Antihypertensives Flashcards
1
Q
What is the leading RF for CVD?
A
- HTN
83% of people with CVD - cause was HTN - 25% of adults over 18 have HTN
2
Q
HTN is more common in what ethnicities?
A
- african americans
- native americans
- hispanics
- more common in younger men than women, no difference after age of 55
3
Q
HTN is a major contributing factor in the development of and death from?
A
- CVD
- stroke
- heart failure
- renal failure
4
Q
What factors effect BP in the body?
A
- arterial BP is product of CO and PVR
- other factors:
SNS activity
kidney fxn (Na and water retention)
electrolyte composition of ICF and ECF
cell membrane transport mech
alterations in vascular endothelium: caused by HTN, insulin resistance, smoking
Hyperinsulinemia (increased Na retention)
dietary Na intake, excessive Na retention - humoral influences: RAA mechanism
5
Q
2 categories of HTN?
A
- essential (primary) HTN: chronic elevation in BP occurs without evidence of other disease
- secondary: elevation in BP results from some other disorder (kidney disease, pheochromocytoma, OCPs, Cushings)
6
Q
How many pts have essential HTN
A
- 90-95% of pts - no identifiable cause of HTN is found
- familial patterns are common
- enviro factors plat a role:
obesity, alcohol consumption, sedentary lifestyle, and salt intake (huge factor)
7
Q
When is Essential HTN usually detected?
A
- during screening procedures or when person seeks medical care for another reason
- typically asx
8
Q
Possible sxs of Essential HTN?
A
- HA: occurs most frequently on awakening, usually felt in the back of head or neck
- common end organ damage in long term undx and untx HTN: common early sx which indicates the kidneys are losing ability to concentrate urine - elevated BUN/Creat and CVD disease
9
Q
How does family hx contribute to HTN likelihood?
A
- 2 or more first degree relatives with HTN before age 55, you have 3.8x greater risk for development of HTN before 50
- persons from high risk families should participate in regular HTN screening
10
Q
How are age and gender major risk factors for HTN?
A
- blood pressure increases with age in both men and women. Lifetime risk for HTN is nearly 90%
- 2/3 of Americans over 60 have HTN
- older women (60 and older) currently have highest rates of HTN, and mortality rates from HTN are higher in women than men
- HTN is also becoming more common in children and teens
- BP increass from 78 mm Hg at 10 days of age to 120 at end of adolescence
- systolic BP continues a slow rate of increase throughout adult life
- diastolic BP increases until age 50, then declines from 60 on up
11
Q
How is race a factor in HTN
A
- more prevalent in Blacks
- occurs earlier
- tend to experience greater cardiovascular and renal damage at any level of pressure:
compared to caucasians, Blacks have 1.8x the rate of fatal stroke, 1.5x risk of fatal heart disease, and 4.2x the rates of end stage kidney disease. In general about 34% of Black men and women have HTN. It may account for over 40% of all deaths in this group - they are often not tx early enough nor aggressive enough
- have higher prevelance of RFs that are associated with HTN
12
Q
How does salt intake and obesity increase rates of HTN?
A
- high salt intake: known as a risk factor because of findings of decreased incidence of HTN among primitive, unacculturated people from widely different parts of the world.
- obesity: wt reduction as little as 10 lbs can produce a sig decrease
- fat distribution may be more of an indicator than actual overweight - central obesity
- sedentary lifestyle plays a part in HTN also
13
Q
How does diabetes, hyperinsulinemia factor into HTN?
A
- up to 75% of CV problems in diabetics may be due to HTN
- activation of smypathetic nervous system and its effects on CO, PVR, and renal Na retention
- insulin stimulated changes in growth of vascular smooth muscle that result in an increased PVR
- the effect of insulin on salt and water retention by the kidney
- changes in Na and Ca transport across cell membrane of vascular smooth muscle
14
Q
How does excess alcohol contribute to HTN?
A
- regular consumption of 3 or more drinks/day increase risk of HTN, mechanism is unknown, suggested correlation with lifestyle factors
15
Q
How do cigarettes and coffee contribute to HTN?
A
- stimulate SNS
- smoking damages vasculature
16
Q
How does low birth wt correlate with HTN?
A
- particularly in girls
- high levels of stress hormones
- LBW is assoc with subsequent obesity
17
Q
How does stress contribute to HTN?
A
- mental stress: in 20 yr study men who had high stress were 2x as likely to have high BP as those with normal stress. The effects of stress on blood pressure in women were less clear. Job stress and lack of career success specifically linked to high BP in both men and women
- anxiety: anxiety rf for HTN, particulary in women
- depression: depression has physiological effects that impair the heart an dthat it contributes to destructive behaviors, such as wt gain, smoking, alcohol abuse. Link particularly strong in African Americans, depression was the strongest RF in this group
18
Q
How does time and seasonal factors contribute to HTN?
A
- BP levels tend to be lowest during the morning and midday hours and highest at end of the day
- seasonal changes also affect BP, with HTN increasing during cold months and declining though the summer, blood pressure readings can vary by as much as 40% depending on time of day and season
19
Q
How do OCPs contribute to HTN?
A
- unknown MOA
- perhaps constant estrogen and progesterone are responsible
- usually disappears with d/c, may take as long as 6 months
20
Q
What are complications of HTN?
A
- target organ damage
- TIA, stroke, dementia
- angina, MI
- PVD
- diabetic retinopathy: fundal hemorrhages or exudates (neovascularization, AV nicking, silver wiring)
- renal impairment, proteinuria (microalbumineria first early sign)
- arteriosclerosis
21
Q
What is isolated systolic HTN? Why is it so bad?
A
- may pose sig danger for heart events and stroke events even when the diastolic is normal
- most common form of HTN in people 50 and older. Favors the development of LVH
- increased myocardial O2 demands
- eventual left heart failure
22
Q
What is a elevated pulse pressure?
A
- diff between systolic and diastolic BP
- produces greater stretch of arteries
- causing damage to elastic elements of the vessel
- predisposing to aneurysms and development of intimal damage that leads to atherosclerosis
23
Q
What are the 2 causes of renovascular HTN?
A
- renal artery stenosis: (atherosclerotic renal artery disease) - usually affect the proximal aspect of renal artery, most common in older men, is often bilateral
- fibromuscular dysplasia: fibrosis and aneurysm formation in middle and distal renal arteries
- most common in younger women
24
Q
What are the 2 adrenal causes of HTN?
A
- hyperaldosteronism
- pheochromocytoma
25
What % of pts are there that a secondary cause of HTN can be found?
- 5%
- think secondary in pts with new onset HTN that are younger than 30, older than 55
- had previously well controlled HTN that develps sudden increase in BP
- pts with poorly controlled BP despite mult. antiHTN meds
26
What conditions increase CO?
```
- Hypervolemia:
renal artery stenosis
renal disease
hyperaldosteronism
hypersecretion of ADH
aortic coarction
pregnancy (preeclampsia)
- stress:
sympathetic activation
- pheochromocytoma: increased catecholamines
```
27
What conditions increase systemic vascular resistance?
```
- stress:
sympathetic activation
- atherosclerosis
- renal artery disease (increased AII)
- pheochromocytoma: increased catecholamines sympathetic
- thyroid dysfunction
- diabetes
- cerebral ischemia
```
28
What do you want to R/O before looking for secondary HTN?
- increase Na+ intake
- non-compliance with meds
- drugs that may interfere with antihtn meds, or meds that cause HTN:
OCPs
corticosteroids (symp stim)
NSAIDs: cox cause kidneys to retain Na and water
- OTC cold remedies containing ephedrine or sympathomimetics
29
How common is renovascular HTN?
- 1-2% of cases of HTN
- most common cause of secondary HTN
- stenosis of renal artery - kidney isn't getting adequate blood flow and senses low O2 - so JG cells send out renin to lungs and this stimulates conversion of AI to AII and this than causes vasoconstriction in periphery and stimulates adrenals to release aldosterone to retain Na and water - this causes increase PVR and increased volume leading to icnrease in BP
30
What are some clinical clues that HTN is due to renovascular HTN?
- sudden development of HTN in a pt with no family hx
- drug resistant HTN
- abdominal bruit
- renal insufficiency
- worsening renal fxn after ACEI**** (check BUN, creatinine and K+)
31
Diagnostic tests for renovascular HTN?
- renal fxns, BUN, creatinine
- plasma renin levels (high because O2 deprived)
- angiography is definitive
32
Why should ACEIs be avoided in renovascular HTN?
- kidney is receiving inadequate blood supply so it activates RAAS system. Therefore a single dose of this ACEI will abruptly reduce renal fxn in the ischemic kidney
- this is why ACEI are CI in renal artery stenosis/ Although they are good at controlling BP, they exacerbate renal failure in already compromised (ischemic) kidney
33
Tx of renovascular HTN?
- eliminating stenosis: percutaneous technique (balloon angioplasty)
surgery with stent placement: this will stabilize or improve renal fxn, assoc with small but significant decrease in BP, may need antiHTN for life (b/c of damage done to kidney)
34
What hyperaldosteronism conditions are more common in men? women?
- unilateral adrenal adenoma: more common in women
- bilateral adrenal hyperplasia: more common in men: secreting aldosterone so increased retention of Na and increased volume so leads to HTN and excreting more K+
35
How does primary hyperaldosteronism cause HTN?
- increase aldosterone stimulates excessive renal Na+ retention with resultant volume expansion and HTN
- increase intravascular volume augments renal perfusion, thereby renin secretion is suppressed
- increases Na+ retention and increases K+ excretion
(will have low serum renin since there is increased intravascular volume
36
Dx tests for primary hyperaldosteronism?
- serum renin will be low
- urine aldosterone levels
- increased sreum aldosterone level that doesn't suppress after saline-induced volume expansion
- CT to diff b/t adrenal adenomas and hyperplasia
37
How is primary hyperaldosteronism tx?
- adrenal tumors are resected, resolved HTN 50% of the time
- adrenal hyperplasia: spironolactone (diuretiic, K+ sparing, aldosterone antagonist)
additional diuretics
38
Tx of pheochromocytoma?
- surgical resection: alpha and beta blockage and volume expansion before surgery
- unresectable tumors: chronic therapy with phenoxybenzimine (alpha adrenergic blocker)
39
Sxs of episodic pheochromocytoma?
- HA
- sweating
- palpitations, tachycardia
- chest pain
- anxiety, fear of impending death
- tremor
- fatigue or exhaustion
- nausea, vomiting
- abdominal pain
- visual disturbances
- sxs b/t paroxysms:
- increased sweating
- cold hands and feet
- wt loss
- constipation
40
What is an aortic coarctation?
- narrowing of the aorta (typically just distal to left subclavian artery), congenital defect that obstructs aortic outflow leading to elevated pressures proximal to coarction (head and arms). Distal pressures, however, are not necessarily reduced as would be expected from hemodynamics assocd with stenosis
- reason for this is that reduced systemic blood flow, and in particular reduced renal blood flow, leads to an increase in release of renin and activation of RAAS system - this in turns elevates blood volume and arterial pressure. ALthough the aortic arch and carotid sinus baroreceptors are exposed to higher than normal pressures, the baroreceptor reflex is blunted due to structural changes in the walls of vessels where baroreceptors are located
- also, baroreceptors become desensitized to chronic elevation in pressure and become "reset" to the higher pressure
41
How is proper BP measurement taken?
- pt should be seated with back supported, arm bared and supported
- pts should refrain from smoking or caffeine for 30 min prior
- pts should rest at least 5 min prior
- appropriate size cuff and calibrated equipment should be used
- 2 or more readings should be averaged
42
According to JNC 8, what is considered HTN?
- in everyone younger than 60, all ages with diabetes, all ages with CKD w/ or w/o diabetes: 140/90
60 and older: 150/90
43
Pts have how much of a risk becoming HTN if already pre-hypertensive?
- those in 130-139/80-89 BP range are at twice the risk to develop HTN as those with lower values
44
What should be included in eval of pt with HTN?
- thorough hx and physical
- goals of eval:
assess for presence and extent of HTN target organ damage
- ID clinical factors that may influence choice of therapy (heart failure, renal failure)
- determine presence of CVD RFs
- recognize occasional pt with secondary HTN
45
HTN's sxs?
- rarely symptomatic
- occipital HAs
- blurred vision
- fatigue
- dizziness
- epistaxis
- dyspnea
- chest pain
46
Sxs of end organ damage?
- CHF
- CVD
- Cerebrovascular disease
- uremia
- microalbuminemia
- aortic dissection
47
Historical features in person with HTN?
- family hx
- dietary Na + intake
- exercise
- alcohol use
- Rx and non-Rx drug use: OCPs, anabolic steroids, NSAIDs
48
What should you focus on after confirming the presence of HTN?
- should focus on recognizing evidence of end organ damage on PE
(eyes, heart, Peripheral artery disease)
49
PE of pt with HTN?
- BP in both arms and compared with pressure in legs
- funduscopic exam: look for retinal changes, AV nicking, copper wire changes, retinal hemorrhages and exudates
- heart: S4 gallop (decreased ventricular compliance), S3- CHF
- vascular exam: carotid bruits. PVD, abdominal bruits
- neuro exam: evidence of prior strokes
50
dx lab work up of pt with HTN?
- initial lab screening and dx:
CMP: renal function, serum glucose, electrolytes
- fasting lipids
- U/A
- CBC: hematocrit (hemachromotosis)
- EKG: LVH, prior MI (large Q wave)
- echo; evidence of left ventricular enlargement or failure should be noted
51
Tx goal of primary HTN?
- to prevent long term mobirdity and mortality assocd with prolonged elevations in BP
- method of aggressiveness depends on these several factors:
absolute level of BP
presence of end organ damage
coexisting medical conditions
overall cardiac risk
52
Lifestyle changes?
- exercise at least 40 min/day
- maintain normal wt
- reduce NaCl intake
- increase K+ intake
- DASH diet: consume a diet rich in fruits, veggies, and low fat dairy products
- reduce total and sat fat intake
- limit alcohol consumption: mod alcohol consumption: 1-2 glasses a day may actually lower risk of heart attack among men with HTN
- stop smoking
- good sleep habits
- stress reduction
- psychological considerations
53
What are causes of secondary HTN?
- renal pathology: stenosis, or fibromuscular dysplasia
- endocrinal: pheo or hyperaldosteronism
- drugs: OCPs, NSAIDs, steroids
- neurogenic, psychogenic (anxiety)
- co-arction of aorta
- pregnancy
- OSA (most common): decrease O2 - sympathetic stimulation - HR and BP rises
54
What is short term goal of antiHTN therapy? long term?
- short term: reduce BP
- long term: controlling all of pts modifiable CV risk factors, want to reduce mortality due to HTN induced disease:
stroke, CHF, CAD (beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg
nephropathy, PAD, retinopathy
55
When should you tx patient?
- in absence of end-organ damage, a pt shouldn't be labeled as having HTN unless BP is persistently elevated after 3-6 visits over a several month period
- antiHTN meds should begin if the systolic pressure is persistently over or = to 140 and/or the diastolic pressure is persistently greater or equal to 90 in office and at home despite attempted nonpharmacologic therapy
56
BP = ?
BP = COx PVR
57
Where are the sites of regulation of CO and PVR?
- arterioles
- postcapillary venules
- heart
- kidneys
58
Tx choices for primary HTN? secondary htn tx?
drugs that:
1) reduce blood volume (which reduces central venous pressure, and CO)
2) reduce systemic vascular resistance
3) reduce CO by depressing HR and SV
secondary htn tx:
best tx by controlling or removing underlying disease or patholgoy, although they still may require antihypertensive drugs
59
What are the major classes of antihypertensives used for initial therapy?
- diuretics
- B -blockers
- ACEIs
- ARBs
- CCBs
- Alpha blockers
- alpha agonists
- vasodilators
- direct renin inhibitors
60
MOA of diuretics? most common adverse effect?
- cause diuresis which reduces plasma and SV causing a decrease in CO and BP
- most common adverse effect: (except in K+ sparing) is hypokalemia
- can also cause magnesium depletion
- use of low doses minimized these adverse effects
61
MOA of thiazides? Use in HTN tx?
- HCTZ:
inhibits NaCl reabsorption in distal convoluted tubule of nephron
- has propensity to cause hypokalemia, have to admin K+
- may precipitate hyponatremia
* pts allergic to sulfa may be allergic to HCTZ
- usually first line agent
- inexpensive, can be used in combo with other antiHTN meds
- ineffective if creatinine is greater than 2.5 (kidney won't be effected by thiazide)
62
MOA of loop diuretics? When are they used?
- selectively inhibit NaCl reabsorption in thick ALoH
- usually needed when renal function declines, used in HF, start low dose because hard on kidneys
- stronger incidence of hypokalemia
- oral K+usually sup in pts receiving loop diuretics
- reserve these for pts with chronic renal insufficiency
63
class of loop diuretics?
- furosemide (lasix)
- torsemide (demedex)
- bumetanide (bumex)
- metolazone (zaroxolyn)
- stronger the loop diuretic - more likely hypokalemia
64
MOA of K+ sparing diuretics?
- antagonize the effects of aldosterone at late distal and cortical collecing tubule in nephron
- weak when used alone, but spare K+ and magnesium loss
65
class of K+ sparing diuretics?
- aldactone (spironolactone)
- midamor (amiloride)
- dyrenium (triamterene)
66
Combos of HCTZ and K+ sparing diuretics?
- Altactazide (spironolactone/HCTZ)
- dyazide (Triamterene/HCTZ)
- maxzide (triamterene/HCTZ): stronger dose (most common combo)
- moduretic (amiloride/HCTZ)
67
First line therapy in HTN pts?
- thiazide type diuretics should be initial tx (either alone or in combo)
- diuretics have been almost unsurpassed in preventing CV complications of HTN
- diuretics enhance effect of other antihypertensives, more affordable, but still underutilized
68
Bblocker MOA?
- effect on ANS
- reduce HR and CO: antagonize the effect of catecholamine's at B adrenoceptors, decrease sympathetic drive
- decrease renin release
- cardioprotective: neg inotropic effect (decrease O2 consumption by heart by decreasing the force of contraction), neg chronotropic effect (decrease heart rate)
69
2 diff subclasses of B blockers?
```
B1 selective:
Metopropolol (lopressor, Toprol)
Atenolol (tenormin)
bisopropol (zebeta)
acebutolol (sectrol)
```
nonselective:
propanolol (inderal)
sotalol (betapace)
timolol (blocadren)
70
Combo b blocker and alpha 1 blocker?
- carvedilol (coreg)
- labetolol (trandate)
(decrease contractility severely - not enough fluid - don't give to HF pts)
71
combo drugs of B blocker and thiazide?
- atenolol-chlorthalidone (tenoretic)
- metoprolol/HCTZ (lopressor HCT)
- Bisoprolol/HCTZ (ziac)
72
Adverse effects of B blockers?
- bradycardia
- HF (too large of dose initially)
- bronchospasm: careful with asthma (use B1 selective B blockers)
- effects on CNS:
impotence
depression
sedation
fatigue
reduced ability to exercise
cold extremities (raynauds - constricting peripheral vasculature)
- has propensity to cause and mask hypoglycemia ( occurs because B2 adrenoceptors normally stimulate hepatic glycogen breakdown and pancreatic release of glucagon, which work together to increase plasma glucose. Therefore, blocking B2 adrenoceptors lowers plasma glucose
- can also mask shock and sympathetic responses to hypoglycemia (tachycardia and tremors)
- can cause increase in lipid profile (lower HDLs)
- reduced ability to exercise, hit plateau with HR
- hypotension
- don't abruptly d/c: rebound HTN, depression
73
B blocker drug interactions
- NSAIDs: can blunt effect of beta blockers
- epi causes severe HTN in presence of b-blockade
- CCBs: conduction effects on heart are additive with b blockers
74
MOA of ACEIs?
- block conversion of AI to AII, leading to artery and vein dilation reducing arterial pressure, preload and afterload
- down regulated sympathetic adrenergic activity by blocking effects of angiotensin II on sympathetic nerve release and reuptake of NE
- promote renal excretion of Na and H2O by blocking the effects of angiotensin in the kidney and stim of aldosterone
- blocks the degradation of bradykinin and stimulates the synthesis of other vasodilating substances (causes cough)
75
All of the effects AII has on the body?
- vasoconstriction
- direct renal Na retention
- aldosterone secretion
- increased thirst
- ADH release
- sympathetic facilitation
- increased cardiac contractility (increase volume)
- cardiac and vascular hypertrophy
76
How are ACEIs renal and cardioprotective?
- renal protective: decrease proteinuria and chronic renal failure in diabetics
- cardioprotective: inhibits cardiac and vascular remodeling asscd with chronic HTN, HF and MI
77
Class of ACEIs
- captopril (capoten)
- lisinopril (zestril)
- enalapril
* remember PRIL
78
When should ACEIs be considered for first line therapy to tx HTN?
- diabetics
- CHF
- chronic kidney failure in both diabetics and nondiabetics
- MI that weakens heart muscle (systolic dysfunction)
79
Combo of ACE and HCTZ?
- enalapril/hCTZ (Vaseretic)
- lisinopril/HCTZ (zestoretic)
- Benazepril/HCTZ (lotensin HCT)
80
Adverse effects of ACEIs?
- cough
- acute renal failure: shouldnt use in bilateral renal artery stenosis
- angioedema
- hypotension
- more effective in younger white pts, not effective in older black pts
- rash
- changes in taste
- hyperkalemia (shouldn't be given with K+ sparing diuretics, watch K+ with renal failure pts)
- ABSOLUTELY CI in pregnancy
81
MOA of ARBs?
- blocks AII receptor
| - so AI can't be converted to AII
82
Use of ARBs?
- alt to ACEIs
- blocks angiotensin II receptors - no cough because doesn't block breakdown of bradykinins
- cardioprotective and renal protective
- CI in pregnancy
- SE profile similar to ACE except decreased incidence of cough
- shouldn't be used with bilateral renal artery stenosis
83
Class of ARBs
| and combo with thiazides?
- Irbestartan (avapro)
- candesartan (atacand)
- losartan (cozaar)
- vlasartan (diovan)
- olmesartan medoxomil (benicar)
combos:
candesartan/HCTZ (atacand HCT)
Valsartan/HCTZ (Diovan HCT)
Olmesartin medoxomil/HCTZ (Benicar HCT)
84
MOA of CCBs?
- dilater peripheral arterioles by blocking the influx of Ca into arterial smooth muscle cells. The result is muscle relaxation and vasodilation
- reduce peripheral vascular resistance and arterial pressure
- decrease myocardial contractile force
- reduce myocardial O2 requirements
- particularly good in combo with diuretics for black pts
- one of initial choices for monotherapy for mild to mod HTN
85
```
Subclass of CCBs:
dihydropyridines
```
- potent vasodilators, highly vascular selective (doesn't effect rate as much)
- AmlodiPINE (Norvasc)
86
Subclass of CCBs: non-dihydropyridines
also used to tx dysrhythmias, angina, and HAs, neg inatropic and neg chronotropic
- verapamil (Calan,, Isoptin): relatively selective for myocardium, less effective as systemic vasodilator drug
- diltiazem (Cardizem): intermed b/t verapamil and dihydropyridines in its selectivity for vascular Ca cahnnels (use in Raynauds)
87
Adverse effects of dihydropyridines?
```
reflex tachycardia
flushing
HA
excessive hypotension
edema****
```
88
Adverse effects of non-dihydropyridines?
- excessive bradycardia
- impaired electrical conduction (AV nodal block)
- depressed contractility
- concern with B blockers
- shouldn't be given with heart block and systolic failure
89
MOA of Alpha 1 blockers?
- block alpha receptors in small arterioles and venules
- reduce arterial pressure by dilation: lower PVR
- often used with diuretic due to Na+ retention assocd with these
- produce less reflex tachycardia than non selective alpha blockers
- used when other drugs fail
- suggest taking at bedtime due to orthostatic hypotension
- use in low doses should be reserved for unique cases such as men with BPH as data doesn't suggest protection against CV events
90
Class of Alpha 1 blockers?
- prazosin (minipress)
- terazosin (hytrin)
- doxazosin (cardura)
91
MOA of alpha 2 receptor agonists?
- centrally acting sympatholytics
- stim alpha 2 receptors in brain
- has specificity towards the presynaptic alpha 3 receptors in vasomotor center in the CNS
- decrease in sympathetic outflow from vasomotor center = decreased vasoconstriction
- chronic use causes Na+ and fluid retention
- SE: sedation, dry mouth, possibly depression
92
Class of alpha 2 receptor agonists
- clonidine (catapres)
use if difficult to control HTN
- oral
- sustained release patch, assoc with increased pt compliance, changed weekly
- useful as 2nd or 3rd drug coice for lowering BP when other anti-HTN meds have failed
- also may be useful on an as need basis to control or smooth out fluctuations in BP
- methyldopa (aldomet) - frequently used in pregnancy
93
MOA of vasodilators?
cause direct arteriolar smooth muscle relaxation by increasing cGMP (common regulator of ion channel conductance, glycogenolysis and cellular apoptosis. It also relaxes smooth muscle tissues. In blood vessels, relaxation of vascular smooth muscle leads to vasodilation and increased blood flow.
- compensatory action over time causes increased heart rate, cardiac output, renin release
- therefore hypotensive effect diminishes unless also taking sympathetic inhibitor (B blocker) and diuretic
94
Class of vasodilators
Hydralazine: may cause dose related lupus like syndrome (Greater than 300 mg/day)
- can't be used for mono therapy
- for refractory HTN with other agents
Minoxidil: very potent, caues severe Na and water retention, hirsutism is SE
Reserpine: depletes NE fro nerve endings thereby reducing sympathetic tone, decreasing PVR and BP
- should be given with a diuretic
- major serious SE: mental depression due to loss of serotonin
** discuss these with supervising (way down line of tx)
95
What is a Hypertensive Crisis?
- sudden increase in BP assoc or potentially assoc with end organ damage
- urgent: no apparent end organ damage (systolic greater than 190)
- emergency: end organ damage that is apparent or suspected (greater than 190 systolic - with end organ damage)
96
What pts most likely have hypertensive crisis?
- usually happens to pt with existing HTN
- usually patient has uncontrolled HTN (rebound HTN)
- crisis more commoon in elderly and African Americans
97
Evaluating hypertensive crisis?
```
- hx of HTN
controlled with meds?
what meds?
careful B/P reading
- fundoscopic exam: papilledema
-CBC(anemia), CMP(kidney fxn), U/A (protein), EKG
- possible precipant drugs:
MAO inhibitors for depression
sympathomimetics (sudafeds)
recreational drugs
```
98
Tx for hypertensive urgencies?
- not associated with end organ damage (can reduce BP over 1-2 days)
- tx with oral meds: captopril (ACEI -capoten) quick onset (50 mg q 1-2 hrs)
Amlodipine (CCB) also used (2.5-5 mg q 2 hours)
clonidine
99
Tx for hypertensive emergencies?
- end organ damage apparent or impending: hospital admission (ICU) + IV tx
- nitroprusside: minute to minute control with rate of 0.25-0.8 mug/kg/min, watch for cyanide toxicity
- nitroglycerin: 5-100 mcg/min. Tolerance after 24-48hrs, HA
- labetalol, hydralazine are also IV alternatives
100
Nitroprusside?
- IV admin only
- used in HTN crisis
- short 1/2 life
- immed onset of action
- soln sensitive to light
- must use either intra-arterial BP monitoring or continuous BP monitor
- ICU only
- start low and go slow
101
Nitroglycerin use in HTN crisis?
- nitrate
- venous and arteriolar dilator (in large doses)
- tolerance develops when used over 24-48 hrs
- used in pt with suspected or confirmed MI
102
Fenoldopam use in HTN crisis?
- short acting dopamine agonist, onset 5 min
- increase renal blood flow, natriuresis, diuresis
- useful in renal failure pts
103
Labetalol use in HTN crisis?
- combo nonselective alpha/beta blocker, onset 2-5 minutes
| - can cause orthostatic hypotension
104
Use of Hydralazine in HTN crisis?
- arteriolar vasodilator: onset 10-30 min, duration 2-4 hours
105
What meds work best in African Americans?
- diuretics and CCBs
| - have resistance to BB, ACEI and ARBs
106
What should be used in stable angina? unstable angina/MI?
- beta blockers: stable angina
| - beta blockers, and ACEIs: unstable angina/MI
107
What group of meds should you not use in LVH?
- vasodilators
| because of fluid retention and reflex tachycardia
108
What is preferred, monotherapy or polypharmacy?
- monotherapy becoming more popular
- polypharm should be with 2 or more drugs, each acting by a different mechanism
- begin with mono therapy, if possible
- add drug from diff class with diff MOA
- consider pts cardiac and renal status, and other conditions
- also consider diabetes
- always implement non pharm therapy first (diet, exercise)
109
Monotherapy options for HTN?
- ACEIs
- diuretics
- B-adrenoceptor blockers
- CCBs
110
Why should pts with CAD be tx with beta blockers?
- decrease O2 demand by slowing rate, and also decreasing workload on heart. Lowers BP
111
What should the tx be for pts with depressed ventricular systolic fxn or overt heart failure?
- diuretics
- ACEI
- beta blockers
- never use CCBs!!!
112
Factors to consider in tx HTN?
- starting levels: start small and slow
- co diseases: HF, diabetes, and renal disease
- cost
- pt ownership/FU
- how many drugs to achieve BP goals: combo drugs?
113
When is it appropriate to add drugs on to therapy?
- pt isn't at goal BP
- meds the pt is currently taking are at optimal doses or add after moderate dose of first drug
- what drugs should be added:
avoid drugs with overlapping toxicities
use same decision process as prev used for first line tx
- if not on thiazide - add one!!!!!!
- if drug has no effect on BP
- patient having adverse effects
114
What are good combos to use?
- Bblocker and diuretic
- ARB and diuretic
- ACEI and diuretic
- CCB and ACEI
- ACEI and BBlocker
115
What should you consider if drug has no effect? Good response but adverse effect?
- consider increasing dose to optimal dose
- change to drug with diff MOA
- add a diuretic (take in morning)
- consider causes of resistance:
compliance and med interactions
- if adverse effect but good response:
change to slightly diff drug within same class
116
What are some causes of resistance to drug therapy?
- volume overload: too much Na intake, inadequate diuretic therapy, renal failure
- noncompliance of pt
- pseudo resistance: pts has white coat syndrome or cuff size is wrong for pt (usually too small)
- non drug causes:
comborbidities: obesity, sleep apnea, smoking, chronic pain, anxiety, insulin resistance
117
What are the secondary causes of HTN that may be cause of resistance to drug therapy?
- renal failure
- renal artery stenosis
- pheochromocytoma
- cushing's disease
- hyperaldosteronism
118
Drug interactions that may be causing resistance to drug therapy?
- NSAIDS and COX-2 inhibitors
- caffeine
- steroids
- oral contraceptives
- erythropoetin
119
How should HTN that is dx before pregnancy be handled during pregancy?
- msot meds can be used through pregnancy
- maske sure meds are safe for fetus
- don't use ACEs and ARBs during pregnancy
120
Tx for HTN dx during pregnancy?
- methyldopa is DOC
- Hydralazine
- labetalol - b blocker avoid in early pregnancy
- don't use ACE and ARBs during pregnancy
121
What are the 2 ways the kidney knows to release renin?
-decreased O2, hypotension
122
Do B 1 receptors have ability to cause renin release?
- yes, b receptors in the kidneys
123
Where does nitric oxide come from? Fxn?
- comes from endothelium of blood vessel
| - is causes vasodilation
124
What are 2 primary physiologic effects of aldosterone?
- reabsorb Na+ and excrete K-
125
Can sympathetic overactivity cause hypertension?
yes
126
Where are arterial baroreceptors located?
- carotids, and aorta
127
Activation of vascular sympathetic nerves causes vasoconstriction of arteries and veins mediated by which adrenoceptors?
- beta receptors
128
A pt with isolated systolic HTN is at risk for?
- pulse pressure is widening - more likely to have tears and ruptures in vessels
129
Fibromuscular dypslasia is commonly found in what population?
- young women
130
Would plasma renin levels in a pt with renovascular HTN be elevated or low?
- elevated
131
One of the most common causes of secondary HTN?
- OSA
132
Would renin levels in a pt with hyperaldosteronism be elevated or low?
- low because there is plenty of volume already
133
Primary goal in tx HTN is to prevent what?
- end organ damage
134
What type of B blocker is contraindicated in a pt with asthma?
- nonselective (B2) - cause bronchospasm
135
What are the recommended drugs for HF?
- Diuretic
- BB
- ACEI
- ARB
136
Post MI tx recommendations?
- BB
| - ACEI
137
High coronary disease risk tx recommendations?
- diuretic
- BB
- ACEI
- CCB
138
Tx recommendations for diabetes?
- diuretic
- BB
- ACEI
- ARB
- CCB
139
Tx recommendations for CKD?
- ACEI
| - ARB
140
Tx for recurrent stroke prevention?
- Diuretic
| - ACEI
141
For pts whose initial BP is greater than 160/100 what should the therapy be?
- initial therapy with 2 agents (one should be thiazide diuretic)
- thiazide often potentiates MOA of other med, especially ACEs and ARBs
142
Recommended tx for Black Americans?
- thiazide
| - CCBs
143
recommended tx with left ventricular systolic dysfunction or overt HF?
- diuretics
- ACEI
- BBs (watch for increased CHF)
- NO CCBs
144
Tx recommendation for pts with diabetes with nephropathy?
- ACEIs
| - ARBs
145
Tx for HTN that develops in pregnancy?
- Methyldopa
146
Pts with renal insufficiency/CRF tx for HTN?
- ACEIs
| - ARBs
147
What BBs can be used in HF?
- Carvedilol, Metoprolol, and BIsoprolol
| - avoid others
148
When should CCBs be avoided?
- HF
| - heart block, conduction delays
