Alterations in Cardio System Flashcards
Renin Angiotensin Aldosterone System (RAAS)
In response to low BP or low serum sodium levels.
Used to regulate BP and extra cellular volume.
Also activated by renal perfusion.
Elevated Blood Pressure Level
120-129 and <80
Encourage diet changes
Stage 1 HTN
130-139 or 80-89
Stage 2 HTN
140+ or 90+
Intro to meds
Crisis HTN
180+ and/or 120+
Primary HTN
Idiopathic-no known cause
Most common
Absence of underlying disease process
Risk Factors for HTN
Smoking, excessive sodium intake, obesity, 60+ years old, family hx, sedentary lifestyle, insulin resistance
Secondary HTN
KNOWN cause related to underlying condition
Treat underlying cause
- renal disorder
- adrenocorticol tumors
- adrenomedullary tumors
- drugs
- pregnancy, hormonal therapy
S/SX of HTN
Asymptomatic, none
Look for signs of end organ damage
-headache
-chest pain
-red face
-visual changes
-weakness in extremities
-increased temp
Hypertensive Crisis
rapidly progressive HTN in which SBP>180 and/or DBP>120
more common with primary HTN
HTN Urgency
no s/sx of end organ damage
BP > 180/120
Treat by gradually lowering BP (hrs to days)
HTN Emergency
s/sx evident of end organ damage, more intense, uncontrolled
treat by aggressively lowering BP (min to hrs)
IV therapy-faster administration
Diuretics
Potassium Sparing (mild)
Thiazide (mild)
Loop (moderate to profound)
MOA: blocks Na and Cl reabsorption, increase urinary output, decrease arterial resistance, decrease circulatory volume
water fluid pills
first line.
Hydrochlorothiazide
Thiazide Diuretic
MOA: works on distal convoluted tubule to inhibit reabsorption of Na/Cl to decrease cardiac output and relax arterioles
SE: electrolyte and metabolic imbalances, HYPOkalemia, orthostatic hypotension, may worsen renal insufficiency, can elevate glucose and cholesterol levels
NA: monitor K levels, K supplements and K rich foods
furosemide
LOOP Diuretic
MOA: inhibit kidneys ability to absorb Na in the LOOP OF HENLE, more peeing out
SE: HYPOkalemia, dehydration, HYPOtension, Ototoxicity (hearing loss)
NA: monitor K levels, KCl supplements, notify HCP of low urine output, push slow thru IV
spironolactone
Potassium Sparing Diuretic
MOA: blocks action of aldosterone, potassium retention and excretion of Na and water
SE: HYPERkalemia, deepened voice, hirsutism, gynecomastia, irregular periods
Sympatholytics
BETA BLOCKERS
Alpha adrenic blockers
Centrally acting alpha 2 agonists
Beta adrenic blockers
Impact SNS
Decreases vasoconstriction and peripheral vascular resistance
Metoprolol (selective)
Propranolol (nonselective)
Carvedilol (alpha and beta)
Beta Adrenergic Blocker
BETA 1: heart
BETA 2: lungs
MOA: increase nitric acid, blocks stimulation of beta 1 receptors, decreases BP AND HR
SE: fatigue/lethargy, bradycardia, HYPOtension, can mask HYPOglycemia
NA: wean when discontinuing, possibility of rebound HTN, don’t use with patients with asthma or breathing problems (COPD), HOLD if SBP<100 or HR<60
clonidine
Alpha 2 Adrenergic Antagonist
MOA: decreases SNS outflow and stimulation of alpha and beta receptors
SE: drowsiness, rebound HTN, can worsen preexisting liver disease
NA: advise to take at night, don’t abruptly discontinue
doxazosin
Selective Alpha 1 Beta Blocker
MOA: selective alpha 1 blockage, venous and arterial dilation
SE: HYPOtension, dizziness
RAAS Blockers
ACE inhibitor
ARBs
Renin inhibitor
Captopril
Lisinopril
ACE inhibitor
1st line
MOA: blocks angiotensin-converting enzyme, inhibits production of angiotensin 2 and aldosterone secretion
Drug of choice for diabetic patients
SE: first dose HYPOtension, dry persistent nonproductive cough, dizziness, rash, angioedema
DO NOT TAKE IF PREGNANT
NA: be cautious with renal disease patients, neutropenia, risk of HYPERkalemia
losartan
Angiotensin Receptor Blocker
MOA: blocks action of angiotensin 2 after formation, causing vasodilation, increased Na and water retention
SE: well tolerated, some risk of angioedema
DO NOT USE IF PREGNANT
aliskiren
Renin Inhibitor
MOA: direct inhibition of renin, induces vasodilation, decreases blood volume, inhibits cardiac and vascular hypertrophy
SE: relatively well tolerated, GI discomfort, watch for HYPERkalemia if given with ACEi
NA: takes several weeks to see effect
DO NOT TAKE IF PREGNANT
Calcium Channel Blockers
nifedipine
nicardipine
verapamil
diltiazem
nifedipine
nicardipine
verapamil
diltiazem
Calcium Channel Blockers
MOA: blocks Ca access to cells, decreases contractility and conductivity of heart, decreases 02 demand, vasodilation of smooth muscles
SE: bradycardia, headache, orthostatic hypotension, GI discomfort, peripheral edema
*cardiac rhythm problems, chest pain
NA: best for elderly and AA
hydralazine
vasodilator
MOA: causes relaxation directly on arterial and venous smooth muscles, decreases peripheral resistance
SE: HYPOtension, dizziness, headache, tachycardia, dyspnea, GI discomfort
Cholesterol
essential part of phospholipid layer in all cell membranes
highly insoluble
Exogenous- 25%
Endogenous- 75% (more impactful)
manufactured by liver
HMG CoA reductase- pathway liver uses to create cholesterol
Lipoproteins
combo of lipids (cholesterol and triglycerides) and proteins
HDL (good)
LDL (bad): stick to artery walls and creates plaque buildup
VLDL
Hypercholesterolemia
also called hyperlipidemia/dyslipidemia
too much cholesterol in blood stream
Total Cholesterol Score
HDL + LDL + triglyceride / 5
Familial Hypercholesterolemia
defect in LDL receptors in liver cells
liver cannot efficiently remove LDL from blood serum
LDL:HDL
Male <5.0
Female <4.5
Risks of Hyperlipidemia
Diet (high saturated fats)
Age
Family Hx
HTN
Diabetes
Physical inactivity
Atherosclerotic Plaque
built up cholesterol (LDL) on blood vessels, vasodilation problem
Atherosclerosis
elevated LDL cholesterol leads to thickening/hardening of arterial walls
plaque formation: injury to endothelium layers of vessels, increased permeability of LDL molecules into vessels
NA: decrease cholesterol (LDL), increase HDL, meds, weight control, exercise, smoking cessation
Effects of atherosclerosis
99% blockage- angina
fatigue, inability to complete common tasks, stroke, heart attach, ischemic heart disease
HMG-CoA Inhibitors
atorvastatin
simvastatin
rosuvastatin
drugs that treat HDL and prevent fatal atherosclerosic cardiovascular events associated with high cholesterol
atorvastatin
simvastatin
rosuvastatin
first line
MOA: stops liver from making endogenous cholesterol
*familial hypercholesterolemia patients won’t respond due to LDL defect
prevents strokes and heart attacks,
decreases diabilities from stroke,
reduces total mortality with hx of ASCVD event
SE: myopathy, Rhabdomyolysis, acute kidney failure, heptotoxicity
NA: taken at night, drug interactions, avoid alcohol
Cholesterol production in liver is highest at what time of day?
Night.
ezetimibe
Cholesterol Absorption Inhibitor
MOA: blocks absorption of cholesterol in jejunum
2nd line
NA: fasted lipid panel, creatine kinase (CK) level monitoring, consider secondary causes
Creutzfeldt Jacob Disease
Mad cow disease from PRION microbes
Normal Potassium Level
3.5-5.0
