Hypertension Flashcards
3 mechanisms the body uses to control BP
- blood volume
- Peripheral resistance/diameter of arterioles
- Cardiac output
what is the preload?
= volume of blood coming back into the ventricles of the heart at the end diastole (diastolic pressure)
what is afterload?
peripheral vascular resistance left ventricles must overcome to circulate blood
-how much resistance heart has to pump against to get blood flowing out to the body
5 classes of antihypertensives:
- –Diuretics
1. Thiazide
2. Loop
3. Potassium Sparing - –Adrenergic Agents
1. Alpha Blockers
2. Beta Blockers
3. Alpha2 Agonist
4. Alpha Beta Blockers - –Calcium Channel Blockers (CCB)
1. “dipines”
2. verapamil & diltiazem - –Renin-angiotensin system (RAAS)
1. ACE inhibitors
2. Angiotensin II Receptor Blockers (ARBs)
3. Direct Renin Inhibitors
4. Aldosterone Inhibitors
—Vasodilators
3 types of classes of diuretics
- Thiazide
- Loop
- Potassium Sparing
4 classes of adrenergic agents
- Alpha 1 Antagonist
- Beta Blockers
- Alpha2 Agonist
- Alpha Beta Blockers
classes of calcium channel blockers
- “dipines”
2. non-dipines: verapamil & diltiazem
4 classes of RAAS drugs for HTN
- ACE inhibitors
- Angiotensin II Receptor Blockers (ARBs)
- Direct Renin Inhibitors
- Aldosterone Inhibitors
2 ways diuretics fxn in body to decrease BP
- Decrease BLOOD VOLUME by urinary excretion of water and electrolytes
- inhibit absorption of sodium and chloride in kidney –> excrete h2o electrolytes
- Decrease arterial resistance due to loss of volume
which drug is our first line therapy for HTN?
diuretics!
- -> most efficacious is loop/furosemide
- -> most widely used = thiazide/ hydrochlorothiazide
where do loop diuretics work?
Inhibits reabsorption of Na & Cl at loop of Henle (early on in tubule)
prototype for loop diuretics?
furosemide (Lasix)
which diuretic gives us the most diuresis?
furosemide (Lasix) b/c it has more impact on more volume of solute
which diuretic will we use to treat acute pulmonary edema?
furosemide (Lasix)
Iv vs PO onset for loop diuretics
PO: 1hour
IV: 5 min
Side effects for loop diuretics?
- electrolyte imbalances (Na, Cl, K+) (hypo)
- hypotension, dehydration, postural hypotension
- ototoxicity- transient: IV push too quick or very high dose
- increases risk of digoxin toxicity, lithium toxicity –> lose salt, and body keeps lithium (monitor bipolar meds)
- increases uric acid (gout) –> if patients already have gout can cause gout attack, usually not a problem for causing new gout
which HTN drugs can cause ototoxicity?
furosemide - if given too fast or too high of a dose
Furosemide and hydrochlorothiazide (HCTZ) both have risk for what 2 toxicities?
litium and digoxin
where does hydrochlorothiazide (HCTZ) fxn in kidney?
-works on the distal tubule.
prototype for Thiazide Diuretics
hydrochlorothiazide (HCTZ)
how does hydrochlorothiazide (HCTZ) work? (2)
1) reduces BLOOD VOLUME -works on the distal tubule.
- ->Results in excretion of H20, Na, K+
2) Reduces arterial resistance (over time)
onset/peak and duration for hydrochlorothiazide (HCTZ)
Onset: 2 hrs., peak 4-6, lasts 12 hours
less sudden onset than loop
side effects of hydrochlorothiazide (HCTZ)
- electrolyte imbalances (K+, Na, Cl) (hypo)
- dehydration, hypovolemia
- Hyperglycemia ( w/ DM)
- increases uric acid (gout)
- risk for digoxin toxicity and lithium toxicity
which diuretic has risk for hyperglycemia w/ DM?
hydrochlorothiazide (HCTZ)
which diuretic will work if GFR is <15-20?
loop/furosemide will work
thiazide will not work with severe kidney impairment
thiazide vs fursoemide- whats goin on with K?
thiazide = increase K in diet furosemide = K supplement
how/were do potassium sparing diuretics fxn?
Competes with aldosterone at receptors in the distal tubule (at very end) blocking aldosterone (fluid lost, K remains)
-Aldosterone usually makes body hold onto fluid and loose potassium, if BLOCK aldosterone will lose fluid and keep potassium
what is prototype for potassium sparing diuretic?
spironolactone (Aldactone)
how long does spironolactone (Aldactone) take to work?
Takes up to 48 hours to work
*do not use with fluid volume overload and struggling to breathe
which diuretic is least efficacious?
spironolactone (Aldactone)
side effects of spironolactone (Aldactone)
- Risk for hyperkalemia (high K+) (especially if using a salt substitute which replaces salt with potassium)
- Endocrine effects: gynecomastia, impotence, hirstruism, deepening of voice
spironolactone (Aldactone) + salt substitute =
risk for hyperkalemia
What drugs do we typically not give with Potassium sparing diuretics and why?
RAAS b/c of risk of hyperkalemia
who is definitely not taking furosemide?
pregz in the eggz
Adrenergic agents- SNS or PNS?
SNS - right side of the chart
adrenergic = norepi/epi , betaz n alphaz
how do 1. Alpha1 Adrenergic Antagonists fxn? (2)
- blocks the sympathetic nervous system action on arterioles and veins resulting in vasodilation
- causes relaxation of smooth muscles in bladder neck and prostatic capsule (BPH)
what is the prototype for Alpha1 Adrenergic Antagonists
prazosin (Minipress) “osins”
side effects of prazosin (Minipress)?
- orthostatic hypotension (due to vasodilation)
- **Ist dose phenomenon (don’t get up for 3 hours) - give at night time
- reflex tachycardia (due to vasodilation)
- nasal congestion (due to vasodilation)
- inhibits ejaculation due to activation of Alpha 1 receptors, reversible
prototype for Alpha2 Adrenergic Agonist
clonidine (Catapres)
how does clonidine (Catapres) fxn?
Alpha2 Adrenergic Agonist
centrally acting on alpha2-adrenergic receptors in the brain
- reduces sympathetic outflow to heart and blood vessels
- Results–> vasodilation and decreased cardiac output
clonidine (Catapres) routes
- pill-PRN, reduce HTN w/in 30 minutes
- patch changed every 7 days
who is taking clonidine (Catapres)
Used in severe HTN management (PRN orders) , older patients who struggle with pills
side effects of clonidine (Catapres)
Alpha2 Adrenergic Agonist
- dry mouth and sedation (gets better with time- develop tolerance like all CNS drugs)
- Rebound Hypertension if stop cold turkey
Adrenergic Agents: Beta Blockers prototype
Metoprolol (Lopressor, Topol XL) - cardioselective
how does Metoprolol (Lopressor, Topol XL) fxn?
-Decreases HR (NEGATIVE CHRONOTROPE)
-Slows conduction through myocardium (NEGATIVE DROMOTROPE) , slow conduction from SA node to AV node
-Decreases force of contraction (NEGATIVE IONOTROPE)
Other actions: decreases peripheral vascular resistance over time and block beta1 on juxtaglomerular cells that release renin
side effects of Metoprolol (Lopressor, Topol XL)
- Bradycardia, AV heart block
- Decreased cardiac output
- Watch for S/S of heart failure
- Rebound cardiac excitation- beta blocker is blocking excitation, stop taking it then sympathetic nervous system comes back with full force –> angina
- May mask SNS (tremors/jittery) s/s of hypoglycemia in diabetics : prefer to put them on cardioselective
- Prolongation to sa-av node = prolongation of PR interval
- Nonselective BetaBlocker (1/2)—can actually cause hypoglycemia b/c glycogen is not getting broken down b/w meals
- fatigue
- drowsy
- dizzy
- HA
- sexual dysfunction
- depression
which HTN drug causes -Prolongation to sa-av node = prolongation of PR interval ?
Metoprolol (Lopressor, Topol XL)
Hold beta blockers is apical pulse is > ________
60
Can you stop metoprolol suddenly?
no, risk of rebound tachy
Prototype for alpha/beta blocker
carvedilol (Coreg)
what receptors is carvedilol (Coreg) blocking
A1, B1, B2
how does carvedilol (Coreg) fxn?
- Alpha blockade: Dilation of arterioles and veins
- Beta blockade: dec. HR, contractility and conduction
side effects of carvedilol (Coreg)
bradycardia, AV block, bronchoconstriction (beta 2- don’t use in asthmatics), postural hypotension
which patient population should not take carvedilol (Coreg)
asthmatic
2 Ca channel blockers=
Very Nice Drugs
- Verapamil
- Nifedipine
- Diltiazem
how does Ca Channel blockers fxn in general?
inhibiting the influx of Ca into cells, preventing muscular contraction–> Vasodilation occurs when Ca is blocker and muscle is relaxed
- -works on peripheral arterioles, arteries, arteries/arterioles of heart –> increases coronary perfusion
- no effect on veins !!
do Ca Channel blockers work on veins?
no! only work on peripheral arterioles, arteries, arteries/arterioles of heart
NORMAL Ca channels in heart have 3 actions
- causes positive inotropic effect = stronger contraction
- pacemaker activity
- AV node excitability regulated by Ca
if Give Ca BLOCKADE….
= negative inotropic effect in heart - decrease contraction
=negative chronotropic effect = decrease HR
= decrease conduction
Ca Channel blockers have same action as what other drug?
Beta blockers!
do not give Ca Channel blocker and beta blocker at same time
VND + Metoprolol = sadness
Dihydropyridines prototype
Nifedipine (Procardia)
(Ca Channel Blocker
how does Nifedipine (Procardia) fxn?
Ca Channel blocker
- Work primarily on blood vessels: vasodilation of arterioles and arteries , not in heart!
if someone gets reflex tachycardia AFTER STOPING a Ca Channel Blocker like Nifedipine (Procardia) we give them
beta blocker!
Non-Dihydropyridines Verapamil & Diltiazem act on….
- arterioles
- heart:
- Decrease contractility (neg inotrope )
- DecreaseHR (neg chronotrope)
- Decrease conduction through AV node (neg dromotrope)
Plus: Vasodilation
Plus: increases coronary perfusion
prototype for Non-Dihydropyridines
verapamil (Calan)
side effects of verapamil (Calan)
- constipation
- dizziness
- facial flushing,
- edema in ankles/feet,
- Cardiac: bradycardia, heart block and heart failure
Considerations for Ca Chennal blockers
- Check BP and pulse (verapamil & diltiazem)
- Watch for reflex tachy (nifedipine)
- IV administration-tachy and hypotension
- Don’t give with grapefruit juice
grapefruit juice does not mix with which class of HTN drugs?
Ca Channel Blocker
The story of Angie and Al:
-ANGIOTENSINOGEN is made by the liver and lives in blood vessels
-When juxtoglomerular cells of kidney sense low BP then release RENIN
-Renin converts Angiotensinogen –> ANGIOTENSIN I
-ACE covers Angiotensin I –> ANGIOTENSIN II
(ACE= Angiotensin Converting Enzyme)
-Angtiotensin II = vasoconstriction + causes Adrenal cortex to release ALDOSTERONE
-Aldosterone causes retaining water/sodium which increases BP
Another name for ACE, what else does it work on?
Kinase II
works on : bradykinin
When we block ACE are we getting rid of all the Angiotensin II?
Nope, Angie II is made by other pathways so there is still some hanging around
What is wrong with Angie II and Aldosterone?
–Increases inflammation in the arteries
Prothrombotic- more likely to clot- MI/stroke
-Increases insulin resistance at the tissues
-Causes cardiac hypertrophy and vascular remodeling by making tissue more fibrotic
How do Ace Inhibitors fxn?
stop Angie II from being formed
times to definitely use an Ace inhibitor
- HTN
- Post MI
- HF
- Diabetes
- Diabetic Nephropathy prevention
- Stroke and MI prevention
Diabetic Kidneys and Ace inhibitors
- Decrease Angtionensin II with ace inhibitor–> vasodilation of the efferent arteriole –> pressure in glomerulus fall–> slows the progression to chronic kidney disease
- Some recommend all diabetics to be on an ACE inhibitor even if BP normal to protect the kidney from diabetic nephropathy
prototype for ace inhibitor
lisinopril (Zestril)
fxn of lisinopril
- Blocks the conversion of angie 1 to angie 2-> vasodilation and decreased fluid volume
- Block aldosterone
- Increase bradykinin - causes dry cough and angioedema (women and black)
side effects of lisinopril
side effects of lisinopril Dry cough, angioedema (will go away after 2-3 weeks in most people), 1st dose hypotension, Increased K+
who is not taking any RASS drugs?
pregz in the eggz
angioedema related to lisinopril- what is it? who is getting it? when does it happen?
- Hypersensitivity response Caused by bradykinin
- May occur at any time during therapy
- May be life threatening emergency
- Most common in women, smokers and African-American individuals
prototype for Angiotensin II Receptor Blockers
valsartan
how does valsartan fxn?
Angiotensin II Receptor Blockers
– block receptors for AT2 after it is formed
- Potent vasodilator
- Prevents bad effects from AT2
- Blocks aldosterone
- Not as good as ACE Inhibitor
side effects of valsartan?
- Decreased risk of cough compared to lisinopril (not working on Bradykinin)
- 8% cross-sensitivity with ACE for angioedema
direct renin inhibitor prototype
aliskiren (Tekturna)
how does aliskiren (Tekturna) fxn?
Blocks the entire RAAS process by binding with Renin and prevent ATI turning into AT II
which HTN must you avoid taking with high fat meal?
aliskiren (Tekturna) Direct Renin inhibitors
decrease absorption
side effects of Direct Renin inhibitors-aliskiren (Tekturna)
angioedema, cough, diarrhea
prototype for Aldosterone Receptor Blockers
spironolactone (Aldactone)
also our potassium sparing diuretic
2 prototypes for direct vasodilators
hydralazine (Apresoline)
nitroprusside (Nitropress)
how does nitroprusside (Nitropress) differ from hydralazine (Apresoline) in its function?
Prototype: hydralazine (Apresoline)
Action: Causes direct relaxation of arteriole smooth muscle
Prototype: nitroprusside (Nitropress)
Action: Causes venous and arteriolar dilation
*Drug of choice for HTN emergency
side effects of hydralazine (Apresoline)
reflex tachy (give with BB), increased bld. volume (give diuretic), SLE syndrome (lupus syndrome)
-vasodilation throughout system - decrease kidney blood- kidney holds onto fluid - increase blood volume
Serious Adverse effects:
- Severe hypotension
- Reflex tachycardia
route and indication for hydralazine (Apresoline)
Use: Primarily used in emergency situations to quickly decrease BP.
Route: Given IV
nitroprusside (Nitropress) route and duration of use
Given by IV continuous infusion
- Effects begin in seconds
- Not used longer than 72 hours
side effect of nitroprusside (Nitropress)
- toxic accumulation of thiocyanate
- If increased blood volume occurs–> manage with furosemide.
drug of choice for HTN emergency
nitroprusside (Nitropress)
Defined as diastolic greater than 120 mmHg
