perfusion Flashcards
1
Q
what is cardiovascular disease linked to
A
closely linked to diet
2
Q
hormonal and NS factors affecting BP
A
adrenal gland, kidney, hypothalamus, baroreceptors, vasomotor centre in medulla
3
Q
baroreceptors
A
mechanoreceptors on the heart which are stimulated by changes in the stretch of the carotid sinus wall. stimulates vasomotor centre in medulla
4
Q
vasomotor centre in medulla (low bp)
A
stimulated by baroreceptors and release norepinephrine
5
Q
norepinephrine
A
vasoconstrictor. released from vasomotor centre in medulla and adrenal gland
6
Q
factors that influence BP (3)
A
blood volume, peripheral resistance, and cardiac output
7
Q
Blood Volume determined by
maintained by
A
amount of water and sodium ingested
maintained by kidneys
8
Q
how does blood volume influence BP
A
fluid loss (dehydration) decreases blood volume = low BP fluid retention (by aldosterone or ADH) increases blood volume=high BP
9
Q
how does peripheral resistance influence BP (3)
A
- Sympathetic nervous system innervation
- renin/angiotensin ii
- increased blood viscosity
10
Q
sympathetic NS innervation
A
causes vasoconstriction (=increase BP) or vasodilation (=decrease BP)
11
Q
renin/angiotensin II
action of angiotensin II
A
- renin (from kidneys) + angiotensinogen (liver) = angiotensin I + angiotensin converting enzyme (ACE) = angiotensin II
- angiotensin II binds to receptors on blood vessels, heart, adrenal cortex causing vasoconstriction
12
Q
increase in blood viscosity
A
increase in hematocrit = increase viscosity
increase in blood viscosity causes resistance in blood vessels = high BP
13
Q
vasoconstriction cascade
what starts it
A
systemic vasoconstriction, aldosterone synthesis, H20&Na retention
caused when angiotensin II binds to receptors
14
Q
what happens when angiotension II pathway is blocked
A
if pathway is blocked, angiotensinogen isn’t converted and vasoconstriction cascade is not activated = decrease BP & blood volume
15
Q
how does cardiac output influence BP (2)
A
- stroke volume
- heart rate
16
Q
Stroke volume
influenced by
A
- amount of blood thats pumped out the left side of the heart to the body
- preload, contractility, afterload
17
Q
increase SV
A
more blood pumped out of the body = high BP
18
Q
decrease SV
A
less blood pumped out of body=low BP
19
Q
what influences heart rate
A
sympathetic NS, parasympathetic NS & epinephrine
20
Q
actions of heart when BP is too high (3)
A
- vasodilation
- low SV
- low HR
21
Q
actions of kidneys due to high BP (2)
A
- high urine output
- low blood volume
22
Q
hypertension
A
elevation of systolic &/or diastolic BP
23
Q
BP to worry about (2)
A
<160 mmhg too high
sudden change >20mmh
24
Q
causes of sudden change in BP (6)
A
pain, infection, compensation, hypervolemia, drug induced, malignant hypertension
25
circadian BP variations
reason why BP is graphed. assess trends to determine chronic changes in BP
26
causes of hypertension (3)
- essential
- secondary
- sudden onset
27
(causes) essential hypertension (4)
(idiopathic) age, race, family history, lifestyle
28
(causes) secondary hypertension
due to organ not working properly; renal disease, adrenal disease, congenital defects; other end organ disease
29
(causes) sudden onset
sudden onset of hypertension due to meds, recreational drugs, or trauma
30
gestational hypertension
preeclampsia- at 20 weeks pregnant
31
gestational hypertension causes
multifocal
32
inflammatory theory of cause of hypertension
inflammatory cytokine released causes endothelial changes
33
risk of endothelial changes that cause gestational hypertension (4)
clotting (to fix damage), risk of DIC, organ damage, and decreased placental flow
34
gestational hypertension tx
sodium restriction & antihypertensive medication
35
causes of hypertension in elderly (3)
decreased elasticity of vessels, decreased renal blood flow, decreased baroreceptors sensitivity
36
tx of hypertension in elderly (3)
start low and go slow, "titrate to effect", & monitor for orthostatic hypotension (risk of falls)
37
orthostatic hypotension
drop of SBP >20 mmHg or DBP >10
38
orthostatic hypotension causes
caused by venous pooling in lower extremities
39
nature of orthostatic hypotension
transient since baroreceptors have low sensitivity, compensated when they intervene
40
orthostatic hypotension S&S (2)
faintness, dizziness
41
at risk for orthostatic hypotension (3)
-elderly, dehydrated patients, patients on antihypertensive meds
42
orthostatic hypotension tx (2)
have to treat the underlying cause, adrenergic agonists if in the ER
43
lifestyle changes for hypertension (3)
decrease cholesterol and alcohol intake
44
organs affected by hypertension (5)
brain, eyes, kidney, placenta, liver
45
expected BP findings & MAP
BP: 120/80 mmHg MAP: 70-100 mmHg
46
blood pressure
perfusion of tissue and organs
47
MAP
mean arterial pressure, used to measure adequate amount of blood getting to vital tissues and organs
48
MAP formula
SP+2(DP)/3
49
Emergency tx of hypertension
| drug class
treatment stimulates endothelial cell-produced endogenous NITRIC OXIDE
direct acting vasodilator
50
how is nitric oxide produced
converted in endothelial cell by arginine into NO then enters the smooth muscle cell activating cyclic GMP pathway causing
51
direct acting vasodilator function
stimulates nitric oxide release in endothelium
52
direct acting vasodilator uses
only used in ICU of ER settings
53
direct acting vasodilator routes
IV- 2 min 1/2 life
| inhalation- broncho specific
54
direct acting vasodilator examples (2)
nipride, hydralazine
55
direct acting vasodilator s/e
reflex tachycardia (hypotension), syncope, headache
56
nipride & function
| routes
nitroprusside; stimulates nitric oxide release in endothelium
-IV continuous infusion in crisis, endotracheal tube for pulmonary vasodilation
57
hydralazine function & routes
stimulates nitric oxide release in endothelium\
| PO/IV
58
hypertension standard treatment meds classes (4)
diuretics, renin-angiotensin drugs, calcium channel blockers, adrenergic agents
59
hypertension standard treatment meds (combo drugs)
direct acting vasodilators (ER use), synergy effect
60
1st line hypertension tx
diuretics
61
diuretics functions (5)
- decreases blood volume, BP, H20 & electrolytes
| - increases urine output
62
types of diuretics (4)
loop diuretics, thiazides, potassium sparing, osmotic
63
diuretics s/e
dehydration, hypoatremia, hypokalemia, hyperkalemia, nocturia
64
loop diuretics target
loop of henle
65
loop diuretics function
blocks Na+, K+, Cl- reabsorption into blood so Na, K, Cl & H20 stay inside tubule and get excreted as urine
66
loop diuretics s/e
hypokalemia (K excreted with urine), ototoxicity (can be reversible with drug interactions (high PPB))
67
most potent route for loop diuretics
IV, PO
68
loop diuretics example
furosemide
69
furosemide
(lasix) first line of therapy for hypertension, blocks sodium potassium chloride cotransporter stopping Na, K, Cl & H20 from exiting tubule so they're excreted with urine
70
thiazides target
distal convoluted tubule
71
thiazides function
inhibits reabsorption of Na and Cl out of tubule = increase Na, Cl, K & H20 in urine
72
thiazides s/e
hypokalemia, hyponatremia
73
thiazide examples
hydrochlorothyazide, chlorothyazide
74
metabolism of thiazides
unchanged
75
potassium sparing function
(aldosterone antagonist) blocks renal aldosterone receptors = Na exits and K stays
76
potassium sparing target
distal tubule
77
potassium sparing s/e
hyperkalemia
78
metabolism of potassium sparing
active metabolites, long half life (1-2 days)
79
potassium sparing example
spironolactone (aldactone)
80
diuretic combo
aldactazide (thiazide + potassium sparing)
81
aldactazide uses
maintenance therapy for hypertension, balances out K
| PO
82
osmotics target
proximal tubule & loop of henle
83
osmotics function
drug contains high solute so to prevents reabsorption of water into blood = low blood volume = low bp
84
osmotic tx
cerebral edema, intraocular hypotension
85
angiotensin ii drugs (2)
angiotensin ii receptor blockers (ARB), angiotensin-converting enzyme inhibitors (ACE inhibitors)
86
ARB site of action
angiotensin ii receptors
87
what does blocking of angiotensin ii receptors cause
prevents vasoconstriction cascade= lowers BP
88
ARB examples
losartan
89
ARB s/e
hypotension
90
ACE inhibitor fx
inhibit ACE from producing angiotensin ii= reduce vasoconstriction
91
1st line drugs in heart failure
ACE inhibitors
92
ACE inhibitor examples
enalapril, captopril, monopril, ramipril
93
ACE inhibitor s/e
severe hypotension
94
hyazaar
losartan + hydrochlorothiazide
95
osmotics ex
mannitol (IV) , isosorbide (PO)
96
calcium channel blocker fx
prevents calcium influx causing muscle relaxation
97
types of calcium channel blockers
vascular selective, cardio-selective
98
vascular selective ccb fx
vasodilation of blood vessels around the body
99
vascular selective ccb ex
nifedipine, amlodipine
100
cardio selective ccb fx
cause relaxation of myocardial cells which decreases HR, CO and BP
101
cardio selective ccb ex
verapamil, diltiazem
102
adrenergic antagonists fx
block sympathetic ns function; decrease HR, conduction rate and contractility
103
adrenergic antagonists targets
alpha (1 & 2), beta (1 & 2) receptors
104
alpha receptors fx
cause vasoconstriction of blood vessels
105
alpha 1 receptors
bind with norepinephrine to cause vasoconstriction of blood vessels
106
alpha 2 receptors
in arteries and veins stimulation causes vasoconstriction
| in CNS stimulation releases norepinephrine which cause vasoconstriction
107
beta 1 receptors
located in pacemakers cells and myocardial cells in heart, stimulation causes increased heart rate, increased contractility, increased conduction rate, and vasodilation
108
beta 2 receptors
located in bronchioles cause bronchodilation
109
beta blockers fx
decrease conduction rate & contractility= low HR = low bp
110
selective beta blockers ex
atenolol, metoprolol
111
nonselective beta blockers
propanolol
112
beta blocker s/e
bradycardia, lethargy, hypotension
113
lopresser HCT
hydrochlorothiazide + metaprolol
114
centrally acting alpha 2 agonist fx
stimulate cns alpha 2 receptors in vasomotor center to activate negative feedback lopp and decrease norepinephrine release
115
centrally acting alpha 2 agonist ex
clonidine, methyldopa
116
methyldopa
prodrug, metabolizes into norepinephrine and activates negative feedback loop
117
centrally acting alpha 2 agonist s/e
hypotension and headaches
118
centrally acting alpha 2 agonist tx's
resistant hypertension
119
atrial fibrillation medications
calcium channel blockers (verapamil, diltiazem) & beta blockers (propanolol, metoprolol)
120
Calcium channel blockers s/e
dizziness, hypotension, reflex tachycardia,, peripherial edema, dysrhythmias, exacerbation of heart failure
