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Pharm II

What are alpha antagonist medications?

Medications that selectively block alpha adrenergic receptors (a1 and a2)

When an alpha 1 receptor is activated, what happens in the body?

-Activation of an alpha receptor causes an increase in intracellular calcium
-Causes contraction of smooth muscle
-Causes vasocontriction of the periphery
-Causes constriction of the bronchioles
-Prevents insulin from being released
-Stimulates glycogenolysis and gluconeogenesis
-Causes dilation of the pupils (mydriasis)
-Relaxes the GI

When an alpha 2 receptor is activated, what happens?

-Neuron firing in the CNS and Peripheral Nervous system is inhibited, causing
-In other organs, you'll see
*decreased salivation and secretion
*decreased GI motility
*prevents renin release,
*increases GFR
*increases sodium and water secretion
*decreased insulin release

Will Alpha antagonist cause the opposite effects of alpha agonist?

An alpha antagonist will prevent an alpha receptor from being activated, therefore the above s*s will not be seen

What is the prototype Alpha 1 ANTAGONIST?

Phenoxybenzamine ( Dibenzyline), this medication irriversible binds to Alpha 1 receptors

In what cases will you use Phenoxybenzamine (Dibenzyline)?

-In long term preoperative treatment to control effects of pheochromocytoma
-To relieve ischemia in peripheral vascular disease
-In BPH to improve flow

Will Phenoxybenzamine increase or decrease peripheral vascular resistance?

It will decrease PVR causing a reduction in blood pressure

Since Phenoxybenzamine blocks alpha 1 receptors synaptically, will there be more or less NE in the synaptic cleft?

There will be more free NE in the synaptic cleft, causing an increase in heart rate and cardiac output

Does Phenoxybenzamine cross the blood brain barrier?

Yes, it crosses the blood brain barrier
*therefore blocks serotonin, histamine and cholinergic receptors

What are some side effects of Phenoxybenzamine?

*CNS: sedation, depression, tiredness, lethargy and headache
*GI: n/v
*CV: postural hypotension, tachycardia and arrhythmias

What are the pharmacokinetics of Phenoxybenzamine?

* Has a long half life 24 hrs
* DOA 4 days
* Given po
*Important to know when pt took this last because it stays in the system so long, may worsen anesthesia effects

What is Phentolamine?

An alpha 1 &2 blocker that is used more for treatment of extravasation and not used much for HTN

What effects does Phentolamine cause in the respiratory system?

Phentolamine causes a decrease in airway resistance and improves asthma symptoms

What are other uses of Phentolamine?

*Treat htn from pheochromocytoma
*Treat htn from clonidine withdrawl
*Erectile dysfunction
*Extravasation of catecholamines

What type of medication is Prazosin (Minipres)

Prazosin or Minipress is an Alpha 1antagonist

What are the effects of Prazosin?

Prazosin or Minipress is a peripheral vasodilator (dilates arteries > veins)
*Increases the heart rate
*Improves urinary flow
*Possilbe improvement of lipids

What are the Alpha 1antagonist we use today?

*Phenoxybenzamine (Dibenzyline)
*Prazosin ( Minipres)

What is the main action of Alpha 2 receptors?

Alpha 2 receptors bind to NE preventing it from acting anywhere else

Why would anesthesia use Alpha Agonist medications?

*Because since Alpha 2 receptors bind NE, it causes a parasympathetic like state (no fight or flight)
*Causes sedation
*Has anesthetic sparing effect
*Used in regional anesthesia
*Intrathecal, epidural, caudal administration
*Peripheral nerve block
*Postop analgesia
*Analgesia for labor
*Chronic pain
*Prevention/treatment of drug withdrawl
*Prevention/treatment of postop shivering

What are the effects of Alpha 2 Agonist on the heart?

Alpha 2 Agonist reduce cardiac &overall mortality * reduces MI
*beneficial in vascular surgery
*monitor for excessive hypotension and bradycardia

What are some Alpha 2 Agonist medications seen today?

*Dexmedetomidine (Precedex)
*Methyldopa (Aldomet)

What is the primary action of Clonidine?

Clonidine is an Alpha 2 Agonist with central effect that decreases sympathetic outflow because it prevents NE from being released,less NE means less renin release ( NE would normally cause renin release to cause vasoconstriction)

Does Clonidine have a higher affinity for Alpha 1 or Alpha 2?

Clonidine has a 220:1 ratio for Alpha 2 over Alpha 1; so binds more to 2 than 1.

What are the routes of administration for Clonidine?

Clonidine can be administered orally, transdermal, IV, intrathecal or epidural (epidural route not recommended in the perioperative period d/t risk of thrombosis)

What is the result of Clonidine administration?

A decrease in heart rate, blood pressure, cardiac output and SVR. (Baroreceptors are preserved)

Abrupt discontinuation of Clonidine with result in what?

Rebound hypertension

What is Clonidine withdrawl?

*Occurs when Clonidine is suddenly dc'd
*The Alpha 2 receptors no longer block NE
*So the surge of NE causes excessive hypertension, tachycardia, restlessness, insomnia, headache and nausea
*If a pt is on Clonidine >6 days, they are at risk

What are the pharmacokinetics of Clonidine?

Clonidine is reabsorbed completely and rapidly after a PO dose
*Peaks in 60-90 mins
* Half life is 9-12 hrs
*Patch takes 2 days to reach full potential

What are the adverse drug reactions of Clonidine?

*Dry mouth

Clonide should be used with caution is what circumstances?

*Severe coronary insufficiency
*Conduction disturbances
*Recent MI/CVA/CKD

What are the effects of Clonidine on anesthesia?

*Reduces induction med dose (propofol, thiopental)
*Can be used in place of N20 to speed up induction time
*To reduce the adrenergic response to intubation during inhaled anesthesia
*Supplement in regional blocks

What receptor does Dexmedetomidine (Precedex) work on?

Dexmedetomidine (Precedex) works on Alpha 2 receptors causing sedation; used IV for < 24 hrs in the ICU. Prolonged use causes tachyphylaxis and decrease tolerance

What is the affinity of Dexmedetomidine (Precedex) to alpha 1 & 2 receptors?

Dexmedetomidine (Precedex) has a 1620:1 Alpha 2 over Alpha 1 affinity

What is the picture of a patient on Precedex?

*Respirations are maintained intubated/extubated
*Arousable and alert when stimulated
*Sedation is more of a sleep like state
*Can be used for procedural sedation during Fiber Optic Intubation and regional anesthesia
*Has analgesic effect
*Safe to use by nonanesthesia providers
*Useful in children who failed or were inadequately sedated by other techniques (no studies regarding the safety of use in children)

How can anesthesia providers utilize Precedex?

*preop to reduce anxiety, reduce sympathetic outflow, provide analgesia and sedate
*intraop to reduce stress response, improves respirations, hemodynamic stability, improves efficacy of anesthetics, increases recovery time, less pain meds needed
*post op may reduce opiod use by half, reduce post op shivering

How is Dexmedetomidine (Precedex) administered?

Bolus 0.5mg/kg over 5-10 mins (may cause hypertension and bradycardia)
GTT of 0.5 -1.0mg/kg/hr (may cause hypotension)
*side effects n/v/fever

What are some safety precautions for Precedex?

*Caution in advanced heart block or ventricular dysfunction
*If pt is young, healthy with high vagal tone may cause significant bradycardia and sinus arrest with rapid bolus

What type of medication is Methyldopa(Aldomet)

Methyldopa (Aldomet) is an Alpha 2 Agonist medication that binds NE from being released

What is Methyldopa metabolized to in the CNS?

Alpha-methylepinephrine this is what acts on Alpha 2 receptors preventing sympathetic outflow

What is Methyldopa used for ?

Used as a safe htn treatment duing third trimester
*500mg- 2 grams in 4 divided doses po or IV

What are common side effects of Methyldopa?

*Sedation, headache, dizziness
*Dry mouth, diarrhea, n/v
*Fluid retention, orthostasis, bradycardia
*+coombs test, hemolytic anemia, bone marrow suppression, impotence and rash

Explain the action in the Renin Angiotensin System

*Renin is released into the circulation b/c of decrease in volume, etc.
*Renin converts angiotensinogen released by the liver into Angio I
*Angio I goes to the lungs where it is converted to Angio II (angiotensin converting enzyme inhibitors work here) to prevent the conversion

Where do ACE Inhibitors work?

*In the arteries causing vasodilation (not directly, but by inhibiting the conversion of Angio I to Angio II)

How are ACE Inhibitors used?

*Treat CHF and MR by reducing afterload
*Increase CO without excessive decrease in preload

Give an example of an ACE Inhibitor

Enalaprilat (Vasotec)
*Initial dose 1.25 mg IV q 6 hrs
*Max 6 mg IV q 6 hrs
*Avoid in hemodynamic/renal impairment

When should ACE Inhibitors not be used?

*In the perioperative period b/c of slow onset/off set of action and limited titratability
*Should not be the first antihypertensive to be used perioperatively
*Risk of ARF with ACEI and ARB's

How do ACE Inhibitors affect renal function?

*In a hypertensive patient will decrease renal vascular resistance, improves RBF and GFR
*In a normotensive patient whose BP decreases, renal function will decrease causing HYPERKALEMIA
*Avoid in pts with decreased renal function/renal artery stenosis

What are the advantages/side effects of ACE Inhibitors?

*COUGH, congestion, rhinorrhea most common side effects
*ANGIOEDEMA is the most serious side effect
*CHF, bronchospasm, low K, low Na, rebound htn NOT SEEN with abrupt withdrawl.
*ARF and high K are reversible if you stop the drug

Should you administer ACE Inhibitors to pregnant women?

*No, they are a category X; will kill the fetus

Effects of ACE Inhibitors in the perioperative period

ACE Inhibitors cause prolonged low bp + anesthesia
*low bp, low volume contribute to AKI (especially if there are great volume loss or lrg fluid shift, if you give diuretics and vasodilators)
*hold acei day of surgery
*if patient is on Lisinopril (ACEI) may prolong NMB's
*careful with the potassium content of the IVF you administer

What are Angiotensin II Receptor Antagonist?

PO meds that block AT1(angiotensin II receptors)
*have the same hemodynamic effects and uses as ACEI
*Produce less cough/angioedema
*Same side effects and anesthesia considerations as ACEI

What are Dopaminergic Agonists?

Medications (compounds that activate dopamine receptors in the absence of Dopamine, used in states of low dopamine levels)

What are the dopamine receptors?

D1 and D2

What happens when a D1 receptor is stimulated?

D1 receptors that are G coupled receptors that stimulate adenylate cyclase which increases the concentration of the second messenger (cAMP{cAMP transfers the signal conduction into cells from hormones that cannot pass through the cell membrane})

What are the effects of increased/activated cAMP?

*The smooth muscle of blood vessels dilates
*Naturesis and diuresis

What happens when a DA2 is stimulated?

The opposite of D1 stimulation; this G coupled receptor prevents adenylate cyclase which casuses a decrease in cAMP

What effects dose a presynaptic DA2 receptor activation?

*presynaptically, it will prevents NE release and promotes vasodilation
*it reduces the beneficial effects of DA on renal blood flow

What is Fenoldopam (Corlopam)?

A selective D1 agonist with moderate affinity for presynaptic Alpha 2 receptors
*Decreases SVR and renal vasculature resistance
causing decreased bp
*increases LVEF and RBF (with rapid titration it can cause reflex tachycardia)
*It's as effective as SNP in controlling BP + it increases RBF

What is Fenoldopam used for?

*For the short term (<48hrs) tx of severe HTN
Start with lower doses andS titrate slowly to prevent reflex tachycardiaDON'T BOLUS*
*Preserves RBF and UO but doesn't protect the kidneys against agents like IVP DYE
*A line is not required, can use peripheral IV

Fenoldopam should be used with caution because?

*If you give a dose >than 0.1mcg/kg/min you may get tachycardia
*this drug may cause hypokalemia, possibly from pressure naturesis or increase NA-K exchange
*It's expensive
*may cause MILD TOLERANCE with long term infusion

What are some side effects of Fenoldopam?

*HA, dizziness, sweating, nausea, flushing,increased IOP, Twave inversion, RLS

What are the advantages of using Fenoldopam?

*Quick onset, short duration, no sudden fall in bp, titrates easy, preserves renal function, no coronary steal, no negative inotropic/chronotropic effects, no invasie line needed, no known interactions

What are calcium channel blockers (CCB)?

Chemicals (medications) that disrupt the movement of calcium through the calcium channels in the cardiac muscle and blood vessels.

What is the function of calcium?

* Sends signal to the CNS and heart
* Causes muscle contraction in the smooth, cardiac muscles and the vessel walls
* Important in clotting cascade and bone health

What is the primary action of calcium channel blockers?

*Negative inotropic effect
* Negative dromotropic effect (because it blocks AV conduction)
*Dilates systemic, splanchnic, coronary and pulmonary beds

What are the two types of Calcium Channel blockers?

* Non dihydropyridines (Phenylalkylamines {verapamil} and Benzothiazines {diltiazem})
* Dihydropyridines { Nifedipine, nicardapine, amlodipine, clevidipine}

Where do the Dihydropyridines work?

*Pure arterial vasodilators
*Have minimal reflex tachycardia (but its possible with higher doses)
*Negative dromo and ionotropic effects
*Used as antihypertensive

How does Nicardipine work?

*Clasic dihydropyridine
* potent specific arteriole vasodilator; systemic, coronary and cerebral circulation with no real negative iono/dromotropic effects
* No coronary steal, favorable myocardial/O2 supply demand

In what situations can you use Nicardipine?

*0.5-1 mg to blunt the hypertensive response to intubation
*Dose dependent decreases BP
*To decrease arterial pressure up to 30mmhg or you have given 5 mg in the ICU or PACU
*It works in 20-30 seconds and last 15-20 minutes (good reason to use in post op period)
*Easy to use without swings of BP, mild natriuretic effect
*No rebound hypertension when stopped
*Minimal reflex tachycardia

What are some disadvantages of Nicardipine?

Slow onset/offset
*may accumulate
*variable duration of action
*venous irritation
*may cause tachycardia b/c of the baroreceptor response

What is Clevidipine?

The newest IV CCB, it's a diphydropyridine type
*Specific arteriole vasodilator
*Decreases PVR
*Ultrashort acting (onset < 5mins),peak at 10 mins and last 10-20 mins.
*Half life 1 min. so it's cleared quickly after administration

What are the advantages of Clevidipine?

Rapid onset/offset, reduced need for other antihypertensive meds, no dose adjustment for renal and hepatic disease, ready to use vial, no MI depression because its highly vascular selective, no effect on preload, low potential for drug interactions

What are the disadvantages of Clevedipine?

*Lipid emulsion (may support bacterial growth)
*Because of lipid load restrictions,don't administer more than 1L (average in 1L is 21 mg) in 24 hrs (may increase lipid levels)

What is Verapamil?

A CCB Phenylalkylamine Class; its a vasodilator
*It decreases ionotropy(contraction)
*It decreases dromotropy (conduction)

What is Verapamil used for?

It is used for Aortic Stenosis and IHISS
*Conversion of atrial arrhythmias
*Treat Prinzmetal angina (coronary artery vasopasm)

What is Dilitiazem (Cardizem)?

A CCB Benzothiazine Class
*used to control rate in afib/atrial tach versus a conversion agen at in verapamil

Of the CCB which medication has the most negative inotropy?

*Verapamil followed by Diltiazem

Of the CCB which medication has the most AV block effect?

*Verapamil followed by Dilatizem

Of the CCB which medication has the most vasodilation effect?

Nifedipine and Nicardipine are equally strong

What are the adverse drug reactions of CCB on CNS?

headache, dizziness, nervousness, insomnia, fatigue

What are the ADRs of CCB on the CV?

Flushing, edema, palpitations with (dihydropyridines) and bradycardia with (nondihydropyridines)

What are the ADRs of CCB on the resp. system?

Nasal congestion, cough (with nifedipine mostly) and dyspnea

What are the ADRs of CCB on other sx?

Arthralgias, joint stiffness and itching

What type of effect do CCB cause on the oxygen balance?

Verapamil and Diltiazem enhance myocardial oxygen balance by
*decreasing o2 consumption by reducing afterload and the thounegative ionotropi effect
*increasing oxygen delivery through coronary vasodilation

All Dihydropyridine's may worsen Mv02 (left ventricle oxygen consumption) by causing hypotension and bradycardia except?


What are the CCB effects on renal function?

CCB cause an increase in RBF and GFR d/t naturesis
*these + efffects can be reversed if the CCB cause hypotension,hypotensiion will cause reflex catecholamine release activating Angiotensin sx leading to decreases in RBF and GFR.

When should a patient taking CCB stop taking them before surgery?

CCB can be taken up until the time of surgery without significant interactions

What are some anesthetic considerations with CCB?

*CCB may potentiate NMB (because the calcium cascade is slowed down)
*CCB may enhance hypotension, CV depression and vasodilating effects of anesthetics and analgesics
*Clevedipine decreaces gastric emptying
*Diltiazem increases effects of Versed

What does the activation of Beta Receptors cause?

Beta 1 receptor activation causes
*increase heart rate, conduction velocity, myocardial contractility
Beta 2 receptor activation causes
*smooth muscle relaxation, peripheral vasodilation, decreases BP, bronchodilates, increases insulin secretion, increases glycogenolysis and glyconeogenesis and decreases GI mobility

By blocking the beta receptors, what effects will you see?

*Decrease CO (hr & contractility)
*Decrease renin release (BUT NO VASODILATION)

What are the advantages of B Blockers over vasodilators?

*no reflex tachycardia
*improve Mv02
*intrinsic antiarrhythmic activity

How are B Blockers classified?

B blockers are classified according the receptor they block

What are some Beta 1 selective meds and how do they act? (AABEM)

Beta 1 selective blockers are:
*Atenolol, Acebutolol, Bisoprolol, Esmolol, Metoprolol
*these decrease velocity across the AV node, therefore you have decreased heart rate, contractility, renin release and lipolysis

What are non-selective B Blockers?

Medications that block either Beta 1 and or Beta 2

Which meds are non selective B Blockers? (CNPPT)

*Carteolol, Nadolol, Pindolol, Propranolol, Timolol These (CNPPT) meds act not only on Beta 1 but also on Beta2 receptors

What is the effect of the non selective B Blocker?

*In addition to beta 1 receptor blocked effects
*they (CNPPT) will cause bronchoconstriction, peripheral vasoconstriction, and decrease glycogenolysis

Non selective b blockers with alpha 1 affects are?

Carvedilol and labetalol

Which b blockers are considered long acting?

* Atenolol (selective Beta 1) 1/2 life 6-10hrs
* Nadolol (nonselective) 1/2 life 12-18 hrs
**Both eliminated by the KIDNEY

Which b blockers are considered intermediate acting?

*Propranolol (nonselective) 4-6hr 1/2 life
*Metoprolol ( selective beta 1) 4-6hr 1/2 life
**Both eliminated by the LIVER

Which bblockers are considered ultra short acting?

*Flestolol (nonselective ) 5-6 min 1/2 life
*Esmolol (selective b1 ) 8-9 mins //2 life
**Both eliminated by RED CELL ESTERASE

B blockers are also classified according to their lipophylicity, what are the differenct categories

*Low lipophylicity include Acebutolol, Atenolol, Bisoprolol, Carteolol, Nadolol
*Moderate lipophylicity include Metoprolol, Pindolol, Coreg, Labetalol
*High lipophylicity include pentbutolol and Propranolol

What are the adverse effects of non-selective blockade beta 2 receptors

* Vasoconstriction and worsening PVD
*Myocardial suppression
*life threatening bradycardia and asystole
*hyperkalemia in renal failure

Caution should be used when using beta blockers with which medications

*Verapamil - decreases HR and contractility
*Digoxin - Decreases HR and conduction

How do you treat Beta Blocker overdose

*consider isoproterenol and dobutimine and or a glucagon infusion
*A last ditch effort would be a pace-maker

When and why would you use a beta blocker perioperatively

*Use it intra and postoperative to treat HTN and tachycardia
*can be used in combination with a vasodiolator to potentiate its effects
*consider its use in an anxious patient
*esmolol is effective limiting HTN during induction and emergence
*Rate control for SVT, tachycardia, A-fib and A-flutter (not for ventricular arrhythmias)
*myocardial protection in ischemic heart disease
aortic stenosis (IHSS)
*Used to block the sympathetic response to ECT
*control peripheral manifestations of hyperthyroidism (until you figure out how to treat the thyroid issue [i.e., surgury[)

What are contraindications to beta-blockers

*Severe bradycardia
*2nd and 3rd degree heartblocks
*cardiogenic shock
*reynaud's Disease

Beta-blockers should be used with caution with

*Asthma and COPD
*Heart Failure (worsens the disease in the first month of treatment, after which, improvement is seen)

What is propranolol

*prototype non-selective beta-blocker, it is lipid soluble and penetrates the CNS.
*up to 70% is metabolized in the liver during 1st pass

What is esmolol (Brevibloc)

*It is a Beta 1 selective agent.
*blunts the cardiovascular response to intubation
*controls the rate of SVT and V-Fib
*more likely than varapamil to convert a-fib to a sinus rhythm
*controls intra and postop HTN and tachycardia
*Comes in 100mg/10ml for intermittent dosing and 2.5g/10ml ampule for dilution

What is the onset and offset times of esmolol

*short half life of 9-10 minutes
*peaks at 5-10 minutes
*duration is 20-30 minutes
*metabolized red cell esterases

What is metoprolol (Lopressor/toprol)

*Beta 1 selective agent
*used to treat angina, acute MI, and HTN
*longer duration of action, titrate to effect up 15 mg

What is labetolol

*Non-specific beta blocker with weak alpha blockade with a ratio of 7:1
*produces negative inotropic and chronotropic effects
*alpha blockade provides vasodiolating effect
(vasoconstricted HTN: vasodilation without reflex tachycardia, Hyperdynamic HTN: Beta blocker without reflex vasoconstricion)

What are indications of Labetolol

*Hyperdynamic HTN - blunts CV response to tracheal intubation
*used in the treatment of aortic dissection
*tachyphylaxis with SNP
*Intracranial HTN - does not increase ICP

Special considerations for Labetalol dosing

*Use "Test dose" 2.5-5mg IV
*If no change in HR in 5-10 min, progressively double the dose every 5-10 min. to a max dose of 100 mg

What are the adverse effects of Labetalol

*unwanted negative inotropy
*prolonged duration of action with high doses
*bronchospasm in high doses (not beta-1 selective)
*acute hyperkalemia in renal failure (high doses)
*use caution when treating post-op HTN in hypothermic patients (when pt. rewarms, persistent Beta-blockade may blunt increases in cardiac output and exacerbate rewarming hypotension due to vasodilation)

What are general considerations of Beta Blockers

*negative inotropic effects and conduction delays are potentiated by many general anesthetics
*continue beta blockers peroperatively and adjust the doses of anesthetic drugs as needed
*Don't stop abruptly due to rebound HTN and tachycardia
*May mask hypoglycemia and hyperthyroidism
*anticholinesterases (neostigmine) may increase bradycardia
*use adequate fluids to prevent orthostasis

When would you need BP managment in the OR

*Hypertension with induction/intubation or emergence/extubation
*controlled hypotension to minimize blood loss or for cross-clamping or cannulating the aorta
*Fluid loading prior to unclamping after repair of AAA
*manage BP during carotid or cerebral aneurysm surgery

What are causes of HTN intrapoeratively

*check depth of anesthesia
*sufficient analgesia
*r/o hypercarbia, distended bladder, hyperthermia, hypoxia, thryoid storm, malignant hyperthermia
*When vasodilators are used, watch for reflex tachycardia as BP decreases

What are methods of treatment for intraoperative HTN?

1. Beta blockers are 1st line therepy
2. Vasodilators 2nd line therapy
3. Calcium channel blockers 3rd line therapy
4. diuretics (Lasix [for patients with evidence of pulmonary edema or increased ICP and HTN)
5. alpha-2 agonists (clonidine, methyldopa, precedex)
6. ACE inhibitors (Only enalaprilat)

What are the favored medications to treat HTN in pregnancy

1. alpha-methyldopa
2. labetalol can be used in 2nd and 3rd trimesters (are associated with growth retardation in the 1st trimester)
3. NO ACE inhibitors
4. Hydralazine may be used during delivery
5. nifedipine can be used p.o. (not SL)
6. SNP is rarely used

What are the effects of negative inotrpes/chronotropes

* Decrease HR
* Decrease Contractility
* Decrease Wall Stress

What are hemodynamic effects of negative inotropes/chronotropes

* Decrease contractility, HR,
* Decrease CO and BP (may increase RA and LA pressures
*in tachycardic patients, slowing the HR may increase CO (increased ventricular filling time)
*calcium channel blockers are vasodilators and will decrerase arterial resistance

When would you use negative inotropes/chronotropes

*desired decrease in mycardial O2 consumption
*treatment of arrhythmias (Sinus Tach [esmolol] SVT [verapamil, propranolol, esmolol])
*myocardial preservation

What are contraindications/complications of negative inotrpes/chronotropes?

*Low CO
*bronchospastic pulmonary disease
*Prolonged conduction blocks (2nd or 3rd degree [consider esmolol for a trial with heart blocks due to the short half life])

What is a HTN emergency

*systolic >180, diastolic >120 with target organ damage

What is the goal in a HTN emergency

*reduce map by no more than 25% within minutes to hours. Reach 160/100 within 2-6 hours. Maintain the goal BP for 1-2 days then further reduce the bp over weeks.
*excessive correction leads to renal, cerebral, and coronary ischemia
*Use IV therapy and immediate correction

What is HTN urgency

*Accelerated, malignant, or perioperative increase in BP without target organ damage
*PO therapy is preferred, and immediate BP lowering is not required
*Do not use IV niphedipine (Unsafe)

What are examples of target organ damage

*Unstable angina
*Acute MI
*Acute LV failure with pulmonary edema
*dissecting aortic aneurysm

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