LP 2 vocab Flashcards
Adrenergic inhibitors
inhibit the sympathetic NS and product many of the same rest-and-digest symptoms as the parasympathomimetics
Afterload
the degree of pressure in the aorta that must be overcome for blood to be ejected from the L ventricle - affects cardiac output
Aldosterone
stimulated by Angiotensin II. Increases Na+ reabsorption in the kidney, causing the body to retain water, increasing blood volume and raising blood pressure
Alpha-1 receptors
all sympathetic target organs EXCEPT the heart - constriction of blood vessels, dilation of pupils
Alpha-2 receptors
presynaptic adrenergic nerve terminals - adrenergic induce adrenalin-like responses (alpha2 receptors inhibit the release of norepinephrine [AKA noradrenaline])
Alpha-blocker
used for their effects on vascular smooth muscle - relaxing the muscle, causing vasodilation, decreasing blood pressure
Block alpha receptors so catecholamines can’t bind. Arteriole dilation, decrease in afterload
Angiotensin converting enzyme inhibitors
block conversion of angiotensin I to angiotensin II
Primary: causes arterial vasodilation, decreasing afterload
Secondary: causes vasoconstriction, decreasing preload
Baroreceptors
sense pressure within blood vessels, responding to changes in the circulating blood volume and regulating sympathetic and parasympathetic neural activity and endocrine activities. located within left atrium, carotid, and aortic arches.
Beta blockers
Blocks stimulation of beta1 adrenergic receptors which causes arterial vasodilation, decreasing afterload
also decrease the heart rate and contractility, reducing cardiac output and lower system blood pressure
Beta-1 receptors
location: heart and kidneys
response: increased heart rate and force of contraction; release of renin
Beta-2 receptors
location: all sympathetic target organs except the heart
response: inhibition of smooth muscle
Calcium channel blocker
Inhibits transport of calcium into myocardial and vascular smooth muscle cells
Causes arterial vasodilation, decreasing afterload
Cardiac output
the volume of blood pumped per minute. the higher the CO, the higher the blood pressure
HR x stroke volume (amount of blood pumped by a ventricle in one contraction)
Catecholamines
involved in neurotransmission (NE, epinephrine, dopamine) = all are adrenaline
Central alpha agonists
Blocks the signal from brain stem that signals release of catecholamines (inhibiting cardio acceleration and vasoconstriction centers), so decreased squeeze and resistance.
Dilates arteries, decrease afterload
Diuretic
Inhibits reabsorption of sodium and chloride ions in the nephron
Decrease blood volume, decreasing preload
Hypertensive crisis
two types, both of which SBP >180 or DBP >120
1) hypertensive urgency: considered stable, no symptoms, often due to nonadherence to drug therapy. Find out WHY this has happened
2) hypertensive emergency: high B/P + symptoms
*If left untreated 80% will die within one year
*Admit, continuous BP
Postural (orthostatic) hypotension
an abnormal drop in BP that occurs as the pt changes from a supine to a standing position
*decrease in SBP of 20 or DBP 10 (dizziness, weakness, syncope)
Preload
the degree of stretch of the ventricles (also the volume of blood) at the end of diastole
Primary hypertension
no identifiable cause
Pulmonary vascular resistance
the resistance of the pulmonary BP to right ventricular ejection
Renin
secreted when the kidneys sense low perfusion or diminished blood pressure. it circulates to the liver and converts angiotensinogen into angiotensin I
Secondary hypertension
high BP from an identifiable underlying cause
*btwn 5-10% of adults w/ hypertension have this kind
Stroke volume
amount of blood ejected from one of the ventricles per heartbeat
