Pathophysiology of Hypertension Flashcards
systolic blood pressure
peak value in the arteries during cardiac contraction
diastolic BP
pressure in arteries during ventricular filling
pulse pressure
difference between systolic and diastolic pressure
mean arterial pressure
tells us what the average BP is in a cardiac cycle
the relationship between BP, cardiac output, and total peripheral resistance
BP = CO x TPR
cardiac output
measurement of blood flow; determined by stroke volume (amount of blood pumped out of ventricle in one contraction)
proper BP measurement technique
Patient’s back rested, feet flat on the ground for 5 minutes, arms need to be resting, cuff size must be appropriate, check BP in both arms initially (want to always check the arm that has the higher reading), important to get two readings
primary hypertension
- essential / benign
- we don’t know what the discreet underlying cause is
secondary hypertension
has a discrete and identifiable cause
risk factors that increase hypertension
- overweight / obesity
- salt intake
- sedentary lifestyle
- alcohol intake
- aging
- stress
- Low K and Ca intake
- race (blacks / hispanics)
the effects of angiotensin II
- direct vasoconstrictor if overly produced
- stimulates sympathetic nervous system: peripherally releases catecholamines, can increase activity in the medulla
- stimulates aldosterone (which can lead to water and sodium retention)
triggers for renin release
- Released from juxtamedullary cells in kidney
- Decrease in renal perfusion will stimulate this process
- Renin is released when sodium or chloride is delivered to the nephron
- Direct stimulation of juxtamedullary cells
- Decreased circulation of angiotensin II
effects of stimulating adrenergic receptors in the central nervous system
- Pre-synaptic alpha II inhibits NE release
- Pre-synaptic beta causes NE release
effects of stimulating adrenergic receptors in the autonomic nervous system
Post-synaptic stimulation:
- Alpha I – vasoconstriction
- Alpha II – vasoconstriction
- Beta I – minimal peripheral effect
- Beta II – vasodilation
baroreceptor reflex: acute increase in BP
Baroreceptors will send a signal to decrease sympathetic outflow and cause vasodilation of arterioles and venules.
baroreceptor reflex: acute increase in BP -> Consequence if baroreceptors are not functioning adequately
Blood pressure will stay elevated.
baroreceptor reflex: acute decrease in BP
Baroreceptors will send a signal to cause vasoconstriction, increased heart rate, and increase contractility to preserve organ perfusion.
baroreceptor reflex: acute decrease in BP -> Consequence if baroreceptors are not functioning adequately
Organ perfusion may be reduced. Can result in syncope or near-syncope (passing out). Common among elderly patients and those with diabetes.
other mechanisms that could have a role in the genesis of primary hypertension
- tissues and organs defective in self-regulating their own blood flow
- endothelial dysfunction
causes of secondary hypertension
- Medications
- Renovascular / kidney disease
- Sleep apnea
- Hyperaldosteronism (primary or secondary)
- Endocrine (Cushing’s disease, excessive functioning thyroid)
- Pheochromocytoma
- Head injury
- Coarctation of the aorta
medications that cause secondary hypertension
- adrenergic agonists (e.g., methylphenidate)
- amphetamines
- anorexiants (e.g., sibutramine)
- corticosteroids (e.g., prednisone)
- cyclosporin
- decongestants (e.g., pseudoephedrine)
- ergot alkaloids (e.g., ergonovine)
- erythropoiesis-stimulating agents (e.g., erythropoietin)
- estrogen-containing substances
- monoamine oxidase type A inhibitors (e.g., tranylcypromine is an older drug that is rarely used, but is one of the original MOA inhibitors). ▪ Type B inhibitors are much less likely to cause a hypertensive response at lower doses (e.g., selegiline)
- NSAIDs/COX-1 inhibitors (e.g., ibuprofen, celecoxib)
- some anti-depressants (e.g., venlafaxine, desvenlafaxine, bupropion)
- street drugs (e.g., cocaine, ephedra alkaloids, herbal ecstasy)
- tripans (for migraines) (e.g., sumatriptan)
physiologic changes that occur in hypertension
- Endothelial dysfunction
- Stiffening / hardening of arteries
- Increased work on heart, leading to thickening of ventricular wall
What happens in endothelial dysfunction?
Leads to development of atherosclerosis
What effect is produced in the dysfunction of renal arteries?
thickening of the renal arteries will worsen hypertension by making the renal response to blood flow and pressure dysfunction (ineffective autoregulatory control)
What effect is produced in the dysfunction of carotid arteries?
Provide the most blood flow to the brain. Dysfunction in the carotid arteries can cause cerebrovascular problems
clinical consequences of hypertension
- Cerebrovascular disease: stroke
- Cardiovascular disease: left ventricular hypertrophy
- Nephropathy
- Retinopathy
- Peripheral Vascular Disease
