Week 6: Cardiovascular 2 - Arrhythmia, Antiplatelets, Anticoagulants, Dislipidaemia Flashcards
What is an arrhythmia?
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
Normal Heart rhythm - physiology
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
Signs and Symptoms of arrhythmia
- 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
Classification of arrhythmia’s
Tachyarrhythmia - rapid heart beat - Sinus tachycardia - Atrial flutter - Atrial fibrillation - Ventricular tachycardia Bradyarrhythmia - slow heart beat - Sick sinus syndrome - AV block
Atrial fibrillation
- First line therapy
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)
When to start drug therapy in atrial fibrillation
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)
First line drug therapy for atrial fibrillation
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
Digoxin (AF treatment)
- MOA
- Indications
- Adverse effects
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
Digoxin (AF treatment) contraindications and cautions
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
Amiodarone (AF treatment)
- MOA
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
Amiodarone (AF treatment)
- Adverse effects
Lots of serious adverse effects (closely monitor)
- Thyroid dysfunction
- Pulmonary toxicity
- Liver dysfunction
- Ocular effects
- Neurotoxicity
Amiodarone (AF treatment)
- Contraindications/cautions
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
AF treatment - Non drug therapy
- Artificial pacemakers
- Implantable cardiac defibrillators
- Cardio version
- Catheter ablation
- Surgery
Describe the coagulation cascade in terms of the blood vessel
- 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)
Coagulation cascade in terms of clotting factors
- Extrinsic pathway
- Intrinsic pathway
- Common pathway
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
What are anticoagulants?
- 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
When are anticoagulants used?
What are the common anticoagulant drugs?
- 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)
Anticoagulant practice points
- 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
Anticoagulants - Warfarin
- MOA and points
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)
Anticoagulants - Heparin/LMWH
- MOA
- Route
- Monitoring
- Drugs
- Pharmacokinetics
- Cautions
- Contraindications
- Adverse effects
- Use in pregnancy and breastfeeding
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
Anticoagulants - Factor Xa Inhibitors
- MOA
- Adverse effect
- Route and adherance
- Drugs
- Practice points
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
Anticoagulants - Direct thrombin inhibitors
- MOA
- Caution
- Route
- Drugs
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
What are antiplatelets?
What are common antiplatelet drugs?
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
Uses of antiplatelets
- Prevent stroke
- ACS
- Aspirin used for CVD prevention in long term management of MI
