Hypertension Flashcards
types of cardiovascular disease:
hypertension
CHF
MI and angina pectoris
cardiac arrhythmias
thrombosis
hyperlidemia
what is hypertension?
high BP >140/90
normal= 120/80 mmHg
what are the stages of hypertension?
SBP:
I: 140-159
II: 160-179
III: 180-200
DBP:
I: 90-99
II:100-109
III:110-119
what is prehypertension?
BP between 120/80 - 139/89
a strong risk factor for developing HTN
what is isolated systolic HTN?
SBP >140 and normal DBP
what are risk factors for HTN?
blood relatives with HTN men > 55 y/o post menopausal women obesity smoking diabetes high blood cholesterol
what are complications of HTN?
cerebrovascular hemorrhage stroke renal failure heart failure MI retinal damage
what are the types of HTN?
PRIMARY (idiopathic) HTN- 95%
SECONDARY HTN (5%)
what are possible contributors of primary HTN?
- high sodium in diet or sodium retention
- enhanced sympathetic nerve activity
- perturbations in renin-angiotensin-aldosterone system
what are possible contributors of secondary HTN?
- precipitated by chronic renal disease (diabetic nephropathy)
- pheochromocytoma
- stress
- aortic coarctation
what is a nephron?
the functional unit of the kidney
what is a diuretic?
For high blood pressure, diuretics, commonly known as “water pills,” help your body get rid of unneeded water and salt through the urine. Getting rid of excess salt and fluid helps lower blood pressure and can make it easier for your heart to pump.
what are the 3 major diuretics?
1- loop- high ceiling diuretics
2- thiazides and thiazide-like
3- K+ Sparing
what are examples of loop diuretics?
Durosemide (Lasix)
Bumetanide (Bumex)
where do loop diuretics work?
in the loop of Henle
what is the mechanism of action for a loop diuretic?
inhibition of Na+, K+, Cl reabsorption in the loop of Henle resulting in electrolyte and fluid excretion
excretion of water, sodium and chord
what are indications for the use of loop diuretics?
treatment of:
acute pulmonary edema.
CHF
HTN
what are adverse effects of loop diuretics?
electrolyte imbalances: hyponatremia (Na), hypokalemia (K) (leads to cardiac arrhythmia)
reactive increase in renin levels
alkalosis
hyperuricemia (uric acid)
what are examples of thiazide diuretics?
Chlorothiazide (Diuril)
Hydrochlorothiazide (Hydrodiurl)
Metolazone (Zaroxolyn(
where do thiazide diuretics work?
distal convoluted tubule
what is the mechanism of action for a thiazide diuretic?
inhibition of Na+, CL- reabsorption in the distal convoluted tubule
what are indications for the use of thiazide diuretics?
either alone or in combo with other drugs in the treatment of HTN and/or CHF
what are adverse effects of thiazide diuretics?
same as loop diuretics
electrolyte imbalance: hyponatremia, hypokalemia–>leads to cardiac arrhythmia
reactive increase in renin levels
alkalosis
hyperuricemia
what are the 2 categories of K+ sparing diuretics?
1- mineralocroticoid receptor antagonists
2- renal Na+ channel inhibitors
what are mineralocroticoid receptor antagonists?
Spironolactone (Aldactone)- blocks aldosterone
what is aldersterone?
a hormone secreted from adrenal cortex and works on the collecting ducts to enhance exchange of Na+ and K+
retains sodium
secretes potassium
what is the mechanism of action of mineralocroticoid receptor antagonist?
competitive blocker of aldosterone receptors in collecting duct, decrease the Na+/K+ exchange
what are indications for the use of mineralocroticoid receptor antagonists?
co-administered with thiazides or loop diuretics in tx of HTN and CHF
what are adverse effects of mineralocroticoid receptor antagonists?
life threatening hyperkalemia
gynecomastia- enlarged breast in men
impotence- erectile dysfunction
decreased libido
acidosis
what are renal Na+ channel inhibitors?
amiloride (Midamor)
Triamterene (Dyrenium)
what is the mechanism of action of renal Na+ channel inhibitors?
inhibit Na+ channels in collecting duct, leading to inhibition of Na+ reabsorption, and K+ sparing
what are indications for use of renal Na+ channel inhibitors?
in combination therapy with thiazides to treat HTN and CHF
what are adverse effects of renal Na+ channel inhibitors?
hyperkalemia
acidosis
what are examples of combination therapy?
amiloride & hydrocholorothiazide
spironolactone and isobutylhydrocholorthiazide
what are the 2 ways to manage hyperkalemia?
1- IV injection of insulin and dextrose
2- exchange resin (sodium polystryrene, kayexalate)
what is renin?
an enzyme secreted by renal cells
what is RAS?
Renin-angiotensin II- Aldosterone System
a hormonal cascade that functions in the homeostatic control of arterial pressure, tissue perfusion, and extracellular volume. Dysregulation of the RAAS plays an important role in the pathogenesis of cardiovascular and renal disorders.
Liver produces a pre enzyme- angiotensinogen ->gets converted to angiotensin I (occurs thru the action of renin that is released by the kidney bc of low fluid volume –> converted to angiotensin II by ACE floating in the blood
Angiotensin II acts on the adrenal gland that causes it to release aldosterone (a steoid hormone) which then acts on the collecting ducts of the nephron within the kidney and causes the nephron to retain water
If the body retains water the BP goes up
angiotensin II leads to:
1- aldosterone –> increased blood volume
2- vascular smooth muscle–> vasoconstriction
loop and thiazide diuretics increase:
sodium excretion
what are the therapeutic components of loop and thiazide diuretics?
decreased blood volume
decreased vascular resistance
what are the counter-therapeutic components of loop and thiazide diuretics?
increased renin production
increased angiotensin II
what are examples of ACE inhibitors?
Captopril (Capoten)
Enlapril (Vasotec)
Lisinopril (Prinivil)
Quinapril (Accupril)
what is the mechanism of action of ACE inhibitors?
inhibition of angiotension converting enzyme (ACE), which reduces levels of vasoconstricting angiotensin II and increases levels of the vasodilator bradykinin.
diminished angiotensin II also decreases secretion of the sodium retaining, potassium secreting corticosteroid, aldosterone
what are indications for the use of ACE inhibitors?
diabetic hypertensive populations- slows development of diabetic neuropathy
hypertensive populations with L ventricular hypertrophy - reverse hypertrophy
what are adverse effects of ACE inhibitors?
cough
dizzyness
can result in angioedema. ACE is responsible for breakdown of bradykinin- a mediator that increases permeability of blood vessels
hyperkalemia
renal insufficiency
what are examples of angiotensin-receptor blockers (ARB)?
Losartan (Cozaar)
Valsartan (DIovan)
Candesartan (Atacand)
what is the mechanism of action of ARBs?
competitive inhibitor of AT-1 receptor of vascular smooth muscle leading to smooth muscle relaxation and decrease vascular resistance
what are indications for the use of ARBs?
as efficacious as ACE inhibitors in tx of HTN when combined with a thiazide diuretic
what are adverse effects of ARBs?
hypotension, generally well tolerated
should be discontinued in second and third trimesters
what are examples of Beta adrenergic blockers?
B1 selective:
Metoprolol (Lopressor)
Atenolol (Tenormin)
Esmolol (Brevibloc)
Non-selective:
Propranolol (Inderal)
what is the MOA of beta adrenergic blockers?
decrease renin production and release in the kidney- ultimately decreasing angiotensin II formation– resulting in decrease of vascular resistance.
other contributing mechanisms including decrease in myocardial contractility
what are indications of use of beta adrenergic blockers?
hypertensive patients with angina, following heart attack (promotes survival)
should be avoided in diabetics as it masks hypoglycemic tachycardia
what are adverse effects of beta adrenergic blockers?
in patients with AC conduction defects, B1 blockers may cause life threatening bradyarrhythmias
abrupt discontinuation of long term B1 blockers use in angina can exacerbate and may increase risk of sudden heart attack
B2 receptors blockade can worsen bronchoconstriction in asthmatic populations.
what are examples of alpha1 adrenergic blockers?
Prazocin (minipress)
Doxazocin (Cardura)
Terazocin (Hytrin)
what is the MOA of alpha1 adrenergic blockers?
interference with the ability of NE (sympathetic neurons) or epinephrine to activate alpha adrenoreceptors on vascular smooth muscle, thus demising their vasoconstriction and growth promoting actions
what are the indications for use of alpha1 adrenergic blockers?
a combination therapy with diuretics
B1 adreoceptor blockers to treat HTN
should not be used alone since they increase the risk of CHF
what are adverse effects of alpha1 adrenergic blockers?
characteristic first dose phenomenon
leads to orthostatic hypotension (seen in 50% of patients)
what are examples of Ca++ Channel Blockers
Verapamil (Isoptin)
Nifedpine (adalat)
Dilitiazem (Cardiazem)
Amlodipine (Norvasc)
what is the MOA of Ca++ Channel Blockers?
block calcium channels in arteriolar smooth muscles, leading to block calcium entry into the cells.
entry of calcium from extracellular fluid to the cytosol is a requirement for smooth muscle contraction
net effect is a decrease in vascular resistance
what are the indications for use of Ca++ channel blockers?
mono therapy for elderly populations with low circulating renin levels
what is the MOA of direct acting vasodilators?
direct relaxation of vascular smooth muscles thus decreasing vascular resistance
what are adverse effects of direct acting vasodilators?
reflex tachycardia
hypotension
fluid retention
hypertrichosis
what are vasodilators used to treat outpatients?
Hydralazine (Apresoline)
Minoxidil (Loniten)
what are vasodilators used in emergency?
Sodium nitroprusside
diazoxide (hyperstat IV)
what are the 2 centrally acting sympatholytic agents?
1- clonidine (catapress)
2- Reserpine
what is clonidine? what is its MOA?
(catapress)
centrall acting sympatholytic agent
MOA:
agonist of alpha2 receptor in brainstem resulting in reduction of sympathetic outflow from CNS – especially in emergency situations
what is reserpine? what is its MOA? Adverse effect?
a centrally acting sympatholytic agent
depletes CNS of NE which lowers BP (pretty dramatically)
MOA:
inhibit vascular storage of NE and dopamine in central adrenergic neurons
adverse effect:
depression
what is CHF?
the inability of the heart to maintain adequate BF to meet the demands of peripheral tissues and itself
among the major causes of mortality
the most common form of CHF is ____? characterized by:?
systolic heart failure
characterized by:
decreased CO
increased pressure and volume loads on R and L ventricles
what are causes of CHF?
uncontrolled HTN
coronary artery diseases
idiopathic cardiomyopathy
what are symptoms of CHF?
orthopnea (SOB/ dyspnea) paroxymal nocturnal dyspnea tachypnea- rapid breathing peripheral edema ankle swelling weight gain hepatomegaly - swelling of the liver
as CO gets worse, what 2 compensatory mechanisms also get worse?
1- increased sympathetic nerve activity
- tacycardia
- vasoconstriction –> increased vascular resistance
2- decreased kidney perfusion
- increased renin release–> increased angiotensin II release–> increased vascular resistance
- decreased urine output –> edema
*really worried about the kidney- fluid is retained–>edema
idea of tx is to slow this down!
what are 2 objectives to therapy?
1- increase CO
2-decrease ventricular filling volume
3- slow pathological remodeling of ventricles
what drugs are used in CHF?
diuretics- to get rid of fluid
vasodilators- to decrease resistance problems with sympathetic activation
inotrophic agents- to stimulate the heart
what is the problem with diuretics for CHF?
development of resistance to the actions of the loop diuretic when chronically used in patients with CHF
how do you overcome the problem of diuretics with CHF?
a thiazide diuretic (Metolazone) can be given either before or with the loop diuretic
the loop is no longer as effective so you add a thiazide
what are thiazides more frequently combined with for CHF?
can be used in mild CHF
most frequently combined with loop diuretics to overcome resistance problem
how can spironolactone be used for CHF?
can be used in combination therapy (K+ sparing)
recent evidence indicates beneficial effects on advanced CHF (promotes survival) independent of its natriuretic effect
What vasodilators are used for CHF?
ACE inhibitors
ARBs
Nitrovasodilators
Ca++ channel blockers
ACE inhibitors for CHF=
first line therapy
shown to promote survival in CHF patients
ARBs for CHF=
used as alternative to ACE inhibitors when side effects of ACE inhibitors are not tolerated
how do nitrovasodilators work for CHF?
to increase BF to the heart (to get more oxygen to heart muscle itself
sodium nitroprusside
organic nitrates- isosorbide denigrate, nitroglycerin
what is the MOA of nitrovasodilators?
release of nitric oxide (NO) - a potent vasodilator
Ca++ for CHF=
second line option- have no been proven as efficacious as other vasodilators in the treatment of CHF
what is the major benefit of using a beta blocker for CHF?
has the ability to slow down pathological remodeling of ventricles (slow down hypertrophy)
recommended for use in moderate forms of CHF where it was shown that they reduce mortality
decreases CO– decreases renin production
what are inotropic drugs used in CHF?
Cardiac Glycosides (digitalis glycosides)
- Digoxin (Lanoxin)
- Digitoxin (Crystodigin)
inotropic= affects force of muscle contraction
what is the MOA of inotrophic drugs?
1- inhibition of Na/K ATPase pump in ventricular myocytes leading to elevation of intracellular Ca++ and increased myocardial contractility
2- potentiation of vagal nerve effects on the heart
(slows the heart by stimulating vagus nerve)
what problems are associated with digoxin use?
**narrow therapeutic index (fine line b/w positive effect and toxicity- has a long half life- have to be very careful about specific dosing
Cardiac arrhythmia (due to inhibition of Na/K pump
A: atrial arrhythmia (atrial fibrillation, sinus bradycardia)
B: ventrical arrhythmia (associated with angina or MI) ***bigger concern
K+ level monitoring during digoxin therapy (hypokalemia and hyperkalemia potentiate digoxin toxicity)
what is the negative chronotropic effect of digitalis glycosides?
decreased heart rate
what are the positive chronotropic effects of digitalis glycosides?
increased CO
increased kidney perfusion
increased urine output
dopamine is a good inotropic because..
it is a good vasodilator
Dobutamine (dobutrex)
what are indications for the use of doputamine?
short term support of circulation in advanced CHF
dopamine is a cardiac stimulant
what is the MOA of dopamine/dobutamine?
inhibitors of phosphodiesterase enzyme leading to stimulation of myocardial contractility and acceleration of myocardial relaxation
also causes a decrease in vascular resistance
how is heart failure staged?
ACC/AHA classification
stages A, B, C, D
based on disease progression
patients cannot revert back to a lower stage
emphasizes preventability
directs treatment approaches
what is stage A of HF?
high risk for developing HF
but no structural heart disease
describe stage B of HF:
structural heart disease is present but no symptoms
-asymptomatic LV dysfunction
describe stage C of HF:
past or current symptoms of HF
CO is increased
tachycardia
describe stage D of HF:
end stage HF
needs transplant
what are non-pharmacologic managements to heart failure?
daily weight monitoring
encourage exercise as tolerated
sodium restriction <1.5 L per day
(sodium and fluid decrease will decrease amount of fluid build up)
what are pharmacologic managements to heart failure?
appropriately manage and treat co-morbid illness
d/c drugs that may contribute to HF
recommend tx options based on ACC/AGA stage
what are treatment options for stage A HF?
stage A= high risk for development of HF
drug therapy to slow disease progression
both classes shown to reduce morbidity and mortality
ACE inhibitors- first line therapy
ARB
what are treatment options for stage B HF?
stage B=asymptomatic structural heart disease
all general measures for stage A
drug therapy
ACE inhibitors or ARB
PLUS
Beta blocker- to decrease BP
what are 3 types of beta blockers?
bisoprolol
carvedilol
metoprolol succinate
what is bisoprolol?
selective beta1 receptor blocker
what is carvedilol?
non selective beta receptor blocker AND alpha adrenergic receptor blocker
what is metoprolol succinate?
selective beta1 receptor blocker
what are common adverse effects of beta blockers?
hypotension
bradycardia
fluid retention
fatigue
what are relative contraindications for the use of BB?
HR <100mm Hg
what are precautions for the use of BB?
asthma/COPD
peripheral vascular disease
what happens if you give too much BB?
fluid retention
what are treatment options for stage C of HF?
stage C= structural heart disease w/ prior or current symptoms
general measures for stages A and B
drug therapy for all patients
- diuretics
- ACE-I or ARB
- BB
drug therapy for selected patients
- aldosterone antagonist
- digitalis
- hydralizaine/nitrates
devices for selected patients:
- biventricular pacing (BivP)
- implantable cardioverter difibrillator (ICD)
loop diuretics for HF:
more potent–> CHF
effective in renal dysfunction
shorter acting: T1/2: 4-6 hours for furosemide
effect potentiated by thiazides
thiazide diuretics for HF:
sustained action–> HTN
only matolazone is effective in renal dysfunction
what is a common adverse effect of diuretics?
urinary frequency
what are contraindications for diuretics?
anuria- failure of kidneys to produce urine
renal decompensation –> renal failure
what are monitoring parameters for diuretics?
electrolytes
renal function
weight
what are aldosterone antagonists?
spironolactone
initial dose: 12.5-25 mg qd
max dose: 25 mg
Eplerenone
initial dose: 25
max dose: 50
what are common adverse effects to aldosterone antagonists?
gynomastia- esp w/ spironolactone
what are contraindications for the use of aldosterone antagonists?
hyperkalemia
what are monitoring parameters for aldosterone antagonists?
renal function
K+
BP
what is the usual dose for digitalis?
0.125-0.25 mg qd
what is the half life for digitalis?
40h
digitalis is excreted by the:
kidney
-maintenance dose depends on the patient
what is the therapeutic range of digitalis?
NARROW
<1.2 ng/ml
the toxicity of digitalis is enhanced by:
quinidine
amiodarone
low K
high Ca
what is the MOA of digoxin?
inhibits Na/K+ ATPase
increases Na/Ca exchange
increases in intracellular calcium
-increased myocardial contractility
what are side effects of digoxin?
visual disturbance, MI, dz, n/v/d
what are precautions for digoxin?
narrow therapeutic index
what are monitoring parameters for digoxin?
serum concentrations
what is the MOA of hydrazine?
direct vasodilation of arterial smooth muscle
reduce afterload
what is the MOA of long acting nitrates?
vasodilation
decrease cardiac oxygen consumption by increasing intracellular cyclic GMP
what are side effects of hydralazines?
reflex tachycardia
lupus
headache
flushing
what are side effects of nitrates?
headaches
what are contraindications for nitrates?
use of PDE-5 inhibitors
head trauma
cerebral hemorrhage
what are monitoring parameters for hydralazines/nitrates?
orthstasis
what are treatment options for stage D HF?
stage D= refractory HF
appropriate measures for stages A, B, C
hospice care?
heart transplant?
what are self care strategies ?
medication adherence
-pill organizer
dietary adherence:
- fluid restriction
- sodium restiction
monitoring of daily weights:
- purchase scale
- keep logbook
what is myocardial ischemia?
insufficient blood flow through coronary arteries to heart leading to imbalance between oxygen supply and demand
what is angina pectoris?
choking and squeezing pain in the chest produced by ischemia
what is MI?
extreme form of ischemia leading to significant cardiac tissue damage and death
what are the 3 types of angina?
1- stable angina (exertional)
2- unstable
3- prinzmetal (variant, vasospastic)
what is stable angina?
exertional
simple blockage of coronary arteries by artherosclerotic lesions
pain and discomfort following exercise or stress
what is unstable angina?
caused by arherosclerotic lesion and/or a clot that can occlude the smaller coronary vessels and is the most common cause of MI
what is prinzmetal angina?
variant, vasospastic
caused by spasm of coronary arteries that are sudden and unpredictable
myocardial oxygen demand depends on?
heart rate
preload, afterload
myocardial oxygen supply depends on?
coronary blood flow
- coronary vascular resistance
- aortic pressure
what drugs are used to treat angina?
organic nitrates –> relaxation of vascular smooth muscles
coronary arteries:
increased BF–> increased oxygen supply
peripheral arterioles:
reduction in afterload –>decreased o2 demand
veins:
reduction in preload–> decrease o2 demand
what are examples of organic nitrates?
nitroglycerine
isosorbide dinitrate
isosorbide monoitrate
amyl nitrite
what happens to organic nitrates taken orally?
subject to first pass metabolism
thereby greatly decreasing their efficacy
what is organic nitrates effect on BP?
can produce severe drops in BP (sometimes fatal) either alone or when combined with other drugs
what is the half life of organic nitrates?
nitroglycerin: 3 min
isosorbide dinitrate: 45 min
sublingual tablets and inhalation sprays of organic nitrate are used for?
immediate relief of angina symptoms (onset of action is 1-2 min)
oral nitrates are used for?
prophylaxis for patients having more than occasional angina attacks
transmucosal or buccal organic nitrates are used for?
short term prophylaxis in anticipation of an angina attack
IV nitroglycerine organic nitrate is used for?
acute management of unstable angina
innervation of the heart and coupling of electrical signaling and muscle contraction:
signal is generated from SA node under the control of sympathetic and parasympathetic systems
signal travels to AV node resulting in atrial contraction
signal enters ventricles, travels through bundle of His and Purkinje fibers leading to ventricular contraction
P wave:
atrial depolarization
QRS complex:
ventricular depolarization
T wave:
ventricular repolarization
atrial fibrillation
skips a p wave
ventricular tachycardia
all over
what are the 4 classes of anti arrhythmic drugs?
Class I- Na+ channel blockers
Class II- beta adrenoceptor blockers
Class III- K+ channel blockers
Class IV- Ca+ channel blockers
what is class I anti arrhythmic drugs?
Na+ channel blockers
Quindine, phenytonin, lidocaine, procainamide
these drugs decreases conduction velocity
what are class II anti arrhythmic drugs?
beta adrenoreceptor blockers
Metoprolol, nadolol, propranolol
antagonize sympathetic nerve activity, decrease SA automaticity, negative inotropic effect
what are class III anti arrhythmic drugs?
K+ channel blockers
bretylium, amiodarone, clofiliu
these drugs extend the duration of AP
what are class IV anti arrhythmic drugs?
Ca++ channel blockers
verapamil, ditiazem
these drugs’ effects are restricted to SA and AV nodes and produce similar effects to class II drugs
what is the MOA of digoxin and digitoxin?
enhance effects of vagus nerve on heart
this results in slowing of SA node, conduction through AV node
cardiac glycosides are used in treatment of atrial arrhythmia associated with tachycardia
