HTN Flashcards
Hypertension
When blood pressure or the force of blood pushing against the walls of your blood vessels is consistently too high
Genetic and environmental factors
Factors that create HTN
Blood volume
Peripheral resistance
Cardiac output
Blood Volume
Total amount of blood in the vascular system
Vol can change from disease, drugs, and regulatory factors
Inc blood vol = inc blood pressure
Peripheral resistance
Blood traveling around the vasculature at a high rate of speed comes in contact with the smooth endothelium of the vessels, where friction slows it down
Constrict blood vessels = inc blood pressure
Cardiac Output
The volume of blood pumped in a ventricle per minute
HR x SV = CO
Inc CO = inc blood pressure
4 things RAAS system does?
1) vasoconstriction of blood vessels
2) releases epi, norepinephrine, and aldosterone
3)
4)
Primary HTN
No identifiable cause
90% of HTN
Secondary HTN
A specific cause can be identified
Ex: Cushings disease, chronic kidney disease, hyperthyroidism, drugs
Normal BP range and treatment
<120/<80
None
Elevated BP range and treatment
120-129/ <80
Lifestyle changes
HTN stage 1 BP range and treatment
130-139/80-89
Lifestyle changes and 1 medication
HTN stage 2 BP range and treatment
> 140 / >90
Lifestyle changes and 2 medications
Classes of meds to treat HTN (there’s 5)
Diuretics
ACE inhibitors
ARBs
Beta Blockers
Calcium Channels
Diuretics
Work by reducing blood volume
- potassium wasting (excrete K+)
- thiazide
- loop - potassium sparing (hang on to K+)
Thiazide Diuretics
Old drug
Inexpensive
Can cause hypokalemia
Loop diuretics
Causes more peeing than thiazide or potassium sparing drugs
Many adverse effects like hypokalemia and dehydration
Ototoxic
Used for intermittent fluid off-loading
Potassium Sparing
Produce only modest diuretics
Hyperkalemia
Can lead to cardiac conduction abnormalities
Don’t use with ACE or ARBs
ACE inhibitors
“Pril”
These drugs work with the RAAS system
decrease BP and increase urine vol
Blocks conversion of Ang I to Ang II
Can cause mild cough, postural hypotension, and hyperkalemia
Effect: angioedema
ARBs
“Sartan”
Block Ang II receptors in the SM
Relatively few side effects
No cough and much lower list for angioedema
Beta Blockers
“Olol”
Block adrenergic receptors
Blockade of B1 receptors in the heart
Dec HR and contractility which Dec CO and BP
Effect: predictable; slow HR and bronchconstriction
Calcium channel Blocker
Block calcium ion channels, which block muscle contraction relaxing the smooth muscle and lowers peripheral resistance
Used with other drugs
Biggest side effect is dizziness, peripheral edema, heartburn, nausea, and flushing
Can inc the effect of statin drugs by messing with the liver
Hypertensive crisis
BP is > 180/120
Causes organ damage
Due to poorly managed essential HTN
Don’t want to drop BP too fast… could cause orthostatic hypotension
