CICMWrecks Tables (Click to Open)
Clonidine
Pharmacopeia - Central Antihypertensives
| CLONIDINE | |
|---|---|
| GROUP | Central Antihypertensive |
| CICM Level of Understanding | Level 3 |
| INTRODUCTION | partial alpha agonist with an affinity for alpha2 receptors 200 times that for alpha1 receptors |
| USES | - refractory hypertension - adjunct in pain management and during anaesthesia - in patients withdrawing from opiods - diagnosis of phaechromocytoma |
| PHARMACEUTICS (PC) | |
| PC: Chemical | |
| PC: Presentation | both in oral form as a white tablet in dosages of 100-150mcg and IV/IM forms as a colourless solution with 150mcg/ml |
| PHARMACODYNAMICS (PD) | |
| PD: Main Action | |
| PD: Mode of Action | useful effects of clonidine rest on its ability to stimulate alpha2 receptors in the lateral reticular nucleus resulting in decreased central sympathetic outflow by a positive feedback mechanism, and in the spinal cord where it augments endogenous opiate release and modulates descending noradrenergic pathways. |
| PD: Route & Doses | PO/IV/IM doses usually 150-300mcg twice daily |
| PD: Metrics (Onset/ Peak/ Duration) | |
| PD: Effects | CVS - transient increase in BP due to alpha2 agonism peripherally but this is followed by a more prolonged fall in BP. - CO is usually maintained despite bradycardia. CNS - sedation and anxiolysis at low doses but anxigenic at higher doses. - Provides analgesia without respiratory centre depression and is synergistic with opiods. Renal - inhibition of ADH may be the cause of diuresis. Endocrine - stress response to surgery inhibited. Insulin release in reduced, usually BSL ok |
| PD: Side Effects / Toxicity | - multiple effects of this drug make it intolerable to many patients, with somnolence and dry mouth being a frequent concern. - It may cause profound bradycardia if used with beta blockers. - If withdrawn suddenly it may cause a rebound hypertension |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | bioavailabilty Immediate release: 75% to 85% routes of administration Oral, IV and IM |
| PK: Distribution | lipid solubility highly lipid soluble in order to cross the BBB |
| Protein binding (PK: Distribution) | 20% to 40% |
| Volume of distribution (PK: Distribution) | 2.1 L/kg |
| PK: Metabolism | Extensively hepatic to inactive metabolites |
| PK: Excretion | Urine (40% to 60% as unchanged drug) |
| - Clearance (PK: Excretion) | |
| - Half Life (PK: Excretion) | 12-16 hours (increased in pts with renal disease) |
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Calcium Channel Blockers
Pharmacopeia - Direct Vasodilators incl. Calcium Channel Blockers
| VERAPAMIL | NIMODIPINE | NIFEDIPINE | DILTIAZEM | |
|---|---|---|---|---|
| GROUP | (CCB) Ca channel blocker – Class I Antiarrhythmic – Vaughan Williams Class IV | (CCB) Ca channel blocker – Class II | (CCB) Ca channel blocker – Class II | (CCB) Ca channel blocker – Class III Antiarrhythmic – Vaughan Williams Class IV |
| CICM Level of Understanding | Level 3 | Level 2 | Level 3 | Level 3 |
| INTRODUCTION | Phenylalkylamine (Non-dihydropyridine calcium channel blocker) Synthetic papaverine derivative | Dihydropyridine calcium channel blocker | prototypical dihydropyridine calcium channel blocker | Benzothiazepine (Non-dihydropyridine calcium channel blocker) |
| USES | HTN Angina Paroxysmal SVT and AFib/Aflutter | Treatment and prevention of cerebral vasospasm after SAH Also used in migraine, CVA and drug resistant epilepsy can pass the blood-brain barrier | primarily arterial vasodilatory e¬ffects with little effect on electrical conduction in the heart. Used primarily for HTN, angina and in preterm labour | It is used for angina and hypertension |
| PHARMACEUTICS (PC) | ||||
| PC: Chemical | ||||
| PC: Presentation | Racemic mixture. PO: 40-240mg. Also in combo w Trandolapril. IV Clear solution at 2.5mg/ml | IV 200mcg/ml with ethanol and macrogol PO 30mg tablets | available in sustained and immediate release oral formulations, 10-60mg | sustained and immediate release oral formulations, 60-360mg |
| PHARMACODYNAMICS (PD) | ||||
| PD: Main Action | ||||
| PD: Mode of Action | Binds to V binding site of L-type channel. Levoisomer: main effects (arterial vasodilation). Slows conduction through the AV and SA node to a greater extent than other CCBs. Dextro: Only acts on fast sodium channels, accounting for local anesthetic effects (1.6x potent as procaine) | Binds to N binding site of L-type Ca channel on vascular smooth muscle to reduce intracellular Ca. | Selectively dilates arterial resistance vessels. The ↓in arterial BP elicits sympathetic reflexes, with resulting tachycardia and positive inotropy. | Similar to the other Ca Channel blockers in terms of blood pressure. |
| PD: Route & Doses | 40mgPO or 5-10mg IV. | 60mg Q4h PO or 20mcg/kg/hr IV | PO 10-20mg BD. | PO/IV 30-80mg TDS |
| PD: Metrics (Onset/ Peak/ Duration) | ||||
| PD: Effects | CVS: slow conduction of AP at SA and AV node, negatively inotropic, peripheral vasodilation (↓SVR), arrhythmia (heart block, VF in WPW). CNS: ↑CBF, may potentiate effects of depol/NDMBs. GIT - Constipn/Nausea | CVS: systolic and diastolic hypotension, 1mcg/kg/h → ↑CO+30% CNS: increases CBF+18% without steal, blunts cardiovascular responses to surgical stimulus/intubation | Thus, arteriolar resistance and blood pressure are lowered, contractility and segmental ventricular function are improved, and heart rate and cardiac output are modestly increased. | Produces more peripheral vasodilation than verapamil and more conduction delay than the dihydropyridines such as nifedipine |
| PD: Side Effects / Toxicity | Dizziness, nausea, flushing, postural hypotension. in patients without CCF: ↑LV fn by improving ischemia. In pts with CCF: ↓contractility and LV fn. Should be avoided in pts with WPW- cause VT/VF. Inhibits CYP3A4. | Decreases SVR and can increase CO (overall, May drop BP) | should not be used for acute blood pressure reduction in hypertensive emergencies. Peripheral oedema is a common side e¬ffect, 2-3 weeks post initiation of therapy. Other side e¬ffects are related to its vasodilating properties: flushing, vertigo, headaches, hypotension and parathesias. Risk of coronary vasospasm with acute withdrawal. | Peripheral oedema is a common side effect, 2-3 weeks post initiation of therapy. Other side effects include ushing, vertigo, headaches, hypotension and parathesias. |
| PHARMACOKINETICS (PK) | ||||
| PK: Absorption | PO/IV. BA 20-25% Well absorbed with high fi¬rst pass metabolism on/ dur 1-2 hrs / 6-8 hrs (PO) | PO/IV. BA 30% Well absorbed high first pass metabolism | PO. BA 60% Well absorbed moderate first pass metabolism on/dur ~20 minutes / not stated | PO/IV. BA 40% Well absorbed high -first pass metabolism on/dur PO: 30-60 min; IV: 3 mins |
| PK: Distribution | Highly lipid sol – use cerebral vasospasm | lipid solubility moderately low, minimal BBB | ||
| Protein binding (PK: Distribution) | ~90% | 98% | ~90% | 70% to 80% |
| Volume of distribution (PK: Distribution) | 3.89 L/kg | 1-2 L/kg | 0.62-1.12 L/kg | 3-13 L/kg |
| PK: Metabolism | Hepatic via multiple CYP isoenzymes, one active metabolite with 20% activity | Demethylation and dehydrogenation to inactive pyridine analogue. | Hepatic via CYP3A4 to inactive metabolites | Hepatic active metabolites desacetyl-diltiazem |
| PK: Excretion | Urine (70% metab, 3% to 4% unchanged); feces (16%) | Inactive metabolites urine and faeces. | Urine (60% to 80% as inactive metabolites); faeces | Urine ( 4% as unchanged, 7% as metab); faeces |
| - Clearance (PK: Excretion) | ||||
| - Half Life (PK: Excretion) | 3-7 hours | 2-4 hrs | 2-5 hours (↑ in liver failure) | 3-4.5 hours (↑ in renal failure) |
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FRUSEMIDE
Pharmacopeia - Diuretics
| FRUSEMIDE | |
|---|---|
| GROUP | Diuretic - Loop |
| CICM Level of Understanding | Level 1 |
| INTRODUCTION | Sulfonamide derivative |
| USES | Oedema of cardiac, renal or hepatic origin, Renal insufficency Hypertension Raised ICP Hypercalcaemia |
| PHARMACEUTICS (PC) | |
| PC: Chemical | |
| PC: Presentation | Photosensitive solution 10mg/ml 20/40/500mg tabs, Syrup |
| PHARMACODYNAMICS (PD) | |
| PD: Main Action | |
| PD: Mode of Action | Diuresis Inhibition of active chloride ion reabsorption in PCT and ascending limb of LoH ↓ reabsorption of NaCl → ↓ tonicity in the renal medulla → ↓water reabsorption and diuresis. Other effects are mediated by the induction of the COX-2 enzyme which assists in synthesis of prostaglandins. |
| PD: Route & Doses | 20-2000mg daily PO/IV/SL/IM. |
| PD: Metrics (Onset/ Peak/ Duration) | |
| PD: Effects | Pulmonary and systemic vasodilation Diuresis ↑ RBF and ↑ corticomedullary blood flow ↓O₂ demand in the LoH (ischaemic protection) |
| PD: Side Effects / Toxicity | ↓ K+/Na+/Cl-/Ca++, Hyper- urea/glu/chol, Metabolic alkalosis Tox: Deafness, Pancreatitis BM depression Interstitial nephritis (worse with aminoglycoside) |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | PO/IV/SL/IM. PO BA 50% Onset PO/SL 30-60mins, IV 5 mins . Dur PO/SL 6-8hrs, IV 2hrs |
| PK: Distribution | |
| Protein binding (PK: Distribution) | 91-99% (Albumin) |
| Volume of distribution (PK: Distribution) | 0.1L/kg |
| PK: Metabolism | Renal to glucuronide Minimal hepatic |
| PK: Excretion | 80% unchanged in urine |
| - Clearance (PK: Excretion) | |
| - Half Life (PK: Excretion) | 0.5-2hrs. ESRF: 9hrs |
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Acetazolamide vs Frusemide
Pharmacopeia - Diuretics
| ACETAZOLAMIDE | FRUSEMIDE | |
|---|---|---|
| GROUP | Diuretic – Carbonic Anhydrase Inhibitor | Diuretic - Loop |
| CICM Level of Understanding | Level 3 | Level 1 |
| INTRODUCTION | Sulfonamide | Sulfonamide derivative |
| USES | Glaucoma Miniere’s disease Altitude sickness Adjunct in epilepsy | Oedema of cardiac, renal or hepatic origin, Renal insufficency Hypertension Raised ICP Hypercalcaemia |
| PHARMACEUTICS (PC) | ||
| PC: Chemical | ||
| PC: Presentation | 250mg white tablets 500mg vials for reconstitution | Photosensitive solution 10mg/ml 20/40/500mg tabs, Syrup |
| PHARMACODYNAMICS (PD) | ||
| PD: Main Action | ||
| PD: Mode of Action | Diuresis Reversible, non-competitive inhibitor of carbonic anhydrase PCT: ↓H+ and HCO3- prodn ↓ cytosol H+ → ↓Na+ reabs in PCT→ ↑H2O loss ↓cytosol HCO3→↑luminal HCO3→ H2O diffusion with HCO3 ,Na, K to urine Eye: ↓Na pump, ↓AH formation | Diuresis Inhibition of active chloride ion reabsorption in PCT and ascending limb of LoH ↓ reabsorption of NaCl → ↓ tonicity in the renal medulla → ↓water reabsorption and diuresis. Other effects are mediated by the induction of the COX-2 enzyme which assists in synthesis of prostaglandins. |
| PD: Route & Doses | 250-1000mg q6hrly IV/PO | 20-2000mg daily PO/IV/SL/IM. |
| PD: Metrics (Onset/ Peak/ Duration) | ||
| PD: Effects | Metabolic: Acidosis via ↑ excretion of bicarb (and reabsorption of Cl) Resp: ↑MV → comp resp alk CNS: anticonvulsant properties, ↓ CSF and IOP by ↓d formation GIT: ↓ Pancreatic and gastric GU: mild diuresis, Na retention | Pulmonary and systemic vasodilation Diuresis ↑ RBF and ↑ corticomedullary blood flow ↓O₂ demand in the LoH (ischaemic protection) |
| PD: Side Effects / Toxicity | metabolic acidosis, urinary alkalinisation, parathesias, fatigue, hypokalaemia, N+V, abdo pain Tox: Rashes, renal stones | ↓ K+/Na+/Cl-/Ca++, Hyper- urea/glu/chol, Metabolic alkalosis Tox: Deafness, Pancreatitis BM depression Interstitial nephritis (worse with aminoglycoside) |
| PHARMACOKINETICS (PK) | ||
| PK: Absorption | IV/PO PO BA = 100% | PO/IV/SL/IM. PO BA 50% Onset PO/SL 30-60mins, IV 5 mins . Dur PO/SL 6-8hrs, IV 2hrs |
| PK: Distribution | Lip sol: crosses BBB | |
| Protein binding (PK: Distribution) | 70-90% | 91-99% (Albumin) |
| Volume of distribution (PK: Distribution) | 0.1L/kg | |
| PK: Metabolism | Not metabolised | Renal to glucuronide Minimal hepatic |
| PK: Excretion | Unchanged in urine | 80% unchanged in urine |
| - Clearance (PK: Excretion) | ||
| - Half Life (PK: Excretion) | 6-9hrs | 0.5-2hrs. ESRF: 9hrs |
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Carvedilol vs Spironolactone
Pharmacopeia - Carvedilol vs Spironolactone
| CARVEDILOL | SPIRONOLACTONE | |
|---|---|---|
| GROUP | Mixed alpha and beta blocker | Diuretic – Aldosterone antagonist |
| CICM Level of Understanding | Level 3 | Level 3 |
| INTRODUCTION | third generation non selective beta blocker with alpha 1 antagonist properties. | A synthetic steroid |
| USES | - used to reduce the excessive adrenergic activity that occurs in response to heart failure. - hypertension | Oedema – CHF, cirrhosis with ascites, refractory. HTN, Nephrotic syndrome. With loop/thiazide to conserve K+, diagn of Conn's syndr |
| PHARMACEUTICS (PC) | ||
| PC: Chemical | ||
| PC: Presentation | oral form in both immediate and sustained release formulations | 25/100mg tablets |
| PHARMACODYNAMICS (PD) | ||
| PD: Main Action | ||
| PD: Mode of Action | Beta blockage leads to ↓Gs activity in receptor associated organs and associated ↓in adenylyl cyclase and intracellular Ca2+. Alpha blockage leads to ↓ Gq activation and subsequent ↓in IP3 and intracellular Ca2+ | Acts in the DCT. It is a competitive antagonist of aldosterone at the receptors in the DCT. Decreased Na reabsorption and increased K reabsorption = Increased Na loss and Diuresis. |
| PD: Route & Doses | oral doses start at 6.25 BD and doubled 1/52 until not tolerated | PO. 25-200mg/day |
| PD: Metrics (Onset/ Peak/ Duration) | ||
| PD: Effects | β: It produces decreases in heart rate and cardiac output and myocardial oxygen consumption. α: Peripheral vasodilation | Sedation and muscle weakness (due to electrolyte abnm) Antihypertensive, Diuresis (in 3-4 days) Potassium retention Anti-androgenic effect- inhbn of ovarian androgen secretion ↑renal Ca excr, ↑plasma urea Reversible hyperchloraemic MA |
| PD: Side Effects / Toxicity | - Withdrawal. - Care with: Opioids, Halo, OAD, CCB - Due to its metabolism, it should be used in caution in liver failure patients and elderly | ↑K+(esp in renal failure). N/V and GI disturbances Menstr irreg, Gynaecomastia ↑digoxin conc. ↓pressor response ↑effects of CVS depressants |
| PHARMACOKINETICS (PK) | ||
| PK: Absorption | bioavailabilty rapid and extenisve absorption but high fi-rst pass metabolism leading to bioavailability of 25-35% | PO - BA 70%, extensive 1st pass metb. Onset 3-4hrs, dur upto 3 days |
| PK: Distribution | lipid solubility moderate | |
| Protein binding (PK: Distribution) | 98% to albumin | 90% |
| Volume of distribution (PK: Distribution) | 105 L/kg | |
| PK: Metabolism | Extensively hepatic, via CYP2C9, 2D6, 3A4, three active metabolites | Hepatic: Rapidly and extensively metabolised by deacetylation and dethiolation. Active metab: canrenone and 7-alpha-spirolactone |
| PK: Excretion | faeces | Urine and faeces |
| - Clearance (PK: Excretion) | ||
| - Half Life (PK: Excretion) | 7-8 hours | 1-2hours, metab upto 24hrs |
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AMIODARONE
Pharmacopeia - Antiarrhythmics
| AMIODARONE | |
|---|---|
| GROUP | Antiarrhythmic – Vaughan Williams Class III K channel blocker |
| CICM Level of Understanding | Level 1 |
| INTRODUCTION | benzofuran derivative - 37% iodine by weight class III antiarrhythmic displays actions of all four classes. |
| USES | critical care for treating many arrythmias |
| PHARMACEUTICS (PC) | |
| PC: Chemical | structurally resembles thyroxine. |
| PC: Presentation | tablets – 100/ 200mg. clear colourless solution 50mg/ml for inf. Therapeutic range (1-2.5mg/L) but monitoring rarely necessary |
| PHARMACODYNAMICS (PD) | |
| PD: Main Action | |
| PD: Mode of Action | blocks potassium channels, calcium channels, sodium channels and adrenoceptors |
| PD: Route & Doses | doses PO 200mg TDS 1/52, BD 1/52, then OD IV 5mg/kg over 1hr → 15mg/kg over 24 hrs IV |
| PD: Metrics (Onset/ Peak/ Duration) | onset / duration 2 days to 3 wks / 1 wk to 5 mon |
| PD: Effects | - Sinus rhythm slowed by 15% secondary to slowed diastolic depolarization of nodal cells - AV nodal automaticity is decreased and AV nodal conduction speed is slowed 25% - After IV administration decreased SVR and LV contractility - Coronary artery vasodilation with increased coronary blood flow - QT prolongation |
| PD: Side Effects / Toxicity | CVS - not arrhythmogenic despite QT prolongation (likely because of its multiple actions), bradycardia and hypotension Resp- pneumonitis, fibrosis or pleuritis. Endo - it may cause hypothyroidism (6%) or hyperth (1%). Hepa - cirrhosis, hepatitis, jaundice. LFT monitoring. Corneal microdeposits common- resolve on cessation. |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | poorly absorbed, BA 40-70% |
| PK: Distribution | |
| Protein binding (PK: Distribution) | 96% |
| Volume of distribution (PK: Distribution) | 66L/kg |
| PK: Metabolism | complex metabolism, hepatic via de-ethylation catalysed by CYP 2C8 and 3A4. active metabolite N-desethylamiodarone |
| PK: Excretion | via skin, faeces, urine, lachrymal glands |
| - Clearance (PK: Excretion) | |
| - Half Life (PK: Excretion) | ~40-55 days |
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DIGOXIN (Limited)
Pharmacopeia - Antiarrhythmics
| DIGOXIN | |
|---|---|
| GROUP | Antiarrhythmic – Vaughan Williams Class V Other |
| CICM Level of Understanding | Level 3 |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | IV, PO BA 60-80% |
| PK: Distribution | |
| Protein binding (PK: Distribution) | prot bind ~25%; uremia- displaced fm pl prot bind sites |
| Volume of distribution (PK: Distribution) | 6-7 L/kg thyroid (↑ in hyper, ↓ hypo). |
| PK: Metabolism | Stomach:Sequential sugar hydrolysis+ redn of lactone ring by intestinal bacteria min hepatic, most excr unchanged |
| PK: Excretion | Urine (50% to 70% unchanged) |
| - Half Life (PK: Excretion) | 36-48 hours |
| PHARMACODYNAMICS (PD) | |
| PD: Mode of Action | i) Na/K ATPase inhibition → ↑ intracell Na → ↓ Na-Ca pump → ↑ intracell Ca → inotropy ii) direct: ↑ AV node ERP, ↓ V ERP iii) Indirect: Via Vagus – bradycardia, ↓ A refr. Augmentn of direct ↑ AV node ERP |
| PD: Effects | CVS - The main action of digoxin is to increase the force of cardiac contraction; automaticity and contractility also increase. - The heart rate is slowed due to a combination of improved haemodynamics, depression of sinus node discharge, slowing of AV nodal conduction, an increase in the AV nodal refractory period, and an indirect vagotonic effect. - Rapid intravenous administration of digoxin may cause vasoconstriction, leading to hypertension and decreased coronary blood flow. - The characteristic ECG changes produced by the drug include prolongation of the PR interval, ST-segment depression, T-wave flattening, and shortening of the QT interval GIT - Anorexia/N/V/Diarrhoea (especially if therapeutic range exceeded) CNS - Headache, confusion, coma (toxicity) - Visual disturbances (deranged red-green colour perception) Renal- Mild diuretic effect Miscellaneous- Rashes, eosinophilia; Gynaecomastia |
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DIGOXIN | AMIODARONE
Pharmacopeia - Antiarrhythmics
| DIGOXIN | AMIODARONE | |
|---|---|---|
| GROUP | Antiarrhythmic – Vaughan Williams Class V Other | Antiarrhythmic – Vaughan Williams Class III K channel blocker |
| CICM Level of Understanding | Level 3 | Level 1 |
| INTRODUCTION | glycoside derived from the dried leaves of the foxglove Block Na-K-ATPase pump | benzofuran derivative - 37% iodine by weight class III antiarrhythmic displays actions of all four classes. |
| USES | used in AF and atrial flutter, SVT and in heart failure | critical care for treating many arrythmias |
| PHARMACEUTICS (PC) | ||
| PC: Chemical | structurally resembles thyroxine. | |
| PC: Presentation | PO: tablets 62.5mcg or 250mcg. IV:25-250mcg/ml. Narrow therapeutic window. Monitoring necessary - 0.5-2mcg/L(~1) | tablets – 100/ 200mg. clear colourless solution 50mg/ml for inf. Therapeutic range (1-2.5mg/L) but monitoring rarely necessary |
| PHARMACODYNAMICS (PD) | ||
| PD: Main Action | ||
| PD: Mode of Action | i) Na/K ATPase inhibition → ↑ intracell Na → ↓ Na-Ca pump → ↑ intracell Ca → inotropy ii) direct: ↑ AV node ERP, ↓ V ERP iii) Indirect: Via Vagus – bradycardia, ↓ A refr. Augmentn of direct ↑ AV node ERP | blocks potassium channels, calcium channels, sodium channels and adrenoceptors |
| PD: Route & Doses | IV/PO. loading 250-500mcg QID then 62.5-125mcg daily | doses PO 200mg TDS 1/52, BD 1/52, then OD IV 5mg/kg over 1hr → 15mg/kg over 24 hrs IV |
| PD: Metrics (Onset/ Peak/ Duration) | onset / duration Oral: 1-2 hours; I.V.: 5-60 mins / 3-4 days | onset / duration 2 days to 3 wks / 1 wk to 5 mon |
| PD: Effects | CVS - The main action of digoxin is to increase the force of cardiac contraction; automaticity and contractility also increase. - The heart rate is slowed due to a combination of improved haemodynamics, depression of sinus node discharge, slowing of AV nodal conduction, an increase in the AV nodal refractory period, and an indirect vagotonic effect. - Rapid intravenous administration of digoxin may cause vasoconstriction, leading to hypertension and decreased coronary blood flow. - The characteristic ECG changes produced by the drug include prolongation of the PR interval, ST-segment depression, T-wave flattening, and shortening of the QT interval GIT - Anorexia/N/V/Diarrhoea (especially if therapeutic range exceeded) CNS - Headache, confusion, coma (toxicity) - Visual disturbances (deranged red-green colour perception) Renal- Mild diuretic effect Miscellaneous- Rashes, eosinophilia; Gynaecomastia | - Sinus rhythm slowed by 15% secondary to slowed diastolic depolarization of nodal cells - AV nodal automaticity is decreased and AV nodal conduction speed is slowed 25% - After IV administration decreased SVR and LV contractility - Coronary artery vasodilation with increased coronary blood flow - QT prolongation |
| PD: Side Effects / Toxicity | Thyroid-Vd Narrow therapeutic window -monitoring - 0.5-2mcg/L(~1) Toxic > 2.5- arrhythmias, AV block. anorexia,N/V/D, lethargy. Altered Red green colour perception. ECG: ↑ PR, ST dep, T fl-attening, ↓QT. (may not indicate toxicity) | CVS - not arrhythmogenic despite QT prolongation (likely because of its multiple actions), bradycardia and hypotension Resp- pneumonitis, fibrosis or pleuritis. Endo - it may cause hypothyroidism (6%) or hyperth (1%). Hepa - cirrhosis, hepatitis, jaundice. LFT monitoring. Corneal microdeposits common- resolve on cessation. |
| PHARMACOKINETICS (PK) | ||
| PK: Absorption | IV, PO BA 60-80% | poorly absorbed, BA 40-70% |
| PK: Distribution | ||
| Protein binding (PK: Distribution) | prot bind ~25%; uremia- displaced fm pl prot bind sites | 96% |
| Volume of distribution (PK: Distribution) | 6-7 L/kg thyroid (↑ in hyper, ↓ hypo). | 66L/kg |
| PK: Metabolism | Stomach:Sequential sugar hydrolysis+ redn of lactone ring by intestinal bacteria min hepatic, most excr unchanged | complex metabolism, hepatic via de-ethylation catalysed by CYP 2C8 and 3A4. active metabolite N-desethylamiodarone |
| PK: Excretion | Urine (50% to 70% unchanged) | via skin, faeces, urine, lachrymal glands |
| - Clearance (PK: Excretion) | ||
| - Half Life (PK: Excretion) | 36-48 hours | ~40-55 days |
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DIGOXIN | SOTALOL
Pharmacopeia - Antiarrhythmics
| DIGOXIN | SOTALOL | |
|---|---|---|
| GROUP | Antiarrhythmic – Vaughan Williams Class V Other | Antiarrhythmic – Vaughan Williams Class III K channel blocker |
| CICM Level of Understanding | Level 3 | Level 3 |
| INTRODUCTION | glycoside derived from the dried leaves of the foxglove Block Na-K-ATPase pump | beta blocker but it also has class III effects and is often categorised in this class |
| USES | used in AF and atrial flutter, SVT and in heart failure | used for the prevention of SVT and in the treatment of ventricular tachyarrhythmias |
| PHARMACEUTICS (PC) | ||
| PC: Chemical | Racemic mixture of d- and l- sotalol both isomers: similar Class III effects l-isomer: all of the Class II effect | |
| PC: Presentation | PO: tablets 62.5mcg or 250mcg. IV:25-250mcg/ml. Narrow therapeutic window. Monitoring necessary - 0.5-2mcg/L(~1) | PO: 80 or 160mg tablets. IV: clear liquid 10mg/ml |
| PHARMACODYNAMICS (PD) | ||
| PD: Main Action | ||
| PD: Mode of Action | i) Na/K ATPase inhibition → ↑ intracell Na → ↓ Na-Ca pump → ↑ intracell Ca → inotropy ii) direct: ↑ AV node ERP, ↓ V ERP iii) Indirect: Via Vagus – bradycardia, ↓ A refr. Augmentn of direct ↑ AV node ERP | Non-selective beta adrenergic antagonist Cause anti-arrhythmic effect by: --- Decreased pacemaker potential current --- Decreased slow-inward Ca2+ current --- Decreased repolarising K+ and Cl- currents --- Decreased Ca2+ stored in the sarcoplasmic reticulum --- Increased serum [K+]* |
| PD: Route & Doses | IV/PO. loading 250-500mcg QID then 62.5-125mcg daily | Doses 80-160mg PO or 50-100mg IV over 20mins |
| PD: Metrics (Onset/ Peak/ Duration) | onset / duration Oral: 1-2 hours; I.V.: 5-60 mins / 3-4 days | Onset IV: 5-10mins, PO 1-2hrs Duration 8-16hrs |
| PD: Effects | CVS - The main action of digoxin is to increase the force of cardiac contraction; automaticity and contractility also increase. - The heart rate is slowed due to a combination of improved haemodynamics, depression of sinus node discharge, slowing of AV nodal conduction, an increase in the AV nodal refractory period, and an indirect vagotonic effect. - Rapid intravenous administration of digoxin may cause vasoconstriction, leading to hypertension and decreased coronary blood flow. - The characteristic ECG changes produced by the drug include prolongation of the PR interval, ST-segment depression, T-wave flattening, and shortening of the QT interval GIT - Anorexia/N/V/Diarrhoea (especially if therapeutic range exceeded) CNS - Headache, confusion, coma (toxicity) - Visual disturbances (deranged red-green colour perception) Renal- Mild diuretic effect Miscellaneous- Rashes, eosinophilia; Gynaecomastia | Effect: Prolonged Action potential. Reduced Inotropy Ventricular rate is slowed QT interval is prolonged |
| PD: Side Effects / Toxicity | Thyroid-Vd Narrow therapeutic window -monitoring - 0.5-2mcg/L(~1) Toxic > 2.5- arrhythmias, AV block. anorexia,N/V/D, lethargy. Altered Red green colour perception. ECG: ↑ PR, ST dep, T fl-attening, ↓QT. (may not indicate toxicity) | class III: QT prolongation predisposes torsades de pointes (with a risk of 2% in pts with sustained VF/VT). This risk is increased in electrolyte imbalance. May precipitate heart failure. Other:bronchospasm, visual disturbances and sexual dysfunction. |
| PHARMACOKINETICS (PK) | ||
| PK: Absorption | IV, PO BA 60-80% | IV, PO BA 95% |
| PK: Distribution | ||
| Protein binding (PK: Distribution) | prot bind ~25%; uremia- displaced fm pl prot bind sites | Nil |
| Volume of distribution (PK: Distribution) | 6-7 L/kg thyroid (↑ in hyper, ↓ hypo). | 1.2—2.4 L/kg |
| PK: Metabolism | Stomach:Sequential sugar hydrolysis+ redn of lactone ring by intestinal bacteria min hepatic, most excr unchanged | None |
| PK: Excretion | Urine (50% to 70% unchanged) | urine unchanged |
| - Clearance (PK: Excretion) | ||
| - Half Life (PK: Excretion) | 36-48 hours | 12 hrs |
| SPECIAL POINTS |
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Glyceryl Trinitrate (GTN)
Pharmacopeia - Direct Vasodilators incl. Calcium Channel Blockers
| GLYCERYL TRINITRATE (GTN) | |
|---|---|
| GROUP | Nitro |
| CICM Level of Understanding | Level 2 |
| INTRODUCTION | organic nitrate similar to isosorbide mononitrate and isosorbide dinitrate. |
| USES | It is used for the treatment of Stable (and unstable) angina and acute pulmonary oedema. |
| PHARMACEUTICS (PC) | |
| PC: Chemical | |
| PC: Presentation | PO/SL/TD Patches Clear liquid with a conc 5mg/ml. IV: glass vial due to GTN being absorbed into some plastics. |
| PHARMACODYNAMICS (PD) | |
| PD: Main Action | |
| PD: Mode of Action | MoA is same for inorganic nitrates although GTN must first combine with Thio containing compound to produce NO. NO activates guanylyl cyclase in smooth muscles which ↑cGMP leading to a ↓intracellular Ca and vasodilation. Venous > arterial dilation and the benefits in angina are believed to be related to decreased MVO2. |
| PD: Route & Doses | 400-800mcg SL, 5mg Top, 5-80mcg min uptitrated IV |
| PD: Metrics (Onset/ Peak/ Duration) | on/dur SL 1-3 mins / 25 mins. IV immediate/ 5mins |
| PD: Effects | Venous > arterial dilation Can cause bronchodilation ↑ICP due to ↑in CBF Disrupt renal autoregulation in CCF pts. relaxation of sphincter of Oddi |
| PD: Side Effects / Toxicity | Tolerance develops rapidly due to depletion of sulphydryl (thiol) groups reqrd for metabolism of GTN to NO2. Breaks for patches CNS – headache (intracerebral vasodilatation) and ↑in ICP CVS – at high doses ↓SVR → ↓afterload, however a compensatory tachycardia (baroreceptor induced) may reduce myocardial blood supply. GIT – relaxes sphincter of oddi HAEM – may precipitate methaemoglobinaemia (See Special points below for further details) |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | Top, SL, IV BA PO 5%. Rapidly absorbed from the sublingual mucosa and enters the circulation via the SVC. Also absorbed in the gut but high first pass metabolism. |
| PK: Distribution | |
| Protein binding (PK: Distribution) | 60% |
| Volume of distribution (PK: Distribution) | ~3 L/kg |
| PK: Metabolism | Hepatic via thiols into NO products |
| PK: Excretion | Urine (as inactive metabolites) |
| - Clearance (PK: Excretion) | |
| - Half Life (PK: Excretion) | 1-4 minutes |
| SPECIAL POINTS | TOXICITY: Methemoglobinemia can rarely occur at conventional doses. MetHb is dose-related and it can be even more pronounced in patients with genetic abnormalities of hemoglobin that favor methemoglobin formation. Methemoglobinemia can be managed with the administration of methylene blue unless the patient has a known G-6-PD deficiency |
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Sodium nitroprusside (SNiP)
Pharmacopeia - Direct Vasodilators incl. Calcium Channel Blockers
| SODIUM NITROPRUSSIDE (SNiP) | |
|---|---|
| GROUP | Nitro |
| CICM Level of Understanding | Level 2 |
| INTRODUCTION | inorganic complex that acts as a prodrug. 5CN groups and 1NO group attached to Fe molecule covalently bonded to Na. |
| USES | used primarily to treat hypertensive emergencies but can also be used in many situations when short-term reduction of cardiac preload and/or afterload is desired |
| PHARMACEUTICS (PC) | |
| PC: Chemical | |
| PC: Presentation | only available in injectable form. It is unstable and must be stored out of light and not in alkaline conditions or it rapidly degrades. |
| PHARMACODYNAMICS (PD) | |
| PD: Main Action | |
| PD: Mode of Action | The nitroso group (−N = O−) in sodium nitroprusside reacts with sulphydryl groups (–SH) in vascular smooth muscle, forming nitric oxide and nitrosothiol derivatives. Both metab stimulate guanylate cyclase, ↑cGMP levels and produce generalized relaxation of vascular smooth muscle (both arterial and venular dilatation) |
| PD: Route & Doses | IV. 10-200mcg/min uptitrated to effect |
| PD: Metrics (Onset/ Peak/ Duration) | on/dur onset <30 secs; peak effect 2 mins, effect disappears within 3 mins after the infusion is stopped |
| PD: Effects | Equal Arterial and venous dilation Attenuates HPV in lungs Increases ICP due to increase in CBF Renal blood flow maintained |
| PD: Side Effects / Toxicity | Main side effects are from excessive hypotension and include nausea, vomitting, abdominal pain, and postural hypotension. Abrupt withdrawal may lead to a rebound hypertension. Longer term there is significant risk of cyanide accumulation and associated toxicity and impaired oxidative phosphorylation. (See Special points below for further details) |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | IV. BA 100%. |
| PK: Distribution | |
| Protein binding (PK: Distribution) | |
| Volume of distribution (PK: Distribution) | 15L (ECF) |
| PK: Metabolism | As per MOA via reaction with OxyHb, then products as: • Fe recycled by liver • CN + MetHb → Cyanomethaemoglobin • CN + Hepatic rhodenase enzymes → Thiocyanate • CN + B12 → Cyanocobalamin (non-toxic) |
| PK: Excretion | Urine (as thiocyanate - inactive) |
| - Clearance (PK: Excretion) | |
| - Half Life (PK: Excretion) | Parent drug: <10 minutes; Thiocyanate: 2.7-7 days |
| SPECIAL POINTS | TOXICITY: • Cyanide poisoning (↑ lactate, “decoupling” of mitochondrial OxPhos via action on cytochrome oxidase, ↑ mixed venous saturation) • ↓VR → ↓ CO → Tachycardia + ↑ myocradial contractility → ↑ myocardial oxygen demand • Coronary steal → worsening myocardial ischaemia • Rebound hypertension on withdrawal ANTIDOTE: 1. Disodium edetate – acts via chelation of CN molecules 2. NaNitrate - ↑ methaemoglobin → ↑ cyanmethaemoglobin 3. NaThiosulphate – acts as thiodonor increasing hepatic rhodenase enzyme activity 4. Hydroxycobalamin – Increases conversion of CN to cyanocobalamin 5. Methylene blue – Increases formation of methaemoglobin |
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Sodium Nitroprusside (SNiP) | Glyceryl Trinitrate (GTN)
Pharmacopeia - Direct Vasodilators incl. Calcium Channel Blockers
| SODIUM NITROPRUSSIDE (SNiP) | GLYCERYL TRINITRATE (GTN) | |
|---|---|---|
| GROUP | Nitro | Nitro |
| CICM Level of Understanding | Level 2 | Level 2 |
| INTRODUCTION | inorganic complex that acts as a prodrug. 5CN groups and 1NO group attached to Fe molecule covalently bonded to Na. | organic nitrate similar to isosorbide mononitrate and isosorbide dinitrate. |
| USES | used primarily to treat hypertensive emergencies but can also be used in many situations when short-term reduction of cardiac preload and/or afterload is desired | It is used for the treatment of Stable (and unstable) angina and acute pulmonary oedema. |
| PHARMACEUTICS (PC) | ||
| PC: Chemical | ||
| PC: Presentation | only available in injectable form. It is unstable and must be stored out of light and not in alkaline conditions or it rapidly degrades. | PO/SL/TD Patches Clear liquid with a conc 5mg/ml. IV: glass vial due to GTN being absorbed into some plastics. |
| PHARMACODYNAMICS (PD) | ||
| PD: Main Action | ||
| PD: Mode of Action | The nitroso group (−N = O−) in sodium nitroprusside reacts with sulphydryl groups (–SH) in vascular smooth muscle, forming nitric oxide and nitrosothiol derivatives. Both metab stimulate guanylate cyclase, ↑cGMP levels and produce generalized relaxation of vascular smooth muscle (both arterial and venular dilatation) | MoA is same for inorganic nitrates although GTN must first combine with Thio containing compound to produce NO. NO activates guanylyl cyclase in smooth muscles which ↑cGMP leading to a ↓intracellular Ca and vasodilation. Venous > arterial dilation and the benefits in angina are believed to be related to decreased MVO2. |
| PD: Route & Doses | IV. 10-200mcg/min uptitrated to effect | 400-800mcg SL, 5mg Top, 5-80mcg min uptitrated IV |
| PD: Metrics (Onset/ Peak/ Duration) | on/dur onset <30 secs; peak effect 2 mins, effect disappears within 3 mins after the infusion is stopped | on/dur SL 1-3 mins / 25 mins. IV immediate/ 5mins |
| PD: Effects | Equal Arterial and venous dilation Attenuates HPV in lungs Increases ICP due to increase in CBF Renal blood flow maintained | Venous > arterial dilation Can cause bronchodilation ↑ICP due to ↑in CBF Disrupt renal autoregulation in CCF pts. relaxation of sphincter of Oddi |
| PD: Side Effects / Toxicity | Main side effects are from excessive hypotension and include nausea, vomitting, abdominal pain, and postural hypotension. Abrupt withdrawal may lead to a rebound hypertension. Longer term there is significant risk of cyanide accumulation and associated toxicity and impaired oxidative phosphorylation. (See Special points below for further details) | Tolerance develops rapidly due to depletion of sulphydryl (thiol) groups reqrd for metabolism of GTN to NO2. Breaks for patches CNS – headache (intracerebral vasodilatation) and ↑in ICP CVS – at high doses ↓SVR → ↓afterload, however a compensatory tachycardia (baroreceptor induced) may reduce myocardial blood supply. GIT – relaxes sphincter of oddi HAEM – may precipitate methaemoglobinaemia (See Special points below for further details) |
| PHARMACOKINETICS (PK) | ||
| PK: Absorption | IV. BA 100%. | Top, SL, IV BA PO 5%. Rapidly absorbed from the sublingual mucosa and enters the circulation via the SVC. Also absorbed in the gut but high first pass metabolism. |
| PK: Distribution | ||
| Protein binding (PK: Distribution) | 60% | |
| Volume of distribution (PK: Distribution) | 15L (ECF) | ~3 L/kg |
| PK: Metabolism | As per MOA via reaction with OxyHb, then products as: • Fe recycled by liver • CN + MetHb → Cyanomethaemoglobin • CN + Hepatic rhodenase enzymes → Thiocyanate • CN + B12 → Cyanocobalamin (non-toxic) | Hepatic via thiols into NO products |
| PK: Excretion | Urine (as thiocyanate - inactive) | Urine (as inactive metabolites) |
| - Clearance (PK: Excretion) | ||
| - Half Life (PK: Excretion) | Parent drug: <10 minutes; Thiocyanate: 2.7-7 days | 1-4 minutes |
| SPECIAL POINTS | TOXICITY: • Cyanide poisoning (↑ lactate, “decoupling” of mitochondrial OxPhos via action on cytochrome oxidase, ↑ mixed venous saturation) • ↓VR → ↓ CO → Tachycardia + ↑ myocradial contractility → ↑ myocardial oxygen demand • Coronary steal → worsening myocardial ischaemia • Rebound hypertension on withdrawal ANTIDOTE: 1. Disodium edetate – acts via chelation of CN molecules 2. NaNitrate - ↑ methaemoglobin → ↑ cyanmethaemoglobin 3. NaThiosulphate – acts as thiodonor increasing hepatic rhodenase enzyme activity 4. Hydroxycobalamin – Increases conversion of CN to cyanocobalamin 5. Methylene blue – Increases formation of methaemoglobin | TOXICITY: Methemoglobinemia can rarely occur at conventional doses. MetHb is dose-related and it can be even more pronounced in patients with genetic abnormalities of hemoglobin that favor methemoglobin formation. Methemoglobinemia can be managed with the administration of methylene blue unless the patient has a known G-6-PD deficiency |
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Sodium Nitroprusside (SNiP) | Glyceryl Trinitrate (GTN)
Limited
Pharmacopeia - Direct Vasodilators incl. Calcium Channel Blockers
| SODIUM NITROPRUSSIDE (SNiP) | GLYCERYL TRINITRATE (GTN) | |
|---|---|---|
| GROUP | Nitro | Nitro |
| CICM Level of Understanding | Level 2 | Level 2 |
| INTRODUCTION | inorganic complex that acts as a prodrug. 5CN groups and 1NO group attached to Fe molecule covalently bonded to Na. | organic nitrate similar to isosorbide mononitrate and isosorbide dinitrate. |
| PHARMACODYNAMICS (PD) | ||
| PD: Mode of Action | The nitroso group (−N = O−) in sodium nitroprusside reacts with sulphydryl groups (–SH) in vascular smooth muscle, forming nitric oxide and nitrosothiol derivatives. Both metab stimulate guanylate cyclase, ↑cGMP levels and produce generalized relaxation of vascular smooth muscle (both arterial and venular dilatation) | MoA is same for inorganic nitrates although GTN must first combine with Thio containing compound to produce NO. NO activates guanylyl cyclase in smooth muscles which ↑cGMP leading to a ↓intracellular Ca and vasodilation. Venous > arterial dilation and the benefits in angina are believed to be related to decreased MVO2. |
| PD: Effects | Equal Arterial and venous dilation Attenuates HPV in lungs Increases ICP due to increase in CBF Renal blood flow maintained | Venous > arterial dilation Can cause bronchodilation ↑ICP due to ↑in CBF Disrupt renal autoregulation in CCF pts. relaxation of sphincter of Oddi |
| PD: Side Effects / Toxicity | Main side effects are from excessive hypotension and include nausea, vomitting, abdominal pain, and postural hypotension. Abrupt withdrawal may lead to a rebound hypertension. Longer term there is significant risk of cyanide accumulation and associated toxicity and impaired oxidative phosphorylation. (See Special points below for further details) | Tolerance develops rapidly due to depletion of sulphydryl (thiol) groups reqrd for metabolism of GTN to NO2. Breaks for patches CNS – headache (intracerebral vasodilatation) and ↑in ICP CVS – at high doses ↓SVR → ↓afterload, however a compensatory tachycardia (baroreceptor induced) may reduce myocardial blood supply. GIT – relaxes sphincter of oddi HAEM – may precipitate methaemoglobinaemia (See Special points below for further details) |
| SPECIAL POINTS | TOXICITY: • Cyanide poisoning (↑ lactate, “decoupling” of mitochondrial OxPhos via action on cytochrome oxidase, ↑ mixed venous saturation) • ↓VR → ↓ CO → Tachycardia + ↑ myocradial contractility → ↑ myocardial oxygen demand • Coronary steal → worsening myocardial ischaemia • Rebound hypertension on withdrawal ANTIDOTE: 1. Disodium edetate – acts via chelation of CN molecules 2. NaNitrate - ↑ methaemoglobin → ↑ cyanmethaemoglobin 3. NaThiosulphate – acts as thiodonor increasing hepatic rhodenase enzyme activity 4. Hydroxycobalamin – Increases conversion of CN to cyanocobalamin 5. Methylene blue – Increases formation of methaemoglobin | TOXICITY: Methemoglobinemia can rarely occur at conventional doses. MetHb is dose-related and it can be even more pronounced in patients with genetic abnormalities of hemoglobin that favor methemoglobin formation. Methemoglobinemia can be managed with the administration of methylene blue unless the patient has a known G-6-PD deficiency |
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Labetalol | Esmolol
Pharmacopeia - Adrenoreceptor Antagonists
| LABETALOL | ESMOLOL | |
|---|---|---|
| GROUP | Mixed alpha and beta blocker | Beta Blocker |
| CICM Level of Understanding | Level 2 | Level 2 |
| INTRODUCTION | an alpha 1 blocker and a non selective beta blocker. | Cardio-selective beta blocker with rapid onset and offset. |
| USES | - Used in the setting of an acute hypertensive crisis - Pregnancy related hypertension | - Short term management tachycardia and hypertension in a monitored patient - For SVT termination - No intrinsic sympathomimetic activity or membrane stabilising properties |
| PHARMACEUTICS (PC) | ||
| PC: Chemical | It is a racemic solution with four stereoisomers present in equal proportions. The SR isomer is likely responsible for the alpha blocking effects and the RR isomer for the betablockade | |
| PC: Presentation | available as a 50-400mg tablets and as a colourless solution containing 5mg/ml. | only available as an IV formulation. presented as a clear liquid usually at a concentration of 10mg/ml |
| PHARMACODYNAMICS (PD) | ||
| PD: Main Action | ||
| PD: Mode of Action | Beta blockage leads to ↓Gs activity in receptor associated organs and associated ↓in adenylyl cyclase and intracellular Ca2+. Alpha blockage leads to ↓ Gq activation and subsequent ↓in IP3 and intracellular Ca2+ | Beta blockage leads to ↓Gs activity in receptor associated organs and associated ↓in adenylyl cyclase and intracellular Ca2+. |
| PD: Route & Doses | IV and oral doses IV in 20mg pushes, oral for HTN 100-400mg BD | IV dose In 10mg increments titrate to effect |
| PD: Metrics (Onset/ Peak/ Duration) | ||
| PD: Effects | β: It produces decreases in heart rate and cardiac output and myocardial oxygen consumption. α: Peripheral vasodilation | It produces decreases in heart rate and cardiac output and myocardial oxygen consumption |
| PD: Side Effects / Toxicity | - Withdrawal. - Care with: Opioids, Halo, OAD, CCB - Due to its metabolism, it should be used in caution in liver failure patients and elderly | - Care with: Opioids, Halo, OAD, CCB - It is an irritant to veins and may lead to tissue necrosis with extravasation |
| PHARMACOKINETICS (PK) | ||
| PK: Absorption | bioavailabilty complete absorption but high first pass metabolism results in bioavailability 25% | bioavailabilty Only available as IV therefore 100% |
| PK: Distribution | lipid solubility moderately lipid soluble, can enter CNS | lipid solubility is high so it crosses the BBB |
| Protein binding (PK: Distribution) | 50% | 60% to albumin |
| Volume of distribution (PK: Distribution) | 3-16 L/kg | 3.5 L/Kg |
| PK: Metabolism | Hepatic, primarily via glucuronide conjugation | neither hepatic or renal! by red blood cell esterases to a mostly inactive metabolite |
| PK: Excretion | Urine (60% as glucuronide conjugates, <5% as unchanged drug) | urine |
| - Clearance (PK: Excretion) | ||
| - Half Life (PK: Excretion) | 6-8 hours | 10 minutes |
| SPECIAL POINTS |
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Adenosine
Pharmacopeia - Antiarrhythmics
| ADENOSINE | |
|---|---|
| GROUP | Antiarrhythmic – Vaughan Williams Class V Other |
| CICM Level of Understanding | Level 2 |
| INTRODUCTION | natural purine nucleoside slows conduction through the AV node |
| USES | e¬ffective treatment for the termination of paroxysmal SVT. Used for slowing rapid atrial arrhythmias to aid diagnosis. |
| PHARMACEUTICS (PC) | |
| PC: Chemical | |
| PC: Presentation | IV: clear liquid with 6mg in 2mL |
| PHARMACODYNAMICS (PD) | |
| PD: Main Action | |
| PD: Mode of Action | acts on the A1 adenosine receptors found in the SA and AV markedly slows or completely blocks conduction in the AV node, probably by hyperpolarizing this tissue (through increased IK1) and by reducing calcium current |
| PD: Route & Doses | IV. doses 3-6mg bolus |
| PD: Metrics (Onset/ Peak/ Duration) | onset / duration seconds / seconds |
| PD: Effects | Effects: causes a temporary heart block and/or asystolic pause which acts to terminate SVT |
| PD: Side Effects / Toxicity | side effects are transient but can be distressing for patients (sense of impending doom). May induce AF/AFL due to ↓ refractory period. Contraindicated in sick sinus syndrome. Avoid in asthma/ COPD - may cause bronchospasm. |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | IV only |
| PK: Distribution | |
| Protein binding (PK: Distribution) | NA |
| Volume of distribution (PK: Distribution) | NA |
| PK: Metabolism | Rapidly deaminated in plasma and taken up by RBCs |
| PK: Excretion | |
| - Clearance (PK: Excretion) | |
| - Half Life (PK: Excretion) | <10 seconds |
| SPECIAL POINTS |
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Metoprolol
Pharmacopeia - Adrenoreceptor Antagonists
| METOPROLOL | |
|---|---|
| GROUP | Beta Blocker |
| CICM Level of Understanding | Level 3 |
| INTRODUCTION | relatively selective beta blocker with no intrinsic sympathomimetic activity. |
| USES | - Early use of metoprolol in haemodynamically stable myocardial infarction reduces infarct size and incidence of VF. - rate control in atrial fibrillation - hypertension |
| PHARMACEUTICS (PC) | |
| PC: Chemical | |
| PC: Presentation | available in oral form as an immediate release or sustained release in increments of 25mg. It is also available as an IV formulation usually 1mg/ml |
| PHARMACODYNAMICS (PD) | |
| PD: Main Action | |
| PD: Mode of Action | Beta blockage leads to ↓Gs activity in receptor associated organs and associated ↓in adenylyl cyclase and intracellular Ca2+. |
| PD: Route & Doses | PO or IV dose Orally in 12.5mg increments, IV in 1-2mg boluses |
| PD: Metrics (Onset/ Peak/ Duration) | |
| PD: Effects | It produces decreases in heart rate and cardiac output and myocardial oxygen consumption. Whilst it does have some β 2 action it has little or no effect on these receptors at doses less than 100mg |
| PD: Side Effects / Toxicity | - Withdrawal - Care with: Opioids, Halo, OAD, CCB - Use with Ca Channel blockers may result in complete heart block |
| PHARMACOKINETICS (PK) | |
| PK: Absorption | bioavailabilty Absoption is rapid and complete, however there is extensive first pass metabolism bioavailability = 50% |
| PK: Distribution | lipid solubility is high so it crosses the BBB |
| Protein binding (PK: Distribution) | 10-20% to albumin |
| Volume of distribution (PK: Distribution) | 5.5 L/Kg |
| PK: Metabolism | hepatic or renal Extensively hepatic via CYP2D6 |
| PK: Excretion | urine 5-10% unchanged |
| - Clearance (PK: Excretion) | |
| - Half Life (PK: Excretion) | 3-8hours |
| SPECIAL POINTS |
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