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245 Cards in this Set
- Front
- Back
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How is the venocity of the shortening of skeletal muscle related to the stretch of the muscle?
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Inversely proportional
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What does starling's law show
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Stretch of myocardial muscle = wall tension = ventricular volume [preload]
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What happens in an inotropic state
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More forward flow occurs at a llower ventricular filling volume
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What happens in HF?
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intropy is decreased and higher filling pressures are necessary to reach the same cardiac output
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What is myocardial intoropy?
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The intrinsic ability of myocardial cells to contract vigorously.
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What is contractility dependent on?
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Ca++ availability
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Describe cardiac muscle contraction
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Ca + Troponin C -> conformation change -> space b/t actin+myosin -> cross-bridging of acting and myosin
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What are the mechanisms of inotropic agents?
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Increase intracellular Ca or increase sensitviity of proteins to Ca
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What are clinical uses of inotropic agents?
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CHF, cardiogenic shock, severe hypotension.
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What are the three classes of inotropic agents?
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Catecholamines, sympathomimetics, and PDEs
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What is the MOA of catecholamines?
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Stimulation of B1/b2 receptors.
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Describe the B1 receptor when stimulated
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Gs -> cAMP -> opens slow Ca channels -> increased ICF Ca
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List endogenous catecholamines
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Epi/Norepi/Dopamine
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Describe the roles of dopamine
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1) precursos of Epi/norepi 2) peripheral neurotransmitter
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What are the actions of dopamine?
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1) stimulates dopamine receptors 2) binds alpha/beta receptors 3) inhibits NE reuptake/metabolism
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What is the Beta range of dopamine?
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3-10 mcg/kg/min
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What is the renal range of dopamine?
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1-3 mcg/kg/min
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What is the alpha range of dopamine?
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10-15 mcg/kg/min
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Does IV dopamine have CNS effects?
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No
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What should dopamine be used carefully with?
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MAOIs
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What are the synthetic catecholamines?
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Isoproterenol, Dobutamine, dopexamine, fenoldopam
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Describe the action of isoproterenol
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B1+B2 -> decrease in SVR, increase in HR+ contractility
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What are the clinical uses of Isoproterenol?
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severe heart block, bradycardia, low CO
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What is the dose of isoproterenol?
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2-4 mcg/min
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How is isoproterenol metabolized?
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COMT
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What are the SEs of isoprel?
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arrythmias
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Describe the action of dobutamine
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1) Primarilly B1 2) minimial indirect effect = inhibition of NE reuptake; Increases contractility > than increase in HR
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What is the dose of dobutamine?
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2-15 mcg/kg/min [usually minimal increase in HR]
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Does dobutamine tend to increase BP?
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No
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What test is dobutamine used for
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Stress echo
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How is dobutamine metabolized
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hepatic
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Describe the action of dopexamine
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B2 and dopamine agonist; Little b1/alpha activity; inhibits reuptake of catecholamines; B2 stimulation -> vasodilation
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What is the use of dopexamine in CHF
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Decreases preload and afterload; Increase HR; No direct inotropic effect
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Describe the action of fenoldopam
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Selective Dopamine1 agonist; causes systemic and renal vasodilation; used as an antihypertensive
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Describe the aciton of ephedrine
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1) stimulates a/b receptors 2) direct a1 agonist, b1 agonist, causes release of catecholamines
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What are the effects of the PDEs?
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Inotropic, vasodilation.
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What happens when a PDE and a beta agonist is given together
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Synergistic effect d/t increase in cAMP
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Describe the effects of amrinone
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immediate vasodilation, inotropy in 10-15 minutes; used in heart failure
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What is a risk of amrinone
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vasodilation w/ inotropy may lead to decreased coronary artery perfusion; Use vasopressors.
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What is the dose for amrinone?
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1.5 mg/kg for 2-3 minutes, then continuous infusion at 2-10 mcg/kg/min
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What should be monitored w/ amrinone
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CVP
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Does amrinone degrade w/ light?
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Yes
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What are possible SEs of amrinone?
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hypotension, thrombocytopenia, GI upset, myalgia, fever, hepatic disfunction, ventricular irritibility.
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Describe milrinone
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20x inotropic effect of amrinone, but no fever or thrombocytopenia. PO available.
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What can be used post cardiopulmonary bypass if the heart fails?
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CaCl
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What are possible risks of CaCl
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Attenuates Epi beta effects; Pancreatic cellular injury
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Wha tis the dose of CaCl?
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2-4 mg/kg Q 10.
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What is the diff b/t CaCl and CaGluconate
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CaCl has a higher level of ionize Ca, so is prefered in adults.
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What are the effects of CaCl
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Vasoconstriction, increase in BP.
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Which inotrope has the highest a1 effect?
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Epi/NE
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Which inotrope has the highest a2 effect
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Epi/NE
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Which intrope has the highest B1 effect?
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Isoprel/Dobutamine
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Which inotrope has the highest B2 effect?
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Isoprel/Dopexamine
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Which inotrope has the highest DA1 effect?
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Dopamine
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What is the epi dose for asthma?
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0.3-0.5 mg s.c. or 1 mcg/min IV
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What is the dose for Isprel?
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0.01-0.2 mcg/kg/min
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Wha tis the dose for dobutamine?
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2-15 mcg/kg/min
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What is the dose for dopexamine?
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1-10 mcg/kg/min
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What is the bolus dose for ephedrine
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10-25mg
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What are the effects of ephedrine?
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Increase CO, SVR, HR
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What is the loading dose for amrinone?
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0.75 mg/kg (maximum 3 mg/kg in CHF)
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What is the bolus dose for milrinone
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50-75 mcg/kg
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What is the rate of dysrhythmias in patients undergoing anesthesia?
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50%
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What is the rate of dysrhythmias in patients taking dig?
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25%
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What is the rate of dysrhythmias in patients post AMI?
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>80%
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What is the concentration of Na+ in the ECF and ICF?
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ECF=140, ICF=10 mmol/L
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What is the exchange rate for Na/KAtpase?
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3 Na+ for 2 K+
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When does spontaneous depolarization occur in pacemaker cells?
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During diastole
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What causes depolarization of a pacemaker cell?
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1) increasing permeability to Na/Ca 2) decreased permeability to K
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What is normally necessary for the AP upstroke?
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Na+ influx
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Describe Phase 1 of the AP (name, event, ions)
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1) early rapid repolarization 2) Inactivation of Na+ channel, increase K+ permeability 3) K+ out
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Describe Phase 2 of the AP (name, event, ions)
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1) Plateu 2) activation of slow Ca channels 3) Ca in
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Describe Phase 3 of the AP (name, event, ions)
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1) Final repolarization 2) Ca channel inactivation, increasing K permeability -> repolarization 3) K+ out
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What reflects the duration of the ventricular action potential?
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The QT interval
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What does the QRS measure?
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The length of time for all ventricular cells to be activated
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Describe Phase 0 of the AP (name, event, ions)
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Upstroke, Opening of fast Na+ channels, Na+ in, decreased K+ permeability
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Describe Phase 4 of the AP
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1) Resting potential/diastolic repolarization 2) Normal permeability: Intrinsic slow Na/Ca leak? 3) K out, Na/Ca in
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What factors precipitate arrythmias?
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I HATE ChAOS: Ischemia, hypoxia, acidosis, electrolyte abnormalities, excessive catecholamines, autonomic, drug toxcicity, overstretching myocardial fibers, disease.
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All arrythmias result from x or y (or both)
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1) disturbances in impulse formation 2) disturbances in impulse conduction
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Shortening what causes an increase in the pacemaker rate
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1) AP duration 2) diastolic interval
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What 3 factors determine the diastolic interval?
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1) Maximal diastolic potential 2) slope of phase 4 depolarization 3) threshold potential
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How does vagal discharge slow the pacemaker rate?
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By making the maximum diastolic potential more negative and reducing the phase 4 slope
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How do beta blockers reduce heart rate?
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Reduce the phase 4 slope
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What causes an increase in the phase 4 depolarization slope?
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FAB PH: hypokalemia, beta receptor stimulation, fiber stretch, acidosis, partial depolarization by currents of injury
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What does it mean to decrease phase 4 slope?
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It means that the the current rises more rapidly from baseline to threshold
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Which cells are most prone to accelleration?
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Ones with latent potential (e.g. w/ slow phase 4 depolarization even under normal conditions, e.g. purkinje cells)
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What are afterdepolarizations?
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Depolarizations that interupt Phase 3 (early) or 4 (delayed afterdepolarizations)
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What causes delayed afterdepolarizations (DADs)
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Intracellular Ca++ excess, fast HR, dig, catecholamines, myocardial ischemia
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What causes early afterdepolarizations?
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Slow heart rates
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What do EADs cause?
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QT-related arrhythmias
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What happens with depressed conduction?
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simple blocks: AV block or BBB
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What may relieve partial AV block? Why?
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Atropine, b/c parasympathetic control of the AV node is significant
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What conditions must exist for reentry?
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1) obsticle to normal conduction 2) unidirectional block at some point in the circuit 3) conduction time in the circiut is long enough that the impulse does not enter refractory tissue
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What happens if the conduction velocity is too slow or to fast in reentry?
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A bidirectional (not unidirectional) block occurs
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What can cause slowing of conduction?
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Depression of the Na+ current, depression of the Ca+ current (esp at the AV node), or both.
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What is the effect of lengthening the refractory period on reentry
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It makes it less likely.
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What are the basic methods of antiarrhythmic drugs?
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1) Na+ channel blockade 2) Beta blockade 3) AP prolongation 4) Ca++ channel blockade
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Why do antidysrhymics have a greater effect on ectopic than normal cells?
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Because they bind more tightly to activated/inactivated channels than rested channels.
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How do drugs reduce the phase 4 slope?
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By blocking Na+ or Ca+ channels. Some drugs may also increase threshold.
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How do beta blockers indirectly reduce phase 4 slope?
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By blocking the chronotropic action of norepinephrine on the heart.
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What do reentrant dysrhythmias depend on?
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Depressed conduction
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How do antidysrhythmics slow conduction in reentrant dysrythmias?
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1) reduce number of available unblocked channels 2) prolongation of the recovery time of channels -> increase in refractory period -> extrasystoles unable to propogate
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What type of loop do reentrant rhythms rely on?
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An anatomic (WPW) or functional (myocardial ischemia) loop
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Describe antidysrhythmic effects d/t reduction of outward repolarizing currents or augmentaiton of inward currents
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1) block of K+ channels/activation of Na/Ca channels during Phase 2 2) increase in effective refractory period 3) Prevents tachycardia by prolonging AP duration
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Therapeutic antidysrhythmic levels may become problematic in...
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tachycardia, hyperkalemia
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What effect does hyperkalemia have on the depressent effects of Na/channel blocking drugs?
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It increases the depressant effects
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In the presence of antidysrhythmic drug toxicity in Na channel blockers, what can help?
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Reducing extracellular K+ levels (evelation of serum pH) -> hyperpolarizing of the myocardium
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Describe Class I antidysrythmics
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Na+ channel blockers
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Describe Class II antidysrythmics
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Reduces adrenergic activity (b-blockers). Acts on atrial, AV nodal and ventricle.
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Describe Class III antidysrythmics
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Prolongs effective refractory period (K+ channel blockers). Primarily acts on ventricles.
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Describe Class IV antidysrythmics
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Ca++ channel blockers. Acts on the atria, AV node.
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Describe Class IA antidysrythmics
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Lengthens AP duration. Effects Atrial, AV node, and ventricle.
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Describe Class IB antidysrythmics
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shortens AP duration. Na channel blockers, more selective for ischemic/abnormal tissue. Ventricular only.
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Describe Class IC antidysrythmics
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No effect/minimaly increases AP duration. Conduction system only
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Give examples of Class IA antidysrythmics.
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Quinidine, procainamide, disopyramide
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Give examples of Class IB antidysrythmics.
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Lidocaine, phenytoin, tocainide
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Give examples of Class IC antidysrythmics.
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Encainide, flecainide, propafenone
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Give examples of Class II antidysrythmics.
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propanolol, esmolol, sotalol
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Give examples of Class III antidysrythmics.
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Bretylium, amiodarone, dofetilide, ibutelide
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Give examples of Class IV antidysrythmics.
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Verapamil, diltiazem, adenosine [indirectly, causes K+ channel opening -> hyperpolarization]
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What is the route of quinidine?
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Oral
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Describe the actions of Quinidine
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1) depresses pacemaker rate, conduction and excitability 2) lengthens refractory period, decreases excitability 3) lengthens AP duration 4) lengthens QT interval d/t block of potassium channels
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What are the SEs of quinidine?
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1) alpha-blocking properties -> vasodilation, reflex tach 2) antimuscarinic actions 3) drug-induced torsades
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What effect does quinidine have on serum dig levels
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May increase them
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What is quinidine syncope?
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Lightheadedness (d/t alpha-blocking properties)
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When does quinidine toxic?
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Serum > 5 mcg/mL, and in the presence of K > 5 mmol/L, widening of QRS duration by 30%
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Describe the pharmacokinetics of quinidine
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Rapidly absorbed, 80% protein bound, metabolized in liver, t1/2 = 6 hours
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What are the therapeutic uses for quinidine?
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PACs, paroxysmal Afib/flutter, re-entrant dysrhythmias, WPW, PVCs, and Ventricular Tachycardia.
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What class is procainamide?
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Class IA
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Describe the actions of procainamide
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Similar to quinidine, less effective in supressing ectopic pacemaker activity, more effective in blocking Na+ channels in depolarized cells; Less antimuscarinic than quinidine
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What are the SEs of procainamide?
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Ganglion-blocking properties -> vasodilation and hypotension w/ rapid IV administration
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Describe toxicity w/ procainamide
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1) Lupus-like syndrome 2) pleuritis, pericarditis, parenchymal pulmonary disease, serologic abnormalities [increased antinuclear antibodies], rash, fever, hepatitis, agranulocytosis
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Describe the pharmacokinetics of procainamide
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Major metabolite is N-acetylprocainamide, a weak Na channel blocker w/ class III activity -> possible torsades. T1/2=3-4 hours; elimitated by kidneys.
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What are the route of procainamide?
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IV, IM , PO
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What are therapeutic uses of procainamide?
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1) atrial/ventricular arrythmias; recurrent Vfib; Wide-complex tachycardias.
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What is norpace?
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Disopyramide
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What is the action of disopyramide?
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Like quinidine, but more antimuscarinic
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What are the SEs of disopyramide?
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Negative inotropy + vasoconstriction -> heart failure; urinary retention, worstening glaucoma, dry mouth, blurred vision, constipation, exacerbated heart block
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Describe the pharmacokinetics of disopyramide
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Renal elimination, t1/2=6-8 hours.
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What are the therapeutic uses of disopyramide
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Only Ventricular arrythmias
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What class is imipramine?
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Tricyclic antidepressant w/ Class IA effects
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Describe imipramine
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Tricyclic antidepressant w/ antiarrythmic activity, strong antimuscarinic effects. Causes sedation.
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Describe the pharmacokinetics of imipramine
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T1/2=12 hrs
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What class is amiodarone?
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All classes, but primarilly class III
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Describe amiodarone's Na channel blocking activity
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Very effective; low affinity for activated channels, most pronounced in tissue w/ long APs, frequent APs, or less negative diastolic potentials.
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Describe amiodarone's action on K+ channels
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Markedly lengthens APs at fast heart rates -> possible torsades
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Describe amiodarone's action on Ca channels
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Weak ca channel blocker
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Describe amiodarone's effect on Beta receptors
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Noncompetitive inhibitor of beta receptors.
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Describe the electrocardiological effects of amiodarone
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Inhibits abnormal automaticity, slows sinus rate and AV conduction, prolongs QT interval, prolongs QRS duration, increases atrial, AV and ventricular refractory period, reduces transmission through refractory pathways
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Describe the effect of amiodarone on angina
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Decreases it (d/t noncompetitive alpha, beta and Ca++ channel blockade?)
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What is amiodarone similar in structure to?
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thyroid hormone
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Describe the SEs of amiodarone
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1) peripheral vasodilation secondary to alpha/ca channel blockade
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Describe amiodarone toxicity
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1) bradycardia or heart block 2) pulomonary fibrosis 3) deposits in eyes -> halos in visual fields 4) paresthesia, tremor, ataxia 5) thryoid disfunction 6) consitpation 7) hepatocellular necrosis
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What drugs reduce clearance of amio?
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Warfarin, theophylline, quinidine, procainamide, flecanaide
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Describe the pharmacokinetics of amio
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t1/2=13-103 days; Effective plasma conc = 1-2 mcg/ml.
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How long does it take to load amio?
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15-30 days
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What is the dose for amio?
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0.8-1.2 g/day x 2 weeks, then 0.2-1g/day (reduced w/ warfarin, dig, other antiarrhythmics)
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What are the therapeutic uses for amio?
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Supraventricular/ventricular arrhythmias; Afib (200-400 mg/day); cardiac arrest; wide complex tachcardia; rate control in low EF; post MI
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What is the amio dose post cardiac arrest (Vfib/pulseless VT)
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300mg IVP, 150 mg after 3-5 min, total dose of 2.2g/day
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What class is lidocaine?
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Class Ib
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Describe the channel effects of lidocaine
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Blocks activated and inactivated Na+ channels
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Describe the electrophysiological effects of lidocaine
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Shortens AP duration; supresses electrical activity of depolarized, arrhythmogenic tissues [minimal effect on normal tissue]
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What is lidocaine effective for
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Arrythmias associated w/ depolarization: ischemia, dig toxicity
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What is lidocaine ineffective for
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Arrythmias occuring in normally polarized tissues: afib/flutter
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What are the SEs of lidocaine
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Neuro: paresthesias, tremor, nausea, light-headedness, hearing disturbances, slurred speach, convulsions
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Describe lidocaine toxicity
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SA standstill; large dose in HF -> hypotension and depressed myocardial contractility.
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Describe the pharmacokinetics of lidocaine
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Extensive 1st pass hepatic metabolism. T1/2=2 hours
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How is lidocaine administered
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Only IV
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Describe the therapeutic uses of lidocaine
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Supression of VTach and fib after shock
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What class is phenytoin?
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Class Ib
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Describe the action of phenytoin
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Shortens AP length; supresses ectopic pacer activity. May interefere w/ Ca current.
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What can phenytoin be used for?
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Dig toxicity
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What class is Flecainide?
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Class IC
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Describe flecainide
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Na/K channel blocker, used for ventricular and atrial arrythmias
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What are the toxic effects of flecainide?
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May cause exacerbation of arrythmias
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What is rythmol?
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Propafenone
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What class is propafenone?
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Class IC
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Describe propafenone
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Na/K channel blocker; Slows conduction; Useful to maintain NSR in pts w/ supraventricular tachycardia and afib; less useful for ventricular arrhythmias.
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Describe the SEs of propafenone
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Accelleration of ventricular response in Afib/flutter; Re-entrant VTach; exacerbation of CHF, sinus bradycardia, bronchospasm.
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Describe the pharmacokinetics
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Reduce dose 20-30% in hepatic failure; PO
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Describe the use of beta blockers
|
effective against atrial dysrhythmias and catecholamine-induced ventricular dysrhythmias
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What are the SEs of beta blockade?
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Bradydysrhythmias, heart block [esp w/ Ca blockers], bronchospasm, CHF
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What class is sotalol?
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Class II
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Describe sotalol
|
Nonselective b-blocker, prolongs AP also by inhibiting K currents; decreases automaticity, slows AV conduction, prolongs AV refractoriness
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What are the SEs of sotalol
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Prolonged QT
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What class is dofetilide?
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Class III
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Describe dofetilide
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Pure K+ blocker [no extracardiac effects]
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What are the SEs of dofetilide?
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Torsades in 1-3% of pts.
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Describe the eliminiation of dofetilide
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Renal, excreted unchanged
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What class is Ibutilide?
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Class III
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Describe ibutilide
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K+/Na+ blocker, prolongs AP
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What is ibutilide used for?
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Conversion of afib/flutter to NSR
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What are the SEs of ibutilide?
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Torsades in 6% of patients [response=immediate cardioversion]
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Describe verapamil
|
Blocks activated/inactivated Ca channels [more effect in frequently firing tissues; AV nodal conduction and refractory period prolonged; reduces ventricular rate in afib/flutter
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What are the SEs of verapamil
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hypotension, vfib [if given in vtach]; negative inotropic; AV block
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How is Ca++ blocker AV block tx'd?
|
atropine, beta agonist, Ca++
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What are the possible SEs of diltiazem?
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hypotension, symptomatic bradycardia, heart block
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What are contraindications for diltiazem
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Afib/flutter w/ WPW or short PR; Wide complex tachycardias; Heart blocks
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What class is adenosine?
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Class IV
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Describe adenosine
|
Derived from ATP; inactivated adenylate cyclase, depresses APs; Opens K+ channels, hyperpolarizes node
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Are wide complex tachycardias affected by adenosine
|
Not usually
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Is adenosine useful in Afib/flutter/MAT?
|
No, only transiently slows rate
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What metabolizes adenosine?
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Erythrocytes and vascular endothelium
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Describe Dig
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Inhibits Na/KAtpase -> Na+ accumulation in cells, increased intracellular Ca -> increased myocardial contractility
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Describe the uses for dig
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afib w/ RVR [esp w/ CHF], supraventricular tachycardias except WPW
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Describe the pharmacokinetics of dig
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Onset 15-30 mins, peak 1-5 hours
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What is a therapeutic level for dig?
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0.5-2.5 ng/ml
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What are possible signs of toxicity for dig?
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Dysrhtymias, PACs, PVCs, AV block, VT, VF, GI or neuro sxs
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What increases dig toxicity?
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Hypokalemia, hypomagnesium, hypercalcemia, alkalosis, renal insufficiency, quinidine, hypothyroidism
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How is dig toxicity treated
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K+, ventricular arrhythmias w/ phenytoin or lidocaine.
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What is magnesium used for?
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Torsades
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What is the dose of mag?
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2-4 g over 30-45 mins, then infusion @ 1g/hr
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Why is mag used when serum mag looks normal?
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In refractory dysrhythmias, serum mag may not reflect total body stores; Mag levels usually parellel changes in potassium
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What is ACLS dosing for adenosine
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6/12/12
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What is ACLS dosing for amio
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Cardiac arrest: 300 mg [diluted in 20-30 cc D4W], then 150 mg in 3-5 mins; Recurrent ventricular dysrhythmias: 150mg/10 mins; slow infusion = 1mg/min; maintenece = 0.5 mg/min
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What is ACLS dosing for metopolol?
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5 mg Q 5 to 15mg
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What is the ACLS use of metopolol
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Suspected MI/unstable angina; reduces incidence of VF
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What is ACLS dosing for atenolol
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5mg Q 10 to 10
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What is the ACLS use of atenolol?
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PSVT, afib/flutter
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What is ACLS dosing for esmolol
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0.5 mg/kg over 1 minute, then 4 minute infusion at 50 mcg/kg; Max 300 mcg/kg.
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What is ACLS dosing for dig
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Load 10-15 mcg/kg; reduce 50% when starting amio
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What is the ACLS use for dig
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Afib/flutter, SVT
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Can cardioversion be used w/ dig?
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Only in life-threatening conditions; use lower dose [10-20 j]
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What is ACLS dosing for diltiazem
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15-20 mg over 2 mins; in 15 mins may try 20-25 mg. 5-15 mg/hr.
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What is the ACLS use for diltiazem?
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Afib/flutter; PSVT
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What is ACLS dosing for Epinephrine?
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1mg q 3-5 in resurritation; Then 2-10 mcg/min.
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What is the ACLS use for epi?
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Cardiac arrest: VF/pulseless VT, asystole, PEA; Symptomatic bradycardia; severe hypotension; anaphylaxis
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What is ACLS dosing for Ibutilide
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1 mg over 10 mins; may repeat in 10 mins. Less than 60 kg, 0.01 mg/kg.
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What is the ACLS use for ibutilide
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SVT, Afib/flutter
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What should ibutilide not be used?
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W/ prolonged QT > 440 msec
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What is ACLS dosing for lidocaine
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Cardiac arrest: 1-1.5 mg/kg; w/ refractory CF may give additional 0.75 mg/kg IV. Repeat in 5-10 minutes. Maximum 3 doses/3 mg/kg. Stable VT: 0.5-0.75 mg/kg Q 5-10 to 3 mg/kg. Maintence infusion = 1-4 mg/min.
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What is the ACLS use for lidocaine?
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Arrest; VT/VF; May be used for stable polymorphic VT w/ QT prolongation is torsades suspected
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What is ACLS dosing for Mag?
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Arrest = 1-2 g in 10 ml D5W over 5-20 mins; Torsades = 1-2g in 50 over 5-60 mins; Follow w/ 0.5-1g/hr
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What is the ACLS use for Mag
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Torsades, Arrest suspected secondary to torsades, dig toxcitity
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When should mag be used cautiously?
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renal failure
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What is ACLS dosing for procainamide?
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Recurrent VT/VF = 20 mg/min IV infusion to max 17 mg/kg. Maintence dose = 1-4 mg/min
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When should procainamide dosing be reduced?
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Cardiac or renal insufficiency [max = 12mg/kg, infusion = 1-2 mg/kg.]
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What is the ACLS use for procainamide?
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Wide-complex arrhythmias/stable VT w/ normal QT/PSVT/Afib w/ WPW
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What should you be cautious about w/ procainamide?
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Possible proarrhythmic; use cautiously w/ drugs that prolong QT.
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When should sotaolol be avoided
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In pts w/ poor perfusion d/t negative inotropic effects [bradycardia, arrhythmias, torsades]; use cautiously w/ drugs that prolong QT
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What drugs prolong QT
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Include procainamide, amio
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What is ACLS dosing for verapamil
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2.5-5 mg over 2 mins then 5-10 mg Q 15-30 up to 20mg. [or 30 mg]
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What is the ACLS use of verapamil?
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PSVT/afib/flutter. DO NOT USE w/ WPW, sick sinus syndrome, heart block.
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What drugs should be avoided w/ WPW?
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Ca channel blockers; dig
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What can Ca channel blockers + beta blockade =?
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severe hypotension
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