N470: vasoactive meds (exam 2)

MAP formula

COxSVR

three elements of stroke volume

1) preload

2) afterload

3) contractility

The sympathetic nervous system holds which kind of receptors?

adrenergic receptors

Where are beta 1 receptors found?

heart

Where are beta 2 receptors found?

-arterioles

- veins

- lungs

Where are alpha 1 receptors found?

- arterioles

- veins

what is the role of beta 1 receptors?

- increase HR

- increase contractility

- increase AV conduction

what is the role of beta 2 receptors?

- vasodilation

- bronchodilation

what is the role of alpha 1 receptors?

vasoconstriction

where are alpha 2 receptors located?

the brain

what is the role of alpha 2 receptors?

decrease pain sensation

Where are dopaminergic receptors located?

kidneys, mesenteric

what is the role of dopaminergic receptors?

increase perfusion

What does a chrono-trope do?

- increases HR

- increases CO

- Increases myocardial demand

* remember: chrono=time, more beats per min

What does a dromo-trope do?

- increase AV conduction

- increase SA to AV node electrical conduction and through heart muscle

- increase Ca movement into cells

define a vaso-pressor

- stimulates smooth muscle (arterial) contraction

- increases afterload via vasoconstriction

- increases peripheral vascular resistance

define a vaso-dilator

- dilates or prevents vasoconstriction of vasc. smooth muscle

- decreases peripheral vascular resistance

define ino-trope

increases contractility

define ino-pressor

both a pressor and an inotrope

effects of alpha 1 stimulation

- vasoconstriction (skin, mucous membranes, kidneys, intestines)

- elevate BP

- homeostasis

- nasal decongestion

examples of alpha 1 agonist medications

- norepinephrine

- epinephrine

adverse effects of alpha 1 meds (4)

- HTN

- tissue necrosis

- bradycardia

- increased MVO2 (myocardial O2 demand)

alpha 2 stimulation inhibits the release of ____________

alpha 2 stimulation inhibits the release of norepinephrine

what does alpha 2 stimulation do in the CNS?

decreases SNS outflow to heart and blood vessels

response to beta 1 stimulation

- + inotrope (squeeze)

- + chronotrope (HR)

- +dromotrope (conduction)

medications that cause beta 1 stimulation (4)

- dopamine

- dobutamine

- epinephrine

- norepinephrine

adverse effects of beta 1 stimulation medications

- tachycardia

- dysrhythmias

- angina

- MVO2

What does beta 2 stimulation cause?

- arertiole dilation

- smooth muscle dilation (bronchus, heart, skeletal, uterine)

response to beta 2 stimulation

- bronchodilation

- glycogenesis

Medications that cause beta 2 stimulation

- albuterol

- preventil

- serevent

adverse effects of beta 2 stimulation

- tremor

- arrythmias

- hyperglycemia

beta 1 blockers do what to HR and BP

decrease both

beta 1 blockers mask symptoms of ______________ in diabetics

hypoglycemia (tremors, sweating, palpitations)

what do beta 2 blockers cause?

bronchoconstriction, inhibition of glycogenolysis

beta blocker drugs (5)

- metoprolol (B1 selective)

- esmolol

- labetalol

- atenolol

- propranolol, carvedilol

What effect do calcium channel blockers have on the body? (4)

- decrease contractility

- decrease HR

- decrease AV node conduction

- vasodilation (vascular smooth muscle)

uses of calcium channel blockers (4)

- SVT

- vasospasm

- increase preload

- HTN

calcium channel blocker drugs (4)

- diltiazem

- verapamil

- nifedipine

- nicardipine

adverse reactions of calcium channel blockers (4)

- low HR and BP

- prolonged PR

- heart block

- CHF

By blocking the calcium signal on __________ _________ cells, calcium channel blockers directly reduce ___________ production, therefore reducing _________ ____________

By blocking the calcium signal on adrenal cortex cells, calcium channel blockers directly reduce aldosterone production, therefore reducing blood pressure

Principles of vasopressor use: Hypotension

- hypovolemia (adequately hydrate first)

- pump failure

- maldistribution of blood

Indications for vasopressor use

- hypovolemia already being treated

- map

titration guidelines for vasopressors

- titrate to achieve end organ perfusion

- add second agent if max dose of first agent is inadequate

How often do we assess patient response while titrating vasoactive meds?

Q 15 min

venodilators that decrease preload and afterload (4)

- NTG (nitro)

- isosorbide

- nitric oxide (pulmonary)

- morphine

vasodilators that decrease preload and afterload (3)

- sodium nitroprusside

- hydralazine

- sildenafil (Viagra) (for pulm. HTN @ high doses)

What class of drugs increase afterload?

alpha-1 stimulants

alpha-1 stimulant meds that increase afterload (4)

- norepinephrine

- epinephrine

- phenylephrine

- dopamine (high dose)

What class of drugs increase contractility?

positive inotropes

positive inotrope meds that increase contractility

- dobutamine

- milrinone

- dopamine (medium dose)

- digoxin

- epinephrine and norepinephrine: dose dependent (beta 1)

normal CO

4-8 L/min

normal cardiac index

2.5-4 L/min

normal CVP (central venous pressure)

2-6 mmHg

normal PCWP (pulmonary capillary wedge pressure)

8-12 mmHg

what are the two measurements of preload?

CVP, PCWP

What re the two measurements of afterload?

SVR and PVR

normal PVR (pulmonary vascular resistance)

37-250

normal SVR (pulmonary vascular resistance)

800-1200

If preload is high, what meds do we give?

diuretics, dilators

If preload is low, what do we give?

volume replacement, dysrhythmia control (pacemaker or drugs)

If afterload is high, what meds do we give?

dilators, IABP (Nitric oxide)

If preload is low, what meds do we give?

vasopressors, IABP (epi, vasopressin)

Normal SVI (Stroke Volume Index)

33-47

What does SVI measure?

contractility

if contractility his high, what meds do we give?

beta blockers

if contractility is low, what meds do we give?

inotropes

effects of epinephrine

Increase SVR, PVR, MAP

adverse effects of epinephrine

-Increases workload of heart = may lead to ischemia & pulmonary edema

-May also cause tachycardia, arrhythmias, hyperglycemia, and profound vasoconstriction

indications for epinephrine

-Cardiac arrest

-Cardiogenic shock

-Septic shock

- Bronchospasm (Choice)

nursing management of epinephrine

-Compatible with most IV fluids

-Central line to avoid peripheral infiltration and necrosis

-Can worsen myocardial ischemia

effects of norepinephrine

↑ SVR, ↑ BP, ↑ CO

side effects of norepinephrine

↑ cardiac workload and may decrease blood flow to kidneys & extremities

indications for norepinephrine

-Hypotension (*hypovolemia being treated)

- Septic shock

Nursing Management of norepinephrine

-Administer through central line to avoid peripheral infiltration and necrosis

-Can worsen myocardial ischemia

-DC ASAP

vasopressin effects

- Non-adrenergic peripheral vasoconstrictor

- Stimulates smooth muscle V1 receptors- Causes vasoconstriction in peripheral vasculature

-ADH- sodium/urine retention

indicators for vasopressin

-Distributive shock- Septic, Neurogenic, Anaphylactic

-VT/VF ACLS

-Adjunct pressor

nursing management for vasopressin

-Not compatible with most meds

-Will affect serum electrolytes

dopamine class/action

B1 & A1 receptor agonist

What does dopamine at a low dose do?*

Stimulates dopaminergic receptors- increased renal & mesenteric perfusion

What does dopamine at a medium dose do?*

stimulates beta-1 receptors

-+ inotrope, chronotrope, dromotrope

-Increase HR, BP

What does dopamine at a high dose do?*

stimulates alpha-1 receptors

-Vasoconstriction

-Increase BP

indications for dopamine

-Hypotension (Hypovolemia treated first)

-Renal perfusion (low dose)

nursing management for dopamine

-Compatible with all IV fluids

-Central line to avoid tissue necrosis due to infiltration

-↑ O2 demand (↑ HR at high doses or if dehydrated)

Action of sodium nitroprusside (Nipride)

-POTENT vasodilator, fastest-acting

-Acts directly on vascular smooth muscle (arterial & venous)

indications for nipride*

HTN crisis, CHF

Nursing Management for nipride

-Metabolized to thiocyanate (cyanide toxicity)

-Faint brown color

-Protect from light

-Solution stable for 24 hrs

indication for NTG*

MI

NTG actions

•Venodilator

–Decreases preload

–decreases MVO2 (myocardial O2 demand)

•Relaxes and prevents coronary artery spasm: ­ oxygen supply

nursing considerations for NTG

–May order mcg/min or mcg/kg/min

–Side Effects: HA, hypotension, tachycardia

-Avoid Viagra within 24H of NTG

Digoxin class

Cardiac Glycosides

Digoxin effects (6)

-promotes accumulation of Ca in the cardiac cell enhancing contractility

-↑ CO

-↓ sympathetic tone

-↓ renin release

- ↑ filling time

- improves symptoms of HF & QOL

adverse effects of digoxin (5)

-bradycardia

-atrial & ventricular dysrhythmias

-↓ K+

- GI symptoms

-Neurological complaints

actions of dobutamine

–Stimulates B1

–Stronger Inotropic vs. chronotropic effect

–decreased CO

–decreased SVR related to increased CO

–decreased PVR

–decreased PAWP related to better pump performance

ADEs of dobutamine

tachycardia and arrhythmias

indications for Milrinone

HTN, CHF, post OH surgery

actions of Milrinone

•Inotrope

•Vasodilator

-Improve left ventricular diastolic relaxation

-Decrease afterload

Actions of amiodarone*

•Management of ventricular dysrhythmias

•Lengthens the cardiac action potential and blocking myocardial potassium channels leading to slowed conduction and prolonged refractoriness

•Administered in mg/min

•Requires loading dose

nursing management of amiodarone (5) *

-Watch for bradycardia, AV blocks.

-Will increase coagulation level and Liver enzymes

-Contraindicated in sinus bradycardia, 2nd and 3rd degree heart block

-Central line infusion recommended

-Not compatible with Heparin!

name the sedatives and paralytics (5)*

1) Propofol (Diprivan)

2) Midazolam (Versed)

3) Lorazepam (Ativan)

4) Vecuronium (Norcuron)

5) Cisatracurium (Nimbex)

Propofol (Diprivan) actions

•Slows GABA channel closing time.

•Also acts as a NA channel blocker. Will bring down BP and HR.

•Protein-bound and metabolized in the liver.

•Rapidly distributed into peripheral tissues.

•Induction agent with short half life.