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BC3 cardiac chap18
BC3 cardio labs chap 18
| Question | Answer |
|---|---|
| Fibrinolytic agents (Altepase,Reteplase,Streptokinase_) | for acute ST segment elevation MI and, lyses the thrombus. |
| Altepase | Clear thrombi in central venous cath, For MI,ischemic stroke, massive PE |
| Streptokinase | MI, acute PE, DVT, arterial thrombul or emboli |
| Contraindications to Fibrinolytic therapy | internal bleeding, stroke, recent spinal surgery, aortic dissedtion, trauma, and Uncontrolled HTN |
| Fibrinolytic agent | give within 30 minutes of ST elevation, or new LBB block |
| Anticoagulants: Unfractioned heparin LMWHs, Direct thrombin inhibitotrs, Warfarin | limit further thrombin formn & help prevent thromboembolism |
| Unfractioned heparin | most common anticoagulantprev clot formn by combining w/ antithrombin III & inhibiting circulating thrombin.Does not lyse thrombi : |
| Protamine So4 | reverses effects of heparin ; may cause LT anaphylactic rxn |
| Low molec Wt Heparins: LMWHs | unstable angina, non-ST segment elevation AMI, or DVT. |
| Advantages of LMWHs | Longer half life; More predictable anticoagulation effect; Greater bioavailability |
| Adverse effects of LMWHs: | Bleeding;Erythema;Hematoma @ inj site;thrombocytopenia |
| . Warfarin | Oral drug for chronic anticoagulation tx;Action: interferes w/ synthesis Vit K dependent clotting factors- factors II, VII, IX, & X.titrated accdg to INR level: 2 – 3.5 |
| . Warfarin indications | prosthetic heart valve: A FIB: CHF1. Post AMI anticoagulation for high risk pts;: |
| Contraindications of warfarin | 1. Uncontrolled HTN:2. Severe hepatic /renal dss;aneurysm;Pericarditis;GI or GU bleeding;pregnancy |
| Platelet inhibitors:Aspirin | most common; inhibits thromboxane A2 plt agonist, & prevents thrombus |
| Platelet inhibitors:Indications | prev. garft closure after CABG, & coronary artery thrombus after angioplastyreduce incid of nonfatal AMI ; Reduce risk of nonfatal stroke & death ; |
| Platelet inhibitors:Ticlopidine (Ticlid)Clopidogrel (Plavix)– | used for pts who cannot tolerate asprevent adenosine diphosphate – induced plt activation & plt aggregation, resulting in an irreversible & non-competitive inhibition of plt functionpirin |
| Adverse effect of Platelet inhibitors: | Bleeding; Agranulocytosis;3. Elev. liver aminotransferases;neutropenia; thrombocytopenic purpuraGI irritation; |
| Clopidogrel (Plavix) Platelet inhibitor | atherosclerosis as documented by recent stroke or AMI or peripheral arterial dss; Used for 4 weeks after coronary artery stenting |
| Glycoprotein IIb/IIIa Inhibitors:Abciximab; | Indications: PCI, USA that does not respond to conventional therapy & when PCI is planned within 24 hrs. |
| Glycoprotein IIb/IIIa Inhibitors Eptifibatide | Indications: Non ST segment elevation ACS, incl pts who are managed medically or w/ PCI. |
| Antidysrhythmics: | restore a normal cardiac rhythm & prevent LT sequelae of dysrhythmias |
| classes of Antidysrhythmics | 1 A, 1B, 1C, II, III, IV |
| Antidysrhythmic Class 1AQuinidine, Procainamide | ;Inhibits fast Na channelDec automaticity, depresses ph 0 Prolongs action pot duration; |
| Antidysrhythmic Class 1B Lidocaine, Tocainaide | Inhibits fast Na channel, shorten action Potential duration. |
| Antidysrhythmic Class 1C ;Flecainide, Moricizine | Inhibits fast Na channel,slows His-Purkinje Conduction-prolonged QRS duration |
| Antidysrhythmic class II Propranolol, Esmolol, B blockers; | depresses ph 4 depo, blocks sympathetic Stimulation of conduction syst. |
| Antidysrhythmic class III; Amiodarone | Blocks K channel, prolongs ph3 repo.prolongs action potential |
| Antidysrhythmic class IV; Ca Channel blockers;Verapamil, Diltiazem | Inhibits inward Ca channel, depresses Ph4 depo, lenthens repo in ph 1 & 2. |
| Procainamide | VT, SVTs incl WPW syndrome, AF,atrial flutter adverse effects:Hypotension w/ IV use, Lupus,rash, fever, heart block, Torsades, HA, agranulocytosis; |
| Lidocaine | VT, VF use for PVC's, SE:Bradycardia, blurred vision, hypotensionTremors, dizziness, tinnitus, convulsionsMental status changes; |
| Flecainide | PSVT,incl WPW syndrome, AF &Atrial flutter, LT sustained VT. Adverse E:Hypotensionbradycardia, CHF,, HA, fatigue, nausea, palpitations |
| Propranolol | SVT, ST, VT digitalis induced Tachydysrhythmias, ventric rateControl w/ AF, atrial flutter. Adverse E.Hypotension, heart block, bradycardiaCHF, bronchospasm, fatigue, nausea,vomiting, gastric pain, constip, diarrhea |
| Amiodarone | Recurrent VF, unstable VT;AF, Atrial flutter, SVTs incl WPW ;Syndrome; Adverse E:Heart block, cardiac arrest, bradycardia, photo-Sensitivity, N/V/C, visual disturbances |
| Verapamil | Ventricular rate control in AF, atrial Flutter, SVT ; Adv. E;Hypotension, heart block, CHF, bradycardia,HA, dizziness, edema, constipation |
| Atropine | AV block, asystole, bradycardic PEA; Symptomatic sinus bradycardiaPalpitations, tachycardia, blurred vision;dry mouth, altered taste, urin retention. |
| Digoxin | Ventricular rate control in AF:Heart block, bradycardia, weaknesstoxicity, dysrhythmias, A/N/V, confusion, |
| Unclassified Antidysrhythmic Adenosine: | 1st line antidysrhythmic that effectively converts narrow complex PSVT to normal sinus rhythm by slowing conduction to AV node |
| Magnesium sulfate | drug of choice for treating torsades de pointes.Also for refractory VT, & V fib & LT dysrhythmias d/t digitalis toxicity.Ca channel blocking properties & inhibits Na & K channels |
| Adverse effects of MgSO4: | Hypotension, nausea, depressed reflexes, & flushing. |
| Unclassified Antidysrhythmic Atropine | 1st line drug to treat symptomatic bradycardia. Reduces effects of vagal stim. – increasing HR & improving cardiac function |
| Unclassified Antidysrhythmic Digoxin | mild inotrope, w/ antidysrhythmic & bradycardic actions. Inhibits Na – K pump – causing inc in intracellular Na. Rise promotes Ca influx & enhances myocardial contractilitym. beneficial for pts w/ Acute Atrial FIB.!!!. |
| Digoxin; Therapeutic level: | 0.5 – 1.5ng/ml |
| INOTROPIC DRUGS; For ventricular dysfunction or cardiogenic shock | increase force of myocardial contraction & cardiac output; Dopamine;Dobutamine; Epinephrine;Isoproterenol;Norepinephrine; Amrinone & Milrinone – phosphodiesterase inhibitors |
| INOTROPIC DRUGS Mech of Action: | Enhance ventricular contraction inc. SV, CO, BP, coronary artery perfusion;Ventricles empty more completely, ventricular filling pressures, preload, pulmo congestion are decreased. Be alert for Increase myocardial O2 demand – as contractility & HR increa |
| Dopamine: | Most widely used inotropic drug given to pts w/ hypotension, dec CO, & oliguriapromotes release of norepinephrine from sympathetic nerve terminals.; |
| Adverse effects of Dopamine: | Tachycardia, palpitations, dysrhythmias, angina, HA, N/V/HTN |
| Dobutamine | Acts on B1 receptors & increases myocardial contractility;Used after cardiac surgery, during some carddiac diagnostic stress procedures;CHF, cardiogenic shock oth conditions that cause poor cardiac contractility or low CO |
| Adverse effects of Dobutamine | Tachycardia, dysrhythmias, BP fluctuations, HA, nausea. |
| Epinephrine:indications | Stim A, A1, B2 receptors. Indicated for variety of conditions – cardiac arrest, symptomatic bradycardia, severe hypotension, anaphylaxis & shock. |
| Epinephrine: route | High dose: Epi stim A receptors causing profound vasoconstriction, inc. BP & SVR, dec renal & splanchnic perfusion. |
| Adverse Effects Epinephrine | Dysrhythmias, tachycardia, cerebral hemorrhage, pulmo edema, HA, dizzinessnervousness, myocardial ischemia, & angina. |
| Vasopressin | used as alternative to epi for pts w/ refractory ventricular fib or shock assoc. w/ vasodilation. |
| Isoproterenol: | Stim 1, 2 receptors . Increase myocardial contractility , CO, HR, BP Indicated mainly to dec HR after cardiac transplantation. Other indications include refractory Torsades de Pointes, B blocker overdose, & symptomatic bradycardia when ext pacemaker N/A |
| Adverse effects:Isoproterenol: | Dysrhythmias, tachycardia, palpitations, myocardial ischemia, hypotension, pulmo edema, bronchospasm HA, nausea, vomiting, sweating |
| Norepinephrine (Levophed) | inc. BP, inc. SVR. Inc SVR may actually increase myocardial O2 demand & work, thus dec. CO.Norepinephrine used for pts w/ cardiogenic shock & significant hypotension accomp by low SVR. |
| Adverse effects:Norepinephrine (Levophed) | Tachycardia, bradycardia, dysrhythmias, HTN, HA tiss necrosis from extravasation. |
| Amrinone: | Phosphodiesterase III inhibitors – increase contractility, venous vasodilation, arterial vasodilation by inhibiting an enzyme that breaks down cAMP. |
| Indications for AMRINONE | Severe CHF refractory to other drugs |
| Milrinone: | Used for short term tx of CHF;Adverse effectsVentricular dysrhythmias;: headache thrombocytopenia;Hypotension;bronchospasm |
| VASODILATORS | dec preload & afterload. |
| Preload | force that stretches ventricular muscle at end of filling. The greater the stretch, the better the contraction |
| Afterload: | force against w/c the heart has to work to eject its content. If afterload is high, heart has to work harder. Low afterload – BP & tiss perfusion maybe low |
| Nitrates: | Pts w/ myocardial ischemia or MI may have increased preload & afterload.Nitrates cause periph vasodilation, w/c in turn dec venous return to heart & reduces preload.improve collateral BF, reduce plt aggregation,enhance perfusion to ischemic myocardium |
| Indications for Nitrates | Acute angina;persistent ischemiaPx of angina;;Large ant AMI;AMI assoc w/ CHF;HTN;angina unresponsive to oth tx |
| Contraindications to IV nitrates: | Hypotension; Uncorrected hypovolemia; Hypertrophic obstructive cardiomyopathy; Pericardial tamponade |
| Extreme caution on Nitrates | R ventric AMI b/c pts requiring adequate venous returnNot to give nitrates for 24 hrs after sildenafil (Viagra) b/c LT hypotension |
| Adverse effects of nitrates: | HA, hypotension, syncope & tachycardia. |
| Nitroprusside Sodium: | Potent arterial & venous vasodilator that is used to treat:Severe L ventricular HF; HTN after CABG;Hypertensive crisis;dissecting aneurysm |
| Nitroprusside sodium effects | Dec. SVR, Inc. CO; Prevent cyanide toxicity: max dose not given longer than 10 min. D/C if not responding |
| ACE INHIBITORS | CHF; HTN; AMI w/ or w/o ventric dysfunction or failure; Pts w/ an AMI ST segment elevation or HF shd receive ACEI w/in 24 hrs. |
| ACE INHIBITORS action | ACEIs block conversion of angiotensin 1 to potent vasoconstrictor angiotensin II, reduce aldosterone synthesis, & may promote fibrinolysis.ACEIs increase CO, decrease sodium retention BP, CVP, SVR, PVR & PCWP; Caution: renal failure |
| ANTIHYPERLIPIDEMICS | Cholesterol reduction – impt part of therapy for pts w/ cardiovasc dss |
| 4 major classes of antihyperlipidemic drugs | 1. HMG – CoA reductase inhibitors ; 2. Nicotinic acid ;3. Bile acid sequestrants 4. Fibrates |
| . HMG (ACE INHIBITORS) | decrease tot & LDL cholesterol, dec triglycerides, inc HDL cholesterol. |
| Nicotinic acid | inhibits lipolysis in adipose tiss & inhibits hepatic prodn of VLDL dec cholesterol, triglycerides, VLDL, LDL, & increasing HDL. |
| Bile acid sequestrants | binds bile acid in intestine & form insoluble complex that is excreted in feces. B/c bile acids are not absorbed, there is an ultimately an increased hepatic synthesis of bile acids from cholesterol that may be evident by sl increased triglyceride level. |
| Fibrates | inhibit periph lipolysis &dec hepatic extraction of free fatty acids w/c dec triglyceride prodn. |
| PERCUTANEOUS CORONARY INTERVENTIONS_(PCI) | invasive procedures to treat CAD; Percutaneous transluminal coronary angioplasty (PTCA);Laser angioplasty; Atherectomy;Stents; Brachytherapy;Percutaneous myocardial vascularization;(7) Gene therapy for myocardial angiogenesis. |
| PTCA | treat pts w/ MI or unstable angina, or those lesions that occlude > 70% of internal lumen of coronary artery. Non-surg technique as an alternative to CABG in tx of obstructive CAD.alleviate myocardial ischemia, relieve angina pectoris, prevent myoc nec. |
| PTCA procedure | A coaxial catheter syst introduced into coronary artery & advanced into an area of coronary artery stenosis. Balloon attached to cath is inflated, increasing luminal dm & improving BF thru dilated segment. several inflations ranging from 30 – 300 sec |
| PTCA outcome | stretches vessel wall leading to fracture of inelastic atherosclerotic plaque & to tearing or cracking within the intima & media of the vessel |
| Major advantages of PTCA over CABG: | Reduced mortality & morbidity;Lower cost to pt;shorter convalescence; 3rd party payers |
| Indications for PTCA: | coronary aa that have at least 70% narrowing./ surgical risk factors, ie severe underlying noncardiac dss, advanced age, poor L ventricular function;totally occluded vessel.had undergone CABG & Sxs have recurred ; |
| Contraindications to PTCA: | L main CAD!!! ( not candidates for angioplasty) WHYYY???. Drawback of PTCA in L main artery dss is possibility of acute occlusion or spasm of the L main artery during the procedure w/c would result in severe L ventricular dysfunction. |
| Meds associated w/ PCI: | Aspirin;LMWH (enoxaparin, Dalteparin);Clopidogrel (Plavix);Nitroglycerin;Heparin (fract);Glycoprotein IIb/IIIa antagonists;Isosorbide (coronary vasodilators); Nifedipine, Diltiazem (Ca channel blockers) |
| Complications of PCI: | Prolonged angina;Abrupt reclosure;Coronary br occlusion;Coronary thrombosis;Marked change in HR: brady, tachy; VT, Vfib;CNS events;Dissection/intimal tear; MI; Restenosis;Exc. Bld loss; |
| STENTS | Hollow stainless steel tubes that act as scaffolding in coronary artery. After predilation w/ PTCA ballon catheter, stents are inserted thru guide catheter along a guidewire to the lesion site. Once placed across stenotic lesion, balloon inflated &left in |
| PERCUTANEOUS BALLOON VALVULOPLASTY | Non surgical tech for increasing BF thru stenotic cardiac valves using dialtion catheters. Similar to PTCA cath syst inserted percutaneously & advanced to region of narrowing using fluoroscopic guidance. |
| Indications 4PERCUTANEOUS BALLOON VALVULOPLASTY | High risk surg pts ;severe valvular narrowing;severe valvular calcification;Mid valvular regurgitation;ContraindicationsInab to access vasculature Thrombus;Severe valvular regurgn;Hx of embolic events |
| INTRAAORTIC BALLOON PUMP (IABP) | Std tx for pts w/ Acute Left Ventricular Failure (A LVF) unresponsive to pharma & volume therapy. |
| Tx goals: for (IABP) | Inc O2 supply to myocardium; Dec L ventricular work;Improve CO ;Designed to increase coronary artery perfusion pressure & BF during diastolic phase of cardiac cycle by inflation of balloon in the thoracic aorta. |
| Deflation of balloon in IABP | just before systolic ejection, dec. impedance to ejection (afterload) & L ventricular work, w/ subseq dec in myocardial O2 consumption.results are inc coronary artery perfusion & dec afterload w/ subseq inc in CO. |
| Greater work is required to maintain CO in HF | O2 demand inc w/ added work reqt. |
| Cycle leading to cardiogenic shock: | dec. CO dec.Aortic root pressure dec.coronary perfusion dec.O2 delivery Ischemia Acidosis contractility; W/ greater impedance to ejection, afterload increases – resulting in increased myocardial O2 demand. |
| Causes of Impedance to ejection: | 1)Aortic valve, (2)aortic end diastolic pressure, & (3)vascular resistance |
| Vasodilation or lower vasc. resistance | decrease afterload by dec impedance to ejection.Deflation of the balloon in aorta just before ventricular systole lowers aortic end-diastolic pressure. This dec impedance to ejection & dec L ventricular workload;IABP can dec O2 demand of the heart |
| AVLF | increase volume in ventricle at end diastole b/c of heart’s inability to pump effectively. This excessive inc in preload inc workload of heart. |
| IABP therapy helps to | dec excessive preload by decreasing impedance to ejection.W/ dec impedance, there is more effective flow of blood & more efficient emptying of L ventricle |
| Direct Physio Effects of IABP: | Cardiogenic shock after AMI;L Ventricular Failure in post op cardiac surg:Severe unstable angina:Post infarction ventricular septal defect/mitral regurgitation; Short term bridge to cardiac transplantation |
| Post op Left Ventricular Failure | – successful reduction in mortality rate has been achieved by using IABP therapy for pts w/ ALVF after cardiac surgery. |
| 2 major conditions might lead to post op pump failure | Severe pre-op L ventricular dysfunction; Intraoperative myocardial injury |
| IABP use? | Used to wean pts from cardiopulmonary bypass & provide post op circ assistance until L ventricular recovery occurs. |
| Unstable Angina | IABP counterpulsation tx used during PCI for pts w/ unstable angina or mechl problems |
| Contraindications to IABP: | Aortic insufficiency – little augmentation of coroanry perfusion; Severe peripheral vascular occlusive dss. – insertn of catheter is difficult & interrupt BF; Aortic aneurysm – may predisp pt to dislodgemt/rupture of aneurysmal debris - emboli. |
| Procedure:IABP | Balloon in thoracic aorta distal to L subclavian artery & proximal to renal aa ;trigger mechanism, drive syst that moves gas in & out of balloon.showing pt’s ECG & an arterial waveform showing effect of balloon inflation-deflation. |
| 2 methods of timing can be used w/ IABP Tx: | 1. Conventional timing – uses arterial waveform as trigger mech to det inflation & deflation ;22. Real timing – uses same pt of reference (dicrotic notch on arterial waveform for balloon inflation but uses ECG signal as trigger for balloon deflation |
| Dicrotic notch | closure of aortic valve creates an artifact on arterial waveform.Inflation should not occur before the notch b/c systole has not been completed |
Created by:
goryan
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