Exam II: CV drugs - ACEIs, CCBs, and vasodilators Flashcards by Linsley Lloyd

Concerns with Antihypertensives and Anesthesia

Interference with the sympathetic nervous system’s activity resulting in ___ ____, or exaggerated hypotension related to _____, position change, or decreased _____ ____ (pos. pressure ventilation)

orthostatic hypotension
hypovolemia
venous return

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Concerns with Antihypertensives and Anesthesia

Possible depletion of _____ stores – minimal response to indirect sympathomimetics

norepinephrine

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Concerns with Antihypertensives and Anesthesia

Exaggerated response to direct sympathomimetics – due to no counter-balancing ____ ____.

beta2 activity

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Historical perspective

Prior to the mid-1970’s, antihypertensives were withheld prior to surgery due to their ___ ___ nature.

myocardial depressant

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Historical perspective

The drugs of the day caused severe ___ ___.

perioperative lability

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Historical perspective

Today, we know that beta-blockers may ____ the outcome of patients with hypertension.

improve

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Historical perspective

Other than ____, antihypertensive medications* should be continued even on the morning of surgery-fewer alterations in BP and HR, fewer _____.

diuretics
arrhythmias

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Beta-adrenergic blockers – negative ___, _____

chronotropic, inotropic

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Combined alpha1- and beta-adrenergic blocker (Labetalol)-negative inotropic, chronotropic, vasodilation; _________ as beta-blockers or phentolamine

not as potent

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Alpha1-adrenergic blocker (prazosin, phentolamine)-_____

vasodilation

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Centrally acting alpha2-adrenergic agonist (clonidine, dexmedetomidine) – decrease _____ outflow

sympathetic

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ACEIs MOA:
inhibit the ACE in both the plasma and in the vascular endothelium, thus block the conversion of ____ to ____, thus preventing the vasoconstriction from angiotensin II and the stimulation of the ____,
decreased aldosterone-decreased ____ & ____ retention (however, increased K)

angiotensin I to angiotensin II
SNS
Na and water

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ACEIs advantage -
minimal ___ ___ compared to beta-blockers, diuretics

side effects

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ACEIs indications -
hypertension (in ____), CHF, mitral ____ (F,F,V), development of CHF (regression of ____)

diabetes
regurgitation
LVH

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ACEIs CIs:
patients with ___ ____ ____ (their renal perfusion is highly dependent on angiotensin II)

renal artery stenosis

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slide 10 poses question about continuing ACEI therapy. The notes provide summary:

“despite the known hypotensive effect of both ACE inhibitors and ARBs, the 2014 ACC/AHA guidelines on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery recommend ______ this therapy in the _____ period.”

maintaining
perioperative

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ACEI Recommendation: _____ ACE inhibitors on the day of surgery or _____ on day before surgery

withhold
discontinue

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ACEIs: Hypotension was to be controlled to within __% of baseline with fluid and vasopressors.

30%

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Continuation of ACEI to day of surgery:
More intraoperative _____
No difference in ____ consequences

hypotension
adverse

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Meta-analysis – both ACEI and ARBs:
Withholding prior to surgery -
____ intraoperative hypotension
___ ____ in mortality or major adverse cardiac event

less
No change

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Large cohort prospective study of noncardiac surgery patients:
Continuation of either ACEI and ARBs prior to surgery - Increase in ____ or ___ ____ events

mortality or major adverse

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Despite the known hypotensive effect of both ACE inhibitors and ARBs, the 2014 ACC/AHA guidelines on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery state it ___ ___ ___ ___ these drugs until time of surgery.

“is reasonable” to continue

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ACE Inhibitors – Side Effects

benefit is _____ SEs, most common are c____, upper resp c____, rhinorrhea, _____ ____ symptoms.

minimal
cough
congestion
allergic-like

(r/t Potentiation of kinins and Inhibition of breakdown of bradykinins)

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ACE Inhibitors – Side Effects

______ – potentially life-threatening
Epi 0.3 to 0.5 mL of __:___ dilution*

Angioedema
1:1,000

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ACE Inhibitors – Side Effects Hyperkalemia – due to decreased production of _____ (esp. CHF w/ renal insuff)

aldosterone

ACE Inhibitors – Side Effects Angioedema may occur _____ after prolonged drug use.

unexpectedly

ACE Inhibitors – Side Effects Hereditary angioedema is due to __ ____ ____ deficiency

C1 esterase inhibitor

ACE Inhibitors – Side Effects ACE inhibitor induced is due to increased availability of bradykinin because ____ ____ is blocked.

bradykinin catabolism

How is angioedema treated? (4) (r/t ACEIs - *MARVEL*)

Epi (catecholamines, antihistamines, and antifibrinolytics may be ineffective in acute episodes) Tranexamic acid or aprotinin – inhibits plasmin activation Icatibant – a synthetic bradykinin receptor antagonist FFP – 2-4 units – to replace the deficient enzyme

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten) PO dose:

12.5-25 mg PO (TC says not important to know)

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten) Decreased ____ – especially in renal __, __ not effected

SVR CO, HR

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten) Baroreceptor sensitivity ____

reduced (HR does not increase with decreased BP)

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten) May cause _____ (related to blocking of aldosterone release)

hyperkalemia

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten) Onset ___ min Duration ___ hours

Onset 15 min Duration 6-10 hours

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten) Cough, upper respiratory congestion, rhinorrhea, and allergic-like symptoms are most common. This is due to the ____ of ____ ____, which normally breaks down bradykinins.

inhibition of peptidyl-dipeptidase activity

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec) PO Dose:

20 mg

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec) Available in IV ___-___ mg

0.625-1.25 mg

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec) Onset approx __ hour; Duration ____ hours

1 18-30

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec) Lacks the rash and pruritus side effects of _____; rarely _____ of the face, lips, tongue and glottis; watch for hypotension

captopril angioedema

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec) Not commonly given perioperatively. _____ onset and duration is _____ (compared to vasodilators like nipride and ntg).

Unpredictable negative

Other ACEIs: (6)

Benazepril (Lotensin) Fosinopril Lisinopril (Prinivil, Zestril) Moexipril Perindopril Quinapril (Accupril)

Angiotensin Receptor Blocker - Losartan (Cozaar) MOA – blocks the binding of angiotensin II to the receptors (type AT1 – found in vascular smooth muscle) to prevent ____ and _____ release

vasoconstriction and aldosterone

Angiotensin Receptor Blocker - Losartan (Cozaar) Similar effects as ___ ___

ACE inhibitors

Angiotensin Receptor Blocker - Losartan (Cozaar) Risk of ____ reduction* - 25% (compared to atenolol)

Risk of stroke reduction* - 25% (compared to atenolol)

Angiotensin Receptor Blocker - Losartan (Cozaar) Dose:

Dose 50 mg

Angiotensin Receptor Blocker - Losartan (Cozaar) May be combined with ___ ___ or inhibitor of _____** (Entresto)

thiazide diuretic neprilysin

Angiotensin Receptor Blocker - Losartan (Cozaar) ____ is losartan and hydrochlorothiazide—combined with diuretic.

Hyzaar

Angiotensin Receptor Blocker - Losartan (Cozaar) Cough due to ____ ____ is significantly less than w ACE inhibitors

bradykinin accumulation

Angiotensin Receptor Blocker - Losartan (Cozaar) *effectiveness is ___ ___ in black patients (with HTN and LVH) – LIFE study out of New Zealand

not seen

Calcium Channel Blockers - Classifications _______ - occludes the channel (Verapamil) _______ - arterial vascular smooth cells (Nifedipine, nicardipine, nimodipine) _______ - AV node-?MOA (Diltiazem)

Phenylalkylamines 1,4-Dihydropyridines Benzothiazepines

CCBs - Dihydropyridines Treat HTN in the ____, ____ ____, and ___-____ patients

elderly, African Americans, and salt-sensitive

CCBs MOA: Bind to the alpha1 subunit of the ____ ___-____ calcium ion channels Block calcium entering the cardiac and vascular smooth muscle cells - _____ specific Reduction of calcium - Fails to ____ ____ - which reduces contraction, ____ depolarization of SA and AV nodal tissue

slow L-type Arterial activate myosin Slows

CCBs MOA: Calcium ion influx is responsible for the ___ ___ of the cardiac action potential, which is important in the ____/____ ____ in cardiac and vascular smooth muscle and depolarization of the SA and AV nodal tissue

phase 2 excitation/contraction coupling

Calcium Channel Blockers - effects Negative ____, _____ effects

inotropic, chronotropic

Calcium Channel Blockers - effects Decreased ___ node activity

Calcium Channel Blockers - effects Conduction slowed through the ___ node

Calcium Channel Blockers - effects Vasodilation, decreased ___

Calcium Channel Blockers - effects Relaxes ___ ___ spasm Complements ____ (different MOA)

coronary artery nitrates

CCBs Uses treatment of coronary artery spasm, unstable ____ ____, chronic stable _____, essential _____

angina pectoris angina hypertension

CCBs Increased risk with dihydropyrimidine derivatives (______) _____ complications (placebo) Perioperative bleeding, GI hemorrhage Development of _____ (compared to beta-blockers, ACE inhibitors)

nifedipine Cardiovascular cancer

Calcium Channel Blockers - Verapamil (Calan) derivative of _____

papaverine

Calcium Channel Blockers - Verapamil (Calan) _____ contractility

Decreases

Calcium Channel Blockers - Verapamil (Calan) _____ HR

Decreased

Calcium Channel Blockers - Verapamil (Calan) Decreased conduction through ___ node

Calcium Channel Blockers - Verapamil (Calan) Relaxation of vascular _____ ____, coronary arteries

smooth muscle (Vascular smooth muscle relaxation is more arterial.)

Calcium Channel Blockers - Verapamil (Calan) Uses-treatment of ___ (AV node), ___

SVT HTN

Calcium Channel Blockers - Verapamil (Calan) Dose ___-___ mcg/kg (__-__ mg) IV slowly

75-150 2.5-5

Calcium Channel Blockers - Verapamil (Calan) Onset __-__ minutes

1-3

Calcium Channel Blockers - Verapamil (Calan) Oral nearly complete ____ metabolism

hepatic

Calcium Channel Blockers - Verapamil (Calan) IV ___% renal metabolism, ___% in bile

70% 15%

Calcium Channel Blockers - Verapamil (Calan) Elimination ½ life __-__ hours

6-12

Calcium Channel Blockers - Verapamil (Calan) Combination with ___ ___ - has additive myocardial depressant and vasodilation effects, even in normal LV function

volatile anes

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Vasodilation of ____ and ____ _____ (>verapamil)

coronary and peripheral arteries

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine _____ BP

Decreased

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Indirect ____-____ increased HR

baroreceptor-mediated

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine ____ decreased contractility, decreased chronotropic, and dromotrophic effects

Directly

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine routes of admin

PO, IV or SL

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Uses – angina, especially coronary artery vasospasm, hypertension emergencies (____/____ -cerebrovascular ischemia, MI, severe hypotension)

CAUTION/STOP

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Dose __-__ mg PO or SL

10-20

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Onset __ min

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Metabolism ____ - Elim ½ life: __-__ hours

hepatic 2-5

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Negative effects are due to ___ ____ ____ of BP

too rapid lowering

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Side effects – f____, h____, v_____, hypotension; may cause ____ dysfunction.

Side effects – flushing, headache, vertigo, hypotension; may cause renal dysfunction.

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine Abrupt stop has caused ____ ____ ____

coronary artery vasospasm

Calcium Channel Blockers - Nicardipine (Cardene) Selective ____ vasodilation - SVR

arterial

Calcium Channel Blockers - Nicardipine (Cardene) Greatest _____ effects - especially _____ arteries

vasodilating coronary

Calcium Channel Blockers - Nicardipine (Cardene) Does not effect the __ ___ or ___ ___, minimal myocardial depressant effects

SA node or AV node

Calcium Channel Blockers - Nicardipine (Cardene) 25 mg in 240 ml solution (0.1 mg/ml) Titrate – start at __ mg/hr (__ ml/hr), increase by ___ mg/hr every __-___* mins to a max of __ mg/hr

5 mg/hr 50 ml/hr 2.5 mg/hr 5-15 mins 15 mg/hr

Calcium Channel Blockers - Nicardipine (Cardene) Not compatible with ____ ____

Lactated Ringer’s

Calcium Channel Blockers - Nicardipine (Cardene) *every __ _____ titration for more rapid reduction; every __ _____ otherwise

5 mins 15 mins

Calcium Channel Blockers - Nicardipine (Cardene) Contraindicated with advanced ___ ___

aortic stenosis

Calcium Channel Blockers - Clevidipine (Cleviprex) 3rd generation _____

dihydropyridine

Calcium Channel Blockers - Clevidipine (Cleviprex) ____ onset, _____

Rapid onset, titratable

Calcium Channel Blockers - Clevidipine (Cleviprex) ___ emulsion (similar to _____)

Lipid emulsion (similar to propofol)

Calcium Channel Blockers - Clevidipine (Cleviprex) metabolism:

Metabolism: plasma and tissue esterases (organ independent)

Calcium Channel Blockers - Clevidipine (Cleviprex) Related to increased _____: maximum administration rate should not exceed ___ ____

triglycerides 32 mg/h

Calcium Channel Blockers - Clevidipine (Cleviprex) Researchers reached their target intraoperative mean arterial pressure (50-65 mm Hg) within 5 to 10 minutes in a group of adolescents using clevidipine infusion rate of 0.5 to 1 µg/kg/min, titrated by 0.5 to 1 mg/kg/min increments every 2 to 3 minutes. ____ of the patients experienced ____ _____ events that required intervention, and BP measurements returned to baseline within __ to __ _____ of stopping clevidipine infusion.

None excessive hypotensive 5 to 10 minutes

Calcium Channel Blockers - Nimodipine (Nimotop) Highly ___ ___ to cross ___ ___ barrier

lipid soluble blood brain

Calcium Channel Blockers - Nimodipine (Nimotop) Used to treat vasospasms related to ____ _____

subarachnoid hemorrhage

Calcium Channel Blockers - Nimodipine (Nimotop) Dose 0.7 mg/kg PO then ___ mg/kg ___ hrs for ___ days

0.35 q4 21

Calcium Channel Blockers - Nimodipine (Nimotop) If _____ compliance is a concern, an increase in ___ could occur

intracranial ICP

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac) Class

Benzothiazepine

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac) Blocks channels in the __ ____

AV node

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac) Uses:

Uses - treatment of SVT, angina pectoris

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac) Dose ___ mg/kg IV over 2 minutes, may repeat in 15 min if needed Infusion __ mg/hr

0.25 10

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac) Elimination via ___ (60%) and ____ (35%)

bile urine

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac) Elimination ½ time __-__ hours

3-5

Calcium Channel Blockers - Drug interactions Additive myocardial depression and vasodilation with ___ ____, especially with preexisting ____ ____

volatile anesthetics LV dysfunction

Calcium Channel Blockers - Drug interactions Potentiate ___ and ___ ___ ______-_____ drugs like ____ antibiotics (Ca ions are needed to release acetylcholine at the NM junction)

dep and non dep neuromuscular-blocking mycin

Calcium Channel Blockers - Drug interactions Increased risk of ___ ____ ____ (inhibition of Na ion movement via Na channels)

local anesthetic toxicity

Calcium Channel Blockers - Drug interactions Hyperkalemia with K replacement due to ____ of ____ ____ ____ ___

inhibition of K moving into cell

Calcium Channel Blockers - Drug interactions ____ and _____ cause hyperkalemia

Verapamil and dantrolene

Calcium Channel Blockers - Drug interactions Increase ____ ____ concentration – decreasing its clearance.

digoxin plasma

Vasodilators Indications: (3)

Treat hypertension Induce controlled hypotension Encourage LV stroke volume

Vasodilators Effects: (3)

Decrease BP Decrease SVR (arterial) Decrease venous return and CO (venodilator)

Nitric Oxide _____ cause both pulmonary and systemic vasodilation by producing ___ ____ (__).

Nitrovasodilators nitric oxide (NO)

Nitric Oxide NO – increases intracellular ____ causing smooth muscle relaxation Results ultimately from decreased ____ ____ (similar to the effect of cAMP from beta2 stimulation)

cGMP intracellular calcium

Nitric Oxide Can be inhaled in the gaseous state to cause ___ ___ specifically

pulmonary vasodilation

Nitric Oxide Increased cGMP can potentially coexist with _____ due to stimulation of ___ receptors.

bronchoconstriction M3

Nitric Oxide ____ ____ ____ ____ – previous name for NO

Endothelial derived relaxing factor (EDRF)

Nitric Oxide Administration of NO affects ____ specifically – it doesn’t affect SVR due to rapid ____ by ____

PVR uptake by hemoglobin

Nitric Oxide - endogenous CV effects Release of NO from endothelial cells due to ___ ___ and ____ ____ ____

shear stress and pulsatile arterial flow

Nitric Oxide - endogenous CV effects Regulates ____ and ____ – baseline

SVR and PVR

Nitric Oxide - endogenous CV effects Impacts distribution of ____ ____

cardiac output

Nitric Oxide - endogenous CV effects Autoregulation – increased ___ _____ with decreased ______

NO production oxygenation

Nitric Oxide - endogenous CV effects ____ produce more NO than ____ (IMA remains patent longer than saphenous vein grafts)

Arteries veins

Nitric Oxide - endogenous pulm effects Broncho_____

Bronchodilation

Nitric Oxide - endogenous pulm effects Selective dilation of vessels to ___ ____

ventilated alveoli

Nitric Oxide - endogenous platelet effect Inhibits plt activation, aggregation, and adhesion (_____)

antithrombotic

Nitric Oxide - endogenous nervous system effects Neurotransmitter in ____, ___ ____ and peripheral nervous system

brain, spinal cord,

Nitric Oxide - endogenous nervous system effects May be involved in _____ and anesthetic effects

antinociception

Nitric Oxide - endogenous Produce relaxation of ___ ___ and ___ tract

smooth muscle GI

Nitric Oxide - endogenous immune response Produced in response to activation of ______

macrophages

Nitric Oxide - endogenous immune response Can damage b____, f____, and p_____

bacteria, fungi, and protozoa

Pathophysiologic effects related to NO Essential hypertension - _____ NO release Sepsis shock – _____ NO release Atherosclerosis – _____ NO – platelet aggregation, vasoconstriction Cirrhosis – _____ production of NO

decreased excessive decreased excessive

Anesthetic Effects on NO Involved in the _____ neurotransmission

excitatory

Anesthetic Effects on NO Anesthetics cause _____ of formation of NO to _____ excitatory neurotransmission and ____ GABA inhibitory transmission

suppression decrease enhance

Anesthetic Effects on NO Administration of NO synthase inhibitors have a ___-___ ____ in MAC

dose-dependent reduction

Uses of NO Inhaled form to treat ______ ______ (use in any other than ______ is “off label” use

pulmonary hypertension neonates

Uses of NO In neonates, its use has decreased the use of _____

ECMO

Sodium Nitroprusside (SNP, Nipride) ___-___, arterial and venous vascular smooth muscle relaxant

Direct-acting

Sodium Nitroprusside (SNP, Nipride) Vasodilation of ____ and ____

arterial and venous

Sodium Nitroprusside (SNP, Nipride)

Sodium Nitroprusside (SNP, Nipride) onset

60-90 seconds

Sodium Nitroprusside (SNP, Nipride) Duration short requiring ___, ____

infusion, titration

Sodium Nitroprusside (SNP, Nipride) Careful monitoring, ___ ___

infusion device

Sodium Nitroprusside (SNP, Nipride) Dose ___-___ mcg/kg/min – up to 5 mcg/kg/min (body can handle only __ ____ continuous)

0.25-1 2 mcg/kg/min

Sodium Nitroprusside (SNP, Nipride) MOA – reacts with ____ to _____ _____ and releases cyanide and nitric oxide (NO). NO causes the _____.

hemoglobin to form methemoglobin vasodilation

Sodium Nitroprusside (SNP, Nipride) Nipride is 44% cyanide (CN-) and during metabolism ___ ____ ____ are released making cyanide toxicity possible-causing ____ ____, _____ metabolism, and ____ acidosis

five cyanide ions tissue anoxia, anaerobic metabolism, and lactic acidosis.

Sodium Nitroprusside (SNP, Nipride) - who is susceptible to CN- toxicity Receiving infusion of ______ Children or young adults – baroreceptor reflexes cause ____ of SNS –require ___ ___ Pregnancy - ____ cyanide toxicity

>2 mcg/kg/min stimulation larger dose fetal

Sodium Nitroprusside (SNP, Nipride) - CN- toxicity S&S: Unresponsive to previously ____ ___ of SNP Increased MvO2 – inability of tissues to ___ ___ Metabolic ____ CNS dysfunction, ____

therapeutic doses use oxygen acidosis seizures

Sodium Nitroprusside (SNP, Nipride) - treatment of CN- toxicity: (4)

Stop infusion 100% oxygen Sodium bicarbonate to correct met acidosis Sodium thiosulfate to be a sulfur donor to convert cyanide to thiocyanate

Sodium Nitroprusside (SNP, Nipride) Nipride must be protected from the light to prevent breakdown into ____. Light-protected solutions are safe for ___ ____.

cyanide 24 hours

Sodium Nitroprusside (SNP, Nipride) CV effects - ____ arterial and venous vasodilation

direct

Sodium Nitroprusside (SNP, Nipride) Decreased ___, ___, Indirect increase in HR and contractility, May have increased ___

BP, SVR CO

Sodium Nitroprusside (SNP, Nipride) Coronary artery vasodilation which creates ___ ___ from ischemic areas.

coronary steal

Sodium Nitroprusside (SNP, Nipride) Decrease in ____ pressure

diastolic

Sodium Nitroprusside (SNP, Nipride) - CNS Increased ____ blood flow Increased ____ blood volume

cerebral cerebral

Sodium Nitroprusside (SNP, Nipride) - CNS ICP increases are ____ if MAP decreases less than 30%; if >30% decrease in MAP, the ICP ____ to ____ levels.

maximal returns to awake

Sodium Nitroprusside (SNP, Nipride) CPP = ____-____

CPP = MAP - ICP

Sodium Nitroprusside (SNP, Nipride) - CNS To prevent the increase in ICP, infuse the SNP to slowly lower BP over ___ _____ along with ____ and _____

5 minutes hyperoxia hypocarbia

Sodium Nitroprusside (SNP, Nipride) - CNS Once the dura is open, ICP problems are ___ ___ ____.

not a problem

Sodium Nitroprusside (SNP, Nipride) - CNS contraindications Patients with increased ___ and inadequate cerebral ____ ___, and patients with ___ ___ stenosis

ICP blood flow carotid artery

Sodium Nitroprusside (SNP, Nipride) - pulm effects decrease in the _____, alteration of ____ ____ ____

PaO2 hypoxic pulmonary vasoconstriction

Sodium Nitroprusside (SNP, Nipride) - pulm effects Bigger problem with ____ lungs

healthy

Sodium Nitroprusside (SNP, Nipride) - pulm effects ___ ____ develop vascular changes that prevent this effect

COPD lungs

Sodium Nitroprusside (SNP, Nipride) - pulm effects Treat: add ____

PEEP

Sodium Nitroprusside (SNP, Nipride) - pulm effects Inhibits platelet aggregation (___mcg/kg/min) No ____ ____-bleeding not increased

>3 clinical significance

Sodium Nitroprusside (SNP, Nipride) - clinical uses Deliberate _____ Most likely to maintain ____ perfusion Initial rate – __ to ___ mcg/kg/min Should not exceed ___ mcg/kg/min Combined with other agents to min. risk of CN- tox

hypotension cerebral 0.3 to 0.5 2

Sodium Nitroprusside (SNP, Nipride) - clinical uses Hypertensive emergencies _____ initial treatment – effective ___ ____ the cause – onset, titration, quick offset

Temporary no matter

Sodium Nitroprusside (SNP, Nipride) - clinical uses Cardiac disease – decreased ____ MR, AR, CHF, MI with LV failure (may also need ____)

afterload inotrope

Sodium Nitroprusside (SNP, Nipride) - clinical uses ____ surgery Treat HTN related to ___-___ ? spinal cord ischemia – distal _____

Aortic cross-clamp hypotension

Sodium Nitroprusside (SNP, Nipride) - clinical uses Cardiac surgery _____ period to cause vasodilation to distribute warmth to periphery Treat pulmonary hypertension after ___ ____ (pulmonary vasodilator)

Rewarming valve replacement

Vasodilators - Nitroglycerin ____ nitrate

Organic

Vasodilators - Nitroglycerin Dilates venous side except, at ____ doses, it will relax ___ ___ ___

elevated arterial smooth muscle

Vasodilators - Nitroglycerin MOA – produces ___ ___ (__) which causes peripheral vasodilation

nitric oxide (NO)

Vasodilators - Nitroglycerin Sublingual – onset __ ____

4 minutes

Vasodilators - Nitroglycerin Transdermal – sustained protection from ___

Vasodilators - Nitroglycerin Infusion requires special ___ and ___ ____ to prevent absorption into the plastic

tubing and glass bottles

Vasodilators - Nitroglycerin Elimination ½ life – 1.5 minutes requires ____

infusion

Vasodilators - Nitroglycerin May cause the production of _____ when the nitrite metabolite oxidizes the ____ ion in hemoglobin

methemoglobin ferrous

Vasodilators - Nitroglycerin Treatment: ___ ___ 1-2 mg/kg IV over 5 minutes to convert back to hemoglobin

methylene blue

Vasodilators - Nitroglycerin CV effects Venous ____ (up to 2 mcg/kg/min) Decreased venous return, ____, ____ CO ____ (in normal heart with no CHF; if patient in heart failure, the CO is improved, and pulmonary congestion is relieved)

dilation LVEDP, RVEDP decreased

Vasodilators - Nitroglycerin CV effects Decreased ___ (related more to volume than SNP) Decreased ___, coronary blood flow

BP DBP

Vasodilators - Nitroglycerin CV effects Dilates larger conductance vessels of the coronary circulation – provides better blood flow to ____ ___ Relaxes ____ vessels

ischemic areas pulmonary

Vasodilators - Nitroglycerin CV effects Baroreceptor-reflex ____, increased ____ effect (increased demand, decrease supply)

tachycardia inotropic

Vasodilators - Nitroglycerin - smooth muscle effects Relaxes ____ smooth muscle Relaxes biliary tract smooth muscle (___ of ___) Relaxes ____ muscles Relaxes uterine and ureteral smooth muscles

bronchial sphincter of Oddi esophageal

Vasodilators - Nitroglycerin - CNS effects _____ vasodilation Inhibition of ___ ____

Cerebral platelet aggregation

Vasodilators - Nitroglycerin - clinical uses ____ ____ - decrease myocardial oxygen demand and vasodilate coronaries to ischemic areas (decrease size of MI-not SNP)

Angina pectoris

Vasodilators - Nitroglycerin - clinical uses Cardiac failure – decrease ____ and relieve pulmonary ____

preload edema

Vasodilators - Nitroglycerin - clinical uses Acute hypertension – maternal patient during C-section with __ ____ on fetus

no effects

Vasodilators - Nitroglycerin - clinical uses Deliberate hypotension – less potent than SNP; decrease in diastolic is less than SNP; ____ ____ has a bigger effect

intravascular volume

Vasodilators - Isosorbide dinitrate Oral nitrate – prophylaxis of ____ ____

angina pectoris

Vasodilators - Isosorbide dinitrate Prolonged _____ effect, increased exercise tolerance up to __ ___

antianginal 6 hours

Vasodilators - Isosorbide dinitrate Vasodilation of venous circulation and dilation of coronary arteries to ___ ___ ___ to ischemic areas

redirect blood flow

Vasodilators - Isosorbide dinitrate Given preop to ____ patients

CABG

Vasodilators - Hydralazine (Apresoline) ___ ___ of arterial side, some venous

Direct dilation

Vasodilators - Hydralazine (Apresoline) Vasodilates (5) things

coronary, cerebral, renal, and splanchnic, pulmonary vessels

Vasodilators - Hydralazine (Apresoline) MOA – interference with ____ ion transport

calcium

Vasodilators - Hydralazine (Apresoline) Decreases ____ more than ____ pressure

diastolic systolic

Vasodilators - Hydralazine (Apresoline) Increases in HR (baroreceptor and direct), SV, CO (can cause MI, prevented with ___-___)

beta-blocker

Vasodilators - Hydralazine (Apresoline) Onset 10 to 20 minutes (_____) Duration 2 to 4 hours (_____) Dose 10 to 20 mg

prolonged unpredictable

Vasodilators - Hydralazine (Apresoline) Mostly ____ metabolism

hepatic

Vasodilators - Hydralazine (Apresoline) Side effects – ___-___ ____, peripheral neuropathies, vertigo, diaphoresis, nausea, tachycardia – uncommon in ____ use

Lupus-like syndrome intermittent

Vasodilators - Trimethaphan Ganglionic blocker – blocks ____ nervous system reflexes

autonomic

Vasodilators - Trimethaphan Vasodilation of ___ ___ vessels Decreases CO, ___

venous capacitance SVR

Vasodilators - Trimethaphan Blocks receptors for ____

acetylcholine

Vasodilators - Trimethaphan May have ____ that offsets the benefit of decreased BP

tachycardia

Vasodilators - Trimethaphan Historical use in ____ ____

deliberate hypotension

Vasodilators - Adenosine ______ _____ in all cells – maintain the balance of oxygen supply and demand of the heart and other organs

Endogenous nucleoside

Vasodilators - Adenosine - Effects Dilation of coronary arteries (___ possible) Negative ____

steal chronotropic

Vasodilators - Adenosine MOA- stimulation of __ ____ in supraventricular cells to hyperpolarize atrial cells and slowing of SA node Can also stimulate release of ___ from endothelial cells

K+ channels NO

Vasodilators - Adenosine - Uses SVT – paroxysmal SVT and narrow complex tachycardia (not atrial fib or v. tach) Dose _________ Can repeat within ___ ____ Elimination ½ life ___-___ ____

Dose 6 mg IV, then 12 mg, then 18 mg* Can repeat within 60 seconds Elimination ½ life 0.6-1.5 seconds

Vasodilators - Adenosine Deliberate _____ ____ responsiveness, onset and recovery Decreased SVR, increased HR*, coronary flow increased**, cardiac filling pressures unchanged ____ mcg/kg/min – no _____

hypotension Rapid 220 tachyphylaxis

“Adenosine infusion evokes a receptor-specific sympatho-excitatory reflex in humans that overrides its ___ ___ ___ effect.”

direct negative chronotropic

Principle Adenosine effects - A1 (4)

Slowing of the rhythm Negative inotropic effects Vasoconstriction Bronchoconstriction Sedation Anticonvulsive effectDecrease of neurotransmitter release

Principle Adenosine effects - A2 (5)

Vasodilation Bronchodilation Complex stimulant effects Increase of neurotransmitter release Platelet aggregation inhibition

A1 receptors – located in ______ (more in atrial membranes than ventricular) – produce negative chronotropic, dromotropic and inotropic effects. The activation of the A1 receptors inhibits ____ ____, decreases the concentration of intracellular cAMP and induces opening of potassium channels, which indirectly ____ ____ ____ into the cell.

cardiomyocytes adenyl cyclase reduces calcium penetration

A2 receptors – in endothelial and vascular smooth muscle – produce coronary artery vasodilation and vascular smooth muscle relaxation -The stimulation of the A2 receptors has an opposite effect, it activates ____ ____.

adenyl cyclase.

Adenosine - Adverse reactions (seen in ___ of ____): Most common: ____ ____, ___ pain (awake patient), and dyspnea – duration averages 50 seconds

1/3 of patients facial flushing chest

Adenosine - If brady arrhythmias persist, can treat with _____ – antagonizes receptor. ______ will be ineffective

aminophylline Anticholinergics