROL HEART RATE?

A

Block adrenaline from binding to beta- adrenergic receptors in the heart

Reduce hearts response to adrenaline

This results in a slower heart rate

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32
Q

How do we treat LIFE- THREATENING HAEMODYANMIC INSTABILITY atrial fibrillation?

A

Electrical cardioversion

(in reference to previous card, make sure to rule out left atrial thrombus before doing this procedure)

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33
Q

How do we treat NON-LIFE THREATNING haemodynamic instability atrial fibrillation?

A

< 48 hours
Rate or rhythm control
(for rhythm control use electrical or amiodarone/ flecainide)

> 48 hours
Rate control
(Verapamil, beta- blocker)

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34
Q

What is the first line treatment for MAINTENANCE DRUG TREATMENT for atrial fibrillation?

A

FIRST LINE IS RATE CONTROL:

Beta blockers (NO SOTALOL)

Rate limiting CCB

Digoxin

(monotherapy- dual therapy- rhythm control)

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35
Q

What is the second line treatment for MAINTENACE DRUG TREATMENT for atrial fibrillation?

A

SECOND LINE IS RHYTHM CONTROL

Beta blockers OR oral anti- arrhythmic drug

(SOTALOL, OR amiodarone, flecainide, propafenone, dronedarone)

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36
Q

If post- cardioversion therapy; a patient still requires RHYTHM control what treatment do we give?

A

The second line treatment for maintenance drug treatment for atrial fibrillation is RHYTHM CONTROL

SO GIVE THIS!

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37
Q

How do we treat paroxysmal and symptomatic atrial fibrillation?

(so if symptoms stop within 48 hours without treatment and if they got symptoms of their AFib)

A

VENTRICULAR CONTROL or RHYTHM CONTROL
- standard beta blocker or oral anti- arrhythmic drug

‘PILL IN POCKET’ if infrequent episodes (self treatment)

  • flecainide or propafenone restores sinus rhythm if episode occurs
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38
Q

How do we TREAT ATRIAL FLUTTER?

A

similar treatment to atrial fibrillation BUT
CATHETER ABLATION = MORE SUITABLE

(ablation creates controlled tissue lesions in the atria- so im guessing it gets rid of the tissues that were generating the abnormal electrical signals)

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39
Q

When do we give anticoagulants?

A

if the risk of thromboembolic stroke > the risk of bleeding

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40
Q

How is the risk of stroke calculated?

A

CHA2- DS2- VASc tool

C= chronic heart failure or left ventricular dysfunction

H= hypertension

A2= Age 75+

D= Diabetes Mellitus

S2= stroke/ transient ischaemic attack/ venous thromboembolism history

V= vascular disease

A= 65- 74 years

Sc= Sex category (male/ female)

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41
Q

What score of CHA2- DS2- VAsc tool suggest patient NEEDS ANTICOAGULANT therapy?

A

If score is 2 OR MORE

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42
Q

What score of CHA2- DS2- VAsc tool suggest patient DOES NOT NEED ANTICOAGULANT therapy?

A

Male= 0

Females= 1

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43
Q

What anticoagulant do we give FOR NEW ONSET ATRIAL FIBRILLATION?

A

Parenteral anticoagulation

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44
Q

What anticoagulant do we give for DIAGNOSED ATRIAL FIBRILLATION?

A

warfarin or NOAC

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45
Q

What are NOAC?

A

new oral anticoagulants

46
Q

When do we give NOACs?

A

in NON VALVULAR Afib

with ≥ 1 risk factors which are: 75+, heart failure, hypertension, diabetes mellitus, previous stroke or TIA

47
Q

What is TIA?

A

Transient ischemic attack

A mini stroke

It is the temporary disruption of blood flow to a aprt of the brain

It is a WARNING sign of INCREASED RISK of FUTURE stroke

48
Q

what is the HAS- BLED tool?

A

a risk assessment to estimate the risk of bleeding

It helps to evaluate the POTENTIAL BENEFITS of anticoagulation vs POTENTIAL RISKS

(use in conjunction with CHA2- DS2- VASc tool)

49
Q

What does the HAS- BLED tool stand for?

A

H= hypertension
A= abnormal renal/ liver function
S= stroke history

B= bleeding history or predisposition
L= Labile international normalized ratio
E= elderly (age>65 years)
D= drug or alcohol use

The higher the score (it is out of 9 in total), the higher the risk of bleeding complications

50
Q

what is labile INR?

A

labile INR means fluctuations in values of INR.
Suggests difficulty in maintain consistent anticoagulation levels= increasing risk of bleeding

51
Q

Why do drugs and alcohol increase risk of bleeding?

A

As they can increase the risks of falls/ trauma

Therefore, CONTRIBUTE to BLEEDING COMPLICATIONS

52
Q

What are the different types of VENTRICULAR TACHYCARDIA?

A
  • pulseless ventricular tachycardia
  • unstable sustained ventricular tachycardia
  • stable sustained ventricular tachycardia
  • non- sustained ventricular tachycardia
53
Q

what is PULSELESS ventricular FIBRILLATION?

A

LIFE- THREATENING

In VF, the heart’s electrical signals become chaotic and disorganized.

the ventricles (the lower chambers of the heart) quiver or fibrillate instead of contracting effectively.

the heart is unable to pump blood to the body.

The absence of a pulse indicates that the heart is not generating enough blood flow to maintain organ function.

VF is a medical emergency

immediate intervention with CPR (cardiopulmonary resuscitation) and defibrillation (shocking the heart) is required to restore normal heart rhythm and save the person’s life.

PULSE is NOT PRESENT
Patients with pulseless VF are in cardiac arrest. They are unresponsive, not breathing normally, and have no palpable pulse.

54
Q

What is pulseless ventricular TACHYCARDIA?

A

LIFE- THREATENING

a rapid heart rhythm that originates in the ventricles.
In VT, the heart beats at a very fast rate, but the contractions may not be coordinated or effective.

The heart may still be beating fast enough to generate a pulse, but in “pulseless VT,” there is no detectable pulse.

Pulseless VT is a medical emergency, as it indicates inadequate circulation.

Treatment for pulseless VT includes CPR and immediate defibrillation, similar to VF.

PULSE is NOT PRESENT
Patients with pulseless VT are in cardiac arrest. They are unresponsive, not breathing normally, and have no palpable pulse.

55
Q

What is defibrillation?

A

Defibrillation is a medical procedure that involves the use of an electrical shock to restore the normal rhythm of the heart in cases of life-threatening cardiac arrhythmias, particularly ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT).

The goal of defibrillation is to “reset” the heart’s electrical activity, allowing it to resume a coordinated and effective pumping action.

56
Q

In such cases where defibrillation has not been successful in restoring a normal heart rhythm and pulse, what must be done?

A

Iv amiodarone is given refractory to defibrillation

Amiodarone is a potent antiarrhythmic drug that can be administered intravenously. It works by affecting the electrical properties of the heart and can help stabilize the rhythm.

57
Q

What is UNSTABLE sustained ventricular tachycardia?

A

a serious cardiac arrhythmia characterized by a rapid and abnormal heart rhythm originating in the ventricles, the lower chambers of the heart.

In this context, “unstable” refers to the fact that the patient’s condition is deteriorating or at risk of deteriorating due to the arrhythmia. It is a medical emergency that requires immediate attention and intervention.

PULSE is present

have symptoms of haemodynamic instability: such as severe chest pain, palpitations, shortness of breath, dizziness, or altered consciousness.

58
Q

How is unstable sustained ventricular tachycardia treated?

A

direct current cardioversion

If this fails give IV amiodarone and repeat direct current

59
Q

What is stable sustained ventricular tachycardia?

A

Stable sustained ventricular tachycardia (VT) is a cardiac arrhythmia characterized by a rapid and regular heart rhythm originating in the ventricles, the lower chambers of the heart.

In this context, “stable” means that the patient is not experiencing severe symptoms or hemodynamic instability, and they are conscious and alert despite the abnormal rhythm.

60
Q

How do we treat stable sustained ventricular tachycardia?

A

IV anti- arrhythmic drug (amiodarone preferred)

61
Q

What is non- sustained ventricular tachycardia?

A

Non-sustained ventricular tachycardia (NSVT) is a cardiac arrhythmia characterized by episodes of rapid heartbeats originating in the ventricles (the lower chambers of the heart) that last for a brief duration, typically less than 30 seconds.

62
Q

How do we treat non- sustained ventricular tachycardia?

A

beta- blocker

can slow down the heart rate by blocking the effects of adrenaline (epinephrine) on the heart

63
Q

What is the maintenance treatment for patients at high risk of cardiac arrest?

A

MOST PATIENTS: cardioverter defibrillator implant

SOME PATIENTS also require a drug: sotalol, beta- blocker alone or beta- blocker with amiodarone

64
Q

What is TORSADE DE POINTES (prolonged QT interval)?

A

a specific type of ventricular tachycardia, a rapid and abnormal heart rhythm originating in the ventricles, the lower chambers of the heart.

often associated with a prolonged QT interval on the ECG. The QT interval represents the time it takes for the ventricles to repolarize (reset) after each heartbeat. A prolonged QT interval can lead to a susceptibility to TdP.

65
Q

What are the CAUSES of TORSADE de POINTES

A

sotalol and other drugs that prolong QT interval

hypOkalaemia

bradycardia

66
Q

why can sotalol prolong QT interval?

A

It can prolong the QT interval on an electrocardiogram (ECG) due to its action on potassium channels in the heart.

67
Q

What is paroxysmal supraventricular tachycardia? PSVT

A

is a type of cardiac arrhythmia characterized by sudden and intermittent episodes of abnormally fast heart rate.

This rapid heart rate originates above the ventricles, usually in the atria or atrioventricular (AV) node, which are the upper chambers of the heart.

68
Q

How is paroxysmal supraventricular tachycardia treated?

A

Terminates spontaneously or with reflex vagal nerve stimulation e.g. Valsalva manoeuvre, carotid sinus massage or immersing face in ice cold water

/
IV adenosine (BUT contra- indicated in COPD/ asthma)

/
Iv Verapmil

69
Q

What is reflex vagal nerve stimulation

A

stimulating the vagus nerve (cranial nerve X), leads to various physiological responses, including changes in heart rate, blood pressure

this nerve can be stimulated by e.g. Valsalva manoeuvre, carotid sinus massage or immersing face in ice cold water

Valsalva maneuver involves forceful exhalation against a closed airway (like trying to exhale against a closed mouth and nose). This increases pressure within the chest and can stimulate the vagus nerve.

Carotid sinus massage involves gently massaging the carotid sinus, a small area near the carotid artery in the neck. This stimulation can lead to activation of the vagus nerve and result in a slowing of the heart rate

Plunging the face into ice-cold water or applying cold stimuli to the face can stimulate the trigeminal nerve, which is closely connected to the vagus nerve. This can lead to a vagal response, including bradycardia (slowing of the heart rate).

70
Q

How does adenosine help treat PSVT?

A

It works by briefly blocking electrical signals in the heart’s AV node, which can interrupt the abnormal rhythm causing PSVT and restore a normal heart rate

71
Q

How do we treat haemodynamically unstable PSVT?

A

direct current cardioversion

72
Q

How do we treat recurrent episodes of PSVT?

A

catheter ablation OR drugs (verapamil, diltiazem, beta- blockers, flecainide or propafenone)

73
Q

What is amiodarone?

A

a class III anti- arrhythmic drug

74
Q

what is the initial loading dose of amiodarone?

A

200mg TDS for 7 days
200mg BD for 7 days and then
200mg OD as maintenance

75
Q

Where can pts experience side effects of amiodarone?

A

EYES, SKIN, NERVES, LUNGS, LIVER, THYROID DYSFUNCTION

76
Q

What are the EYE side effects of amiodarone?

How will you counsel patients?

A

1) Corneal micro- deposits

PATIENT COUNSELLING: night time glares when driving

2) Optic neuropathy/ neuritis (blindness)

PATIENT COUNSELLING: STOP if impaired vision

Amiodarone contains iodine, which can deposit in various tissues, including the cornea of the eye.

77
Q

What are the SKIN side effects of amiodarone?

How will you counsel patients?

A

1) Phototoxicity (burning, erythema)

2) Slate - grey skin on light exposed areas

PATIENT COUNSELLING: shield skin from light during treatment. Use wide spectrum, high SPF sunscreen for months after stopping

(Phototoxicity (photoirritation) is defined as a toxic response that is elicited after the initial exposure of skin to certain chemicals and subsequent exposure to light)

The skin reactions are thought to be related to the drug’s accumulation in the skin and its effects on pigmentation.

78
Q

What are the NERVE side effects of amiodarone?

How will you COUNSEL patients?

A

Peripheral neuropathy

PATIENT COUNSELLING: to look out for numbness, tingling hand, and feet’s, tremors

may involve direct drug toxicity to nerves and muscles

79
Q

What are the LUNG side effects of amiodarone?

How will you COUNSEL patients?

A

Pneumonitis, pulmonary fibrosis

PATIENT COUNSELLING: shortness of breath, dry cough

The exact mechanism of amiodarone-induced lung toxicity is not fully understood, but it is thought to involve inflammation and fibrosis in the lung tissue.

80
Q

What are the LIVER side effects of amiodarone?

How will you COUNSEL patients?

A

Hepatoxicity

PATIENT COUNSELLING: patients must REPORT jaundice, nausea, vomiting, malaise, itching, bruising, abdominal pain, 3x raised liver transaminases

The precise cause of amiodarone-induced liver toxicity is not well understood, but it may involve direct toxicity to liver cells.

81
Q

What are the THYROID side effects of amiodarone?

A

Amiodarone contains iodine, which can disrupt the normal regulation of thyroid hormones. It may also cause inflammation of the thyroid gland

Can cause THYRPOD DYSFUNCTION - Can cause hypo and hyperthyroidism

Hyperthyroidism e.g. weight loss, heat intolerance, tachycardia. Give carbimazole if necessary. Withdraw amiodarone

Hypothyroidism e.g. weight gain, cold intolerance, bradycardia. Start levothyroxine without withdrawing amiodarone if essential

82
Q

How can we monitor patients on amiodarone?

A

EYES: annual eye test

LUNGS: chest x- ray before treatment

LIVER: liver function tests every 6 months

THYROID: monitor TSH, T3, T4 before treatments and every 6 months

as can also cause HYPOTENSION and BRADYCHARDIA: monitor blood pressure and do ECGs

amiodarone causes HypOkalaemia, this enhances arrhythmogenic effects of amiodarone. MONITOR SERUM POTASSIUM

83
Q

Why are there danger of interactions with AMIODARINE several months AFTER STOPPING?

A

Amiodarone has an EXTREMELY LONG HALF-LIFE (around 50 days)

84
Q

Why should you avoid grapefruit juice whilst taking amiodarine?

A

grapefruit juice REDUCES amiodarone metabolism

leads to INCREASED plasma amiodarone concentration

the concentration of amiodarone in your bloodstream can increase significantly. Higher amiodarone levels can increase the risk of side effects and toxicity associated with the medication.

85
Q

Why does amiodarine interact with warfarin, phenytoin and digoxin (half)?

A

amiodarine is a is a potent inhibitor of enzymes that are responsible for metabolising for these drugs

increasing their levels in the blood + increase risk of side effects

86
Q

Why does amiodarine interact with statins?

A

like statins, amiodarone is associated with an increased risk of myopathy, which is a condition characterized by muscle pain, weakness, or inflammation.

87
Q

Why does amiodarone interact with BETA BLOCKERS and RATE LIMITING CCBs?

A

Basically all these drugs SLOW DOWN HEART RATE

When amiodarone is used in combination with beta blockers or rate-limiting CCBs, the cumulative effect of all these medications can result in significant bradycardia. This means the heart rate can become dangerously slow.

Therefore can lead to BRADYCARDIA, AV BLOCK and MYOCARDIAL DEPRESSION

Atrioventricular (AV) block is a type of heart block that occurs when there is a disruption or delay in the transmission of electrical signals between the atria (the upper chambers of the heart) and the ventricles (the lower chambers of the heart).

Myocardial depression refers to a condition where the heart muscle (myocardium) becomes weakened and less able to pump blood effectively.

88
Q

Amiodarone is known to interact with a variety of MEDICATIONS, potentially leading to a prolongation of the QT interval on an electrocardiogram (ECG)

This increases risk of ventricular arrhythmia

Give examples of such MEDICATIONS

A

Quinolones

Macrolides

TCAs

SSRIs

Lithium

Quinine

Hydroxychloroquine

Anti- malarials (chloroquine, mefloquine)

Antipsychotics (especially sulpiride, primozide, amisulpride)

89
Q

What is digoxin?

A

1-2mcg/L

Cardiac glycoside

High risk drug

90
Q

What is a positive inotrope?

A

A positive inotrope is a substance or medication that increases the force of contraction of the heart muscle, improving its ability to pump blood.

e.g digoxin

91
Q

What is a negative inotrope?

A

A negative inotrope is a substance or medication that decreases the force of contraction of the heart muscle, reducing its ability to pump blood

e.g. beta blockers, calcium channel blockers

92
Q

What is the mechanism of action of digoxin?

A

It enhances myocardial contractility by inhibiting the sodium-potassium pump (Na+/K+ pump) in heart muscle cells. This inhibition leads to an increase in intracellular calcium levels, which improves the force of cardiac muscle contraction.

93
Q

What are the therapeutic levels of digoxin?

A

Therapeutic levels of digoxin refer to the range of blood concentrations at which the medication is effective in treating specific heart conditions while minimizing the risk of toxicity.

1-2 mcg/ L (Cp 6 hours after dose)

94
Q

Is regular monitoring required for digoxin maintenance therapy?

A

NO

unless toxicity suspected or in renal impairment (as digoxin is cleared renally)

95
Q

Why are loading doses required for digoxin?

A

As it has a long half life

96
Q

What is the maintenance once daily dose of DIGOXIN for ATRIAL FLUTTER and NON- PAROXYSMAL AF in sedentary patients?

A

125- 250 mcg

97
Q

What is the maintenance once daily dose of DIGOXIN for WORSENING OR SEVERE HEART FAILURE (in sinus rhythm)?

A

62.5- 125 mcg

98
Q

What are the bioavailability’s of digoxin when it is in the following different dosage forms?

ELIXIR

TABLET

IV

A

ELIXIR= 75%

TABLET= 90%

IV= 100%

99
Q

When is there a risk of digoxin toxity?

A

risk of toxicity in hypO K+

hypo Mg2+

hyper Ca2+

hypoxia and renal impairment

100
Q

What are signs of toxicity?

A

“SLOW AND SICK”

  • bradycardia/ heart block
  • nausea, vomiting and diarrhoea, abdominal pain
  • blurred or yellow vision
  • confusion, delirium
  • rash
101
Q

What is the treatment for digoxin toxicity?

A

Withdraw: correct electrolyte imbalances

Using digoxin- specific antibody for life- threatening ventricular arrhythmias unresponsive to Atropine

102
Q

HypOkalaemia predisposes to digoxin toxicity.

What drugs cause this?

A

Diuretics (loop/ thiazide)
B2 agonist
Steroids
Theophylline

(If K+ <4.5mmol/L: give K+ supplements or K+ sparing diuretic (preferred))

103
Q

What drugs INCREASE plasma digoxin concentration?

A

Amiodarone (give half digoxin dose)

rate limiting CCBs. macrolides, ciclosporin (enzyme inhibitors)

104
Q

What drugs decrease plasma digoxin concentration

A

St Johns wart, rifampicin (enzyme inducers- speed
up metabolism of digoxin)

105
Q

What drugs decrease renal excretion?

Why can this cause digoxin toxicity?

A

NSAIDs, ACE inhibitors/ ARBs

Digoxin is renally excreted therefore drugs that decrease renal excretion= increase digoxin plasma conc

106
Q

What drugs does digoxin interact with

A
  • drugs that cause hypokalaemia e.g. diuretics, b2 agonists etc
  • drugs that are enzyme inhibitors and INCREASE plasma digoxin conc e.g. amiodarone, rate limiting CBBs
  • drugs that are enzyme inducers and DECREASE plasma digoxin conc e.g. st johns wart
  • drugs that reduce renal excretion and INCREASE plasma digoxin conc as digoxin is renally excreted e.g. NSAIDs, ACE inhibitors/ ARBs
107
Q

“CRASED” is an acronym for digoxin interations.

Write out this acronym

A

C= calcium channel blockers (verapamil)
R= rifampicin
A= amiodarone
S= St johns wart
E= erythromycin
D= diuretics

108
Q

Digoxin is said to have a narrow therapeutic index. What does this mean?

A

means the difference between a therapeutic and toxic dose is relatively small.

Therefore, careful monitoring of blood levels and clinical symptoms is essential when using these medications

109
Q

How is TORSADE de POINTES treated?

A

magnesium sulphate

because it addresses one of the underlying factors that can trigger this specific type of ventricular tachycardia—namely, electrolyte imbalances, particularly hypomagnesemia (low levels of magnesium in the blood)

110
Q

What is tachycardia?

A

a FAST heart rate

Often exceeding >100beats/ min in ADULTS

Cardiovascular Nafisa (9 decks)

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