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Systemic Vascular resistance
Cardiac output
- 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
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Preload
Afterload
- 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
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Heart failure
- 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
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Beta Blocker 1
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
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SE beta blockers 1
Bradycardia, hypotension, CNS (dizzy, headache), bronchospasm, reduce HDL and increase cholesterol and triglycerides
NI- see previous handouts.
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Alpha 1 Blocker
minipress
MOA- blocks Alpha 2 receptor (vasodilates)
CI: HTN
SE: significant hypotension, first dose effect (dizziness, headache, drowiness)
NI: see neuro
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Centrally acting agents (alpha 2 stimulants)
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
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Centrally acting agents (alpha 2 stimulants)
- 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
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Ace inhibitor
- 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)
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Ace Inhibitor End results
- decreases peripheral vascular resistance
- lowers blood pressure
- increases renal blood flow- can use for renal patient
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Ace Inhibitor CI SE NI
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
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Angiotensin II receptor antagonist ARB
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)
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A II NI
- 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)
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