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CSB601 > Week 6: Cardiovascular 2 - Arrhythmia, Antiplatelets, Anticoagulants, Dislipidaemia > Flashcards

Week 6: Cardiovascular 2 - Arrhythmia, Antiplatelets, Anticoagulants, Dislipidaemia Flashcards

1
Q

What is an arrhythmia?

A

An arrhythmia is a problem with the electrical impulses in the heart - abnormal impulse formation or conduction
Leads to ineffective and inefficient filling and ejection of blood from heart

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2
Q

Normal Heart rhythm - physiology

A

Sinus rhythm is the normal heart rhythm

  • Atria contract and pump blood into ventricles
  • Right ventricle pumps blood into lungs
  • Left ventricle pumps blood to body

A heartbeat is initiated by electrical signals that follow conduction pathways within the heart

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3
Q

Signs and Symptoms of arrhythmia

A
  • Palpitations due to cardiac rhythm imbalance
  • Breathlessness/Fatigue as tachycardia can cause LV systolic impairments
  • Falls/Blackouts
  • Chest pain
  • Resuscitation sudden death - arrhythmia’s can be fatal
  • No cardiac symptoms at all
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4
Q

Classification of arrhythmia’s

A 
Tachyarrhythmia - rapid heart beat
- Sinus tachycardia
- Atrial flutter
- Atrial fibrillation
- Ventricular tachycardia
Bradyarrhythmia - slow heart beat
- Sick sinus syndrome
- AV block
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5
Q

Atrial fibrillation

- First line therapy

A

Most common sustained arrhythmia associated with high incidence of stroke and heart failure

  • Can be paroxysmal, persistent or permanent
  • First line therapy is to remove underlying cause (pneumonia, thyroid imbalance, alcohol, caffeine, medications)
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6
Q

When to start drug therapy in atrial fibrillation

A

When to start treatment

  • Nature of arrhythmia is life threatening
  • Systemic symptoms or hemodynamic effects
  • Presence of underlying heart disease (heart failure, coronary artery disease or valvular heart disease)
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7
Q

First line drug therapy for atrial fibrillation

A

Beta blocker (atenolol or metoprolol)
OR
Non-dihydropyridine CCB (diltiazem or verapamil)

  • Do not use these together as both slow the heart rate and force of contraction allowing more time for heart to fill
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8
Q

Digoxin (AF treatment)

  • MOA
  • Indications
  • Adverse effects
A

MOA
- Slows heart rate and reduces AV node conduction by increased vagal tone and reduction in sympathetic activity

Indications

  • Patients with comorbidity of heart failure and require ventricular rate control as it increases the force of myocardial contraction by increasing release and availability of stored intracellular calcium
  • Effective in elderly/non active patient
  • Not strong enough in active younger patients
  • AF and Atrial flutter
  • Heart failure
  • Narrow therapeutic index - regularly assess for toxicity

Adverse effects
- Common include anorexia, nausea, vomiting, diarrhea, visual disturbances, drowsiness, dizziness, headache, rash, bradycardia, arrhythmia

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9
Q

Digoxin (AF treatment) contraindications and cautions

A

Pregnancy - safe

Geriactric - may be preferred but care if renal function is reduced

Renal reduced dose in renal impairment

Avoid using with drugs that slow cardiac conduction

Precautions

  • Hypo/Hyperthyroidism
  • Electrolyte imbalances
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10
Q

Amiodarone (AF treatment)

- MOA

A

MOA

  • Slows how quickly the heart can contract by acting on refractory period of muscle contraction, or how quickly the muscle cells can recover from one contraction to contract again
  • Also has some beta blocking activity
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11
Q

Amiodarone (AF treatment)

- Adverse effects

A

Lots of serious adverse effects (closely monitor)

  • Thyroid dysfunction
  • Pulmonary toxicity
  • Liver dysfunction
  • Ocular effects
  • Neurotoxicity
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12
Q

Amiodarone (AF treatment)

- Contraindications/cautions

A

Pregnancy/Breastfeeding - Do not use

Elderly - more likely to have bradycardia

Avoid in patients with bradycardia or prolonged QT intervals

Renal impairment

Precautions

  • Thyroid disorders
  • Lung disease
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13
Q

AF treatment - Non drug therapy

A
  • Artificial pacemakers
  • Implantable cardiac defibrillators
  • Cardio version
  • Catheter ablation
  • Surgery
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14
Q

Describe the coagulation cascade in terms of the blood vessel

A
  • Damaged blood vessel (triggers release of clotting factors)
  • Formation of platelet plug (vasoconstriction limits blood flow and platelets form a sticky plug)
  • Development of clot (Fibrin strands adhere to plug to form insoluble clot)
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15
Q

Coagulation cascade in terms of clotting factors

  • Extrinsic pathway
  • Intrinsic pathway
  • Common pathway
A

Extrinsic pathway

  • Damage to tissue outside vessel
  • Tissue thromboplastin
  • Converts inactive Factor X to activated Factor X

Intrinsic pathway

  • Damage to blood vessel
  • Cascade of clotting factors (produced using vitamin K)
  • Converts inactive Factor X to active Factor X

Common pathway

  • Once both extrinsic and intrinsic pathway produce active factor X prothrombin is converted into thrombin
  • Thrombin then converts fibrinogen to fibrin
  • Fibrin and Factor XIII produces a blood clot
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16
Q

What are anticoagulants?

A
  • Target clotting factors
  • Work in venous system
  • They are not blood thinners they just prevent the formation of clots
  • Considered a more aggressive therapy than anti platelet therapy
17
Q

When are anticoagulants used?

What are the common anticoagulant drugs?

A
  • Patients at high risk of stroke or who have already had a stroke/pulmonary embolism/VTE (include patients with AF)
  • Acute coronary syndrome

Common drugs include

  • Warfarin
  • Newer oral anticoagulants (NOACs) such as Factor Xa inhibitors
  • Heparin
  • Low molecular weight heparin (LMWH)
18
Q

Anticoagulant practice points

A
  • Counseling to ensure patient understands how to take/inject their medication as well as check for signs of bleeding
  • Avoid other drugs which cause bleeding
  • Monitor signs of bleeding
  • Surgery must be ceased prior to surgery
19
Q

Anticoagulants - Warfarin

- MOA and points

A

MOA

  • Vitamin K antagonist therefore inhibits synthesis of clotting factors including Factor X
  • As it works high up in cascade it is associated with high risk of bleeding
  • Many interactions including green leafy vegetables (high in vitamin K)
  • INR (clotting time) needs to be monitored no more than 4 weeks apart
  • Compliance as it must be taken at same time everyday
  • Avoid in pregnancy
  • Brands should never be substituted (Marevan and Coumadin)
20
Q

Anticoagulants - Heparin/LMWH

  • MOA
  • Route
  • Monitoring
  • Drugs
  • Pharmacokinetics
  • Cautions
  • Contraindications
  • Adverse effects
  • Use in pregnancy and breastfeeding
A

MOA

  • Inactivate thrombin and Factor Xa with Heparin inhibiting both equally while LMWH inhibit thrombin more than Factor Xa
  • Only available via injection
  • LWMH can be used as outpatient therapy
  • Heparin usually requires hospital monitoring
  • Drugs include Enoxaparin and Dalteparin
  • Faster onset and shorter half life than Warfarin
  • LWMH cautioned in RF
  • Contraindicated in severe hepatic impairment or disease
  • Can cause thrombocytopenia (Heparin induced thrombocytopenia - HIT)
  • Used to treat/prevent thromboembolism in pregnancy and safe for breastfeeding
21
Q

Anticoagulants - Factor Xa Inhibitors

  • MOA
  • Adverse effect
  • Route and adherance
  • Drugs
  • Practice points
A

MOA
- Selectively inhibit Factor Xa

Adverse effect
- Bleeding (it is better tolerated than Heparin)

Route and adherance
- Oral and requires compliance with same time per day administration

Drugs include

  • Apixaban
  • Rivaroxaban

Practice points

  • Not suitable for severe RF
  • No antidote - not suitable if high risk of bleeding
  • Shorter half life than Warfarin
  • Interaction are increasing in number being identified
22
Q

Anticoagulants - Direct thrombin inhibitors

  • MOA
  • Caution
  • Route
  • Drugs
A

MOA
- Directly and selectively inhibit thrombin (lower in cascade)

Caution
- Renal and liver failure

Route
- Oral but capsules cannot be opened (do not crush or chew)

Drugs
- Dabigatran

23
Q

What are antiplatelets?

What are common antiplatelet drugs?

A

Work to inhibit the ability of platelets to stick together - still circulate but cannot help form a blood clot
* They are not blood thinners
Work in arterial system

Drugs include

  • Aspirin
  • Clopidogrel
  • Dypirimadole
24
Q

Uses of antiplatelets

A
  • Prevent stroke
  • ACS
  • Aspirin used for CVD prevention in long term management of MI
25
Q

Platelet plug formation

A
  1. Platelets adhere to collagen
  2. Activation of thromboxane A2 receptor by Thromboxane A2 which is activated by arachidonic acid via COX-1
  3. Activation of ADP receptor
  4. Activation of IIb/IIIa receptor allowing aggregation of platelets at these receptors via fibrinogen cross linking

See Diagram

26
Q

Antiplatelets - Aspirin

  • MOA
  • Combination products
  • ADR
A

MOA

  • Inhibit platelet aggregation by irreversibly inhibiting cyclo-oxygenase (COX) which stops synthesis of thromboxane A2
  • Works for lifetime of platelet (up to 3 months)

Combination products

  • Aspirin + Clopidogrel
  • Aspirin + Dypirimadole

ADR (lots)
- Gastric upset, GI bleeds, ulcer, severe skin reaction, hemorrhage

27
Q

Antiplatelets - Clopidogrel

  • MOA
  • ADR
  • Interaction
A

MOA

  • Bind to platelet ADP receptor to inhibit platelet aggregation for the life of the platelet
  • It is a pro drug and needs to be activated by CYP enzymes

ADR
- Usually well tolerated but there are some rare side effects including skin reactions, multi-organ hypersensitivity, anaemia, thrombocytopenia, neutropenia

Interactions
- Grapefruit juice (blocks CYP enzyme from working)

28
Q

Antiplatelet - Dypirimadole

  • MOA
  • ADR
  • Contraindications
A

MOA
- Helps inhibit platelet function by inhibiting the platelet phosphodiesterase, which is necessary for activation of the platelet

ADR
- Commonly causes headache, GI upset, hypotension and tachycardia

Contraindications
- Avoid use in patients with unstable angina or recent MI

29
Q

Cholesterol

  • Low Density Lipoproteins
  • High density Lipoproteins
A

LDL

  • Carry cholesterol from liver to peripheral tissue for physiological function
  • Carry excess cholesterol to vascular tissue where atherosclerosis is likely to develo
  • Bad cholesterol

HDL

  • Carry cholesterol from vascular tissue to liver for removal
  • Remove cholesterol from tissue where atherosclerosis is likely to develop
  • Good cholesterol
30
Q

Target lipid levels for patients on lipid modifying therapy

A

LDL cholesterol = <2.0mmol/L

Non-HDL cholesterol = <2.5mmol/L

Total cholesterol = <4 mmol/L

HDL cholesterol = >1mmol/L

Triglycerides = <2.0mmol/L

31
Q

Dietary modification of cholesterol

A
  • Reduce saturated and trans fats (replace with monounsaturated and poly saturated fats)
  • Increase soluble fibre
  • Introduce plant sterol enriched milk, margarine, cheese produces
  • Limit alcohol
  • Lose weight
32
Q

Initiating drug therapy for cholesterol

A
  • Consider treatable secondary causes of raised blood lipid before commending drug therapy
  • First line = statins
  • If not adequately controlled add one or more of Ezetimibe, Bile acid binding resin, Nicotinic acid
  • If intolerant to statins consider Ezetimibe, Bile acid resin or nicotinic acid
  • For raised triglycerides consider Fenofibrate, nicotinic acid or fish oil
33
Q

Synthesis of cholesterol

A
  • Hydroxy-methylglutaryl coenzyme A converted to cholesterol by HMG CoA reductase (rate limiting step)
  • Cholesterol also brought into liver from fats and diet
  • Cholesterol produces steroid hormones, bile salts and membranes
  • Low liver cholesterol synthesis increases synthesis of LDL receptors (reuptake of LDL into liver)

See Diagram

34
Q

Cholesterol control - Statins

  • MOA
  • Drugs
A

MOA

  • Block action of HMG CoA reductase
  • Stops body from making excess cholesterol
  • As body is not making as much on its won it increases uptake from diet which further lowers LDL levels

Drugs include

  • Simvastatin
  • Atorvastatin
  • Rosuvastatin
35
Q

Cholesterol control - statins

  • Indications
  • ADR
A

Indications

  • Hypercholesterolaemia
  • High risk of coronary heart disease, with or without hypercholesterolaemia

ADR

  • Common include myalgia, mild transient GI symptoms, headache, sleep disturbance, dizziness, elevated aminotransferase concentration
  • Rare include myopathy and rhabdomyolysis

Must monitor for liver dysfunction and muscle problems
- Risk factors for myopathy and rhabdomyolysis are pre-existing muscle, liver, kidney disease, high dose, interacting drugs, illness, elderly/frail

36
Q

Cholesterol control - statins

- Contraindications and cautions

A

Pregnancy
- Contraindicated for use in 1st trimester causes fetal malformation

Hepatic
- Use cautiously and start at low dose

Geriatric
- Increased risk of myopathy

Renal impairment

  • Increased risk of myopathy and rhabdomyolysis
  • Start at low dose

Drug interactions - lots due to CYP enzyme metabolism (substrate of CYP3A4)

37
Q

Cholesterol control - Ezetimibe

  • MOA
  • Line of therapy
  • ADR
A

MOA

  • Reduces absorption of cholesterol from diet by inhibiting the transport of cholesterol across intestinal wall
  • Increase uptake of LDL that does get through back into liver and away from peripheral tissue

Line of therapy
- Usually in combination with statin, only used as single therapy if statins are not tolerated

ADR
- Diarrhea, myalgia/myopathy, raised liver enzymes, pancreatitis

38
Q

Cholesterol control - Ezetimibe

- Contraindications and cautions

A

Pregnancy
- No data; avoid

Hepatic
- Do not use

Not to be used with fibrates or in patients with pancreatitis or gall bladder disease

CSB601 (12 decks)

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