Cholinergic Agents Generic (Trade) Edrophonium (Tensilon, Reversol) CV effects HR Site/mechanis m ACHase inhibitor (ACH levels) Indication HR(dx

SVT 2ary to AV nodal reentry of bypass tract; superceded by adenosine), dx myasthenia gravis/myasthe nic crises Vagal response, bradycardia, heart block (inferior wall MI/digitalis tx), antidote for cholinergic tx motion sickness, amnesia Contraindication lacrimation, pupillary constriction, spasm of accommodation, diplopia, laryngospasm, bronchocx, bradycardia pyloric stenosis Adverse rxn Bradycardia, hypotension, severe stomach cramps Pharmacokinetics ; v bolus; t~ short acting (minutes) Other Neostigminereverse neuromuscula r blockage;

muscarinic antagonist

agonist

Atropine

HR, AV nodal refractorine ss, vasodilation

Muscarinic antagonist

Dry mouth/skin, delirium, tachycardia, flushing

iv bolus; t~ mod, ~2.5 hr

dose=0.51mg (<0.5 mg may paradoxically HR)

Scopolamine

Slight HR

muscarinic antagonist

glaucoma

dry mouth, drowsiness, blurred vision, pupillary dilation, CNS (disorientation, memory disturbances, dizziness, restlessness, hallucinations, confusion).

transcutane ous; iv, t = 4.8 hr

crosses blood brain barrier

Via BPT

Rhythmic Drugs

Generic (Class)

Procainam ide (IA) Ina, Ik

Na+ = Conduction velocity (CDV) and Excitability (EXC) K+ = Eff Refractory Period (ERP) and Action Potential Duration(APD) Potency: IC>IA>IB channels available to response acts mostly on tissue that is not normal w/ lower safety factor (normal fast response tissue has high safety factor) For Na Channels: Potency of drug if : Depolarized and HR For K+ Channels: Potency of drug if : HR and hypoK,Mg

CV effects RED = acts on fast response Blue = acts on SLOW response

Site/mechan ism

Indication Fast response Tissue = ERP

Contraindication Adverse rxn

Pharmacokinetics

block open or inactivated Na+ APD, ERP CDV, EXC

prevents reentry intermediate speed Ina

ectopic arrhythmias ventricular arrhythmias

CNS SEs little effect on normal lupus erythematosuslike syndrome in 25-30% of pts

PO short half life

Lidocaine (IB) Ina

block open or inactivated Na+ channels shortens phase 3 repolarization APD block open or inactivated Na+ channels markedly slows phase 0 depolarization in Purkinje and myocardial cells ( threshold) thus causes marked slowing of conduction in all cardiac tissue slow speed has effects even at nl HR INa APD w/o altering Phase 0 or the resting potential

fast speed INa

ventricular arrhythmias

IV dealkylated and eliminated by liver PO

Flecainide (IC) Ina

can be proarrhythmo genic

only for refractory ventricular arrhythmias

Dofetilide (III) Ik

use dependence (work better in frequently depolarizing tissue)

phase 3 repolarization so ERP No efxs on EXC

can also be proarrhythmic by generating early afterdepolarizations torsade de pointes Depress conduction and excitability in slow response tissue

Verapamil (IV) Ica

Ca channel blockers

(AV node, SA node) Atenolol (II) Ica Adenosine Ica, IkACH -Blockers Purinergic receptor agonist outward Ik hyperpolarization EXC (ICa, IK, IF) SA automaticity AVN: cond vel, ERP, coronary and cerebral vasodilation BLOCK Na+/K+/ATPase [Ca]i Upward and leftward shift of starling pharmacolo gic stress test dilate coronaries: half life ~10s IV

suprventricular tachycardias ( AVN CDV and ventricular response)

Digoxin Ica, IkACH ALWAYS CHECK K+ levels

Rate ctrl of A-fib w/ rapid ventricular response (CV) Symptomati c HF despite medical tx (not first line) Can be combined with other drugs

DIG 4 it down low Mg, K, BO Hypothyoridism Hypoxia Abs: Dig toxicity Relative: advanced AV block w/o pacemaker, Bradycardia/sick sinus, Ventricular , arrhythmias/tachy cardia, WPW w/ a-fib

arrhymias Vtach and vfib, SVT, PACs, PVCs MIs Nausea, vomiting, diarrhea, depression, hyperestrogenism, scotomas, blurry vision

RENAL EXCRETION Goal levels: 0.5-1 to achieve benefit and avoid mortality MANY DRUG-DRUG interactions Tx Toxicity: Fab antibody

Adrenergic agonists (pressors & inotropic agents)

Adrenergic Agonists Generic (Trade) CV effects

Muscarinic Agonists Site/mechanism Indication Contraindicati on Adverse rxn Pharmaco-kinetics

ALL IONOTROPES act by Ca (Via cAMP)

Digoxin ALWAYS CHECK K+ levels

CO, LVEF, LVEDP Exercise tolerance, Natriuresis Neurohormor nal activation Plasma NE, PNS, RAAS activity vagal tone Normalize arterial baroreceptors

BLOCK Na+/K+ pump [Ca]i Upward and leftward shift of starling

Rate ctrl of Afib w/ rapid ventricular response (Dig slows down AV node) Symptomatic HF despite medical tx (not first line) Can be combined with other drugs

DIG 4 it down low Mg, K, BO Hypothyoridism Hypoxia Abs: Dig toxicity Relative: advanced AV block w/o pacemaker, Bradycardia/sick sinus, Ventricular , arrhythmias/tac hycardia, WPW w/ a-fib angina, CHF, ischemia (renal, bowel, extremities:fing ers, toes) Arrhythmias, narrow angle glaucoma, local anesthesia of certain areas, e.g., fingers, toes

arrhymias Vtach and vfib, SVT, PACs, PVCs MIs Nausea, vomiting, diarrhea, depression, hyperestrogenis m, scotomas, blurry vision

RENAL EXCRETION Goal levels: 0.5-1 to achieve benefit and avoid mortality MANY DRUG-DRUG interactions Tx Toxicity: Fab antibody

Phenylephri ne (neosynephr ine) Epinephrine

BP, HR, CO

1 agonist baroreceptor reflex causes vagal , causing HR , 1, 2 agonist nonselective

Hypotension, sepsis

cardiac ischemia, mesenteric/periph eral vascular ischemia, angina arrhythmias, tachycardia, ischemia, tremulousness, insomnia, anxiety nervousness, palpitations, angina, platelet aggregation/infa rction, tachycardia, cardiac arrhythmias, excitation, tremulousness, insomnia, nervousness, palpitation, angina.

Iv bolus/infusion; t~

BP (), HR (1), Cx, CO

asthma, anaphylaxis, After bypass/resusc itation, prolong local anesthetic

iv bolus/infusion; t~ VERY short acting

Ephedrine

BP, HR, Cx

- direct & indirect (release NE)

Hypotension/br adycardia, asthma

hyperthyroidism , HTN

im, iv bolus; t~ short

Norepinephr ine (Levophed)

BP, Cx, HR CO no change

, -1>2 agonist VC, modest inotrope NE>E selectivity

refractory hypotension, sepsis

Dopamine (Intropin)

HR, Cx

Dobutamine (Dobutrex)

Cx

DA, -1>2, agonist (Dose-dpt efx) DA1 (LOW;postsynaptic) VD (Vasodilate renal, mesenteric, coronary, cerebral) DA2/Indirect (MID; pre-synaptic) via inhibition of NE reuptake 1, (High HR, CO) 1>2 agonist pure inotrope, AL (afterload) little effect on HR, BP Racemic (net 1 mixture of LEVO (1, 1) DEXTRO (1) -1,2 agonist SA/AV node, HR, Pulmonary VR, powerful chronotrope

Cardiac failure (esp hypothesive pts)

BP 2o hypovolumemi a, mesenteric/peri pheral vascular ischemia ventricular arrhythmias, pheochromocyto ma

ischemic injury, bradycardia, substernal pain

iv infusion; t~ med acting

Ectopy/arrhythmia s, angina, tachycardia, HTN, palpitations, dyspnea, naurea/vomit, infiltration @ IV site can cause necrosis/gangrene

iv, t = 2 min Titratable; short T1/2 Antidote : phentolamine

Cardiac failure (esp normotensive pts)

ventricular arrhythmias, mortality in Decompensated HF

Isoproteren ol (Isuprel)

HR, Cx, CO BP

heart block, heart transplant, pulm htn, bronchospasm

tachyarrhythmia s, tachycardia or heart block caused by digitalis, ventricular arrhythmias, angina

Clonidine (Catapres)

HR, BP

Milrinone More potent

BP

-2 agonist acts on CNS -2 receptors causing a reduction in sympathetic tone PDE III Inhibitor cAMP Ca++ + inotrope

htn

tachycardia, ventricular arrhythmias, HYPOTN PRECIPITATE angina (used for dx of angina) palpitations, dyspnea, naurea/vomit, palpitations, angina, nervousness, headache, dizziness, tachycardia, VT, pulmonary edema, HTN, hypotension Confusion, hypotension, dry mouth ventricular arrhythmias (esp by ORALs, not

iv infusion; t = 2 min 2-3ug/kg/min; titrate up Inhibited by blockers!

iv bolus/infusion; t~ short acting, 5 min

PO, transdermal, iv; t~, cross BBB into CNS T ~ 2.3 hrs Give bolus, then continuous infusion

IV and PO

actually shown to mortality in CHF

more selective>> Amrinone

MLC phosphorylation peripheral vasodilation not widely used Cardiac Glycosides blocks the Na+/K+ pump [Na+]in make Na+/Ca++ exchanger less effective [Ca++]in o may see delayed afterdepolarizations as more Na+ also favors more Ca++ entry [Ca++]in is a positive feedback signal for more Ca++ to enter NE (release and block reuptake) [H+]in via the Ca++/H+ exchange so get even more Ca+ + Electrophysiologic Effects: PO GI absorb (60-80%) Area SAN atrium AVN Non-Toxic sinus rate none cdxn time (antiarr) automaticity vagal tone SNS activity refractory period inotropy direct effect APD (delay repol) (ST seg changes)

efficacious, many not safe) Enoximone is safe but not efficacious thrombocytopen ia

80% renal excretion NO TACHYPHYSLAXIS

Amrinone Digoxin supraventricula r tachyarrhythm ias CHF II, III, IV a fib, rapid ventricular resp in AMI CO, LVEF, LVEDP Exercise tolerance, Natriuresis Neurohormornal activation Plasma NE, PNS, RAAS activity vagal tone Normalize arterial baroreceptors

Toxic sinus arrest cdxn, atrial tachyarr AV block bradycardia

Ventricl es PF/VM

SNS tone automaticity (v-tach/fib) phase 4 automaticities

interactions: quinidine, verapamil,

amiodarone levels abx levels (bacteria metabolize) Digitalis Toxicity: o N/V o vasoconstriction o neurologic sxs o hormonal/sexual dysfxn o characteristic rhythm changes (get whatever you didnt have before) reverse toxicity with digibind

Dopamine

Dobutamine

immediate biosynthetic precursor of NE! direct effect: 1 receptor (+ inotrope) indirect effect: NE vasodilate: DA1 receptor diuresis: DA1 receptor 1, 2, agonist 1, -- + inotropy in heart counteract each other in periphery PDE Inhibitors -- cAMP Ca++ influx in heart + inotrope MLC phosphorylation peripheral vasodilation

effects of DA are antagonized by

blockers! at high does dilation is reversed and vasoconstrict adverse effect: arrhythmia

Amrinone Milrinone

adverse effect: arrhythmia o speed up SAN, AVN, shorten the refractory period of atrial and ventricular muscle dobutamine preferred in refractory heart failure not widely used thrombocytopenia

actually shown to mortality in CHF

IV and PO SE: ventricular arrhythmias

B-blockers Generic (Trade)

CV effects

Site/mechanis m Note that lipid solubility mitigates CNS efx Nonselective 1, 2 antagonist

Indication CHF, MI/angina, Arrhythmias, HTN

Contraindication If has SNSmetic not good for angina

Adverse rxn

Pharmaco-kinetics

Propranolol (Inderal)

HR, Cx

htn, angina/MI, SVT, ventricular arrhythmias, hypertrophic

Pts w/ airway disease cardiogenic shock/CHF, sinus bradycardia.

HR, CHF, heart block; hypotension, weakness, fatigue

PO,iv; t~ 4hrs, med acting

Labetalol (Normodyne) Carvedilol (Coreg )

HR, BP, Cx HR, Cx

1, 1,2 antagonist Nonselective + 1, 1,2 antagonist selective 1 antagonist

subaortic stenosis HTN, aortic dissection HTN, Congestive heart failure 1 mediates vasodilation Tachycardia, atrial flutter or fibrillation, paroxysmal supraventricular tachycardia, HTN, angina, MI

bronchial asthma, cardiac failure, heart block, severe bradycardia sinus bradycardia, cardiac failure

Esmolol (Brevibloc)

HR

HR, cardiogenic shock, acute bronchospasm

postural hypotension, bradycardia, impotence bradycardia, congestive heart failure; peripheral edema, heart block, dizziness Bradycardia, AV block, cardiac arrest, dizziness, hypotension. bronchospasm, bradycardia, palpitations, CHF, peripheral edema, depression, nightmares no CNS effect, no lipophilic

PO, iv bolus/infusion; t~ med acting PO, t~8 hrs, long acting expensive iv infusion only; t~ in min very expensive PO, iv; t~4 hrs, med acting expensive

Metoprolol (Lopressor)

HR, Cx

selective 1 antagonist

sinus bradycardia, heart block, cardiogenic shock, cardiac failure

Atenolol

HR, Cx

selective 1 antagonist

HTN, angina, MI

PO, long duration (q1d)

Alpha-blockers Generic CV effects (Trade) Prazocin BP (arterial (minipress) & venous dilation)

Site/mechanis m 1 >>2

Indication 3rd line Htn, urinary bladder voiding dysfunction pheochromocyto ma pheochromocyt oma

Contraindication BP, mesenteric/periphe ral vascular ischemia BP BP

Adverse rxn Dizziness, headache, fatigue

Pharmacokinetics PO, iv; t~ med

Other

Phentolamine (Regitine, Vasomax) Phenoxyben zamine (Dibenzyline )

BP BP

1,2 antagonist 1,2 noncompetetiv e antagonist

Dizziness, headache, fatigue hypotension, dizziness, fatigue, nasal congestion, orthostatic sinus tachycardia, weakness

Doxazocin and Terazocin - pure a1, ( longer duration, slower onset) PO, iv; t~ med acting iv; t~ long acting

Drugs for Angina Generic (Trade) ONLY alleviate Sx DO NOT Tx disease Organic nitrates CV effects Site/mechanis m Indication Contraindication/ Adverse rxn Pharmacokinetics Other

Vasodilators 1. peripheral venodilation preload (less blood return),afterload (SVR) myocardial O2 demand antithrombotic and anti-inflammatory Cardiac depressants and vasodilators nondihydropyridines act on the heart bind while the channel is OPEN HR, intracardiac conduction, cardiac contractility also peripheral action NO cGMP phosphorylation (inhibition) of MLCK prevent SMC ctxn

used for stable angina, unstable angina (antiplatelet), variant angina, cyanide antidote, acute CHF, AMI (controversial, used IV) (coronary artery dilation is not significant)

tachyphylaxis (rapid tolerance develops), interaction w/ sildenafil, action limited to peripheral vasculature, cant withdraw quickly adverse effects: 2/2 CV effects

converted to NO inside endothelial cells hep metabolism o SL: rapid onset o TD: for prevention o IV: rapid onset o PO: first pass effect, prevention

Ca blockers Verpamil paroxysmal supraventr icular dysrhythm ias

1,2 antagonist most profound myocardial effects effective for angina

pheochromocytoma

BP

PO, iv; t~ med acting

Diltiazem

Nifedipine

dihydropyridine act while chnnel is resting affects VSMCs peripheral

lowest incidence of SEs not a great anti-HTN drug can cause a reflex tachycardia use w/ blocker to

vasodilation SVR prevent arterial vasospasm

-Blockers

prevent angina excellent for vasospasm (Printzmetal s angina) highest incidence of SEs contraindica ted post-MI, CHF

Drugs for HTN Generic (Trade) Organic nitrates ONLY alleviate Sx DO NOT Tx disease CV effects Site/mechanis m Indication Contraindication/ Adverse rxn tachyphylaxis (rapid tolerance develops), interaction w/ sildenafil, action limited to peripheral vasculature, cant withdraw quickly adverse effects: 2/2 CV effects Pharmacokinetics Other

Vasodilators 1. peripheral venodilation preload (less blood return),afterload (SVR) myocardial O2 demand

NO cGMP phosphorylation (inhibition) of MLCK prevent SMC ctxn

used for stable angina, unstable angina (antiplatelet), variant angina, cyanide antidote, acute CHF, AMI (controversial, used IV) (coronary artery dilation is not significant)

converted to NO inside endothelial cells hep metabolism o SL: rapid onset o TD: for prevention o IV: rapid onset o PO: first pass effect, prevention

antithrombotic and anti-inflammatory

Thiazide (hydrochloro thiazide, metolazone, chlortalidon e) lithium)

first line rx for elderly, AA effective and inexpensive relatively easy to take useful in combination

Renal insufficiency (not useful) T2D pts

-Blockers Captopril

arterial and venous vasodilation and natriuresis block ant ATI can block ACE and nonACE generated ATII no effect on bradykinin clearance vasodilation used in HTN Block AT1-Rs

used in HTN, CHF

Captopril cough in CI in Pregnancy

Bilateral renal artery stenosis

PO, TID dosing 5% angioedema

Losartan competitive AT II blocker

CI in Pregnancy

-blockers ACE ARB Lasix (thiazides) DIG Hydralazine, nitrates PDEIII inhibitors (milirone) CCBs (amlodipine) Dihydropyridine Aldactone

mortality YES YES YES NO NO YES NO (may ) NO mortality NO YES

SEs HR, block AV conduction, HB Coughing, K, Creatinine, angioedema, K, Creatinine, angioedema, hypovolemia,K, Na, renal failure Arrythmias, LUPUS-like syndrome, BP HR, BP Fluid retention Gynecomastia,

Generic (Trade) Atorvastati n (Lipitor)

CV effects

Site/mechanism

Indication

Contraindication / Adverse rxn when drug is introduced get small in intrahepatic cholesterol liver senses this and upregulates LDLR LDL removal from blood

Pharmacokinetics

Other

when drug is introduced get small in intrahepatic cholesterol liver senses this and upregulates LDLR LDL removal from blood

VLDL: - or LDL: HDL: (unclear mechanism) used for hypercholesterolemia (polygenic and monogenic heterozygous), combined hyperlipidemia adverse effects: well tolerated hepatotoxicity (in 1%, dose related) myopathy (v. rare) VLDL: LDL: ,-, HDL: TG: well tolerated used for hypercholesterolemia adverse effects: not fun to take constipation, bloating, flatulence, etc. interfere w/ other drug absorption Related drug: Ezetimibe which just blocks the cholesterol transporter at the intestine (NPC1L1) VLDL: -, LDL: HDL: reduces hepatic synthesis of VLDL

Atorvastatin (Lipitor)

VLDL: - or LDL: HDL: (unclear mechanism) used for hypercholesterolemia (polygenic and monogenic heterozygous), combined hyperlipidemia adverse effects: well tolerated hepatotoxicity (in 1%, dose related) myopathy (v. rare)

Other Gemfibrozi l (fibrates)

Cholestyra mine

PPAR agonist Block lipolysis LPL activity hepatic synthesis and secretion of VLDL HDL bile acid sequestrant PO, remains in intestine and binds bile acids excretion

Other Gemfibrozil

Cholestyramine

PPAR. LPL activity hepatic synthesis and secretion of VLDL HDL bile acid sequestrant PO, remains in intestine and binds bile acids excretion

VLDL: LDL: ,-, HDL: TG: well tolerated used for hypercholesterolemia adverse effects: not fun to take constipation, bloating, flatulence, etc. interfere w/ other drug absorption Related drug: Ezetimibe which just blocks the cholesterol transporter at the intestine (NPC1L1) VLDL: -, LDL: HDL: -

Nicotinic Acid (Niacin)

mechanism unknown

DRUGS FOR HTN Hydrochlorothiazi de

diuretic: urine production

naturetic: Na+ excretion kalluretic: K+ excretion believed that the long term effects attributed to a in peripheral vascular resistance

PO and IV absorption: small intestine distribution: wide and bound to plasma proteins excretion: renal (alter dose in elderly b/c renal fxn means blood levels) o can dose to SEs w/o efficacy widely used a first line tx 50% responder rate w/ monotherapy synergy w/ all other classes qd dosing African Americans and elderly respond best adverse effects: pee a lot o TG and LDL (short term) o plasma glucose and insulin resistance (careful in diabetics) o contraindicated in sulfa allergy o electrolyte disturbances

avoid in: sulfa allergy, hypovolemia,

hyponatremia, gout (retain uric acid) Potassium Sparing Diuretic Spironolactone inhibits the action of aldosterone (competitive antagonist) Na+ absorption and K+ excretion Blockers (Class II) Atenolol selective 1 Metoprolol HR, contractility Propanolol non-selective antagonist HR, contractility

antiandrogenic effects gynecomastia

new $$$ version avoids this: Eplerenone

Carvedilol Labetalol Esmolol

-1 and -1 blocking activity HR, BP, contractility selective 1

used in HTN, angina, MI used in HTN, angina/MI, SVT, ventricular arrhythmias, hypertrophic subaortic stenosis contraindicated in cardiogenic shock/CHF, sinus bradycardia adverse rxns: hypotension, weakness, etc.; reversible mental depression, impotence PO, IV; half life 4hrs hepatic P450 metabolism used for HTN, slows progression of CHF used in aortic dissection used in tachycardia, atrial flutter/fibrillation,

 HR

PSVT, myocardial ischemia short acting metabolism relies on erythrocyte esterases (not renal/hepatic) used in HTN, CHF adverse effects: Captopril cough in 5% o angioedema o PO, TID dosing

ACE Inhibitors Captopril

arterial and venous vasodilation and natriuresis

Angiotensin II Antagonist Losartan competitive AT II blocker used in HTN can block ACE and non-ACE target AT1 subtype generated ATII no effect on bradykinin clearance vasodilation Calcium Channel Blockers (Class IV) Ca++ makes smooth muscle contract, makes SAN and AVN spontaneously depolarize antiarrhythmic effects: o have greatest effect in slow response tissue (SAN, AVN) o the ERP of the AVN can block reentrant tachycardias o ventricular response to atrial tachycardia o in fast response tissue they contractility, triggered activity HTN effects: o dont affect skeletal muscle which relies on intracellular calcium, only affect SMCs and myocytes o act on the L-type Ca++ channel accentuate lithium toxicity Verpamil non-dihydropyridines act on most profound myocardial effects the heart paroxysmal effective for angina supraventricul bind while the channel is OPEN ar HR, intracardiac dysrhythmias conduction, cardiac Diltiazem lowest incidence of SEs contractility also peripheral not a great anti-HTN drug action Nifedipine dihydropyridine act while can cause a reflex tachycardia chnnel is resting use w/ blocker to prevent angina affects VSMCs peripheral excellent for vasospasm (Printzmetals vasodilation angina) SVR highest incidence of SEs prevent arterial vasospasm contraindicated post-MI, CHF

ANTIHYPERLIPIDEMIC DRUGS diet and exercise first! hyperchylomicronemia hypercholesterolemia (LDL) combined hyperlipidemia (LDL and VLDL) dysbetalipoproteinemia (IDL) hypertriglyceridemia (VLDL) mixed hypertriglyceridemia (IDL and VLDL)

Statins are HMG CoA-Reductase Inhibitors Atorvastatin when drug is introduced get small (Lipitor) in intrahepatic cholesterol o liver senses this and upregulates LDLR o LDL removal from blood

VLDL: - or LDL: HDL: (unclear mechanism) used for hypercholesterolemia (polygenic and monogenic heterozygous), combined hyperlipidemia adverse effects: well tolerated o hepatotoxicity (in 1%, dose related) o myopathy (v. rare) VLDL: LDL: ,-, HDL: TG: well tolerated used for hypercholesterolemia adverse effects: not fun to take o constipation, bloating, flatulence, etc. o interfere w/ other drug absorption Related drug: Ezetimibe which just blocks the cholesterol transporter at the intestine (NPC1L1) VLDL: -, LDL: HDL: effective at high doses (2-8g/day) VLDL: LDL: HDL: Lp(a): used for: hypercholesterolemia, type III

Other Gemfibrozil

Cholestyramine

PPAR. LPL activity hepatic synthesis and secretion of VLDL HDL bile acid sequestrant PO, remains in intestine and binds bile acids excretion

Nicotinic Acid (Niacin)

mechanism unknown reduces hepatic synthesis of VLDL

dyslipidemia, hypertriglyceridemia, combined hyperlipidemia contraindicated in diabetes glucose intolerance

Case I: Idiopathic dilated cardiomyopathy

Case II: Acute CHF, Goal: LA Pressures

vs chronic:

Case III: Preventative Therapy AA: THiazides + RAAS ACE-I/ARB