pharm 3 set 2

prevent contraction of smooth muscles

• T affect:
• peripheral arterioles and arteries
• cardiac muscle - decrease force of contract.
• SA & AV node - dec. impulse speed/conduction
• Coupling of cardiac Ca channels to Beta 1 receptors - Decrease force, rate, and conduction

activating B1 receptors will cause a 2nd messenger to open Ca++ channels

Ca++ blockers

affects only the arterioles and NOT the HR

2nd type of Ca++ blocker classification

Affect the arterioles AND the HR

• Ca++ blocker
• affects arteriole smooth muscle via vasodilation BUT NOT HR

• Angina (coronary vasadialtion)
• HTN
• Migraines

SE= Reflex Tachycardia

• Ca++ blocker
• Affects arterioles AND HR
• -vasodilation
• -Dec. HR, force, and conduction
• -Inc. coronary artery perfusion

Angina, HTN, Dysrythmias

SE= dizzy, headache, edema, constipation, and can cause more heart problems in a compromised heart

NO Reflex Tachycardia

• Ca++ blocker
• affects arterioles AND HR

DOC for A-Fib and SVT to slpw HR enough for the heart to convert to nl rhythm

• -Peripheral arterioles= vasodilation
• -Cardiac arteries and arterioles= INc coronary bld flow
• -SA node= Dec. HR
• -AV node= slow myocardial conduction
• -Myocardium= Dec. force of contraction

• prevent angina
• HTN
• Dysrhyth

Se= same as previous Ca++ blocker

Special Ca++ blocker

Provides selective blocking of Cerebral blood vessels ONLY

Only used for rupture of Intracranial Aneurysm and used to prevent future vasospasm and re-bleed

• ACE inhibitors (prils)
• Angio II receptor blockers (sartens)
• Ca+ blockers (pines)
• Sympatholytics (alpha blockers)
•   - prevent sympathetic vasocontriction

• decrease the work load of the heart
• work on resistance vessels (arterioles)
• -reduce resistance to LV pumping
• -decrease afterload
• work on Capacitance vessels (veins)
• -reduce amount of blood return to the heart
• -decrease preload (and therefore BP)

• Postural hypoTN
• -venous relaxation
• -blood pools in venous side

• Reflex Tachycarida
• -Central-sympathetic stimulation
• -Peripheral- baroreceptors

• Increase blood volume (over time)
• -decrease renal blood flow (RAA)
• -Na+ and h2o are reabsorbed

• vasodilator
• selective dilation of arteries (dec. afterload and BP)
• -relax smnooth ms
• -No effect on veins

Used for HTN and HF (decrease workload)

• HR and contractility can increase by reflex (tachycardia)
• SLE like syndrome
• tolerence may develope

• vasodilator
• relaxes arteriole smooth muscle
• Much stronger than Hydralazine with stronger SE

Used ONLY when HTN is refractory of other drugs

Now used for Male pattern baldness

• DOC for HTN Emegencies
• Arteriole and venous dilation
• Immediate effects and short 1/2 life
• Given very slowly IV push
• Need to protect from light

• thiocyanide is a metabolic by-product of use and can poison pt.
• Need to check levels is Nipride in use for >3 days

selective dilation of arterioles

go to drug for acute HTN emergencies if Nipride is not working

can cause severe reflex tachycardia, angina, and MI

given in mini-boluses now

Naturally occuring peptides that respond to Fluid Overload/HTN used for severely decompensated HF

• B-type nat peptide does 3 things:
• -Inc vascular permeability (pull fluid out of vasc space)
• -Inc. h2o and Na+ loss
• -artery and venous dilation
•    => theses 3 dec. BP and workload

SE= hypoTN

if the electricity is going the right speed and direction

Based on the site of action potential disruption

I= blocks Na+ channels

Beta Blockers

K+ channel blockers

Ca++ channel blockers

digoxin and adenosine

ANY and ALL Dysrhythmic drugs can cause or worsen dysrhythmias 

• AICD
• -atuomatic implanted cardiac defibrillators

• Ablation
• -radio waves to destroy abnl foci

• Class 1A Na blocker
• from bark of Cinchona tree
• Slows conduction
• is a broad spectrum drug, so see a lot of SE's (diarrhea, hypoTN, tinnitus, N/V, blurry vision)

• Pro= 2nd gen
• less SE, but still a braod spectrum drug

• Call 1B Na+ blocker
• for SHort Term Ventricular Arrythmias ONLY
• Slows conduction on axons
• given IV for dysrhythmis
• given topically (needle) for local anesthetic

SE= condusion, seizures, arrest: toxic effects when given IV

Mex= 2nd gen oral version, doesn't work well

• Class 1C Na blockers
• Prodysrhythmic actions
• can exacerbate and cause new dysrhythmias

ONLY used for Refactory Arrhythmias when nothing else worked

• Class II Beta Blockers
• used for tachydysrhythmias and PVC's

• Prop= non-selective B1,2 blocker
• =Slows HR, bronchocontrict
• =Suppresses all conduction (not given with AV block)

• Met= Most popular class II
• Esmolol= IV form of Met

• Class III K+ blocker
• DOC for ANY dysrhythmias

• -K+, Na+, and Ca++ channels blocked to produce overall reduction in conduction
• -HIGHLY lipid soluble, accumulates in tissues, long 1/2

• -Pulmonary toxicity
• -Liver Failure
• -can cause HF

• Class III K+ blockers
• used for refractory dysrhythmias ONLY
• -has both K+ and beta blocking effects
• -A-fib/flutter

Pt. has really bad electricity if on this

• Class III K+ block
• Used for Refractory Dyrhythmias ONLY
• -a-fib/flutter
• -some drugs interfere with excretion

• Class III K+ block
• Terminates A-fib, and flutter of recent onset
• -used to convert to a nl sinus rhythm
• -Pt. will flat line before rhythm resest
• -can take up to 90 minutes to convert
• -1 mg given twice after 10 minutes

• Class IV Ca+ block
• do 3 things:
• -slow HR
• -Dec. velocity
• -Dec. force of contraction

• Terminate SVT's
• Slow ventricular rate in A-fib

Class IV Ca block

• Supravent. dysrhytm
• -Dec. rate
• -(+) inotrope -> INc. force of contraction

• SE= dysrhythm with toxicity
• =narrow Ther range (0.5-2.0)
• = will be worse with HypoKalemia
• =many drug interactions

Class IV

• naturally occuring nucleotide
• DOC of r terminating Paroxysmal SVT ONLY
• -Dec, automaticity of SA
• -Dec. conduction of AV
• Will stop heart temporarily

• can give 3 doses in a row:
• 6mgs, 12, and 12

• C=inc with activity, emotions, etc.
• =dec with rest

V= coronary vasospasms (feel like MI but can't find anything wrong)

• U= (Acute Coronary Syndrome)
• = Medical emergency
• =occurs at rest, is new onset, Pt. usually had previous Stable angina, but thiings got worse

Tx= reduce O2 demand of heart

• Nitrates
• Beta Block
• Ca++ block

N= dialte veins and decrease preload

B=decrease rate and force of contrction

C= Dilate arteriole, decrease afterload

• 1st drug given for Angina
• Acts directly on vascular smooth mucsle
• Dilates veins and pulls fluid from heart, DECREASING Preload
• -Give Tylenol to prevent Nitro headache

• SE= Dec. BP
• = drug interaction with Viagra

Highly lipid soluble

Sublingual - 3 doses, 5 min apart

• Oral - sustained release (Prophylaxis ONLY)
•   - Isosorbide/Imdur

Transdermal - off at night

• IV fusion - short term only
•  - 5-50 ug/min