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to convert cm H 2 O to mmHg).
• PCWP: LV preload best estimated at a wave; risk of pulmonary edema from avg PCWP
    Cardiac output
• Thermodilution : saline injected in RA. Δ in temp over time measured at thermistor (in PA) is integrated and is1/CO. Inaccurate if ↓ CO, sev TR or shunt.
• Fick method : O 2 consumption (O 2 ) (L/min) = CO (L/min) × ∆ arteriovenous O 2 content
∴  CO = O2 / C(a-v)O2
O 2 ideally measured (esp. if ↑ metab demands), but freq estimated (125 mL/min/m 2 )
C(a-v)O 2 = [10×1.36 mL O 2 /g of Hb × Hb g/dL × (S a O 2 –S v O 2 )]. S v O 2 is key variable that Δ s .
If S V O 2 >80%, consider if the PAC is “wedged” (ie, pulm vein sat), L→R shunt, impaired O 2 utilization (severe sepsis, cyanide, carbon monoxide), ↑↑ FiO 2 .

    Tailored therapy in cardiogenic shock ( Circ 2009;119:e391)
• Goals : optimize both MAP and CO while ↓ risk of pulmonary edema
MAP = CO × SVR; CO = HR × SV (which depends on preload, afterload and contractility)
pulmonary edema when PCWP >20–25 (↑ levels may be tolerated in chronic HF)
• Optimize preload = LVEDVLVEDPLAPPCWP ( NEJM 1973;289:1263)
goal PCWP ~ 14–18 in acute MI , ≤ 14 in acute decompensated HF
optimize in individual Pt by measuring SV w/ different PCWP to create Starling curve
↑ by giving NS (albumin w/o clinical benefit over NS; PRBC if significant anemia)
↓ by diuresis (qv), ultrafiltration or dialysis if refractory to diuretics
• Optimize afterload wall stress during LV ejection = [(~SBP × radius) / (2 × wall thick.)] and ∴ ∝ MAP and ∝ SVR = (MAP – CVP / CO); goals: MAP > 60 , SVR 800–1200
MAP >60 & SVR ↑: vasodilators (eg, nitroprusside, NTG,  ACEI, hydral.) or wean pressors
MAP <60 & SVR ↑ (& ∴ CO ↓): temporize w/ pressors until can ↑ CO (see below)
MAP <60 & SVR low/nl (& ∴ inappropriate vasoplegia): vasopressors (eg, norepineph-rine [a, b], dopamine [D, a, b], phenylephrine [a] or vasopressin [V 1 ] if refractory)
• Optimize contractility ∝ CO for given preload & afterload; goal CI = (CO / BSA) > 2.2
if too low despite optimal preload & vasodilators (as MAP permits):
inotropes : eg, dobutamine (mod inotrope & mild vasodilator) or milrinone (strong inotrope & vasodilator, incl pulm), both proarrhythmic, or epi (strong inotrope & pressor)
mechanical support devices : eg, IABP, percutaneous or surgical VAD (left-sided, right-sided or both) or ECMO ( Circ 2011;123:533)

HEART FAILURE
    Definitions ( Braunwald’s Heart Disease , 9th ed., 2012)
• Failure of heart to pump blood forward at sufficient rate to meet metabolic demands of peripheral tissues, or ability to do so only at abnormally high cardiac filling pressures • Low output (↓ cardiac output) vs. high output (↑ stroke volume ± ↑ cardiac output) • Left-sided (pulmonary edema) vs. right-sided (↑ JVP, hepatomegaly, peripheral edema) • Backward (↑ filling pressures, congestion) vs. forward (impaired systemic perfusion) • Systolic (inability to expel sufficient blood) vs. diastolic (failure to relax and fill normally) • Reduced (HFrEF) vs. preserved (HFpEF) left ventricular ejection fraction • Some degree of systolic and diastolic dysfxn, may occur regardless of ejection fraction
Figure 1-3  Approach to left-sided heart failure

    History
• Low output: fatigue, weakness, exercise intolerance, Δ MS, anorexia • Congestive:  left-sided → dyspnea, orthopnea, paroxysmal nocturnal dyspnea right-sided → peripheral edema, RUQ discomfort, bloating, satiety Functional classification (New York Heart Association class)
• Class I: no sx w/ ordinary activity; class II: sx w/ ordinary activity; class III: sx w/ minimal activity; class IV: sx at rest Physical exam (“2-minute” hemodynamic profile; JAMA 1996;275:630 & 2002;287:628)
• Congestion (“dry” vs. “wet”)
↑ JVP (~80% of the time JVP >10 → PCWP >22;   J Heart Lung Trans 1999;18:1126)
hepatojugular reflux: >4 cm ↑ in JVP for ≥15 sec w/