pharm exam 2

oh my god bruh

sympathetic nervous system

primary autonomic regulatory of cardiovascular system

• parasympathetic in opposition

fight or flight response supplemented by epinephrine from adrenal glands

sympathetic receptors

preganglion: nicotinic N

postganglion:

beta 1 and 2

alpha 1 and 2

dopamine

sympathetic neuotransmitters (catecholamines)

norepinephrine

• primary nerve-organ neurotransmitter

epinephrine

• released by adrenal glands when stimulated by sympathetic

• circulates in blood and binds to adrenergic receptors in target organs

dopamine

• only catecholamine that specifically increases blood flow to kidneys

• more clinical relevance in central nervous system

catecholamine attributes (endogenous ligand in sympathetic)

• quickly metabolized by monoamine oxidase (MAO) or reabsorbed by cells

• short half life and first pass effect → can’t give it orally

• doesn’t cross blood brain barrier

• different catecholamines bind w different combo of receptors

adrenergic receptor subtypes

beta 1

beta 2

alpha 1

alpha 2

dopaminergic

beta 1 receptor (one heart)

↑ heart rate

↑ heart contractility

chronotropic

relating to heart rate

inotropic

relating to heart contractility

beta 2 receptor (2 lungs)

dilates bronchioles

↑ glycogenolysis in liver (increases blood glucose)

alpha 1 receptor

constrict blood vessels

↑ bp

↑ perfusion

alpha 2 receptor

works in opposition to norepinephrine (slows SNS)

↓ bp

vasoconstriction

dopaminergic receptor

dilates blood vessels in kidneys, promoting targeted blood flow

3 major elements in heart/bp control

preload (water tower)

• circulating volume, venous pressure

• blood at end of diastole ready to be pumped out

cardiac effort

• total pumping action

• rate (chronotropic)

• contractility (inotropic)

afterload (finger on water hose)

• arterial resistance in left ventricle

• pressure to pump blood out

sympathetic nervous system direct agonists

vasopressors

• ↑ bp and perfusion

• ↑ afterload (arterial resistance)

• ↑ contractility (pumping power)

ex: epinephrine

norepinephrine

dopamine

dobutamine

phenylephrine

epinephrine

DIRECT ADRENERGIC AGONIST

mechanism of action: stimulates all alpha and beta receptors

indications

IV- cardiac arrest

IM or SQ epipen- anaphylatic rxn

combined with local nerve blockers to extend duration of action (↑ vascular resistance)

racemic (nebulizer) - severe asthma or croup (infection of upper airway)

epinephrine pharmacokinetics

doesn’t cross blood brain barrier but does cross placenta

epinephrine adverse effects

SNS overstimulation

hyperglycemia

tachycardia

hypertension

angina or MI due to increased demand without increased supply

vasopressor/catecholamine nursing implications

short half life

• need either continous infusion or frequent dosing

monitor

• IV drips can be dangerous

• adverse effects w SNS overstimulation

perfusion status

• urine output (poor perfusion won’t pee), mean arterial pressure, serum lactate (low perfusion will increase lactate), mental status, kidney function test

IV site

• very corrosive to tissue if IV infiltrated

• advocate for central line to avoid necrosis

centrally acting SNS stimulants

meds work in central nervous system which then stimulates peripheral

mechanism of action (3 diff types)

1. promotion of norepinephrine release

• amphetamines + stimulants (adderall)

• nasal decongestants (pseudophedrine)

2. NE reuptake inhibitor

• cocaine, tricyclic antidepressant, ADHD meds

3. inhibit enzymes that breakdown NE

• MAO inhibitor

alpha 1 agonist

↑ action of peripheral vascular resistance (afterload)

(midodrine)

alpha 1 antagonist

↓ peripheral SNS effects

(tamsulosin, prazosin, doxasin)

alpha 2 agonist

↓ peripheral vascular resistance and ↓ bp

(clonidine, tizanidine, dexmedetomidine)

MIDODRINE (alpha 1 agonist)

oral med used to treat symptomatic orthostatic hypotension (by increasing afterload)

• not commonly prescribed

TAMSULOSIN (alpha 1 antagonist)

commonly used for BPH in men

• off label use for essential hypertension (not common)

PRAZOSIN (alpha 1 antagonist)

FDA approved for hypertension

• used off label for PTSD related nightmares

CLONIDINE (alpha 2 agonist)

mechanism of action: binds to alpha 2 receptors in central and peripheral nervous systems (↓ SNS activity)

indications:

hypertension

severe pain→ potentiates effect of opiates

ADHD

off label: alclopiates/smoking withdrawal

clonidine adverse effects

↓ of SNS and CNS activity

• bradycardia, hypotension, sedation, dizziness

xerostomia

vivid dreams + nightmares

clonidine nursing implications

• potential for abuse/addiction

• rebound hypertension if discontinued too quickly

• if pt is dizzy after taking, sit down

• take at night due to sedative effects

beta blockers

mechanism of action: block the SNS action by blocking beta receptors

↓ cardiac rate/contractility

beta blocker sub classes

2 receptor types: B-1 (heart) and B-2 (lungs, liver)

• selective beta blockers: block only B-1

• non-selective: block B-1 and B-2

• alpha/beta (also called 3rd gen): block B-1, B-2, and a-1

beta blocker intended use

slow tachycardia

↓ cardiac effort (workload) after MI or CHF

lowers hypertension (3rd gen)

cardio-selective beta blockers

selective for B-1 receptors

• strong ↓ chronotropic effect on heart

• little to no effect on liver, bronchioles, arteries

ex: metoprolol

atenolol

cardio-selective beta blocker adverse effects

↓ SNS

• bradycardia, hypotension, dizziness

• CHF symptoms ( hand+feet swelling, sob, night cough)

• mask signs of hypoglycemia (less tachycardia, less anxiety)

• chronic hyperglycemia risk (long term use)

non-selective beta blockers

antagonist for B-1 and B-2 receptors

• B-1 heart: negative chronotropic effect

• B-2: bronchioles and liver

ex: propanolol

non-selective beta blocker adverse effects

same as selective PLUS

-acute hypoglycemia risk in pts taking insulin

• inhibits glycogenesis and gluconeogenesis (decreases blood sugar)

-bronchospasm (important for ppl with asthma)

alpha/beta blockers

traditional beta blocker effect + vasodilation

• ↓ cardiac rate + afterload

• greater blood pressure lowering

• better for diabetics

ex: carvedilol: positive data with diabetics

labetalol: emergency IV for hypertensive crisis

alpha/beta blocker adverse effects

addition risk for hypotension

B-1 blockade adverse effects

(all beta blockers)

• ↓ SNS signal to heart

• bradycardia, hypotension, dizziness

• CHF symptoms (hand + foot swelling, sob, night coughing)

• mask symptoms of hypoglycemia

B-2 blockade adverse effects

(nonselective +alpha/beta)

• risk for acute hypoglycemia in pts taking insulin

— inhibits glycogenolysis (breaks down glycogen into glucose) and glucogenesis

• can cause bronchospasm (asthmatic pts)

a-1 blockade adverse effects

(alpha-beta)

• decreases insulin resistance → helpful for diabetics

no a-1 blockade adverse effects

(cardio selective + nonselective)

• increases insulin resistance

— risk for chronic hyperglycemia and or developing diabetes

beta blocker nursing implications

closely monitor vital signs

hold and question order if HR less than 50-60 and BP less than 100-110

orthostatic hypotension

• common w initiation → call provider if dizzy/fainting

• take first dose at night and or w food as indicated

heart failure

• beta blockers can worsen HF symptoms

• ↓ adrenergic support and less effective pumping

some beta blockers approved to treat HF

• metaprolol

• carvedilol

• bisprolol

anxiety

• treat as needed

beta blocker diabetes implications

any beta blocker can mask symptoms

• no tachycardia

nonselective beta blockers reduce glucogenesis (risk for acute hypoglycemia)

alpha/beta blockers

• only class that doesn’t increase insulin resistance

• other classes increase risk for chronic hyperglycemia