PHCT Midterm Reviewer-11-16 PDF

PHCT MIDTERMS Week 9: Cardiovascular Drugs Cardiovascular Drugs Electrical impulses → AV node → bundle of his → Purkinje fibers (ventricle b...

PHCT MIDTERMS Week 9: Cardiovascular Drugs Cardiovascular Drugs Electrical impulses → AV node → bundle of his → Purkinje fibers (ventricle beating) o Anti-arrhythmic Drugs Phases of Action Potential: o Beta-adrenergic Blockers 1. Phase 0: Upstroke, Opening of Na channel depolarization o Vasodilators 2. Phase 1: Early fast repolarization, Closure of Na (+) channel, o Clonidine and Related Drugs opening of K channel (dec. AP) Sinoatrial node → natural pacemaker of the heart, initiates 3. Phase 2: Plateau, sustained inward movement of Ca (+) and outward heartbeat movement of K (Can cause homeostasis) Atrium and ventricle → not synchronized in beating but 4. Phase 3: Repolarization phase, Closure of Ca channel, K channel simultaneously beating remains open Atrioventricular node → center of atrium and ventricle, receives 5. Phase 4: Diastole or resting state, All channels close electrical impulses from SA node ANTI-ARRHYTHMIC DRUGS Type I: Inhibit fast sodium channels, depress myocardial Clinical Presentation: automaticity, conduction, and contractility. Acts on phase 0 Cardiotoxic effects: sinus bradycardia (condition where the heart Type II: Block beta-adrenergic receptors. On heart (-) ionotropic, rate is slower than normal due to the sinus node (the natural chronotropic, and dromotropic effect → decreased force of pacemaker of the heart) generating electrical impulses at a reduced contraction (bradycardia) betablockers for tachyarrhythmia rate) sinus node arrest, PR, QRS, or QT interval prolongation, polymorphous ventricular tachycardia, hypotension. Type III: Block potassium channels to prolong the duration of the action potential. CNS toxicity (Quinidine and disopyramide): dry mouth, dilated pupils, delirium, seizures, coma. Type IV: Calcium channel blockers. Other effects: nausea, vomiting, diarrhea, cinchonism (tinnitus, Type I Anti-arrhythmic Drugs: vertigo, deafness, visual disturbances with chronic dose). Type Ia: Depressed myocardial contractility with alpha-adrenergic or Examples: Quinidine, Procainamide (Pronestyl®), Disopyramide ganglionic blockade may result in hypotension and occasionally (Norpace®) pulmonary edema. Mechanism: All Type Ia agents can produce seizures, coma, respiratory arrest. Procainamide can cause: GIT upset, lupus-like syndrome condition Depress fast sodium-dependent channels, slowing phase zero of the that mimics systemic lupus erythematosus (SLE) but is triggered by cardiac action potential. certain medications. (butterfly rash) (chronic use). At high concentrations, this results in reduced myocardial Treatment: contractility and excitability, and severe depression of cardiac conduction velocity. Emergency and supportive measures. Reduced myocardial contractility → inhibit Na channels → inhibit Specific drugs and antidotes (e.g., hypertonic sodium bicarbonate). depolarization → inhibit contraction (Helps to counteract the acidosis that can occur during cardiac arrest) Repolarization is also delayed, resulting in a prolonged QT interval that may be associated with polymorphic ventricular tachycardia → A cardiac pacemaker (a medical device implanted in the chest or characterized by a rapid and irregular heartbeat originating from the abdomen to help manage abnormal heart rhythms, known as ventricles, the lower chambers of the heart. arrhythmias. It delivers electrical impulses to the heart to ensure it beats at a normal rate and rhythm) is indicated for patients Additional Properties: unresponsive to sodium bicarbonate therapy. Quinidine and disopyramide also have anticholinergic activity. Decontamination (e.g., activated charcoal). Disopyramide has three important side effects: it is vagolytic, Enhanced elimination (e.g., dialysis for quinidine). Acidification of causing urinary retention, constipation, and dry mouth. urine may enhance elimination but is not recommended. Usage: Dysopyramide, procainamide, and N-acetylprocainamide (NAPA) Quinidine and procainamide are commonly used for suppression of are effectively removed by hemoperfusion or dialysis. acute and chronic supraventricular (rhythm disorders originating Type Ib: above the ventricles, typically in the atria or the atrioventricular (AV) node) and ventricular arrhythmias. (abnormal heart rhythms Examples: Tocainide, Mexiletine, Lidocaine originating from the ventricles, the lower chambers of the heart.) Clinical Presentation: Quinidine has alpha-adrenergic receptor-blocking activity and is one o Sedation of the oldest anti-dysrhythmic drugs. o Confusion Procainamide has ganglionic and neuromuscular blocking activity o Coma (muscle relaxation) o Seizures Toxic Dose: o Respiratory arrest 1 g of quinidine, 5 g of procainamide, or 1 g of disopyramide. 11 PHCT MIDTERMS o Cardiac toxicity o AV block Lidocaine: o Asystole o Lidocaine is an aminoacyl amide synthetic derivative of o Prolonged QRS and QT intervals cocaine. Encainide o It is an antidysrhythmic and local anesthetic agent. Encainide was withdrawn from US and Canadian markets in o Lidocaine is metabolized to two active metabolites, December of 1991 due to increased mortality in the cardiac monoethylglycinexylidide (MEGX) and glycine xylidide (GX); dysrhythmia trial. these metabolites may contribute to toxicity. Encainide, an analog of lysergic acid, is at least 10 times more potent III. Clinical Presentation: than procainamide. Its absorption and hepatic metabolism are A. Tocainide and Mexiletine rapid; these metabolites are as active as the original drug. Side effects may include: Type III Anti-arrhythmic Drugs: o Dizziness o Blocks potassium channels to prolong the duration of the action o Paresthesias → abnormal sensations on the skin, such as potential and the effective refractory period. tingling, prickling, numbness, or "pins and needles," without Bretylium: an obvious physical cause. These sensations can occur in Bretylium is a quaternary benzylammonium compound used for various parts of the body, including the hands, feet, arms, and treating lidocaine-refractory arrhythmias. legs. Causes initial release of catecholamines (NE. epinephrine, o Tremor dopamine → vasoconstriction (if inhibited: vasodilation → o Ataxia hypotension) followed by inhibition, with the major side effect being o GIT disturbance hypotension. Orthostatic hypotension (a condition where a person's blood pressure falls significantly when they stand up from a sitting or Overdose may cause: lying position. This sudden drop in blood pressure can lead to o Sedation dizziness, lightheadedness, and in some cases, fainting) may persist. o Confusion After rapid intravenous injection, transient hypertension, nausea, o Coma and vomiting may occur. o Seizures Amiodarone: o Respiratory arrest Non-competitive beta-adrenergic blocker may cause o Cardiac toxicity (sinus arrest, AV block, asystole, and bradyarrhythmias. hypotension) Side effects include photosensitivity, hyperthyroidism, pulmonary Type Ic: fibrosis, and corneal deposits. Examples: Flecainide, Encainide, Propafenone, Moricizine May release iodine, and chronic use has resulted in altered thyroid function. Thyroid hormones: Thyroxine (T4), Triiodothyronine (T3) Side effects: Has a very long half-life (40-50 days). o Dizziness Acute overdose of amiodarone is not expected to cause toxicity. o Blurred vision Chronic use may cause: o Headache o Ventricular arrhythmias (monomorphic or polymorphic o GIT upset ventricular tachycardia) o Ventricular arrhythmias (monomorphic or polymorphic o Bradyarrhythmias (sinus arrest, AV block) ventricular tachycardia) o May aggravate cardiac failure Clinical Presentation: o Pneumonitis o Hypotension o Bradycardia BETA-ADRENERGIC BLOCKERS Widely used for treating hypertension, angina pectoris, migraine o Atenolol headaches, and glaucoma. o Metoprolol Beta Blockers Membrane Stabilizing Activity: anesthetic like effect, cannot be Types and Characteristics: given as ophthalmic drops (contraindicated in glaucoma) Selective: o Propranolol o Betaxolol o Pindolol o Bisoprolol o Acebutolol o Esmolol o Labetalol o Acebutolol o Metoprolol 12 PHCT MIDTERMS Mixed Alpha and Beta Blocking Effect: Toxic Dose: o Labetalol Ingestion of 2-3 times the therapeutic dose can be life-threatening. o Carvedilol Clinical Presentation: Intrinsic Sympathomimetic Activity: partial agonist effect Cardiac Disturbances: Hypotension, bradycardia, atrioventricular block, intraventricular conduction disturbances, cardiogenic shock, o Acebutolol asystole. o Bisoprolol Central Nervous System Toxicity: Convulsions, coma, respiratory o Carteolol arrest. o Pindolol Other Symptoms: Bronchospasm (especially in asthma patients), o Penbutolol hypoglycemia, hyperkalemia. Non-Selective (β1 (heart) and β2 (lungs) blockers): bronchospasm Diagnosis: o Propranolol Specific Levels: Measurement of beta-blocker serum levels may confirm the diagnosis but is not essential for emergency o Nadolol management. o Timolol Treatment: o Pindolol Emergency and Supportive Measures. o Sotalol Specific Drugs and Antidotes: Glucagon (secreted by the pancreas, Mechanism of Toxicity: increases blood sugar levels (endogenous) 0.1-0.3 mg/kg IV bolus, repeated as needed for bradycardia and hypotension, hypertonic Propranolol: Depresses myocardial contractility and conduction; sodium bicarbonate 1-2 meq/kg for membrane-depressant causes seizures and coma due to lipid solubility. poisoning, isoproterenol, magnesium, or overdrive pacing for Pindolol: May cause hypertension due to beta-agonist activity. torsades de pointes. Sotalol: Prolongs QT interval, may cause torsades de pointes and Decontamination: Activated charcoal, ipecac-induced emesis, ventricular fibrillation. Torsades de pointes → fatal polymorphic cathartics. ventricular tachycardia VASODILATORS Types: Toxic Dose: Alpha-Adrenergic Blocking Agents: Minimum toxic or lethal doses not established. Fatalities reported with indoramin overdose and excessive intravenous phentolamine. o Phenoxybenzamine Clinical Presentation: o Phentolamine Headache, nausea, dizziness, weakness, syncope (fainting), o Tolazaline orthostatic hypotension, warm flushed skin, palpitations, lethargy Selective α1 Inhibitors: and ataxia in children, cerebral and myocardial ischemia, acute o Prazosin 1stselective α1 inhibitor was introduced in the early renal failure. 1970’s Diagnosis: o newer α1 selective agents Diagnosis is based on a history of exposure and the presence of orthostatic o Doxazosin hypotension, which may or may not be accompanied by reflex tachycardia. o Indoramin Specific Levels: Blood levels not routinely available or clinically useful. o Terazosin Laboratory Studies: Electrolytes, glucose, BUN, creatinine, ECG. o Trimazosin Treatment: o Urapidil Emergency and Supportive Measures. Mechanism of Toxicity: Specific Drugs and Antidotes: No specific antidote. Dilate peripheral arterioles, lower blood pressure. Decontamination: Activated charcoal, ipecac-induced emesis, Reflex sympathetic response can cause tachycardia and cathartics, Terazosin and doxazosin are long-acting and eliminated arrhythmias. 60% in feces; thus, repeat-dose activated charcoal for enhanced Prazosin and other newer α1 specific agents are associated with elimination. little or no reflex tachycardia CALCIUM CHANNEL BLOCKERS o Anti-hypertensive Non-Dihydropyridine: o Anti-arrhythmic o Verapamil o Anti-angina o Diltiazem Types: 13 PHCT MIDTERMS Dihydropyridine Family: o Vasopressor support (dopamine, norepinephrine, epinephrine, phenylephrine, vasopressin, metaraminol) o Amlodipine o High-dose insulin infusion with dextrose o Felodipine Rapid transport before the patient deteriorates is crucial. Empiric o Isradipine use of glucagon (adults: 5-15 mg IV) may be warranted for patients o Nicardipine with an unknown overdose presenting with bradycardia or o Nifedipine hypotension. o Nisoldipine Consider using calcium only if a witness confirms a calcium channel blocker overdose; calcium may induce fatal arrhythmias in digoxin Mechanism of Toxicity: overdose, which can present with similar findings. Cardiovascular Effects: Treat hypotension with fluid boluses. If profound hypotension fails to Peripheral vasodilatation respond to fluid resuscitation, administer a dopamine or norepinephrine (increases cardiac force and contraction) drip, if Negative chronotropy permitted by local protocol. Negative inotropy If the patient deteriorates to cardiac arrest from a calcium channel Negative dromotropy blocker overdose, perform prolonged cardiopulmonary resuscitation (CPR) in the field because patients have survived Other Physiologic Responses: neurologically intact after an hour of CPR. Suppression of insulin release Avoid ipecac syrup. Decreased free fatty acid utilization, causing hyperglycemia, lactic Administer activated charcoal (AC) if the patient's airway is acidosis (a condition characterized by an accumulation of lactic protected. acid in the blood, leading to a decrease in blood pH (metabolic acidosis), and depressed cardiac contractility Atropine may be tried if hemodynamically significant bradycardia occurs; however, heart block is usually resistant to atropine in Laboratory Studies: calcium channel blocker toxicity. Lactic acidosis (ABG analysis) Mid-dose dopamine (5-10 mcg/kg/min) may improve heart rate and Serum electrolytes contractility. BUN/creatinine Administer IV calcium gluconate (up to 4 g) or IV calcium chloride (1 g) and/or glucagon (5-10 mg) if hypotension persists. CCB blood levels (generally not available promptly) Serum acetaminophen level Consider dopamine or norepinephrine infusion if a long transport time is likely, as permitted by local prehospital care protocols. Liver function tests Gastric decontamination: Serum digoxin level o Gastric lavage may be useful in early presentations (