Critical care medications
Sedation
Anesthetic- propofol
Analgesics- morphine, dilaudid , fentanyl
Neuroleptic- haldol
Benzos- versed, valium, ativan- reverse w/ Romazicon
Alpha adrenergic agonists- dexmedetomidine (Precedex), clonidine
Neuromuscular blockades (paralytics)- vercuronium; need vent support,
monitor “trains of 4”
-nifedipine (Adalat, Procardia)
-amlodipine (Norvasc)
-felodipine (Plendil)
-nicardipine (Cardene)
-verapamil (Calan)*
-diltiazem (Cardizem)*
Vasoactive/cardiac drugs
ACE Inhibitors- vasodilation, excretion of Na & H2O, retention of K
-captopril (Capoten)
-enalapril (Vasotec)
-fosinopril (Monopril)
-lisinopril (Prinivil)
-ramipril (Altace)
Cholesterol lowering
Statins- reductase inc’s activity of LDL in liver
-s/e- rash, gas, elevated liver enzymes, rhabdomyolysis (rare)
-lovastatin (Mevacor)
-simvastatin (Zocor)
-fluvastatin (Lescol)
-atorvastatin (Lipitor)
-rosuvastatin (Crestor)
Bile Acid Binding Resins- chol binds w/ bile acids, removed in feces
-s/e- interfere w/ absorption of other drugs (digoxin, thiazide, vanco), GI
complaints- nausea, belching
-cholestyramine (Questran)
-cholestipol (Colestid)
-colesevelam (Welchol)
Niacin- inhibits synthesis & secretion of LDL & inc’s HDL
-s/e- hot flashes & flushing (ASA 30min prior to minimize), high does liver
problems
-Niacin
-Niaspan
Fibric Acid Derivatives- reduce triglycerides & inc HDL
-s/e-may inc effects of anticoagulants & hypoglycemic
-atromid (Clofibrate)
-Tricor (Tricor)
-Lopid (Lopid)
Cholesterol absorption inhibitor- inhibits intestinal absorption
-can be used w/ other antilipidemic drugs, often w/ statins
-ezetimibe (Zetia)
Adranergic agonist- alpha1 vasoconstriction; beta1 inc HR, contractility,
conduction, release renin; beta2 vasodilation, bronchodilation, smooth muscle
relax, glycogenolysis, skeletal muscle contaction; dopamine renal vessel
dilation
-epinephrine (Adrenaline)- alpha1, beta1 & 2
-dopamine (Intropin)- alpha1, beta1, dopamine
-dobutamine (Dobutrex)- beta1
Alpha blockers (sympatholytics)-vessel dilation, smooth muscle relaxation
-prazosin (Minipress)
-doxazosin mesylate (Cardura)
Alpha2 agonist- dec sympathetic outflow dec HR & CO
-clonidine (Catapres)
-methyldopa (Aldomet)
Anticoagulants- prevent clots & fibrin formation
-heparin- antagonist is protamine sulfate
-enoxaprain (Lovenox)
-warfarin (Coumadin)- oral; antagonist Vit K (phytonadione, aquamephyton)
AntidysrhythmicsClass IA Na channel blockers-dec conduction, inc automaticity, dec rate of
repolarization
-procinamide (Pronestyl)
-quinidine sulfate (Quindex)
-disopyramide (Norpace)
-tocainide (Tonocard)
-propafenone (Rythmol)
Class IB Na channel blockers- dec conduction, dec automaticity, inc rate of
repolarization
-lidocaine (Xylocaine)
Class III K channel blockers- dec rate of repolarization, conduction,
contractility & automaticity
-amiodarone (Cardarone, Pacerone)
-bretylium
Endogenous glucoside- dec conduction
-adenosine (Adenocard)
-ibutilide (Corvert)
antiPLT-prevent plt clumping
-aspirin
Angiotensin II Receptor Blocker (ARB)- vasodilation, excretion of Na &
H2O, retention of K
-isartan (Cozaar)
-valsartan (Diovan)
-irbesartan (Avapro)
-candesartan (Atacand)
-olmesartan (Benicar)
Beta blockers- dec HR, contractility & conduction
cardioselective
-metoprolol (Lopressor)
-atenolol (Tenormin)
Nonselective
-propranolol (Inderal)
-nadolol (Corgard)
Ca channel blockers- vasodilation, *dec force of contraction & HR
Cardiac glycosides- inc contraction, dec HR
-digoxin (Lanoxin, Lnoxicaps, Digitek)
Nitrates- dec cardiac O2 demand by dilating veins & dec venous return
-nitroglycerine (Nitrol, Nitrostat)
-isosorbide dinitrate (Imdur)
Thrombolytics- dissolve clots, used in acute MI
-streptokinase- 50-60% reperfusion in 90 min, depletes fibrinogen up to 72hrs,
$500
- anteplase (Activase, tPA)
- eteplase (Retavase)- recombinant tPA, 70-85% reperfusion in 90 min, $2500
MiscDiuretics
Insulin
Steroids
Immunosuppressive
Hormone replacement therapy
Volume expanders
Acid-base disorders
Resp acidosis: hypoventilation, over sedation, head trauma, anesthesia, drug
overdose, neuromuscular disease
Resp alkalosis- hypoxia, anxiety, pulmonary embolism, hyperventilation
Metabolic acidosis- diabetic or alcoholic ketoacidosis, renal failure,
rhabdomyolysis, toxin ingestion (ie: methanol, slicylates) diarrhea
Metabolic alkalosis- steroid therapy, vomiting, GI suctioning, diuretic
therapy, hypokalemia
Weaning parameters:
RR<25, VC 10-15ml/kg, Vt 405,l/kg, NIF >-20
Coronary Arteries:
L coronary artery anterior descending & circumflex; supplies L atrium &
ventricle
R coronary supplies R atrium & ventr, portions of post wall of L ventr, AV
node
Pulsus paradoxus-
S3- turbulence w/in ventr in early diastole; anemia, fever, inf; can be normal
in young & athletes; assoc w/ MI or surgery
S4- diastolic motion & ventr dilation; CAD, HTN, cardiomyopathy
Pericardial friction rub- pericarditis occurs 2-7 days post-op
Murmurs- regurg/stenosis
Electolytes:
K+ (3.5-5.0)-determines conduction velocity & helps confine pacing
HyperK+: K administration, rhabdomyolysis, K sparing diuretics, renal fail:
 depressed AV conductions leads to v-fib or cardiac standstill
-ECG- peakd T wave, widened QRS, pronlonged PR interval
-tx- insulin/glucose (drives K into cell, out of serum), kayexalate (drives K out
of body thru defecation), hemodialysis (removes K from blood)
HypoK+: GI loss, diuretics, chronic steroid use
-ECG- PVC’s, prominent U wave then v-tach/v-fib
-tx- administer K+
Ca+ (4.0-5.0 ionized, 8.5-10.0 serum)- effects vascular tone, myocardial
contractility, cardiac excitability
HyperCa+: bone tumors, endocrine disorders, excessive VitD
-ECG- short QT interval, bradycardia, 1st 2nd 3rd heart block, BBB, potentiates
effect of digitalis, HTN
HypoCa+: critically ill & post-op from blood transfusion, Mg imbalances,
shock, alkalosis dec’d contractility, CO, & hypotension
-ECG- brady to v-tach to asystole; prolonged QT leads to Torsades De Pointes
*low ionized is emergency & requires immediate IV Ca+
Mg+ (1.5-2.0)- ensures transport of Na & K across cell membrane
HyperMg+: very RARE, secondary to renal insufficiency or iatrogenic over tx
HypoMg+: liberates K to extracellular fluid inc’d renal excretion of K &
Ca; insufficient intake, chronic alcohol abuse, dieresis, diarrhea, rapid admin
of citrated blood products (citrate bonds to Mg)- HTN, vasospasm, sudden
cardiac death, acute MI, CHF
-ECG- prolonged PR & QT, presence of U wave, flat T wave, wide QRS,
Torsades
*cannot correct K & Ca if Mg is uncorrected
Cardiac enzymes:
Cardiac specific- Troponin I
-CK-MB: 3 consec draws, 8hrs apart, begins rising w/in 24 hrs of onset of
symptoms, elevated 4-8 hrs of MI, peak 15-24hrs, remain elevated 2-3 days
Nonspecific- Myoglobin- elevated 1-2hrs after
-CK-Troponin T,
-LDH
Hematologic studies:
RBC
Hgb
Hct
WBC
Coagulation
-PT
-INR
-PTT
-ACT
Serum Lipids
Total cholesterol <200
LDL <130 no risk, <100 mild risk, <70 high risk
HDL >40♂ , >50♀
Triglycerides <150
Chemistry
Thyroid
BUN
Creatinine
Liver enzymes
-AST
-ALT
Hemodynamic Monitoring:
MAP 70-110 = SBP + 2DBP / 3
Pulse pressure= SBP-DBP
CVP 2-6 mmHg (R side)
PWP 6-12mmHg (L side)
PCWP <5 dry, need fluid
18-20 onset of pulm congestion
20-25 mod congestion
25-30 severe congestion
>30 pulmonary edema
PVR 37-250(1/6 SVR), aka PAS-pulm art sys press- measure of RV afterload;
-inc’d w/ COPD, pulm HTN, hypoxia, pulm embolus, ARDS, sepsis
SVR 900-1400- measure LV afterload;
-inc’d w/ HTN, hypovolemmia r/t shock, hypothermia, cardiogenic shock
-dec’d fever, septic shock, anemia, anaphylactic shock, cirrhosis, aortic
regurg, acute adrenal insufficiency
SVO2- mixed venous sat, 60-80%
EF 55-70%
ICP <20mmHg
CAD- symptoms occur when plaque occludes 75% of vessel
Angina- stable, unstable, variant, silent ischemia
-stable- tx w/ nitro, 5 min apart, if unrelieved by 3 rd call 911
-unstable- if unrelieved w/ 1 nitro call 911
-variant- Ca channel blockers & nitro
-silent- (diabetics @ risk) nitrates, beta blockers, Ca channel blockers
-MONA- morphine (dec pain & O2 demand), O2 (inc myocardial
oxygenation), Nitro (vasodilation), ASA (antiplt)
-coronary precautions- bed bath, stool softener, limit caffeine & ice water
MI- tx angioplasty, stents, CABG, artherectomy
-complications- sinus brady (post wall)/tachy (ant wall), /ventr dysrhythmias,
AV block, CHF, cardiogenic shock, papillary muscle dysfxn, pulm embolism,
Dressler syndrome, ventr aneurysm, ventr septal rupture, cardiac wall rupture,
pericarditis
-beta blockers after MI due to inc’d risk of a-fib
Heart Fail- systolic (too weak to contract fully, thin walls) vs diastolic
(impaired ventr filling, thick walls)
Chronic causes- CAD, HTN, rheumatic heart disease, congenital heart
disease, cariomyopathy, anemia, bacterial endocarditis, valvular disorders
Acute causes- MI, arrhythmias, PE, thyrotoxicosis, HTN crisis, papillary
muscle rupture, VSD, myocarditis
Right side-most common cause is L side fail “back up of blood”, PE, R ventr
infarct
-s/s- periph or sacral edema, JVD, acites, jaundice, liver tenderness, pulm
HTN
Left side- LV dysfxn blood backs up into pulm veininc’d pulm
pressdec’d COdec’d periph perfusionmay lead to R ventr fail
-s/s-tachypnea, tachycardia, cough, inc’d pulm press, cyanosis, pulm edema,
fatigue, dyspnea, PND, restlessness, confusion, orthopnea, crackles, wheezes
Heart fail tx- ACE inhibitors, diuretics, inotropic drugs (digitalis, beta
adrenergic agonists, phosphodiesterase), vasodilators, beta blockers, nutrition
Pulmonary Edema- alveoli fill w/ fluid
-s/s- breathlessness, anxiety, sensation of suffocation, *pink frothy sputum,
incd RR w/ access muscles, loud gurgling, profuse diaphoresis, skin cold
ashen cyanotic, dec’d CO
-tx- Swan Ganz, diuretics, morphine, vasodilators, nitrates, IABP, digitalis,
positive inotropic agents
Cardiomyopathy
-s/s- angina, exercise intolerance, dyspnea, orthopnea, syncopy
-tx- transplant if EF <10%; drugs: immunosuppressive & anti-rejection
(started during surgery), ABX, antiviral, steroids (long term usediabetes)
*rejection is largest cause of death in 1st year
Hypertrophic obstructive- L ventr stiff, noncompliant, hypertrophied; septum
enlarged; obstructs blood flow from L ventr; impaired L ventr filling
-rapid forceful contractions dec’d CO & preload
-tx- to improve ventr filling by dec’s ventr contractility & relieving LV
outflow obstruction; beta blockers, Ca channel blocker, ICD,
ventriculomyotomy, myectomy, alcohol septal ablation
Dilated Cardiomyopathy (most common)- cardiomegaly, ventr dilation,
impaired sys fxn, atrial enlargement, statis of blood
-causes- ischemic, genetic, idiopathic, r/t valvular disease, inf, viral, alcohol
“alcoholic heart”, cocaine
-s/s- change in exercise tolerance, fatigue, dry cough, dyspnea, PND,
orthopnea, palpitations, anorexia, S3 & S4, tachycardia, pulm crackles,
edema, weak peripheral pulses, pallor, hepatomegaly, JVD, arrhythmias
-tx-palliative, VAD, ICD, transplant, antiarrhythmics (amiodarone, digoxin),
anticoagulants (heparin), nitrates (dec preload & afterload), loop diuretics (dec
preload), ACE inhibitors (dec afterload), Beta blockers (dec afterload)
-monitor kidney fxn, grafts can migrate
Restrictive Cardiomyopathy (least common)- ventr wall rigidity from fibrosis,
inhibits ventr filling may be r/t amyloidosis, sarcoidosis, endocardial fibrosis
-s/s- angina, syncope, fatigue, dyspnea
-tx- transplant; avoid situations that impair ventr filling (strenuous activity,
*dehydration, )
Primary Pulmonary HTN- PAP>20; vasoconstriction, remodeling,
thrombosis all  icn’d PAP
-s/s- exertional CP, dizziness, syncope, R ventr hypertophy
-tx- diuretics, anticoagulants, vasodilators, Ca channel blockers; *Flolan ,
Remodulin, Tracleer, Slidenifil
Secondary Pulm HTN- underlying condition- hypoxemic disorder,
thromboembolic disorders, pulm venous HTN
-s/s- hypoxia vasoconstriction
-tx- treat underlying disorder, Flolan (only to show improvement in
secondary), oxygenate, vasodilate
Endocarditis- inf endothelial surface of heart
-risk- congenital heart disese, valvular heart disease, prosthetic heart valves,
IV drug use (60 times rate)
-s/s- fever, rigor, elevated WBC, cough, pleuritic CP
-tx- prolonged IV ABX, surgery to excise damaged valve
Valvular Disease
Mitral Regurg (insufficiency)- blood backs up from L ventr to L atrium L
atr hypertrophy ind work for L ventr eventual L ventr hypertrophy
-dec CO, inc PAP
-tx- valve replacement
Acute- no time to compensate (can be due to MI) pulm edema, shock
-s/s- new systolic murmur (L clavicular, 5th intercostals, radiates to axilla),
pulm edema, weakness, fatigue, DOE
Chronic- weakness, fatigue, DOE, palpitations, S3 gallop, systolic murmur
Mitral stenosis- valve stiff; L atr vol & press inc, hypertrophy inc PAP R
ventr hypertrophy R heart fail
-dec CO, Inc PAP, risk for emboli
-s/s- DOE, PND, orthopnea, fatigue, weakness, R sided heart fail, crackles,
cardiac arrhythmias, loud S1, diastolic murmur @ apex (put pt lateral w/
scope @ 5th IC, midclavicular)
Aortic Regurg- blood flows from aorta back to L ventr fluid overload
hypertrophy dec myocardial contraction pulm HTN L ventr fail
-acute- trauma, aortic dissection, infective endocarditis
-chronic- congenital, syphilis, rheumatic fever
-s/s- dyspnea, cough, L sided heart fail, pulsus biferiens (rapid rising &
collapsing pulses), blowing diastolic murmur (2nd IC R sterna border), S3
-tx- treat symptoms, valve replacement
Aortic Stenosis-L ventr hypertrophy, inc’s workload, dec CO poor coronary
artery perfusion (ischemia L ventr, L heart fail) inc PAP
-s/s- occur when opening ~1/3 size; *DOE, PND, fatigue, *syncope, *angina,
palpitations, arrhythmias, L sided heart fail, systolic murmur (very harsh),
dec’d CO
*classic symptoms
Tricuspid Stenosis- rarely isolated; periph edema, ascites, hepatomegaly,
diastolic low-pitched murmur w/ inc’d intensity during inspiration
Tricuspid regurg- usually from advanced L side heart fail
Pulmonic valvular disease- uncommon in adults, usually congenital
anomaly; produces R side fail; fatigue, loud midsystolic murmur
Collaborative management- prophylactic ABX for GI/GU surgeries, Na
restriction, anticoagulation, antidysrhythmics, perc balloon valuloplasty,
surgery (valvulotomy, valvuloplasty, annuloplasty, *valve replacement)
Aortic Aneurysm- localized dilation of arterial wall, alteration in vessel
shape & blood flow
Aortic Dissection- column of blood separates vascular layers
often no symptoms, may see abd pulsation or hear bruit
<5cm monitor
>5cm w/ no dissection/problem- open surgical repair, endograft
>5cm w/ dissection- emergent open surgical repair
Post-op- prevent hemorrhage (s/s- low back pain, hyptension), maintain
patency of graft, promote adequate perfusion, prevent infection
Other Vascular surgeries: endarterectomy, stent, fem-pop bypass
Hypertensive emergency- risk of end organ damage, life threatening;
(urgency- serious elevation but does not put pt @ risk for end organ damage)
-s/s- HTN encephalopathy, renal insufficiency, rapid cardiac decompensation,
aortic dissection, pheochromocytoma
-tx- dec MAP 10-20% first 1-2hrs, vasodilatros (nitro, hydralazine),
adrenergic inhibitors (regitine, labatolol, esmolol), ACE inhibitors (enalapril),
Na nitroprusside, felodapam
VAD- persistant cardiac fail, bridge to transplant, destination therapy
-tx- anticoagulation, monitor hemodynamics, pt ed, weaning-gradual dec in
flow rates
-complications- inf, thromboembolism, malfxn
Balloon Pump (IABP)- L ventr fail, unstable angina refactory to meds,
recurrent angina after MI, complications of MI, cardiogenic shock, papillary
muscle dysfxn/rupture w/ mitral regurg, ventr septal rupture, refractory ventr
dysrhythmias
-inflation augments coronary blood flow, deflation dec’s afterload
ECG’s:
ST elevation- ischemia
ST depression- infarction