Chapter 36 - Hypertension - Exam 2 Flashcards
alright here we go, what is hypertension
high blood pressure
as bp increases so does the risk for
MI, HF, stroke, renal disease, and vision loss
what is bp
the force exerted by the blood against the walls of the blood vessell
BP is mainly a function of
cardiac output and systemic vascular resistance
Cardiac output or CO is
total blood flow thru the systemic or pulmonary circulation per minute
CO is determined by..
SV x HR
systemic vascular resistance or SVR is
the force opposing the movement of blood w/in the blood vessels
as we already know, as arteries narrow resistance to blood flow increases.
HTN often accompanies a ______disease
lipid
how do baroreceptors help regulate bp
vital role in maintaining bp stability, sensitive to stretching.
when stimulated by an increase in BP, they send INHIBITORY impulses to the sympathetic vasomotor center.
sym NS inhibition results in decreased HR, decreased force of contraction, and vasodilation in peripheral arteries
vice versa when barorecepters sense a fall in bp
how does the vascular endothelium help regulate bp
the vascular endothelium is a single cell layer that lines the blood vessels
Responsibilities include:
platelet adhesion, coagulation regulation, immune function, and regulating fluidcontrol within the vessel and extra vascular space.
the endothelium is essential to the regulation and maintanence of vasodilating/constricting substances such as nitric oxide and prostacyclin, endothelin
how does the renal system help regulate bp
control sodium excretion and extracellular fluid volume
eg sodium retention results in water retention, which increases ECF volume
prostaglandins secreted by the renal medulla have a vasodilator effect on the systemic circulation this results in decreased systemic vascular resistance and lower bp
what the fuck is the renin-angiotensin-aldosterone system or RAAS
essential role in bp regulation
okay, the kidney secretes RENIN in response to either:
- sympathetic nervous system stimulation
- decreased blood flow through the kidneys
- decreased serum sodium concentration
RENIN is an ENZYME that CONVERTS angiotensinsinogen to angiotensin 1
angiotensin 1 is then converted to angiotensin 2 by angiotensin-converting enzyme (ACE).
angiotensin 2 increases BP by 2 different mechanisims:
1. A2 is a potent vasoconstrictor and incresases systemic vascular resistance. This results in an immediate increase in bp
2. over the period of hours or days, A2 increases bp indirectly by stimulating the adrenal cortex to secrete aldosterone
aldosterone stimulates the kidneys to retain sodium and water which increased blood volume and cardiac output
what is primary hypertension
(essential or idopathic) is elevated bp without an identifiable cause
contributing factors: damaged vessels, overactive SNS, increased sodium intake
what is secondary hypertension
elevated bp with a specific cause that can be identified and corrected
eg, renal disease, obstructive sleep apnea, cirrhosis, drug related, pregnancy,
excess _______intake is linked to the development of hypertension
sodium
complications:
coronary artery disease
hypertension disrupts the coronary artery endothelium, rigid arterial wall with a narrowed lumen
complications:
left ventricular hypertrophy
sustained high bp increases the cardiac workload and causes left ventricular hypertropy
complications:
heart failure
Heart is overwhelmed and can no longer pump enough blood to meet body’s demands
mechanism of action:
a1-adrenergic blockers
block a1-adrenergic effects, producing peripheral vasodilation
eg doxazosin, prazosin
mechanisim of action:
angiotensin-converting enyzme ACE inhibitors
inhibit ACE
eg benazepil, lisionopril
mechanisim of action:
Calcium channel blockers - non-dihydropyridines
inhibit movement of Ca++ across cell membrane, resulting in vasodilation
eg diltiazem extended release
mechanism of action:
calcium channel blockers - dihydropyridines
cause vascular smooth muscle relaxation resulting in decreased systemic vascular resistance and arterial bp
eg amlodipine
mechanisim of action:
hydralazine
decrease systemic vascular resistance and bp by direct arterial vasodilation
mechanism of action: nitroglycerin
relaxes arterial and venous smooth muscle, reducin preload and systemic vascular resistance
mechanism of action:
loop diuretics
inhibit NaCl reabsorption in the ascending limb of the loop of henle
increased excretion of na+ and cl-
the patho of HTN in the older adult involves:
- loss of elasticity in large arteries from atherosclerosis
- increased collagen content and stiffness of myocardium
- increased peripheral resistance
- decreased adrenergic receptor sensitivity
- blunting of baroreceptors
- decreased renal function
- decreased renin response to sodium and water depletion
the systolic and diastolic values that categorize hypertension are
> or equal to 140
or equal to 90
140/90
what do beta blocker drugs do?
Beta blockers, also known as beta-adrenergic blocking agents, work by blocking the action of adrenaline (epinephrine) and other stress hormones at beta receptors in the body. These receptors are found in various tissues, including the heart, blood vessels, and kidneys.
In the heart, beta blockers primarily block beta-1 receptors, which are responsible for regulating heart rate and the force of heart contractions. By blocking these receptors, beta blockers slow down the heart rate, decrease the force of contraction, and reduce the workload on the heart. This can be beneficial in conditions such as hypertension (high blood pressure), angina (chest pain), and heart failure, where reducing the heart’s workload can improve symptoms and outcomes.
Beta blockers also have effects outside the heart. For example, they can block beta-2 receptors in the blood vessels, leading to vasodilation (widening of blood vessels), which helps lower blood pressure. In addition, beta blockers can reduce the release of renin, a hormone involved in blood pressure regulation, from the kidneys.
Overall, beta blockers help to reduce the effects of adrenaline and other stress hormones on the body, leading to decreased heart rate, reduced blood pressure, and decreased workload on the heart, which can be beneficial in various cardiovascular conditions.
how do ace inhibitors work
CE (angiotensin-converting enzyme) inhibitors work by blocking the action of ACE, an enzyme responsible for converting angiotensin I into angiotensin II. Angiotensin II is a potent vasoconstrictor, meaning it causes blood vessels to narrow, leading to an increase in blood pressure.
By inhibiting ACE, ACE inhibitors prevent the formation of angiotensin II, resulting in vasodilation (widening of blood vessels) and a decrease in blood pressure. This helps to reduce the workload on the heart and improve blood flow to the heart and other organs.
Additionally, ACE inhibitors can also inhibit the breakdown of bradykinin, a substance that promotes vasodilation and reduces blood pressure. By increasing bradykinin levels, ACE inhibitors further contribute to their blood pressure-lowering effects.
Overall, ACE inhibitors are commonly used to treat hypertension (high blood pressure), heart failure, and other cardiovascular conditions by lowering blood pressure and reducing the workload on the heart. They are also beneficial in protecting the heart and kidneys in certain conditions.
