What is hypertension?
a common, often asymptomatic, disorder in which the BP persistently exceeds 140/90
Explain what secondary hypertension is.
-hypertension associated with a primary underlying disease
-Hypertension due to the use of some medications (iatrongic)
Explain what malignant hypertension is,
-Rare bus associated to tumor
-a sudden and rapid development of extremely high BP. The systolic is over 200 and the diastolic is often over 130.
What conditions are individuals more at risk for malignant hypertension?
-affects about 1% of people with high BP
-more common in younger adults
-women with eclampsia of pregnancy
What is the goal of antihypertensive drug therapy?
reduce the risk of mortality and cardiovascular and renal morbidity
What affect does the increase of SNS activity have on CO and BP?
increased contractility (inotropic) and heart rate (chronotropic)
How do ARBs differ from ACE inhibitors?
-ACE Inhibitors: (prevents formation of angiotensin II & prevent breakdown of Bradykinin)
-ARBs: (block angiotensin II receptor which prevents the action of the receptor)
BOTH VASODILATE, thus decrease BP
Would you use a Beta Blocker that was nonselective in a pt. with asthma?
not asthma or COPD
b/c it blocks Beta1 and Beta2
this causes vasodilation, but also vasoconstriction!
What is the number one concern with antihypertensive drugs?
Large!! FIRST DOSE EFFECT
-causes orthostatic hypotension
Pt. education needed to be careful when standing OR take drug at night
What is the caution for giving Beta Blockers hypertension in pt. who is also diabetics?
-Beta2 blockers decrease the conversion of glycogen to glucose in liver and muscle, so can't respond quickly to a drop in BG
-it masks hypoglycemia
They are unable to sweat or have tachycardia
(need to teach other signs to recognize like growling stomach, feeling "off", slurred words)
How do the properties of Beta1 blockers and Beta2 blockers effect the brain function of a pt.?
Beta2 are more lipid soluble, thus able to cross the BBB = Fatigue/drowsiness
What effect does CYP inhibitors have on Beta Blockers?
grapefruit & tagament give with Beta Blockers
-the drug will not be metabolized as easily
-more chance of toxicity due to increased levels of Beta Blocker in bloodstream
What effect do NSAIDS have on Beta Blockers?
1.cause retention of fluids = increase in vol. = increase in BP
2.inhibit prostiglandins, which are important for blood flow in kidneys = increase blood vol. = increase in BP
What effect do Calcium Blockers have on Beta Blockers?
Vasodilation = additive effect of decreasing BP
Why do you have to be careful with pt. getting allergy tested who is taking Beta Blockers?
-hold Beta Blockers for 48 to 72 hours
-You want the Beta blockers to be "open" in case the person has an allergic reaction, so you can give Epinephrine which is an Adrenergic drug that targets Alpha1, 2 and Beta 1, 2 receptors. If the pt. has blocked these receptors, the Epinephrine will not be able to impact the Alpha/Beta receptors to reverse the anaphalaxic shock
What effect can Beta Blockers have on a pt. going in for a Cardiac Stress Test?
-hold Beta Blockers for 48 to 72 hours
-You want the Beta blockers to be "open" in case the person goes into cardiac arrest, so you can give Epinephrine which is an Adrenergic drug that targets Alpha1, 2 and Beta 1, 2 receptors. If the pt. has blocked these receptors, the Epinephrine will not be able to impact the Alpha/Beta receptors to reverse the cardiac arrest.
Calcium Channel BlockersDihydroprpyridines vs. nondihydropyridines
1. Di : act mainly on vascular sm. muscle (D=dilate) dilate arteries and arterioles ONLY
2. NonDi : (N=node & D=dilate)
dilate vascular sm. muscle=hypotension
mycardium = decreases force of contraction (negative inotrope)
blocks AV node = slows conduction = slows HR (negative chronotrope/negative dromotrope)
What are Calcium Channel blockers used for?
Dysrhythmias (fast HR)
Side effects of Dihydropryridine Calcium Channel Blockers
dilate only, thus low BP, edema
2.reflex tachycardia (initially the baroreceptors are attempting to compensate for the decrease in BP)
3.peripheral edema (SVR is decreased, thus hydrostatic pressure is increased, fluid shifts to interstital compartment)
Side effects of Nondihydropryridine Calcium Channel Blockers
dilate and affect node, so more cardiac side effects
1.constipation (no parastalsis)
3. facial flushing (vasodilate: extra blood supply to face)
6. bradycardia heart block
7. CHF (can't pump enough blood out = overloaded)
8. ginigval hyperplasia (puffy/bleed)
8.excema like rash in the eldrely
What is the mechanism of action of centrally acting drugs?
-pre-synaptic inhibition of norepinephrine outflow from CNS
-reduces activity of renin in kidneys
THUS they vasodilate! causing decrease in BP
What are the mechanisms of action for peripherally acting drugs?
-dilate arteries & veins
-decreases peripheral vascular resistance
-decreases systemic and pulmonary venous pressure
-increases cardiac output
-relax smooth muscle of urethra just below prostate
Why might pt. taking a peripherally acting drug develop nasal congestion?
These are Alpha Antagonists
-dilates nasal mucosal arteries
Why might pt. taking a peripherally acting drug develop edema?
These are Alpha Antagonists.
-Vasodilation increases hydrostatic pressure, which causes a fluid shift to the intrastitial compartment being tissue
What type of sexual dysfunction could occur with Alpha Antagonist?
Erectile dysfunction due to the relaxation of the sm. muscle of urethra below the prostate
What do Dual Action drugs like Labetolol and Carvedilol do?
It is a Alpha 1 & Beta1 & 2 BLocker
-calcium channel blocker
What is important to remember about Carvediolol, the dual acting drug?
Start out in low doses..,strong due to specificity (oral drug)
GOOD for Heart Failure
--However, Labetolol (an IV dual action drug) is used for Hypertension crisis in ER
--Carvediolol has shown to slow progress of heart failure and to decrease the frequency of hospitalization in pt. with mild to moderate heart failure
Contraindications for Alpha BLockers
-active peptic ulcers (b/c can't vasoconstrict)
-colitis (b/c can't vasoconstrict to stop bleeding)
-liver or kidney disease (getting rid of the drug)
What is the effect of ACE inhibitors?
Angiotensin-converting Enzyme Inhibitors
1. Cardiovascular by vasodilate :prevent the formation of angiotension II, preventing the breakdown of bradykinin & substance P (a vasodilator)
2. Renal: keeps the body at a hypotensive state thus decreases the amount protein lose at the glomulerus
thus decreases the afterload and preload
Why is the accumulation of bradykinin so important?
mostly in woman & African Americans
-it causes a cough
(to prevent this you can put them on an angiotension II receptor blocker)
When are ACE inhibitors used?
Chronic Heart Failure (prevent sodium & water reabsorption by inhibiting aldosterone secretion with is linked to Angiotensin II formation) =diuresis
Protect kidneys from renal failure
Common Side effects of ACE inhibitors?
-**dizziness (First Dose Effect)
-fatigue (low BP causes them to feel this)
-**Hyperkalemia (caused by retention of Potassium)
-musculoskeletal pain (usually due to shifts of potassium ions across Cell membranes)
Very Serious Side effects of ACE inhibitors?
-***Angioedema (lips swollen, tongue swollen, leads to epiglottis swelling..ER!!!)
-Stevens-Johnson Syndrome (patches of skin that get necrotic/mucous membrans involved)
What are the contraindications to ACE inhibitors?
-***pregnancy (the baby will be born with hypotension)
-Bilateral renal artery stenosis
-high potassium (5.0 mE/q/L)
-Lithium (these people require salt & water: these drugs inhibit aldosterone, thus Na+ thus water!)
What are the drug interactions to ACE inhibitors?
-Potassium sparing diuretics (cause hyperkalemia which this drug causes hyperkalemia already!)
-other Antihypertensive drugs
prevent Angiotensin II mediated vasoconstriction and release of aldosterone
THUS DO NOT produce a cough (since they still allow the breakdown of bradykinin)
What are ARBs contraindication?
caution with elderly & renal dysfunction: more sensitive to adverse effections