CARDIOVASCULAR SYSTEM DRUGS-2

LVF = Left ventricular failure U&Es = Urea and electrolytes  GFR = Glomerular filtration rate t½ = Half-life VTE = Venous thromboembolism

cGMP =Cyclic guanosine monophosphate HMG CoA =3-hydroxy-3-methylglutaryl coenzyme A MAO = Monoamine oxidas DVT = Deep vein thrombosis COMT = Catechol-O-methyl transferase PE = Pulmonary embolism VTE = Venous thromboembolism OCP = Oral contraceptive pil Fibrinolytics  EXAMPLES  Streptokinase, alteplase, reteplase, tenecteplase MECHANISM OF ACTION Activation of plasminogen to form plasmin, a proteolytic enzyme that promotes the breakdown of fibrin clots into fibrin degrading products leading to clot dissolution and reperfusion. INDICATIONS 
  • Acute MI
  • Massive pulmonary embolus (alteplase)
  • Acute ischaemic stroke (under specialist supervision by stroke physician)
CAUTIONS AND CONTRA-INDICATIONS
  • Aortic dissection.
  • Active bleeding.
  • Active peptic ulcer disease.
  • Previous haemorrhagic stroke or recent ischaemic stroke.
  • Coagulation defects.
  • Recent surgery/trauma.
  • Active intracranial neoplasm.
  • Uncontrolled hypertension (relative contraindication)
SIDE-EFFECTS
  • Bleeding (including cerebral haemorrhage).
  • Nausea and vomiting.
  • Reperfusion cardiac arrhythmias and ischaemia.
  • Cerebral and pulmonary oedema.
  • Anaphylaxis.
  • Severe hypotension
METABOLISMANDHALF-LIFE  Variable–t½ for streptokinase is18–23min;t½ for alteplase is 4–5min. Metabolised predominantly by the liver. MONITORING  Monitor for signs of bleeding, anaphylaxis and intracranial haemorrhage. DRUG INTERACTIONS
  • Risk of haemorrhage is increased with oral anticoagulants.
  • Patients on ACEIs are at an increased risk of anaphylactoid reaction when streptokinase is administered
IMPORTANT POINTS
  • Fibrinolytics are licensed for ST-elevation MI within 12h of the onset of chest pain (administered ideally within one hour).
  • Streptokinase is derived from b-haemolytic Streptococci of Lancefield group C; persistence of antibodies to streptokinase may reduce the effect of subsequent doses. It has effectively been superseded by the newer fibrinolytics(e.g.reteplase)in acute mi(where primary percutaneous coronary intervention is not available).
  • Alteplase is a recombinant tissue-type plasminogen activator.
  • Does not cause allergic reactions and can be used in patients with recent streptococcal infections or recent use of streptokinase
Flecainide  MECHANISM OF ACTION 
  • Blocks Naþ dependent channels hence depressing phase 0 of the cardiac action potential.
  • Increased PR and QRS intervals and lengthened ventricular refractory period lead to slower conduction of electrical impulses, with the greatest effect noted on the bundle of His and Purkinje system.
  • In addition to the negative chronotropic effect, flecainide also reduces contractility.
INDICATIONS
  • Wolff–Parkinson–White syndrome.
  • AV nodal reciprocating tachycardia (AVNRT).
  • Ventricular tachyarrhythmias
CAUTIONS AND CONTRA-INDICATIONS
  • Second and third-degree AV block. SA node dysfunction. Impaired LV function.
  • Long-standing AF. History of structural heart disease e.g. previous MI
SIDE-EFFECTS