Hypertension Flashcards
hypertension
- consistent elevation of systemic arterial blood pressure
- complex disease controlled by a combination of genetic and environmental factors
- no specific cause identified for large majority of HTN patients
factors that create high blood pressure
- blood volume
- peripheral resistance
- cardiac output
blood volume and high blood pressure
- total amount of blood in vascular system
- volume can change due to disease, drugs, regulatory factors
- more blood = increase pressure
How do we increase blood volume?
fluids and blood transfusion
peripheral resistance and high blood pressure
blood traveling around the vasculature at a high rate of speed comes in contact with smooth endothelium of the vessels, where friction slows it down
cardiac output and high blood pressure
- the volume of blood pumped in a ventricle per minute
- heart rate (# of beats per minute)
- stroke volume: amount of blood pumped by the heart in one contraction
- increase cardiac output, increase blood pressure
HR x SV = CO
organs that control BP
- brain (emotions)
- kidneys (RAAS)
- chemo/baroreceptors in heart/carotid artery
-hormones (antidiuretic: potent vasoconstrictor)
converts angiotensinogen to Angiotensin I
renin
converts Angiotensin I to Angiotensin II
angiotensin converting enzyme
primary hypertension
no identifiable cause
secondary hypertension
specific cause can be identified:
- Cushing’s disease
- CKD
- hyperthyroidism
- drugs (corticosteroids, oral contraceptives, decongestants, amphetamines)
non-pharmacological management
lifestyle changes
- limit alcohol
- restrict sodium consumption
- reduce intake of saturated fat/cholesterol
- increase fresh fruits and vegetables
- increase physical activity
- discontinue use of tobacco products
- reduce sources of stress
- maintain optimal weight
diuretics
- reduces blood volume
- water excretion in the urine achieved by retaining or excreting electrolytes
types of diruetics
- potassium wasting
- potassium sparing
potassium wasting diuretics
thiazide diuretic:
- old
- inexpensive
- safe
- can cause hypokalemia
loop diuretic:
- cause more diuresis than thiazide or potassium-sparing drugs
- not ideal for control of HTN due to adverse effects such as hypokalemia and dehydration
- ototoxic (affect hearing and ears)
- usually used for intermittent fluid off-loading (diuresis)
potassium sparing diuretics
- hang on to potassium
- produce only modest diuresis
- can cause hyperkalemia
- potassium is our main intra-cellular electrolyte (helps with muscle contraction)
- too much or too little can lead to cardiac conduction abnormalities
- concurrent use of ACE-inhibitors or ARB’s increase the potential for hyperkalemia
- many people control their BP by decreasing sodium and using a salt-substitute that is high in potassium that could lead to hyperkalemia
ACE inhibitors
- angiotensin converting enzyme inhibitors
- work within the RAAS system
- decrease BP and increase urine volume
- widely used in the treatment of HTN, HF, and myocardial infarction
- blocks the conversion of angiotensin I to angiotensin II (powerful vasoconstrictor)
- end in -pril
adverse effects of ACE inhibitors
- mild cough, can switch them to an ARB
- postural hypotension
- hyperkalemia
side effects of ACE inhibitors
- ANGIOEDEMA: caused by pro-inflammatory bradykinins
- swelling of lips, eyes, throat, and other body regions that could lead to throat closure
Angiotensin II Receptor Blockers
- ARBs
- end in -sartan
- blocks angiotensin II receptors in the smooth muscle
- relatively few side effects (can have hypotension)
- no cough associated with ARBs, much lower risk of angiodedema
- often combined with other anti-HTN drugs
beta-blockers
- end in -olol
- work by blocking adrenergic receptors (blocks the fight or flight response)
- blockage of B1 receptors in the heart
- decrease HR and heart contractility which decreases cardiac output and lowers systemic blood pressure
- blocks the B1 in the juxtaglomerular apparatus which inhibits the secretion of renin and the formation of angiotensin II
adverse effects of beta-blockers
- predictable based on inhibition of fight or flight
- slow heart rate
- bronchoconstriction (use with caution in patients with asthma or COPD)
calcium channel clockers
- block calcium ion channels, which block muscle contraction and relaxes arterial smooth muscle, which lowers peripheral resistance and decreases BP
- rarely used alone
- good for elderly or African American patients who are often less responsive to other anti-HTN drugs
- can increase the effect of statin drugs by messing with liver enzymes (CYP3A4)
calcium channel blocker side effects
- HYPOTENSION
- dizziness
- peripheral edema
- heartburn
- nausea
- flushing
all due to vasodilation
hypertensive crisis
- BP >180/120
- can cause end organ damage
- most common cause is uncontrolled, poorly managed essential HTN
- don’t want to drop the BP too fast»_space; hypotension