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217 Cards in this Set

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For each 10mmHg increase in diastolic BP or 20mmHg increase in systolic BP how much does the risk for Cardiovascular disease increase?
double
risks of high blood pressure
heart attack
heart failure (due to ventricular failure)
stroke
kidney disease
What is program that aims to better manage hypertension
JNC 7 joint national committee on prevention, detection, evaluation and treatment of high blood pressure
major risk factors for hypertension
smoking!!!!!!!!!!!!!!!!!
diabetes (HTN and DM both damage smooth muscle of vessels)
males over 55
females over 65 (post-menopausal)
familial CV disease
lipid elevation
obesity
inactivity
organ damage due to HTN
left ventricle hypertrophy, angina,
MI,
coronary angioplasty, stent, graft,
heart failure
stroke/TIA
kidney disease
peripheral artery disease
retinopathy
non drug causes of HTN
sleep apnea
kidney renovascular disease
primary aldosteronism
steroid therapy
cushing's disease
pheochromocytoma: adrenal medulla releases too much epinephrine block alpha and beta receptors
coarction of aorta
Drugs that cause HTN
NSAIDS: Cox 2 inhibitors, block prostaglandin synthesis
cocaine, speed, SANS, decongestants
steroids, cyclosporine, tacrolimus
erythropoietin
licorice (carbenoxolone)
ephedra (alpha/beta agonist)
ma huang
blood pressure goals of therapy
BP under 140/90

under 130/80 if have DM or kidney disease
Pseudo-tolerance
looks like drug is not working, but the body is compensating
2 compensatory reflexes
1. sypathetic reflexive tachycardia

2. Renin-Angiotensin-Aldosterone
Lifestyle modifications for HTN
stop smoking

weight reduction (5-20mmHg/10kg loss)

eat right (8-14mmHg)

reduce sodium (2-8mmHg)

physical exercise (4-9mmHg)

limit alcohol 1-2 drinks/day (2-4mmHg)
Initial drug therapy for HTN
Thiazide: hydrocholorothiazide and indapamide
distal tubule diuretic that recovers Ca and lets Na go

distal tubule job: reabsorb Na and Ca
Drug combinations for HTN
Thiazide diuretic (retain Ca)
+
Ace inhibitor,
or angiotensin receptor blocker,
or beta blocker,
or Ca channel blocker

add drugs until goal pressure
ischemic heart disease drug therapy
start with:
beta blocker
or verapamil or diltiazem (ca channel blockers)
HTN and

Ischemic heart disease MI or post-MI drug therapy
or
heart failure therapy
beta blocker (olols) +
Ace inhibitor (prils/sartans)
LV dysfunction + HTN drug therapy
1.ACE inhibition (pril) +
2. Beta blocker (olols) +
3. spironolactone (Aldosterone antagonist, acts on CT)
4. loop diuretic (furosemide, ethacrynic acid, bumetanide)
diabetic HTN drug therapy
2 or more drugs
1. thiazide diuretic (DCT, indapamide, hydrocholorthiazide)
2. Beta blocker (olol)
3. Ace inhibitor (pril) or angiotensin receptor blocker (sartans)
4. loop diuretic (furosemide, ethacrynic acid, bumetanide)
HTN and stroke drug therapy
ACE inhibitor (pril)
Thiazide (DCT diruretic- indapamide, hydrochlorothiazide)
What is the red carpet effect?
when liver cholesterol is low it creates more LDL receptors and calls cholesterol back
Which types of drugs act on the red carpet effect?
bile acid resins: cholestipol, cholestyramine

HMGCoA inhibitors: statins
What are the goal cholesterol levels?
<100mg/dl

<70mg/dl if high risk: cardiovascular disease, DM, metabolic syndrome, smoking
Which drugs are bile acid resins?
cholestipol

cholestyramine
Which drugs block HMGCoA reductase
Statins

lovastatin
simvastatin
pravastatin
fluvastatin
atorvastatin (newest, potent, long acting, active metabolite)
What are the 3 classes of drugs used to treat high cholesterol
bile acid resins

niacin

statins
What are the bile acid resin drugs and their function
cholestyramine, colestipol

bind bile acids in gut and take them out with cholesterol

the liver makes more LDL receptors (Red carpet)

zero bioavailability- never enter vascular compartment
block absorption of some drugs/vitamins
GI symptoms
Which drug decreases triglyceride assembly?
niacin (nicotinic acid)

SE:
flushing (vasodilation) and itching- give with aspirin to block histamine release
peptic ulcer
myositis: inflammation of voluntary muscle characterized by pain, tenderness, spasm
rhabdomyolysis: breakdown of muscle fibers, toxic to kidney
Which drugs block cholesterol synthesis?
statins

block HMGCoA reductase- rate limiting step in cholesterol synthesis

liver increases the number of LDL receptors

used for high risk patients

SE:
hepatic toxicity
myopathy
rhabdomyolysis
What is the first dose effect?
compensations due to hypotension

sympathetic and renin-angiotensin-aldosterone compensations

reflexive tachycardia

Na and H2O retention
K loss
What is classical/typical angina?
angina due to reduced coronary flow

angina of effort
What is atypical angina?
prinzmetal

caused by vasospasm
Which drugs lower preload (venodilate)?
nitrates
Which drugs lower afterload?
Calcium channel blockers
beta blockers
sympathetic antagonists
Which drugs are used to treat angina of effort?
nitrates (lower preload)

beta blockers, block sympathetic stimulation, calcium channel blockers (lower afterload)
Which drugs are used to treat atypical (prinzmetal's) angina?
calcium channel blockers- relax arterioles

nitrates

NO beta blockers
What is congestive heart failure?
ventricle fails to maintain ejection fraction

pressure backs up and creates venous and pulmonary hypertension and edema
How is congestive heart failure treated?
cardiotonics (digitalis-Ca), dobutamine-beta1, amrinone (cAMP)

diuretics- decrease volume

ACE inhibitor: lose volume, decrease TPR, reverse myocardial remodeling
What are the 4 classes of anti-arrhythmics?
1. Na channel blockers
2. beta blockers
3. K channel blockers
4. Ca channel blockers
How do Na channel blockers work?
elevate the threshold for depolarization and slow impulse conduction
What are some examples of Na channel blockers?
class 1A
quinidine
procainamide

class 1B
lidocaine (IV)
tocainide (oral)
phenytoin

class 1C
flecainide
Class 1A Na channel blockers
Quinidine
procainamide

atrial/ventricular excitation
Class 1B Na channel blockers
lidocaine (IV)
tocainide (oral)
phenytoin

used for ventricular extrasystoles
Class 1C Na channel blockers
flecainide
super effective and dangerous
antiarrhytmic class 2
beta blockers

resist NE and epi effects on SA and AV node
anti-arrhythmic class 3
K channel blockers

delay repolarization in phase 3
prolong phase 2 and AP
prolong refraction

amiodarone
sotalol (beta blocker)
bretylium
anti-arrhythmics class 4
Ca channel blocker
verapamil
diltiazem

SA node sinus tachycardia
AV node paroxysmal supraventricular tachycardia
What does the proximal tubule recover?
Na

NaHCO3
What does the ascending loop recover?
everything
What does the distal convoluted tubule recover?
Na and CA
What does the collecting tubule recover?
aldosterone: recover Na and release K and H

ADH: recover water
How do loop diuretics and thiazides work?
they are weak acids that compete for the organic acid excretion sites in the proximal tubule

uric acid accumulates in the presence of a competing organic acid like lactate (alcohol metabolism related gout) and diuretics
Why do diuretics cause hyperglycemia?
K flows out of cell
K conductance stops when glucose enters
insulin is released

loop diuretics or thiazides lead to hypokalemia outside the cell so there is faster conductance of K out by diffusion, more glucose is needed to turn off the K channel and less insulin is released
ADH (vasopressin)
V1: vasoconstrictor
V2: collecting duct water recovery

desmopressin only does collecting duct water recovery
What is an ADH antagonist?
lithium ion (blocks V2: collecting duct water recovery)
What is lithium induced DI treated with?
desmopressin (not ADH)
Which diuretics act on the proximal tubule?
acetazolamide
Which diuretics act on the ascending loop?
furosemide
ethacrynic acid
bumetanide
Which diuretics act on the distal convoluted tubule?
indapamide (vasodilator)
hydrochlorothiazide
Which diuretics act on the collecting tubule?
amiloride
triamterene

spironolactone- target aldosterone
Which are the urine alkalinizing diuretics?
Acetazolamide
Which are the loop diuretics
furosemide
bumetamide
ethacrinic acid

act on ascending tubule
which are the K sparing diuretics
spironolactone
amiloride
triamterene

act on collecting duct
which are the thiazide diuretics?
hydrochlorothiazide

indapamide (also a vasodilator)
What are the effects of acetazolamide?
Carbonic anhydrase inhibitor
act on proximal tubule
block reabsorption of NA and NaHCO3
recover H creating acidic blood and alkaline urine
acidic blood stimulates respiratory compensation in altitude sickness

used to treat glaucoma
Loop diuretics
furosemide
ethacrynic acid
bumetanide

block recovery of everything

used to treat edema, pulm edema, CHF, hypercalcemia, HTN

ethacrynic acid- ototoxic

furosemide and bumetanide- sulfa sensitivity

hypokalemia, alkalosis, hypovolemia, hyperuricemia, hyperglycemia
Ca sparing diuretics
Thiazides:
indapamide (vasodilator)
hydrochlorothiazide

act on DCT
(DCT recovers Na and Ca)
CALCIUM SPARING
NaCl diuresis

reduce formation of Ca stones, benefit osteoporosis

tx: HTN, CHF, nephrogenic DI
K sparing diuretics
spironolactone- target high aldosterone

amiloride
triamterene

use with thiazide or loop to neutralize K loss
mannitol
osmotic diuretic

used to treat glaucoma or edema
drugs to treat glaucoma
mannitol
acetazolamide
Explain the renin angiotensin system:
when low renal artery BP or when Beta 1 stimulated

JG cells release renin

Angiotensin 1 is converted to Angiotensin 2 by angiotensin converting enzyme (from lungs)

Bradykinin is inactivated by ACE or peptidyl dipeptidase
What are the effects of angiotensin 2?
vasoconstriction
aldosterone release
increase SANS
retain Na and H2O
increase BP
What are the effects of bradykinin?
inactivated by ACE
vasodilator
decrease arterial resistance and increase venous capacitance
proinflammatory: pain, swelling, angioedema
bronchoconstrictor: airway irritability, cough, airway obstruction
What do ACE inhibitors do?
decrease angiotensin 2
increase Bradykinin: cough, resp. irritability, angioedema

dilate arterioles and venules
low aldosterone- reduce BP in patients with elevated PRA
decrease extracellular fluid and blood volume
Name the ACE inhibitors:
direct acting:
captopril
lisinopril

prodrugs:
enalapril
benazepril
Which drugs block the angiotensin 1 receptors?
losartan
valsartan

avoid bradykinin SE
How is Ca released in the cell?
NE binds G protein receptor
PLC activated
PLC causes release of DAG and IP3
DAG activates phosphokinase C
IP3 causes release of Ca from smooth muscle
What does nitric oxide do?
1. enters the cell
2. binds guanylate cyclase
3. GTP is converted to cGMP
4. cGMP causes relaxion of vessel walls by inhibiting calcium
vasodilators
nitrates: isosorbide dinitrate
sodium nitroprusside

hydralazine
minoxidil
diazoxide
causes of high TPR
vasoconstriction
renin-angiotensin
cortisol
sympathetic stimulation
licorice
Na
Ca
What causes high Cardiac output
increased volume (Na hyperaldosteronism, kidney failure)
SANS
pheochromocytoma
renin-angiotensin
What do vasodilators do?
reduce TPR
activate K channels
interfere with Ca channel function
promote NO synthesis by vascular endothelium to target smooth muscle
What are the side effects of vasodilators?
hypotension (excessive vasodilation)

reflex tachycardia: with decreased BP, sympathetic reflex will be invoked and HR will increase

coronary steal syndrome-> angina pectoris

renin-angiotensin-aldosterone compensation
which vasodilator works on the arteriole? and what are the side effects?
hydralazine

minoxidil
Which vasodilators cause excessive hair growth?
minoxidil

nitrate

diazoxide
Which vasodilators act on the venules and arterioles
nitrates

sodium nitroprusside
What are the side effects of hydralazine?
LUPUS syndrome
headache, flushing, dizziness, hypotension, tachycardia, angina pectoris
Which drug is used to reverse emergency hypertension?
diazoxide

causes hyperglycemia and hypertrichosis
How do Ca channel blockers work?
block Ca release from arterioles and heart
cause arterioles to relax
BP drops
heart automaticity and ventricular contractility decrease

used to treat angina and HTN

SE: Hypotension
Calcium channel blockers
Nifedipine
nimodipine

Verapamil
diltiazem
Calcium channel blockers that act on the arteries and heart
verapamil
diltiazem
calcium channel blockers that act only on the arterioles
nifedipine
nimodipine
Which Ca channel blockers resist the sympathetic reflex?
verapamil
diltiazem
What controls sympathetic stimulation
vasomotor center
alpha 2 agonists
clonidine
guanabenz
alpha methyldopa (prodrug)
nonselective alpha antagonist
phentolamine
phenoxybenzamine (irreversible)
alpha 1 selective antagonist
doxazosin
prazosin

relax sphincters
miosis: constrict pupil
lower BP

SE:
1st dose effect: precipitous drop in BP on starting the drug or increasing the dose
postural hypotension
reflexive tachycardia
urinary incontinence/diarrhea
GI hyperactivity
miosis
nonselective beta blockers
propranolol
nadolol
pindolol (ISA)
labetalol (mixed alpha beta blocker)
B1 (cardioselective)blockers
acebutol (ISA)
metoprolol
atenolol
alpha 1 agonists
EPI
NE
cocaine
amphetamine

vasoconstriction
increase TPR, CO, BP
contract GI sphincter, stop gut, retain urine
mydriasis(dilate pupil)
alpha 2 agonist effects
decrease vasomotor action
decrease sympathetic stimulation
inhibit neurotransmitter release
pre-synaptic negative feedback

SE:
CNS depression
rebound phenomenon
low BP
alpha blocker uses
HTN
pheochromocytoma (only allows Beta stimulation)
BPH
epinephrine reversal (hypertension to hypotension)
alpha blocker side effects
loss of TPR- hypotension
congestion
1st dose effect: precipitous drop in BP on starting drug or decreasing dose, postural HTN
reflexive tachycardia
urinary incontinence
GI hyperactivity
miosis
Beta 1 receptor effects
Heart: stimulate contractility, conduction
kidney: release renin-> antiotensin 2 (vasoconstriction) -> aldosterone release
beta 2 receptor effects
bronchodilate
vasodilate
decrease GI tone
convert glycogen to glucose
beta blocker effects
decrease Heart contraction, conduction
decrease renin-angiotensin 2-aldosterone
non-selective antagonize glycogen breakdown and increase GI tone
suppress ventricle arrhythmias
decrease positive feedback at VMC
decrease work in coronary artery disease
nonselective alpha blockers
phentolamine (injectable)

phenoxybenzamine (irreversible)
alpha 1 selective antagonists
doxazosin
prazosin
alpha 2 agonists
clonidine
guanabenz
alpha methyldopa (prodrug)
nonselective beta blockers (drug names)
propranolol
nadolol
pindolol (ISA)- partial agonsit
labetalol (mixed alpha/beta blocker)
&beta;1 blocker drug names
acebutol (ISA)
metoprolol
atenolol
nonselective alpha blocker function
decrease vasoconstriciton
treat HTN
pheochromocytoma

SE: reflex tachycardia, diarrhea, epinephrine reversal
alpha 1 antagonists SE
less reflex tachycardia than non-selective alpha blockers
alpha 2 agonist drugs, effects, and SE
clonidine,
guanabenz,
alpha-methyl dopa

decrease CO and TPR and thus BP
negative feedback inhibition of vasomotor center

SE: CNS depression, dry mouth/eyes/nose, drowsiness, rebound hypertension, tachycardia
alpha 2 antagonists
yohimbime- used for male impotence, increases sympathetic stimulation, can cause HTN
nonselective beta blockers general facts
-olol
decrease renin

used to treat HTN, angina, arrhythmias

SE
receptor upregulation and rebound phenomenon- extreme tachycardia, ventricular arrhythmia
cardiac depression
sedation
diabetic hypoglycemia
beta 1 blockers
AMA
atenolol- less CNS effects
metroprolol,
acebutol: with ISA

use in asthmatics, DM, PVD

decrease renin release

SE:
cardiac depression
rebound phenomenon
mixed beta blocker (alpha and beta)
labetalol

SE:
hypertensive crisis
pheochromocytoma
clonidine withdrawal
rebound phenomenon- upon withdrawal
ganglionic block
mecamylamine

lose dominant tone on an organ

use to treat HTN
NE depleter that blocks biosynthesis
alpha methyl tyrosine

blocks tyrosine hydroxylase and inhibits synthesis of Dopamine, NE, epi

Tx: severe pheochromocytoma

SE: depression, hypotension, extrpyramidal symptoms
NE depletor that blocks storage
reserpine

bind NE and serotonin and block storage

SE: CNS depression (amine hypothesis), GI hyperactivity
NE depletor that displaces NE in vesicles
guanethidine

does not cross BBB

SE: no CNS depression, GI hyperactivity
depolarization cycle
0: Na channels open- depolarize
1: overshoot, Na channels close
2. ca channels open
3. Ca channels close, K channels open
4. Na/K pump resets conc. gradient
Na/Ca pump restores normal Ca levels
effective refractory period
no stimulus regardless of size will cause a response
relative refractory period
a strong enough stimulus will induce a response

can produce arrhythmias
conductance
rate of spread of an impulse
conductance determined by
vmax- rate of phase 0 depolarization (lower vmax, lower conduction)

threshold potential: the less -, the less Na channels needed, the slower the conduction velocity

resting membrane potential: the more negative, the faster the recovery of channels
automaticity
ability to spontaneously depolarize, phase 4 slope

in the heart, the tissue with the fastest phase 4 slope will be the pacemaker of the heart
arrhythmias caused by disturbances in
impulse generation

impulse conduction
factors that increase the slope of phase 4 depolarization
cause tachycardia
-sympathetic
-hyperthyroidism
-atropine (ACH blocker)
-hypokalemia
-digoxin
factors that decrease the slope of phase 4 depolarzation
cause bradycardia

beta blockers
Ca channel blockers
hyperpolarize (supress depolarization)
vagal, parasympathetic activity

muscarinic agonists, acetylcholinesterases

digoxin action on SA or AV node
elevate threshold for depolarization- suppress impulse generation
Na channel blockers

cause bradycardia
early afterdepolarizations
occur in phase 3

can trigger ventricular tachycardia or torsades des pointes

drugs that slow the rate (beta blockers), lengthen QT or action potential duration (class 3, K blockers), and cause hypokalemia (diuretics)
delayed afterdepolarization
phase 4

due to elevated intracellular calcium (digoxin)
hypokalemia- diuretics
excessive catecholamines (sym, hyperthyroidism, drugs)
ischemia (MI, coronary disease)
ventricular tachycardia
3 extra systoles in a row
impulse conduction problems
AV node unloading: AV node normally prevents excessive activity

AV node depression: digoxin, beta blockers (propranolol), artiolar and cardiac calcium channel blockers (verapamil, diltiazem), adenosine

accessory pathway-bypass AV node, avoid everything used to suppress the AV node

reentry: AV node and purkinje system cause a cyclic conduction pathway that depolarizes surrounding tissue, major cause of atrial tachycardias
4 classes of antiarrhythmics
1. Na channel blockers
2. beta blockers
3. K blocker
4. Ca channel blockers
class 1 antiarrhytmics
1. Na blockers
1A: quinidine, procainamide
1B: lidocaine IV, tocainide (oral), phenytoin
1C: flecainide
Sotalol
Class 2 and 3 anti-arrhytmic
Beta and K blocker
AV depressant
Long QT- torsades de pointes
increase AP duration
bretylium
class 3 (k blocking) anti-arrhythmic
depletes NE
decreases BP
use for ventricular ischemic events
Ca channel blocker side effects
bradycardia
asystole
AV depression
vasodilation
hypotension
constipation
arteriolar calcium channel blockers
nifedipine

nimodipine
arteriolar and cardiac channel blockers
verapamil

diltiazem

used for arrhythmias
block Ca channels at SA, AV nodes
decrease conduction
Adenosine
classless anti-arrhytmic
IV- instant, short half-life (8 seconds)
opens K channels in AV node
reverse AV node events

SE: bronchospasm, vasodilation
Digoxin
classless anti-arrhythmic
AV nodal depressant
invokes muscarinic ACH effect
suppress AV node to protect ventricle

SE:
extra ventricular systoles, DADs
ventricular tachycardia esp with diuretic and hypokalemia
AV depression or block- with verapamil (ca channel blocker), propranolol, or adenosine
class 1A anti-arrhytmics
Na channel blockers
Quinidine, Procainamide
decrease vMax
increase effective refractory period
Class 1B anti-arrhytmics
Na channel blockers
target the ventricle
lidocaine, tocoainide, phenytoin
class 1C anti-arrhytmics
flecainide:
super Na blocker, dangerous, last resort, emergency

like 1A: slow Vmax, increase ERP
commonalities between anti-arrhythmics class 2 (beta blockers), 4 (calcium channel blockers), adenosine, and digoxin
all increase AV effective refractory peiod

all used at AV node to protect ventricle
class 3 drugs
K blockers
amiodarone, sotalol, bretylium

increase ERP everywhere
atrial flutter or fibrillation
digoxin- AV depression
verapamil: ca channel blocker (class 4)
beta blocker (class 2)
class 1A: suppress Na driven ectopic focus
supraventricular tachycardia: atrial or AV node reentry circuit
verapamil suppresses AV
other AV depressants
caused by atrial wall reentry

1. inhibit initiation of action with class 1A- quinidine
2. increase refractoriness with class 3: amiodarone
premature ventricular contraction, extra systoles, early after depolarization, delayed after depolarizaiton
may start by extra Ca
Na will cause it to depolarize
lidocaine- class 1B
beta blockers- class 2 if sympathetic, hyperthyroidism, beta 1 drug administration
class 1 drugs
ventricular tachycardia
caused by repeated ectopic depolarizations in conducting tissue or by a conducting path reentry circuit

Na driven

life threatening-cardioversion
lidocaine- class 1B
Class 1A (quinidine or procainamide)
Class 3: K blockers (amiodarone, sotalol, bretylium)
anti-arrhythmic classes that work on ventricle
1, 3
ventricular fibrillation
cardioversion will synchronize the depolarizations and drugs will slow the initiation of such events

treat with
Class 1A (quinidine, procainamide)
Class 1B (lidocaine, tocainide, phenytoin)
Class 3: K blocker (sotalol, amiodarone, bretylium)
digitalis induced arrhythmias
extrasystole or ventricular tachycardia with danger of AV node depression

Class 1B: lidocaine, tocainide, phenytoin, increase AV conduction
congestive heart failure
heart progressively fails to maintain adequate output to support normal blood pressure

progressively fails to move venous return and allows development of high venous blood pressures leading to pulmonary and systemic edema
CHF progression
1. inadequate CO-> decrease in BP
2. HR increases due to low CO
3. resistance in vessels increases
4. BP increases
5. low blood flow to kidney
6. kidney secretes renin-> angiotensin-> aldosterone

excess venous blood
pulmonary and systemic edema
CHF drug targets
1. stimulate ventricle to contract more forcefully
2. use diuretic to improve kidney function and decrease volume
3. vasodilate venous or arteriole side
4. counteract compensations
CHF drug target: stimulate ventricle to contract more forcefully
improve stroke volume improves BP and reduces vasoconstriction of vessels, more blood reaches the kidneys and less renin is released
CHF drug target: use diuretic to improve kidney function
diuretic decreases the volume needed to be pumped, lower work-load for the heart

support the kidney
CHF drug target: vasodilate venous or arteriole side
Vasodilators arterioles:
hydralazine
minoxidil
diazoxide

vasodilate venules and arterioles
Na Nitroprusside
Nitrates
Isosorbide Dinitrate
Counteract compensations
ACE inhibitor- block angiotensin 2 vasoconstriction
block angiotensin 2 receptors: Sartans
block aldosterone: spironolactone
Proximal tubule diuretic: name
Acetazolamide
loop diuretics: names
furosemide
bumetamide
ethacrinic acid
K sparing diuretics
spironolactone
amiloride
triamterene
thiazide diuretics
hydrochlorothiazide

indapamide (also a vasodilator)
Calcium sparing diuretics
hydrochlorothiazide
indapamide (vasodilator)

work on DCT
decrease reabsorption of Na
vasodilate
hypokalemia
hypercalcemia
Loop diuretic drug names and effects
ethacrynic acid (ototoxic)
furosemide (sulfa sensivity)
bumetamide (sulfa sensitivity)

decrease recovery of everything
diuretics that act on the collecting duct
spironolactone- targets aldosterone, K sparing

amiloride
triamterene
retain K
use with loop and thiazide
vasodilator: arteriolar only
hydralazine
minoxidil (always use with vasodilator and beta blocker)
diazoxide (reverse emergency HTN)

decrease afterload
vasodilator: venules
isosorbide dinitrate
sodium nitroprusside

decrease preload
beta blockers used in CHF
metoprolol
carvedilol

usually considered cardio depresants
but MAY SUPPRESS SYMPATHETIC DRIVEN VENTRICULAR TACHYCARDIA
can aggravate digitalis induced depression
Digitalis
blocks Na-K-ATPase
improves calcium contractility in cardiac cells
residual Na decreases the gradient to run the NaCa antiport
Ca remains in the cell
long term improvement in cardiac contractility
AV node depression

SE: ventricular extrasystole, ventricular tachycardia, ventricular fibrillation
AV node depression
difference between digoxin and digitoxin
digitoxin is detoxified by the liver

digoxin is excreted unchanged
beta 1 agonists
dobutamine, NE, epi, isoproterenol

potentiate B1 by improving signaling by cAMP
phosphodiesterase inhibitors
inamrinone (amrinone)

potentiate B-1 action by improving signaling by cAMP
brain natriuretic peptide
nesiritide

increase cGMP
relax smooth muscles in arterioles and venules

short term
AV depressants
beta blockers
Ca channel blockers
adenosine

can aggravate digitalis induced AV depression
Major concept in pharmacology
use drugs with different mechanisms of action and different toxicities
CHF main treatment
diuretics and ACE inhibitor (captopril, lisinopril, enalapril, benazepril)

cardiotonics to support CO
3 drug classes used to treat angina
1. nitrates (venodilate)

2. beta blockers

3. calcium channel blockers
classical angina
stable, classical, typical, angina of effort, lead pipe coronary

coronary blood flow is regulated by perfusion pressure
-limited blood flow adjustment
-heart work that exceeds the limits of blood flow will cause ischemic damage/pain
-induced by cold, stress, exercise
-coronary hypoperfusion can be caused by vasodilator
variant angina
prinzmetal's angina, angina at rest
-atherosclerosis may contribute
-caused by coronary vasospasm
-at rest the predominant tone is parasympathetic
unstable angina
aka crescendo angina
-emergency
-will get worse
-atheromatous disease
-vasospasm
-PLATELET PLUGS AND COAGULATION
-will cause MI
treatment goal for classical angina
reduce heart work
treatment goal for variant angina
reduce coronary vasospasm
treatment goal for unstable angina:
reduce heart work
reduce vasospasm
stop platelets and fibrin
go to the ER
Typical angina: Drug therapy to reduce heart work
reduce preload- venodilate- nitrates

decrease sympathetic drive: Beta blockers

decrease afterload: Ca channel blockers (verapamil, diltiazem, nifedipine)

verapamil and diltiazem also resist cardiac response to sym.
variant angina: drug therapy to reduce coronary vasospasm
vasodilator
venodilate: nitrates
Ca channel blocker

NO BETA BLOCKERS
how do nitrates work?
1. release NO
2. activates guanylate cyclase
3. forms cGMP which dephosphoryates myosin light chain kinase
4. smooth muscles relax
What are the effects of nitrates? and their side effects
venodilation
arteriolar dilation

SE:
dependence
tolerance
headaches
dizziness, fainting, hypotension
Name the nitrate drugs
sodium nitroprusside

nitroglycerin: PO, avoid 1st pass metabolism for rapid onset, many routes of administration

isosorbide mono (longer duration) and dinitrate
What is coronary steal syndrome?
when vasodilators steal perfusion pressure

can cause angina
and sympathetic reflex- tachycardia
Ca channel blockers used in angina
nifedipine
-works at arteriole
-use alone in variant angina or with a beta blocker in common angina
-can cause angina, hypotension, reflex tachycardia, coronary steal
-variant angina- might be able to tolerate tachycardia if they can exercise without angina
Ca channel blockers used prophylactically in variant angina
verapamil, diltiazem

vasodilate heart and arteries
beta blockers are used with other drugs
to prevent reflex tachycardia
heparin
IV anti-coagulant
potentiates antithrombin 3
reversed with protamine sulfate
Warfarin
oral anti-coagulants
blocks clotting factor synthesis by inhibiting recycling of vitamin K (required cofactor)
reverse with vitamin K or clotting factors
fibrinolytics
streptokinase
urokinase
alteplase
promote activation of plasmin (proteolytic enzyme that retracts clots and digests fibrin)
Aspirin
irreversible blocks COX1 and COX2
stops synthesis of thromboxane (platelet aggregation, release response, arterial constriction)
associated with the prevention of an MI
block ADP receptors on platelets
ticlopidine
clopidogrel
binds platelet surface receptors for cell-cell interaction
abciximab
prostacyclin's job
stabilize cell against activation
arterial dilation
inhibits platelet aggregation
lidocaine
IV
used to treat ventricular arrhythmias
class 1B Na channel blocker
minimal toxicity
Amiodarone
#1 drug for ventricular arrhytmias
class 3 (K blocker)
increases APD and ERP
many side effects
bradycardia due to MI
acute MI invokes the vagus M2 receptor

treat with atropine (block ACH)
pulmonary congestion due to acute heart failure
furosemide- rapid reduction of ECF volume
morphine- pain relief
aminophylline: bronchodilation, vasodilation, cardiac stimulation
Pop quiz, hot shot.

low CO, low BP, high venous pressure, acute heart failure, shock

What do you do? What do you do?
vasodilate: arterioles and venules
increase CO:
-dopamine,
-dobutamine: beta 1 agonist
-imarinone and milrinone: block phosphodiesterase, induce cAMP
sildenafil
viagra
blocks phosphodiesterase to increase cGMP and to relax smooth muscle of corpora cavernosa
cGMP is also activated by nitroprusside by NO
therefore, sildenafil can potentiate nitrates to cause severe hypotension or a MI
right ventricular failure
add volume
increase CO and BP
increase Left venricular contractile force: dobutamine (beta 1 agonist), dopamine, imarinone and milrinone (phosphodiesterase inhibitors)
low dose aspirin
80-160mg/day
block platelet thromboxane
does not block vessel prostacyclin (unless dose is too high)
stabilizes platelets
effect lasts 7 days
ticlopidine and clopidogrel
block ADP receptor on platelets
prevent expression of glycoprotein receptor that works in bridging
suppresses platelet aggregation
helps prevent TIA, CVA, MI
always used in angioplasty and stents
Beta blockers use in MI
propranolol and AMA
non ISA
decrease heart work
prevent arrhythmia, angina, ventricular events
Ca channel blockers in MI
diltiazem and verapamil
relax heart and arteries
delay attainment of angina where double product:
HR x systolic BP= DP
What is double product
HR x systolic BP

point of angina
risk factors for a MI
smoking
weight
diet
stress