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PHARM2 > CV > Flashcards

CV Flashcards

0
Q

WHAT ARE PERIPHERAL EXCITATORY ACTION OF E/NE?

A

VASOCONSTRICTION OF SMOOTH MUSCLE OF BLOOD VESSELS PERFUSING SKIN.

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1
Q

WHAT ARE SYMPATHOMIMETIC AMINES?

A

EPI AND NOREPI

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2
Q

WHAT IS PERIPHERAL INHIBITORY ACTION?

A

RELAX SMOOTH MUSCLES OF THE GUT, BRONCHIOLES, AND BLOOD VESSELS PERFUSING SKELETAL MUSCLES.

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3
Q

E/NE CARDIAC EFFECTS ARE WHAT?

A

POSITIVE CHRONOTROPIC, DROMOTROPIC, AND IONOTROPIC.

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4
Q

E/NE METABOLIC EFFECTS ARE?

A

ENHANCES GLYCENOLYSIS AND LIPOLYSIS. WILL RESULT IN INCREASED BLOOD GLUCOSE AND FATTY ACIDS.

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5
Q

NE/E ENDOCRINE ACTIONS?

A

MODULATE THE SECRETION OF INSULIN.

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6
Q

NE/E EFFECT ON CNS?

A

INHIBIT APPETITE. INFLUENCE LEVEL OF AROUSAL

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7
Q

WHAT RECEPTORS DOES EPI ACTIVATE?

A

BOTH ALPHA AND BETA RECEPTORS.

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8
Q

EPI DOSES AND EFFECTS. LOW, MODERATE, HIGH DOSE.

A

LOW: 1-2 MCG/MIN: STIM BETA 2: MODEST VASODILATION.
MED: 4 MCG/MIN: STIM. BETA 1: INCREASED BP, HR, CO.
HIGH: 10-20 MCG/MIN: STIM. BOTH ALPHA AND BETA CAUSING VASOCONSTRICTION AND DILATION.

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9
Q

EPI CARDIAC ARREST DOSE?

A

1MG IV Q 3-5 MIN.

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10
Q

EPI TOXIC EFFECTS ARE….?

A

STRESS SYMPTOMS, CARDIAC ARRHYTHMIAS ESP WHEN COMBINED WITH CERTAIN VA DRUGS LIKE HALOTHANE. PRESSOR EFFECT IN LARGE DOSES CAN CAUSE EXTREME INCREASE IN BP AND CAN CAUSE STROKE, MI ETC.

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11
Q

WHAT RECEPTORS DO NE WORK AT?

A

ALPHA AND B1. NO B2 SO NO BRONCHODILATION.

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12
Q

WHAT ARE TOXIC EFFECTS OF NE?

A

SAME AS EPI EXCEPT LESS PRONOUNCED AND FREQUENT. CONTRAINDICATED WITH HALOTHANE, PREGNANCY.

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13
Q

ACLS DOSE OF NE?

A

.5-30 MCG/MIN TITRATE TO EFFECT.

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14
Q

WHAT IS THE DOSE OF DOPAMINE?

A

RENAL DOSE: 1-3 MCG/KG/MIN
BETA DOSE: 2-10 MCG/KG/MIN
ALPHA DOSE: > 10MCG/KG/MIN

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15
Q

WHAT RECEPTORS DOES DOBUTAMINE WORK AT AND WHAT IS THE DOSE?

A

MAINLY B1 RECEPTOR.

2-20 MCG/KG/MIN

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16
Q

INDICATIONS/CONTRAINDICATIONS FOR DOBUTAMINE?

A

TO INCREASE CO IN PTS WITH CHF, ESP IF HR AND SVR ARE INCREASED.

IE: WANT A GOOD SQUEEZE WITHOUT MUCH ELSE.
CAUTION IN PT WITH A FIB. AND THERE IS AN INCREASED RISK OF SVT/ V ARRYTHMIAS WITH VA. HIGHER DOSES PREDISPOSE PT TO TACHYCARDIA AND DYSRYTHMIAS.

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17
Q

RECEPTOR ISOPROTERENOL WORKS AT?
DOSE?
INDICATIONS/CONTRAINDICATIONS?

A

ACTS SELECTIVELY ON BETA RECEPTORS…1 AND 2.
END RESULT IS INCREASED CO AND O2 CONSUMPTION. 2-10 MCG/MIN INFUSION…TITRATE TO EFFECT.
USED FOR ASTHMA BRONCHODILATION, INCR HR IN HEART BLOCK, DECR PULM VASC RESISTANCE IN PULM HTN. CONTRAINDICATED IN V TACH, VFIB, HYPOTENSION.

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18
Q

WHAT IS MOA OF EPHEDRINE?

A

ACTS DIRECTLY ON B1 AND B2. ACTS INDIRECTLY ON ALPHA 1 BY CAUSING NE RELEASE. CAUSES INCREASED BP AND HR. INCREASE IN BP ONLY IF NE STORES ARE INTACT.

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19
Q

DOES EPHEDRINE ELICIT TACHYPHYLAXIS?

A

YES! IT MAY DEPLETE THE NE STORES IN SYMPATHETIC NERVE ENDINGS.

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20
Q

EPHEDRINE INDICATIONS?

A

HYPOTENSION DUE TO VASODILATION. GOOD FOR USE IN PREGNANCY AS IT DOES NOT REDUCE PLACENTAL BLOOD FLOW.

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21
Q

EPHEDRINE DOSE?

A

5-10MG. MAX DOSE IS 60MG.

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22
Q

HOW DOES NEOSYNEPHRINE WORK?

A

DIRECT ALPHA 1. NO BETA. ALPHA 2 IN HIGHER DOSES. GOOD FOR PT WITH CAD OR ADEQUATE HR.

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23
Q

WHY IS NEO THE DRUG OF CHOICE FOR CAD?

A

IT INCREASES CORONARY PERFUSION WITHOUT INCREASING HR.

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24
Q

WHAT IS DOSE FOR NEO?

A

50-100MCG IV BOLUS PERIOP.

INFUSION 10-200 MCG/MIN TITRATED TO EFFECT.

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25
Q

HOW MUCH PHENTOLAMINE WOULD YOU GIVE IF YOUR EPI JUST WENT SUB Q?

A

5-10 MG PHENTOLAMINE.

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26
Q

WHAT ARE 2 POSSIBLE USES FOR PHENOXYBENZAMINE?

A

ITS AN ALPHA ANTAGONIST CAUSING VASODILATION. CAN BE USED TO CONTROL BP FOR PHEOCHROMOCYTOMA AND POSSIBLE USE FOR RAYNAUDS.

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27
Q

WHAT IS REFLEX TACHYCARDIA AND WHEN MIGHT YOU SEE IT?

A

INCREASED HR DUE TO DECREASE IN BP…BARORECEPTOR REFLEX AND BLOCKED ALPHA 2 LEADING TO INCREASES IN NE. CAN SEE WHEN ALPHA ANTAGONISTS ARE GIVEN.

28
Q

WHAT DOES YOHIMBINE BLOCK AND WHAT DOES THAT CAUSE PHYSIOLOGICALLY?

A

SELECTIVE FOR PRESYNAPTIC ALPHA 2 BLOCK. PERIPHERAL EFFECT IS DECREASED BP. CENTRAL EFFECT IS STIMULATION OF MOOD….MAY POSSIBLY INCREASE MAC.

29
Q

HOW IS PROPRANALOL METABOLIZED? HOW DOES IT AFFECT OTHER DRUGS?

A

MET IN LIVER TO ACTIVE METABOLITES. THIS DECREASES THE AMT OF AMIDE LA THE LIVER CAN METABOLIZE. PROPRANALOL ALSO DECREASES THE PULMONARY UPTAKE OF FENTANYL RESULTING IN HIGHER CIRCULATING LEVELS. ITS HIGHLY PROTEIN BOUND SO IT INCREASES THE LEVELS/EFFECTS OF DRUGS THAT COMPETE FOR PROTEINS.

30
Q

HOW DOES PROPRANOLOL DECREASE BP?

A

NON SELECTIVE BETA BLOCKER. EQUAL BLOCK OF B1/B2.

31
Q

WHAT IS DOSE, ONSET OF ESMOLOL?

A

O: 1-2 MIN.
P: 5 MIN
D: 10-20 MIN

SELECTIVE B1. RAPID ONSET; SHORT ACTING.

32
Q

LABETALOL DOSE, ONSET?

A

O: 2-5 MIN
P: 5-15 MIN
D: 2-4 HRS

DOSE 2.5- 20MG

33
Q

WHAT IS THE BETA ALPHA BLOCK RATIO BY LABETALOL?

A

BETA: ALPHA
PO 3:1
IV 7:1

34
Q

INDICATIONS/CONTRAINDICATIONS FOR ALPHA ANTAGONISTS?

A

HTN CRISIS. PREVENT SLOUGHING AFTER INADVERTENT EXTRAVASATIONS OF SYMPATHOMIMETIC DRUGS.

35
Q

INDIC/CONTRA FOR BETA ANTAGONISTS?

A

DECREASE BP WHEN YOU DONT WANT INCREASE IN HR.

36
Q

WHAT ARE THE 5 CLASSES OF DRUGS FOR HTN?

A

SYMPATHOLYTICS…..ALPHA/BETA BLOCKERS. ACE INHIBITORS, CA CHANNEL BLOCKERS, DIURETICS, VASODILATORS.

37
Q

WHAT AGENTS ARE USEFUL FOR PHEOCHROMOCYTOMA? WHAT AGENT CAN RULE IT OUT?

A

CLONADINE CAN DIAGNOSE PHEOCHROMACYTOMA….WILL SEE DECREASE IN PLASMA CATECHOLAMINE OF NORMAL PTS AFTER CLONADINE IS GIVEN….BUT NOT IN A PHEO PT…..THEY WILL STILL BE HTN.

38
Q

HOW DOES ALPHA BLOCKADE LOWER BP?

A

ALPHA ANTAGONISTS BLOCK THE SMOOTH MUSCLE (VESSEL) CONTRACTION CAUSED BY ALPHA 1 STIMULATION.

39
Q

HOW DOES A CENTRAL ALPHA 2 AGONIST BLOCK BP?

A

IT ENHANCES THE NEGATIVE FEEDBACK LOOP CAUSING CENTRAL MEDIATED DECREASE IN NE AND THUS BLOCKS VASOCONSTRICTION.

40
Q

HOW DOES CLONADINE WORK?

A

ITS A CENTRALLY ACTING ALPHA 2 AGONIST

41
Q

WHAT ARE SOME OTHER USES FOR CLONADINE?

A

ANALGESIA, PROLONGATION OF REGIONAL BLOCKADE, DIAGNOSIS OF PHEOCHROMACYTOMA. OPIOID WITHDRAWL, SHIVERING, PREANESTHETIC MEDICATION (UNCOMMON)

42
Q

HOW DOES HYDRALAZINE WORK?

A

RELAXES THE VESSELS. ARTERIOLE GREATER THAN VENOUS. EXHIBITS REFLEX TACHYCARDIA. USED FOR HTN AND TO DECREASE AFTERLOAD IN CHF PTS.

43
Q

HOW DO ACE INHIBITORS WORK?

A

BLOCK CONVERSION OF ANGIOTENSIN 1 TO ANGIOTENSIN2. PREVENTS SECRETION OF ALDOSTERONE BY THE ADRENAL CORTEX.

44
Q

WHAT ARE THE 4 ANESTHESIA IMPLICATIONS FOR ACE INHIBITORS?

A

CONTINUE DRUG THERAPY. BE AWARE PT MAY HAVE COEXISTING CAD. ADDITIVE HYPOTENSIVE EFFECTS WITH VA. MAY NEED INTRAOP CRYSTALLOID.

45
Q

WHAT ARE 2 MAJOR MECHANISMS OF ECTOPY?

A

REENTRY AND ENHANCED AUTOMATICITY.

46
Q

NAME 6 FACTORS INVOLVED IN DYSRHYTHMIAS?

A 
ELECTROLYTE AND ACID/BACE INBALANCE 
HYPOXIA
MYOCARDIAL ISCHEMIA
ALTERED SNS ACTIVITY
BRADYCARDIA
DRUG EFFECTS
47
Q

WHEN DO DYSRHYTHMIAS REQUIRE INTERVENTION?

A

CANNOT BE CORRECTED BY REMOVING THE CAUSE OF DYSRYTHMIA, HEMODYNAMIC FUNCTION IS COMPROMISED, PREDISPOSES PT TO MORE SERIOUS DYSRHYTHMIAS.

48
Q

MOA OF LIDOCAINE/PROCAINAMIDE?

A

SUPRESSES AUTOMATICITY AND SLOWS CONDUCTION.

49
Q

METABOLISM OF LIDO/PROCAN?

A

BOTH HEPATIC TO ACTIVE METABOLITES.

50
Q

SIDE EFFECTS OF LIDO/PROCAN?

A

L: HYPOTENSION, BRADY, HEART BLOCK, RESP DEPRESSION, TINNITUS, SEIZURES, LOSS OF HEARING, DIPLOPIA….ESP WHEN PLASMA CONC. > 5 MCG/ML.
P: HYPOTENSION. ARRYTHMIAS ESP WITH DIGOXIN. POTENTIATES MUSCLE BLOCKERS.

51
Q

LIDO/PROCAN DOSING?

A

L: 1.5 MG/KG FOLLOWED BY .5MG/KG Q 2-5 MIN. INFUSION 1-4 MG/MIN.
P: 100MG Q 5 MIN UNTIL ARRHYTMIA IS SUPPRESSED. 1 GM IS MAX DOSE. INFUSION 2-6 MG/MIN. THERAPUTIC LEVEL IS 4-12 MCG/ML.

52
Q

WHEN HOW SHOULD ADENOSINE BE GIVEN?

A

SVT. NOT EFFECTIVE FOR A FIB, A FLUTTER, OR V TACH. SHORT HALF LIFE SO MUST BE GIVEN FAST. CONTRAINDICATED IN PTS WITH 2ND 3RD HEART BLOCK OR SICK SINUS SYNDROME UNLESS PACER IS IN PLACE.

53
Q

WHEN AND HOW SHOULD AMIODARONE BE GIVEN?

A

FOR REFRACTORY SVT AND V TACHYDYSRHYTHMIAS. IE V FIB, REFRACTORY A FIB OR FLUTTER. IV ONSET IS IMMEDIATE PO CAN BE UP TO 3 WEEKS. 15 MG/MIN FOR 10 MIN THEN 1 MG/MIN FOR 6 HRS, THEN .5MG/MIN FOR 18 HRS.

54
Q

WHAT ARE CALCIUM CHANNEL BLOCKERS USED FOR?

A

TREATMENT OF HTN, ANGINA, ARRHYTHMIAS, CORONARY ARTERY SPASM AND MIGRANE PROPHYLAXIS.

55
Q

CALCIUM CHANNEL BLOCKERS MOA?

A

INTERFERE WITH CALCIUM ION MOVEMENT ACROSS MYOCARDIAL AND VASCULAR SMOOTH MUSCLE. ANTIARRHYTHMIC EFFECT DUE TO INHIBITION OF CALCIUM THROUGH ALPHA SUBUNIT OF THE L TYPE SLOW CHANNELS. THIS PROLONGS REFRACTORY PERIOD WITHIN AV NODE. CEREBRAL DILATION INCREASES CBF AND ICP.

56
Q

5 ADVERSE EFFECTS OF CALCIUM CHANNEL BLOCKERS?

A

HYPOTENSION, BRADY, REBOUND TACHY FROM DECREASED PVR. BRONCHOSPASM, LARYNGOSPASM. DIZZINESS, HA, SEIZURES.

57
Q

IN TERMS OF CA CHANNEL BLOCKERS….WHEN WOULD YOU USE VERAPAMIL VS. DILTIAZEM VS NIFEDIPINE.

A

USE BOTH VERAPAMIL AND DILTIAZEM FOR PSVT; A FIB; AFLUTTER. NIFEDIPINE HAS LITTLE EFFECT ON NODE CONDUCTION…MORE VASODILATION; USED FOR HTN, PULM HTN, ANGINA (CORONARY ARTERY VASOSPASM)

58
Q

WHEN WOULD YOU GIVE A VASODILATOR?

A

HTN CRISIS, DELIBERATE CONTROLLED HYPOTENSION, FACILITATE LEFT VENT STROKE VOLUME AS IN ACUTE FAILURE, ATTENUATE HTN INTRAOP FROM AORTIC CROSS CLAMPING. COMMON DURING NEURO, VASCULAR, AND CARDIAC ANESTHESIA.

59
Q

HOW DOES NITRIC OXIDE WORK? WHAT ARE ITS EFFECTS?

A

INCREASES CYCLIC GMP RESULTING IN SMOOTH MUSCLE RELAXATION. RESULTS IN BRONCHODILATION AND VASODILATION. IT ALSO ENHANCES THE ANESTHETIC STATE.

60
Q

NIPRIDE/NTG EFFECTS ON VESSELS/HEART?

A

NIPRIDE VASODILATES AND HAS NO EFFECT ON THE HEART….CAN PRODUCE A CORONARY STEAL PHENOMENON. NTG DILATES CORONARY VESSELS LEADING TO INCREASED FLOW TO ISCHEMIC AREAS SO ITS BETTER FOR PTS WITH CAD. DECREASES BP.

61
Q

WHAT ARE THE TOXIC EFFECTS OF NIPRIDE/NTG?

A

CAN DEVELOP CYANIDE TOXICITY WITH NIPRIDE. CHARACTERIZED BY METABOLIC ACIDOSIS, CARDIAC DYSRHYTHMIAS. AN EARLY SIGN IS AN ACUTE RESISTANCE TO HYPOTENSIVE EFFECTS OF INCREASED DOSES OF NIPRIDE. TREATED WITH METHALENE BLUE AND SODIUM THIOSULFATE.
NTG: DIMINISHED EFFECT, METHEMOGLOBINEMIA, REFLEX TACHYCARDIA, INCREASED ICP.

62
Q

DOSES FOR NIPRIDE/NTG?

A

NIPRIDE: 10-300 MCG/MIN
NTG: 5-200 MCG/MIN

63
Q

HOW DOES DIGOXIN WORK?

A

INHIBITS THE NA/K PUMP LEADING TO INCREASED SODIUM IN THE CELL. INCREASED NA=INCREASED CALCIUM INSIDE CELL LEADING TO INCREASED CONTRACTILITY.

64
Q

EFFECTS OF DIGOXIN?

A

DECREASED ACTIVITY AT SA NODE. INCREASED CONDUCTION TIME. DECREASES O2 CONSUMPTION IN HEART FAILURE. POSITIVE INOTROPIC EFFECT.

65
Q

S/S OF DIGOXIN TOXICITY?

A

EARLY: ANOREXIA, N/V.
PROLONGED P-R INTERVAL. HEART BLOCK. VTACH OR VFIB. ATRIAL TACHY IS MOST COMMON DYSRYTHMIA ATTRIBUTED TO DIG TOXICITY. PREDISPOSED TO TOXICITY IF: HYPOKALEMIC, HYPOMAGNESEAMIA, HYPERCALCEMIA, ARTERIAL HYPOXEMIA, RENAL INSUFFICIENCY, USE OF K DEPLEATING DIURETICS IS MOST COMMON CAUSE.

66
Q

HOW DO PHOSPHODIESTERASE INHIBITORS WORK?

A

COMPETATIVE INHIBITION AT PDE III. INCREASES CALCIUM MOVEMENT INTRACELLULARLY. OVERALL POSITIVE INOTROPIC EFFECT WITH VASCULAR AND AIRWAR SMOOTH MUSCLE RELAXATION.

67
Q

PDE EFFECTS AND ADVERSE RXN?

A

EFFECT: INCREASE STRENGTH IN CONTRACTION WITH DECREASED VASCULAR RESISTANCE.
AE: HYPOTENSION, ARRHYTHMIA, THROMBOCYTOPENIA, HEPATIC DYSFUNCTION, HYPOKALEMIA, ANGINA.

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