ICU MEDICATIONS

Figure 11-1 ACLS pulmonary edema, hypotension or shock algorithm

(Adapted from ACLS 2005 Guidelines)

ANTIBIOTICS

The following tables of spectra of activity for different antibiotics are generalizations. Sensitivity data at your own institution should be used to guide therapy.

Penicillins
Generation	Properties	Spectrum
Natural (eg, penicillin)	Some GPC, GPR, GNC, many anaerobes (not Bacteroides)	Group A strep, Enterococci, Listeria, Pasteurella, Actinomyces, Syphilis
Anti-staph (eg, nafcillin)	Active vs. PCNase-producing Staph Little activity vs. Gram ⊖	Staphylococci (except MRSA) Streptococci
Amino (eg, ampicillin)	Penetrate porin channel of Gram ⊖ Not stable against PCNases	E. coli, Proteus, Listeria, H. influenzae Salmonella, Shigella, Enterococci
Extended (eg, piperacillin)	Penetrate porin channel of Gram ⊖ More resistant to PCNases	Most GNR incl. Enterobacter, Pseudomonas, Serratia
Carbapenems (eg, imipenem)	Resistant to most β-lactamases	Most Gram ⊕ & ⊖, incl. anaerobes; not MRSA or VRE
Monobactams (aztreonam)	Active vs. Gram ⊖ but not Gram ⊕	Gram ⊖ bacterial infxn in Pt w/ PCN or Ceph allergy
β-lact. inhib. (eg, sulbactam, clavulanate)	Inhibit plasma-mediated β-lactamases	Adds staph, B. fragilis, & some GNR (H. flu, M. cat, some E. coli); intrinsic activity against Acinetobacter

Cephalosporins
Resistant to most β-lactamases. No activity vs. enterococci.
Gen.	Spectrum	Indications
1st (eg, cefazolin)	Most GPC (incl. staph & strep, not MRSA); some GNR (incl. E. coli, Proteus, Klebsiella)	Used for surgical Ppx & skin infxns
2nd (eg, cefuroxime, cefotetan)	↓ activity vs. GPC, ↑ vs. GNR. 2 subgroups: Resp: H. influenzae & M. catarrhalis GI/GU: ↑ activity vs. B. fragilis	PNA/COPD flare Abdominal infxns
3rd (eg, ceftriaxone, ceftazidime)	Broad activity vs. GNR & some anaerobes. Ceftazidime active vs. Pseudomonas.	PNA, sepsis, meningitis
4th (eg, cefepime)	↑ resistance to β-lactamases (incl. of staph and Enterobacter)	Similar to 3rd gen. MonoRx for nonlocalizing febrile neutropenia
5th (eg, ceftaroline)	Only class of cephalosporin with MRSA activity. NOT active vs. Pseudomonas.	MRSA. Not 1st line for MRSA bacteremia.
Combination (eg, ceftolozane-tazobactam, ceftazidime-avibactam)	MDR GNRs, incl. Pseudomonas. Ceftaz-avi has activity vs. some carbapenemases.	Complicated UTIs, complicated intra-abdominal infections.

Other Antibiotics
Antibiotic	Spectrum
Vancomycin	Gram ⊕ bacteria incl. MRSA, PCNase-producing pneumococci and enterococci (except VRE)
Linezolid	GPC incl. MRSA & VRE (check susceptibility for VRE)
Daptomycin
Quinolones	Enteric GNR & atypicals. 3rd & 4th gen. ↑ activity vs. Gram ⊕.
Aminoglycosides	GNR. Synergy w/ cell-wall active abx (β-lactam, vanco) vs. GPC. ↓ activity in low pH (eg, abscess). No activity vs. anaerobes.
Macrolides	GPC, some respiratory Gram, atypicals
TMP/SMX	Some enteric GNR, Stenotrophomonas, PCP, Nocardia, Toxo, most community-acquired MRSA
Clindamycin	Most Gram ⊕ (except enterococci) & anaerobes (↑ resis. to B. fragilis)
Metronidazole	Almost all anaerobic Gram, most anaerobic Gram ⊕
Doxycycline	Rickettsia, Ehrlichia, Anaplasma, Chlamydia, Mycoplasma, Nocardia, Lyme
Tigecycline	Many GPC incl. MRSA & VRE; some GNR incl. ESBL but not Pseudomonas or Proteus.

FORMULAE AND QUICK REFERENCE

CARDIOLOGY

“Rule of 6s” for PAC: RA ≤6, RV ≤30/6, PA ≤30/12, WP ≤12. Nb 1 mmHg = 1.36 cm water or blood.

Fick cardiac output

Oxygen consumption (L/min) = CO (L/min) × arteriovenous (AV) oxygen difference

CO = oxygen consumption/AV oxygen difference

Oxygen consumption must be measured (can estimate w/ 125 mL/min/m², but inaccurate)

AV oxygen difference = Hb (g/dL) × 10 (dL/L) × 1.36 (mL O₂/g of Hb) × (S_aO₂–S_MVO₂)

S_aO₂ is measured in any arterial sample (usually 93–98%)

S_MVO₂ (mixed venous O₂) is measured in RA, RV, or PA (assuming no shunt) (nl ~75%)

Assessment of RV function (Circ 2017;136:314)

PAPi = Pulmonary artery pulsatility index = [PA systolic – PA diastolic] / RA pressure >1.0 predicts RV failure in acute MI; <1.85 predicts RV failure after LVAD

Shunts

Valve equations

Simplified Bernoulli: Pressure gradient (∇P) = 4 × v² (where v = peak flow velocity)

Continuity (conservation of flow): Area₁ × Velocity₁ = A₂ × V₂ (where 1 & 2 different points)

PULMONARY

Chest Imaging (CXR & CT) Patterns
Pattern	Pathophysiology	Ddx
Consolidation	Radiopaque material in air space & interstitium patent airway → “air bronchograms”	Acute: water (pulm edema), pus (PNA), blood Chronic: neoplasm (BAC, lymphoma), aspiration, inflammatory (COP, eosinophilic PNA), PAP, granuloma (TB/fungal, alveolar sarcoid)
Ground glass (CT easier than CXR)	Interstitial thickening or partial filling of alveoli (but vessels visible)	Acute: pulm edema, infxn (PCP, viral, resolving bact. PNA) Chronic: ILD w/o fibrosis: acute hypersens., DIP/RB, PAP w/ fibrosis: IPF
Septal lines Kerley A & B	Radiopaque material in septae	Cardiogenic pulm edema, interstitial PNA viral, mycoplasma, lymphangitic tumor
Reticular	Lace-like net (ILD)	ILD (esp. IPF, CVD, bleomycin, asbestos)
Nodules	Tumor Granulomas Abscess	Cavitary: Primary or metastatic cancer, TB (react. or miliary), fungus, Wegener’s, RA septic emboli, PNA Noncavitary: any of above + sarcoid, hypersens. pneum., HIV, Kaposi’s sarcoma
Wedge opac.	Peripheral infarct	PE, cocaine, angioinv. aspergillus, Wegener’s
Tree-in-bud (best on CT)	Inflammation of small airways	Bronchopneumonia, endobronchial TB/MAI, viral PNA, aspiration, ABPA, CF, asthma, COP
Hilar fullness	↑ LN or pulm arteries	Neoplasm (lung, mets, lymphoma) Infxn (AIDS); Granuloma (sarcoid/TB/fungal) Pulmonary hypertension
Upper lobe	n/a	TB, fungal, sarcoid, hypersens. pneum., CF, XRT
Lower lobe	n/a	Aspiration, bronchiect., IPF, RA, SLE, asbestos
Peripheral	n/a	COP, IPF & DIP, eos PNA, asbestosis

CXR in heart failure

• ↑ cardiac silhouette (in systolic dysfxn, not in diastolic)

• Pulmonary venous hypertension: cephalization of vessels (vessels size > bronchi in upper lobes), peribronchial cuffing (fluid around bronchi seen on end → small circles), Kerley B lines (horizontal 1–2-cm lines at bases), ↑ vascular pedicle width, loss of sharp vascular margins, pleural effusions (~75% bilateral)

• Pulmonary edema: ranges from ground glass to consolidation; often dependent and central, sparing outer third (“bat wing” appearance)

Dead space = lung units that are ventilated but not perfused

Intrapulmonary shunt = lung units that are perfused but not ventilated

A-a gradient = P_AO₂ – P_aO₂ [normal A-a gradient ≈ 4 + (age/4)]

Minute ventilation (V_E) = tidal volume (V_T) × respiratory rate (RR)(nl 4–6 L/min)

Tidal volume (V_T) = alveolar space (V_A) + dead space (V_D)

GASTROENTEROLOGY

NEPHROLOGY

Anion gap (AG) = Na – (Cl + HCO₃) (normal = [alb] × 2.5; typically 12 ± 2 mEq)

Delta-delta (ΔΔ) = [Δ AG (ie, calc. AG – expected) / Δ HCO₃ (ie, 24 – measured HCO₃)]

Urine anion gap (UAG) = (UN_a + U_K) – U_Cl

However, Δ in Na depends on glc (Am J Med 1999;106:399)

Δ is 1.6 mEq per each 100 mg/dL ↑ in glc ranging from 100–440

Δ is 4 mEq per each 100 mg/dL ↑ in glc beyond 440

Total body water (TBW) = 0.60 × IBW (× 0.85 if female and × 0.85 if elderly)

Trans-tubular potassium gradient (TTKG) = [U_K / P_K] / [U_Osm / P_Osm]

HEMATOLOGY

Peripheral Smear Findings (also see Photo Inserts)
Feature	Abnormalities and Diagnoses
Size	normocytic vs. microcytic vs. macrocytic → see below
Shape	Anisocytosis → unequal RBC size; poikilocytosis → irregular RBC shape acanthocytes = spur cells (irregular sharp projections) → liver disease Bite cells (removal of Heinz bodies by phagocytes) → G6PD deficiency echinocytes = burr cells (even, regular projections) → uremia, artifact Pencil cell → long, thin, hypochromic - very common in adv. iron deficiency Rouleaux → hyperglobulinemia (eg, multiple myeloma) Schistocytes, helmet cells → MAHA (eg, DIC, TTP/HUS), mechanical valve Spherocytes → HS, AIHA; sickle cells → sickle cell anemia Stomatocyte → central pallor appears as curved slit → liver disease, EtOH Target cells → liver disease, hemoglobinopathies, splenectomy Tear drop cells = dacryocytes → myelofibrosis, myelophthisic anemia, megaloblastic anemia, thalassemia
Intra- RBC findings	Basophilic stippling (ribosomes) → abnl Hb, sideroblastic, megaloblastic Heinz bodies (denatured Hb) → G6PD deficiency, thalassemia Howell-Jolly bodies (nuclear fragments) → splenectomy or functional asplenia (eg, advanced sickle cell) Nucleated RBCs → hemolysis, extramedullary hematopoiesis
WBC findings	Blasts → leukemia, lymphoma; Auer rods → acute myelogenous leukemia Hypersegmented (>5 lobes) PMNs: megaloblastic anemia (B12/folate def.) Pseudo-Pelger-Huët anomaly (bilobed nucleus, “pince-nez”) → MDS Toxic granules (coarse, dark blue) and Döhle bodies (blue patches of dilated endoplasmic reticulum) → (sepsis, severe inflammation)
Platelet	Clumping → artifact, repeat plt count # → periph blood plt count ~10,000 plt for every 1 plt seen at hpf (100×) Size → MPV (mean platelet volume) enlarged in ITP

(NEJM 2005;353:498)

Heparin for Thromboembolism
80 U/kg bolus 18 U/kg/h
PTT	Adjustment
<40	bolus 5000 U, ↑ rate 300 U/h
40–49	bolus 3000 U, ↑ rate 200 U/h
50–59	↑ rate 150 U/h
60–85	no Δ
86–95	↓ rate 100 U/h
96–120	hold 30 min, ↓ rate 100 U/h
>120	hold 60 min, ↓ rate 150 U/h

(Modified from Chest 2008;133:141S)

Heparin for ACS
60 U/kg bolus (max 4000 U) 12 U/kg/h (max 1000 U/h)
PTT	Adjustment
<40	bolus 3000 U, ↑ rate 100 U/h
40–49	↑ rate 100 U/h
50–75	no Δ
76–85	↓ rate 100 U/h
86–100	hold 30 min, ↓ rate 100 U/h
>100	hold 60 min, ↓ rate 200 U/h

(Modified from Circ 2007;116:e148 & Chest 2008;133:670)

✔ PTT q6h after every Δ (t_½ of heparin ~90 min) and then qd or bid once PTT is therapeutic

✔ CBC qd (to ensure Hct and plt counts are stable)

(Annals 1997;126:133; Archives 1999;159:46) or, go to www.warfarindosing.org

Warfarin-heparin overlap therapy

• Indications: when failure to anticoagulate carries ↑ risk of morbidity or mortality (eg, DVT/PE, intracardiac thrombus)

• Rationale: (1) Half-life of factor VII (3–6 h) is shorter than half-life of factor II (60–72 h);

∴ warfarin can elevate PT before achieving a true antithrombotic state

(2) Protein C also has half-life less than that of factor II;

∴ theoretical concern of hypercoagulable state before antithrombotic state

• Method: (1) Therapeutic PTT is achieved using heparin

(2) Warfarin therapy is initiated

(3) Heparin continued until INR therapeutic for ≥2 d and ≥4–5 d of warfarin (roughly corresponds to ~2 half-lives of factor II or a reduction to ~25%)

Common Warfarin-Drug Interactions
Drugs that ↑ PT	Drugs that ↓ PT
Amiodarone Antimicrobials: erythromycin, ? clarithro, ciprofloxacin, MNZ, sulfonamides Antifungals: azoles Acetaminophen, cimetidine, levothyroxine	Antimicrobials: rifampin CNS: barbiturates, carbamazepine, phenytoin (initial transient ↑ PT) Cholestyramine

ENDOCRINOLOGY

NEUROLOGY

OTHER

NOTES