Cardiac Medication

• Resistance against which the left ventricle must pump blood thru out  the systemic system
• - diameter/tone of the blood vessels
• - viscosity
• - resistance from the inner lining
• increase SVR- the more the heart will pump therefore more energy used

• Cardiac Output
• The amount of blood the heart pumps in one minute
• HR SV

• Preload- when u blow up a balloon
• end diastolic ventricular volume (when blood is sitting in the ventricle)
• strenching of the muscle fibers in the ventricles
• Starlings Law

• Afterload
• resistance ie like tieing a knot then balloon has to work harder to get the air out
• - systemic vascular resistance
• - pressure that the ventricle must generate to overcome the pressure in the aorta

when u strench the fiber too much the blood will sit in the ventricle causing heart failure

• Cardiac Workload- influence by the heart rate and venous return- how much work does the heart have to do to get the blood out. the greater the cardiac workload the more work the heart has to do. 
• great workload= more O2 demand

• Inability of the heart to meet the body's demand
• - ventricular hypertrophy
• - decrease contractile force
• - too tired to pump
• - s/s right and left sided heart failure
• - tx decrease SVR decrease venous return

Ex- Propanolol (inderal) and Metoprolol (lopressor)

MOA- blocks Beta 1 receptors (decrease, HR, contractlity, blocking renin)

CI- primary line of therapy HTN, prevent angina (increase O2 supply bc it vasodilates, decrease O2 demand because of de hr), blocks aldosterone

Bradycardia, hypotension, CNS (dizzy, headache), bronchospasm, reduce HDL and increase cholesterol and triglycerides

NI- see previous handouts.

minipress

MOA- blocks Alpha 2 receptor (vasodilates)

CI: HTN

SE: significant hypotension, first dose effect (dizziness, headache, drowiness)

NI: see neuro

ex. Clonidine (catapress), Methyidopa (aldomet)

• MOA: acts on the brainstem to suppress sympathetic outflow. decrease sns (stimulation)- vasodilate 
• stimulant alpha 2 receptor- inhibits NE release
• used for alcohol abuse
• Not first line choice

CI: HTN Severe to moderate, decrease s/s from withdrawl from opiates and alcohol

• SE: orthostatic hypotension, CNS, rebound HTN following abrupt withdrawl
• methylopa- hemolytic anemia (red blood gets broken down and see as foriegn)

• NI: 
• Assess BP and associated s/s
• patient teaching safety
• assess CBC
• slow withdraw of medication

• MOA: blocks the conversion of Angiotensin I to Angiotensin II- it vasodilate
• then it block aldosterone

Angiotensin converting enzyme inhibitors

ex- Captopril (Capoten), Enalapril (Vasotec)

• decreases peripheral vascular resistance 
• lowers blood pressure
• increases renal blood flow- can use for renal patient

CI: Htn, CHF, DM nephropathy (renal damage caused by DM less blood flow to the kidneys)

SE: hypotension, CNS, chronic cough A1 converts to A2 in the lungs, Angioedema (swellen in the lips face, neutrapenia (risk for infection)

• NI: 
• Assess BP
• patient teaching 
• best on empty stomach
• careful with other drugs- hypotension
• assess edema, WBC
• enhance of effect of thiazide diurectics

Ex. Irbesrtian (Avapro)

Blocks Angiostensin II

used for pts who cannot tolerate the ace inhibitor- less side effects 

CI: adjunct HTN (used for dm pt with HF who cannot tolerate Ace inhibitor, treat kidney damage in pt with DM)

• Assess BP
• response seen in 2-3 weeks
• assess renal function
• drug interaction
• NSAIDs will decrease diurectics effects
• additive effect with other drugs
• addess K (can cause hyperkalemia)