Myocardial, Valvular, and Pericardial Disease

HEART FAILURE

Definitions (Braunwald’s Heart Disease, 10^th ed., 2014)

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

Stages in the Development of Heart Failure (Circ 2009;119:e391)

A: At high risk for HF, but w/o structural heart disease or symptoms of HF
B: Structural heart disease, but w/o signs or symptoms of HF
C: Structural heart disease w/ prior or current symptoms of HF
D: Refractory heart failure requiring specialized intervention

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 RAP > 10 mmHg → PCWP >22 mmHg; JHLT 1999;18:1126)

⊕ hepatojugular reflux: ≥4 cm ↑ in JVP that persists for ≥15 sec w/ abdominal pressure Se/Sp 73/87% for RA >8 and Se/Sp 55/83% for PCWP >15 (AJC 1990;66:1002)

Abnl Valsalva response: square wave (↑ SBP w/ strain), no overshoot (no ↑ BP after strain) S₃ (in Pts w/ HF → ˜40% ↑ risk of HF hosp. or pump failure death; NEJM 2001;345:574) rales, dullness at base 2° pleural effus. (often absent in chronic HF due to lymphatic compensation) ± hepatomegaly, ascites and jaundice, peripheral edema
Perfusion (“warm” vs “cold”): narrow pulse pressure (<25% of SBP) → CI <2.2 (91% Se, 83% Sp; JAMA 1989;261:884); other signs of low perfusion include soft S₁ (↑ dP/dt), pulsus alternans, cool & pale extremities, ↓ UOP, muscle atrophy
Other signs to look for: periodic breathing/Cheyne-Stokes resp., abnl PMI (diffuse, sustained or lifting depending on cause of HF), S₄ (diast. dysfxn), murmur (valvular disease, ↑ MV or TV annulus, displaced papillary muscles), ↓ carotid upstroke

Evaluation for the presence of heart failure

CXR (see Radiology insert): pulm edema, pleural effusions ± cardiomegaly, cephalization, Kerley B-lines
BNP/NT-proBNP can help exclude HF; levels ↑ w/ age, renal dysfxn, AF, ↓ w/ obesity Se ≥95%, Sp ˜50%, PPV ˜65%, NPV ≥94% for HF in Pts p/w SOB (BMJ 2015;350:h910)
Evidence of ↓ organ perfusion: ↑ Cr, ↓ Na, abnl LFTs
Echo (see inserts): ↓ EF & ↑ chamber size ↑ systolic dysfxn; hypertrophy, abnl MV inflow, abnl tissue Doppler → ? diastolic dysfxn; abnl valves or pericardium; ↑ estimated RVSP
PA catheterization: ↑ PCWP, ↓ CO and ↑ SVR (in low-output failure)

Evaluation of the potential causes of heart failure

ECG: Q waves or PRWP (ischemic heart disease); LVH (hypertensive heart disease or HCM); low limb lead voltage (NICM or infiltrative); heart block (infiltrative)
TTE: LV & RV size & function, valvular disease (and whether likely 1° or 2° to CMP), findings indicative of infiltrative or pericardial disease
Coronary angio (or noninvasive imaging, eg, CT angio); if no CAD, w/u for NICM
Cardiac MRI: multiparameter evaluation of cardiac structure & function including:

LVEF, RVEF and volumes; regional wall motion abnormalities

presence, pattern, & extent of myocardial scar (using late gadolinium enhancement, LGE) w/ Se/Sp of 100%/96% vs coronary angio for dx etiology of HF (Circ 2011;124:1351)

myocardial inflammation or infiltration (eg, myocarditis, sarcoidosis, amyloidosis) restriction vs constrictive pericardial disease

Evaluation of Potential Causes of Heart Failure
Etiology	ECG Pattern	Imaging Pattern
Ischemia, infarct	ST segment deviation, Qw	TTE: regional WMA, ± thinning/aneurysm Cor angio/CTA: obstructive CAD MRI: subendocardial or transmural LGE
Infiltrative	Low limb lead voltage, ± heart block, pseudoinfarct	TTE: LVH, “starry sky,” ↑ biatrial size → amyloid MRI: inapprop nulling of myocardium + diffuse LGE → amyloid; patchy LV + RV LGE → sarcoidosis; ↓ T2 star → iron overload
Idiopathic DCM	Low limb lead volts, precordial LVH, BBB	TTE: 4 chamber dilation, diffuse hypokinesis MRI: mid-myocardial LGE
Tachy-myopathy	Persistent SVT	TTE: diffuse hypokinesis MRI: absent LGE in early stage
Myo(peri) -carditis	Pseudoischemia/-infarct. Pericard: diffuse concave STE w/ ST:T ratio >0.24 in V₆ and PR depression	TTE: typically global HK MRI: mid-myocardial + epicardial LGE, ↑ T2 and ↑ T1 ratios (edema)

Precipitants of acute heart failure

Dietary indiscretion or medical nonadherence (˜40% of cases)
Myocardial ischemia or infarction (˜10-15% of cases); myocarditis
Renal failure (acute, progression of CKD, or insufficient dialysis) → ↑ preload
Hypertensive crisis (incl. from RAS), worsening AS → ↑ left-sided afterload
Drugs (βB, CCB, NSAIDs, TZDs), chemo (anthracyclines, trastuzumab), or toxins (EtOH)
Arrhythmias; acute valv. dysfxn (eg, endocarditis), espec mitral or aortic regurgitation
COPD or PE → ↑ right-sided afterload; RV pacing
Other: extreme emotional stress; anemia, systemic infection, thyroid disease

Treatment of acute decompensated heart failure

Assess degree of congestion & adequacy of perfusion
For congestion: “LMNOP”

Lasix IV w/ monitoring of UOP; total daily dose 2.5× usual daily PO dose → ↑ UOP, but transient ↑ in renal dysfxn vs 1× usual dose; Ø clear diff between cont gtt vs q12h dosing (NEJM 2011;364:797)

Morphine (↓ sx, venodilator, ↓ afterload)

Nitrates (venodilator)

Oxygen ± noninvasive vent (↓ sx, ↑ P_aO₂; no Δ mortality; see “Mechanical Ventilation”)

Position (sitting up & legs dangling over side of bed → ↓ preload)
For low perfusion, see below
Adjustment of oral meds

ACEI/ARB: hold if HoTN, consider Δ to hydralazine & nitrates if renal decompensation βB: reduce dose by at least ½ if mod HF, d/c if severe HF and/or need inotropes

Overview of Treatment of Heart Failure by Stage
Pt characteristics		Therapy
A	HTN, DM, CAD Cardiotoxin exposure FHx of CMP	Treat HTN, lipids, DM, SVT Stop smoking, EtOH; ↑ exercise ACEI/ARB if HTN/DM/CAD/PAD
B	Prior MI, ↓ EF, LVH or asx valvular dis.	All measures for stage A + ACEI/ARB & βB if MI/CAD or ↓ EF. ? ICD.
C	Overt HF	All measures for stage A, ACEI, βB, diuretics, Na restrict ↓ EF: aldo antag, ICD, consider CRT, nitrate/hydral, dig.
D	Sx despite max med Rx 4-y mortality >50%	All measures for stages A-C Consider IV inotropes, VAD, transplant, end-of-life care

Utility of BNP-guided Rx remains debated (Circ 2013;301:500 & 509)
Implantable PA pressure sensor in NYHA III → 37% ↓ risk of hosp (23% for HFrEF; 52% for HFpEF) (Lancet 2011;377:658)

Treatment of advanced heart failure (Circ 2009;119:e391)

Consider PAC (qv) if not resp to Rx, unsure re: vol status, HoTN, ↑ Cr, need inotropes
Tailored Rx w/ PAC; goals of MAP >60, CI >2.2 (MVO₂ >60%), SVR <800, PCWP <18
IV vasodilators: NTG, nitroprusside (risk of coronary steal if CAD; prolonged use → cyanide/thiocyanate toxicity); nesiritide (rBNP) not rec for routine use (NEJM 2011;365:32)
Inotropes: in addition to ↑ inotropy, consider additional properties:

dobutamine: vasodilation at doses ≤5 mcg/kg/min; mild ↑ PVR; desensitization over time

dopamine: splanchnic vasodil. → ↑ GFR & natriuresis; vasoconstrictor at ≥5 mcg/kg/min; does not enhance decongestion or preserve renal fxn in ADHF (JAMA 2013;310:2533)

milrinone: prominent systemic & pulmonary vasodilation; ↑ dose by 50% in renal failure
Ultrafiltration: similar wt loss to aggressive diuresis, but ↑ renal failure (NEJM 2012:367:2296)

Mechanical circulatory support (MCS) (JHLT 2013;32:157; JACC 2015;65:e7 & 2542)

Temporary MCS: depending on the device (Table), can be placed percutaneously or surgically to support LV or RV, as a bridge to recovery, for periprocedural support, or as a bridge to decision regarding transplant or durable long-term MCS

Intra-aortic balloon pump (IABP): inflates in diastole & deflates in systole to ↓ impedance to LV ejection of blood, ↓ myocardial O₂ demand & ↑ coronary perfusion

Axial flow pumps (eg, Impella): Archimedes screw principle in LV

Extracorporeal magnetically levitated centrifugal pumps (eg, TandemHeart & CentraMag)

Extracorporeal membrane oxygenation (ECMO, Circ 2015;131:676)

Short-Term Mechanical Circulatory Support in Cardiogenic Shock
Device	IABP	Impella 2.5 & CP	Impella 5.0	Tandem	CentriMag	ECMO
Max support (L/min)	0.5	2.5 & 3-4	5.0	5.0	10	6
RV support	N	Y (2^nd dev.)	N	Y (2^nd dev.)	Y (2^nd dev.)	Y
Support duration	wks	˜4 wk	˜4 wk	<4 wk	mos	wks
Percutan?	Y	Y	N	Y	N	Y
Contraindic.	≥ mod AI, severe PAD	LV thrombus, mech AV, severe AS		coagulop severe PAD	coagulop	coagulop
(Circ 2011;123:533 & 126:1717; JACC 2015;65:e7)

Durable Long-term MCS: surgically placed LVAD ± RVAD as bridge to recovery (NEJM 2006;355:1873) or transplant (HeartMate II or HeartWare LVAD or Total Artificial Heart if biventricular failure), or as destination Rx (HeartMate I: 52% ↓ 1-y mort. vs med Rx; NEJM 2001;345:1435, HeartMate II: 24% ↑ mort. vs HeartMate 1; NEJM 2009;361:2241)

Cardiac transplantation: curative Rx but supply of organs limited (˜2500/y in U.S.) 10% mortality in 1^st year, median survival ˜10 y

Contraindications: active malignancy or infection, irreversible PHT (TPG>15, PVR>5WU despite pulmonary vasodilator Rx), active substance abuse or lack of social supports

Relative contraindications: age (eg, >70 y), other end organ dysfunction (liver, kidney, lung, unless dual organ transplantation is performed)

Treatment of Chronic Heart Failure with Reduced Ejection Fraction
Diet, exercise	Na <2 g/d, fluid restriction, exercise training in ambulatory Pts
ACEI	↓ mortality: 40% in NYHA IV, 16% in NYHA II/III, 20-30% in asx but ↓ EF (NEJM 1992;327:685 & Lancet 2000;355:1575) High-dose more effic. than low. Watch for ↑ Cr, ↑ K (ameliorate by low-K diet, diuretics, Kayexalate; patiromer, another K binder, under review; NEJM 2015;372:211), cough, angioedema.
ATII receptor blockers (ARBs)	Consider as alternative if cannot tolerate ACEI (eg, b/c cough) Noninferior to ACEI (Lancet 2000;355:1582 & 2003;362:772) As with ACEI, higher doses more efficacious (Lancet 2009;374:1840) Adding to ACEI → ↑ risk of ↑ K and ↑ Cr (BMJ 2013;346:f360)
ARNi (ARB + neprilysin inhib)	Neutral endopeptidase (NEP, aka neprilysin) degrades natriuretic peptides as well as bradykinin & angiotensins. LCZ696 = valsartan + sacubitril (NEPi): ↓ CV mort & HF hosp c/w ACEi; more HoTN and trend to more angioedema (PARADIGM-HF, NEJM 2014;371:993).
Hydralazine + nitrates	Consider if cannot tolerate ACEI/ARB or in blacks w/ NYHA III/IV 25% ↓ mort. (NEJM 1986;314:1547); infer. to ACEI (NEJM 1991;325:303) 43% ↓ mort. in blacks on standard Rx (A-HEFT, NEJM 2004;351:2049)
β-blocker (data for carvedilol, metoprolol, bisoprolol)	EF will transiently ↓, then ↑. Contraindic. in decompensated HF. 35% ↓ mort. & 40% ↓ rehosp. in NYHA II-IV (JAMA 2002;287:883) Carvedilol superior to low-dose metop in 1 trial (Lancet 2003;362:7), but meta-analysis suggests no diff between βB (BMJ 2013;346:f55).
Aldosterone antagonists	Consider if adeq. renal fxn and w/o hyperkalemia; watch for → K 24-30% ↓ mort. in NYHA II-IV & EF ≤35% (NEJM 2011;364:11) 15% ↓ mort. in HF post-MI, EF ≤40% (EPHESUS, NEJM 2003;348:1309)
Cardiac resynch therapy (CRT, qv)	Consider if EF ≤35%, LBBB and symptomatic HF 36% ↓ mort. & ↑ EF in NYHA III-IV (CARE-HF, NEJM 2005;352:1539) 41% ↓ mort. if EF ≤30%, LBBB and NYHA I/II (NEJM 2014;370:1694)
ICD (see “Cardiac Rhythm Mgmt Devices”)	Use for 1° prevention if EF ≤30-35% or 2° prevention; not if NYHA IV ↓ mort. in ischemic & non-isch CMP; no Δ mort. early post-MI (NEJM 2004;351:2481 & 2009;361:1427), wait ≥40 d
Diuretics	Loop ± thiazide diuretics (sx relief; no mortality benefit)
Digoxin	23% ↓ HF hosp., no Δ mort (NEJM 1997;336:525); ? ↑ mort w/ ↑ levels (NEJM 2002;347:1403); optimal 0.5-0.8 ng/mL (JAMA 2003;289:871)
Ivabradine (If blocker w/o [circled dash] ino)	Consider if HR >70, NSR on max βB. 18% ↓ CV mort or HF hosp (Lancet 2010;376:875)
ω-3 fatty acids	9% ↓ mortality (included HF with normal LVEF) (Lancet 2008:372:1223)
IV iron supplementation	? if NYHA II/III, EF ≤40%, Fe-defic (ferritin <100 or ferritin 100-300 & TSAT <20%). ↓ Sx, ↑ 6MWD, independent of Hct (NEJM 2009;361:2436).
Anticoagulation	If AF, VTE, LV thrombus, ± if large akinetic LV segments In SR w/ EF <35%, ↓ isch stroke, but ↑ bleed (NEJM 2012;366:1859)
Heart rhythm	Catheter ablation of AF → ↑ in EF, ↓ sx (NEJM 2004;351:2373) No mortality benefit to AF rhythm vs rate cntl (NEJM 2008;358:2667) Pulm vein isolation ↓ sx c/w AVN ablation & CRT (NEJM 2008;359:1778)
Meds to avoid	NSAIDs, nondihydropyridine CCB, TZDs
Experimental	Serelaxin ± ↓ dyspnea & ? ↓ mortality (Lancet 2013;381:29)
(Circ 2009;119:e391; NEJM 2010;362:228; Lancet 2011;378:713 & 722)

Heart failure with preserved EF (HFpEF; “Diastolic HF”) (Circ 2011;124:e540)

Epidemiology: ˜½ of Pts w/ HF have normal or only min. impaired systolic fxn (EF ≥40%); risk factors for HFpEF incl ↑ age, ♀, DM, AF. Mortality ≈ to those w/ systolic dysfxn.
Etiologies (impaired relaxation and/or ↑ passive stiffness): ischemia, prior MI, LVH, HCMP infiltrative CMP, RCMP aging, hypothyroidism
Precipitants of pulmonary edema: volume overload (poor compliance of LV → sensitive to even modest ↑ in volume); ischemia (↓ relaxation); tachycardia (↓ filling time in diastole), AF (loss of atrial boost to LV filling); HTN (↓ afterload → ↓ stroke volume)
Dx w/ clinical s/s of HF w/ preserved systolic fxn. Dx supported by evidence of diast dysfxn:

(1) echo: abnl MV inflow (E/A reversal and Δs in E wave deceleration time) & ↓ myocardial relax. (↑ isovol relax. time & ↓ early diastole tissue Doppler velocities)

(2) exercise-induced ↑ PCWP (± ↓ response chronotropic & vasodilator reserve)
Treatment: diuresis for vol overload, BP control, prevention of tachycardia and ischemia; no benefit to: ACEI/ARB (NEJM 2008;359:2456) or PDE5 inhib (JAMA 2013;309:1268) spironolactone ↓ CV death & HF hosp (at least in Americas) (NEJM 2014;370:1383);

ARNi (Lancet 2012;380:1387) and serelaxin (Lancet 2013;381:29) under study

PA CATHETER AND TAILORED THERAPY

Rationale

Cardiac output (CO) = SV × HR; LV SV depends on LV end-diastolic volume (LVEDV) manipulate LVEDV to optimize CO while minimizing pulmonary edema
Balloon at tip of catheter inflated → floats into “wedge” position. Column of blood extends from tip of catheter, through pulmonary circulation, to a point just proximal to LA. Under conditions of no flow, PCWP ≈ LA pressure ≈ LVEDP, which is proportional to LVEDV.
Situations in which these basic assumptions fail:

(1) Catheter tip not in West lung zone 3 (and PCWP = alveolar pressure ≠ LA pressure); clues include lack of a & v waves and if PA diastolic pressure < PCWP

(2) PCWP > LA pressure (eg, mediastinal fibrosis, pulmonary VOD, PV stenosis)

(3) Mean LA pressure > LVEDP (eg, MR, MS)

(4) Δ LVEDP-LVEDV relationship (ie, abnl compliance, [ “nl” LVEDP may not be optimal)

Indications (Circ 2009;119:e391; NEJM 2013;369:e35)

Diagnosis and evaluation

Ddx of shock (cardiogenic vs distributive; espec if trial of IVF failed or is high risk) and of pulmonary edema (cardiogenic vs not; espec if trial of diuretic failed or is high risk)

Evaluation of CO, intracardiac shunt, pulmonary HTN, MR, tamponade, cardiorenal syndrome

Evaluation of unexplained dyspnea (PAC during provocation w/ exercise, vasodilator)
Therapeutics (Circ 2006;113:1020)

Tailored therapy to optimize PCWP, SV, S_MVO₂, RAP, & PVR, in heart failure or shock

Guide to vasodilator therapy (eg, inhaled NO) in pulm HTN, RV infarction

Guide to perioperative management in some high-risk Pts, pretransplantation

Guide to candidacy for thoracic organ transplantation and mechanical circulatory support
Contraindications

Absolute: right-sided endocarditis, thrombus/mass or mechanical valve; PE

Relative: coagulopathy (reverse), recent PPM or ICD (place under fluoroscopy), LBBB (˜5% risk of RBBB ↑ CHB, place under fluoro), bioprosthetic R-sided valve

Efficacy concerns (NEJM 2006;354:2213; JAMA 2005;294:1664)

No benefit to routine PAC use in high-risk surgery, sepsis, ARDS
No benefit in decompensated HF (JAMA 2005;294:1625); untested in cardiogenic shock
But: ˜½ of CO & PCWP clinical estimates incorrect; CVP & PCWP not well correl.; use PAC to (a) answer hemodynamic ? and then remove, or (b) manage cardiogenic shock

Pulmonary Artery Catheter Features
Component	cm from distal tip	Function
Distal lumen	0	Sampling of blood for S_MVO₂
1.5-mL balloon	0.5	Inflation allows flow directed placement & determination of PCWP
Thermistor	4	Detection of temp Δ for CO calc
Proximal injectate port	26	Infusions & injection of saline for CO calc
Additional Optional Features
Fiberoptic O₂ sat sensor	0	Allows continuous measurement of S_MVO₂
Thermal filament	˜10-25	Allows continuous CO calc by thermodilution
Pacing port	˜19	Allows placement of pacing wire in RV
Infusion port(s)	˜30	Additional infusion port(s)

Placement

Insertion site: R internal jugular or L subclavian veins for “anatomic” flotation into PA
Inflate balloon (max 1.5 mL) when advancing and to measure PCWP
Use resistance to inflation and pressure tracing to avoid overinflation & risk of PA rupture
Should require 1-1.5 mL air in balloon to float into wedge (<1 mL → pull PAC back; no PCWP at 1.5 mL → advance)
Deflate balloon when withdrawing and at all other times
CXR should be obtained after placement to assess for catheter position and PTX
If catheter cannot be successfully floated (typically if severe TR or RV dilatation) or if another relative contraindication exists, use fluoroscopic guidance

Complications

Central venous access: pneumo/hemothorax (˜1%), arterial puncture (if inadvertent cannulation w/ dilation → surgical/endovasc eval), air embolism, thoracic duct injury
Arrhythmias: ½ PVCs, 20% NSVT, 3% VT (minimize time PAC tip in RV); RBBB (5%)
Inability to advance: difficulty RA → RV seen w/ lg RA and/or severe TR; difficulty RV → PA seen w/ lg RV; deflate balloon, withdraw 10 cm, inflate balloon & readvance. If repeated attempts unsuccessful at bedside, then perform under fluoro (to avoid PAC coiling & potentially knotting, which would require interventional cardiology to extract).
PA rupture: risk factors include prolonged balloon inflation, PHT, anticoag. Presents w/ hemoptysis and, if severe, hypoxemia & hypovolemic shock. Keep balloon inflated, intubate w/ dbl-lumen endotracheal tube, lateral decubitus position with affected side down, STAT interventional radiology and/or thoracic surgery consultation.
Air embolism: presents w/ dyspnea, chest pain, ↑ R-sided pressures, HoTN. Place in

Trendelenburg, high-flow O₂.
Other: infxn (espec if PAC >3 d old); thrombus; pulm infarction; valve/chordae damage

Intracardiac pressures

Zero the transducer and level it with the right atrium (phlebostatic axis)
Transmural pressure (≈ preload) = measured intracardiac pressure – intrathoracic pressure
Intrathoracic pressure (usually slightly [circled dash]) is transmitted to vessels and heart
Always measure intracardiac pressure at end-expiration, when intrathoracic pressure closest to 0 (“high point” in spont. breathing Pts; “low point” in Pts on ⊕ pressure vent.)
If ↑ intrathoracic pressure (eg, PEEP), measured PCWP overestimates true transmural pressures. Can approx by subtracting ˜½ PEEP (× ¾ to convert cm H2O 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 is ≈ 1/CO. Inaccurate if ↓ CO, severe TR or shunt.
Fick method: O₂ consumpt ([V with dot above]O₂) (L/min) = CO (L/min) × Δ arteriovenous O₂ content

CO = [V with dot above]O₂ /C(a-v)O₂

[V with dot above]O₂ ideally measured (espec if ↑ metab demands), but freq estimated (125 mL/min/m²)

C(a-v)O₂ = [10 × 1.36 mL O₂/g of Hb × Hb g/dL × (S_aO₂-S_MVO₂)]

S_MVO₂ is key variable that Δs with acute interventions

If S_MVO₂ >80%, consider if the PAC is “wedged” (ie, pulm vein sat), L→ R shunt, impaired O₂ utilization (severe sepsis, cyanide, carbon monoxide), ↑ ↑ FiO₂

PA Catheter Waveforms
Location	RA	RV	PA	PCWP
Distance	˜20 cm	˜30 cm	˜40 cm	˜50 cm
Normal Pressure (mmHg)	mean ≤6	syst 15-30 diast 1-8	syst 15-30 mean 9-18 diast 6-12	mean ≤12
Waves
Comment	a = atrial contraction, occurs in PR interval c = bulging of TV back into RA at start of systole x = atrial relaxation and descent of base of heart v = blood entering RA, occurs mid-T wave y = blood exiting RA after TV opens at start of diastole	RVEDP occurs right before upstroke and ≥ mean RA pressure unless there is TS or TR	Waveform should contain notch (closure of pulmonic valve). Peak during T wave PA systolic = RV systolic unless there is a gradient (eg, PS). PA diastolic ≈ PCWP unless ↑ trans-pulm gradient (eg, ↑ PVR).	Similar to RA except dampened and delayed. a wave after QRS, ± distinct c wave, v wave after T (helps distinguish PCWP w/ large v waves 2° MR from PA).
PCWP waveform abnormalities: large a wave → ? mitral stenosis; large v wave → ? mitral regurgitation; blunted y descent → ? tamponade; steep x & y descents → ? constriction.

Hemodynamic Profiles of Various Forms of Shock
Type of shock	RA	PCWP	CO	SVR
Hypovolemic	↓	↓	↓	↓
Distributive	variable	variable	usually ↑ (but can be ↓ in sepsis)	↓
Cardiogenic: 1° L-sided (eg, acute MI)	nl or ↑	↑	↓	↑
Cardiogenic: 1° R-sided (eg, RV infarct; PE)	↑	nl or ↓	↓	↑
Tamponade	↑	↑	↓	↑
Surrogates: JVP ≈ RA; pulmonary edema on CXR implies ↑ PCWP; UOP ∝ CO (barring AKI); delayed capillary refill (ie, >2-3 sec) implies ↑ SVR

Tailored therapy and management of shock (Circ 2009;119:e391)

Goals: optimize both MAP and CO to promote end-organ perfusion, while ↓ risk of pulmonary edema & systemic venous congestion MAP = CO × SVR; CO = HR × SV (depends on preload, afterload and contractility) pulmonary edema when PCWP >20-25 (↑ levels may be tolerated in chronic HF) hepatic and renal congestion when CVP/RAP >15 mmHg
Optimize preload = LVEDV ≈ LVEDP ≈ LAP ≈ PCWP (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, norepinephrine [α, β], dopamine [D, α, β], phenylephrine [α] or vasopressin [V₁] 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 (L-sided, R-sided, or both) or ECMO (Circ 2011;123:533)

Vasopressors and Inotropes Used in Shock
Drug	Receptors			Hemodynamics				Comment
Drug	α₁	β₁	β₂	SVR	MAP	HR	CO	Comment
Phenylephrine	+++	0	0	↑ ↑ ↑	↑ ↑	↓ ↓^a	↓^a	↑ PVR
Vasopressin^b	0	0	0	↑ ↑ ↑	↑ ↑	↓ ↓^a	↓^a	↔PVR; attractive if RV dysfxn or PHT
Norepinephrine	+++	++	+	↑ ↑ ↑	↑ ↑	↔/↑	↔/↑	Better outcomes than w/ dopa
Epinephrine	+++	+++	+++	↓ / ↑^c	↑	↑ ↑	↑	β predom at low doses
Isoproterenol	0	+++	+++	↓ ↓	↓	↑ ↑ ↑	↑ ↑	⊕ chronotrope
Dobutamine	+	+++	++	↓	↔/↓	↑ ↑	↑ ↑	↓ PCWP
Dopamine^d	+	++	0	↔/↑^d	↔/↑^d	↑ ↑ ↑	↑
Milrinone^e	0	0	0	↓ ↓	↓	↔	↑ ↑ ↑	↓ ↓ PCWP; ↓ PVR; attractive if RV dysfxn or PHT
^aBradycardia seen due to vagal reflex if hypertension; ↓ CO due to ↑ afterload ^bV₁ agonist ^cLow doses ↓ SVR, high doses ↑ SVR ^dAlso a (D) dopa receptor agonist; 0.5-2 mcg/kg/min → D; 2-10 → D & β₁; > 10 → α₁, β₁, D ^ePDE₃ inhibitor