Management of Acute Cardiogenic Pulmonary Oedema

Management of AcuteCardiogenic PulmonaryOedemaG.A. RichardsMBBCh PhD FCP(SA) FRCP FCCPDirector Critical Care CMJAH

• Hypertension• IschaemiaCauses of LV Failure• Muscle (CMO, drugs, toxins, infiltrative,nutritional, endocrine, HIV, peripartum)• Valvular• Congenital

Prognosis• 50% are dead at 4 yrs• 40% of those admitted with HF are dead orreadmitted within 4 yearsEuropean Journal of Heart Failure (2008), 933–989

Dickstein ESC Guidelines: Eur J Heart Failure 2008

Diastolic HF: HFPEF• Symptoms ± signs of HF & preserved LVEF(40–50%) (no consensus on cut-off for“preserved EF”)• Clinical diagnosis alone inadequate, esp in♀, elderly, obese• HFPEF is present in 50%• Prognosis similar to systolic HFRemes Eur Heart J 1991Wheeldon Q J Med 1993Owan N Engl J Med 2006

Diagnosis of HFPEF• Requires 3 conditions• Signs and/or symptoms of chronic HF• Normal or mildly abnormal LV systolic function• Diastolic dysfunction (abnormal relaxation ordiastolic stiffness)

Diagnosis of Heart FailureDickstein ESC Guidelines: Eur J Heart Failure 2008

Therapeutic Modalities:• Oxygen• Non-invasive ventilation• Loop diuretics• Vasodilators• Inotropic agents• Cardiac glycosides• Morphine

ACPO is Frequently not Associatedwith Systemic CongestionDickstein ESC Guidelines: Eur J Heart Failure 2008

Worsening/decompensated CHF• Peripheral oedema/congestion:• Systemic congestion with low BP• Often both RV and LV dysfunction so LApressure not increased• Poor prognosis• Pulmonary congestion less common

Pulmonary CongestionRARVLUNGINCREASEDLATV PA PV MitralPRESSURELV

Acute Pulmonary Oedema:Hypertensive HF• High BP: systolic function mostly preserved• Increased sympathetic tone, tachycardia,vasoconstriction• No systemic congestion; Euvolaemic ormildly hypervolaemic• Pulmonary congestion

Isolated right HF:• Low output syndrome• Increased JVP± hepatomegaly• Low LV filling pressures• No pulmonary congestion

ACS and HF• 15% of patients with ACS have signs andsymptoms of HF• HF frequently associated with/precipitatedby arrhythmia (bradycardia, AF, VT)• Not hypervolaemic at onset of ischaemia

Classification of HF severity inMI: KillipKillip Am J Cardiol 1967

Classification of HF severity inMI: ForresterForrester Am J Cardiol 1977

Tako-tsubo• “Stress-induced CMO”, “broken heart” or“transient LV apical ballooning syndrome”• 0.7–2.5% patients with apparent ACS• Preceding hypertension in 43-76%• Primarily older ♀ (90%), acute emotional/physiologic stress; also younger patientsand ♂, not always with stressful eventsPilgrim Int J Cardiol 2008Sharkey J Am Coll Cardiol 2010

Tako-tsubo: Diagnostic Criteria• Transient hypo-, akinesis in LV mid segments± apical involvement in >1 vessel distribution• Absence of OCAD or plaque rupture on angio• New ECG abnormalities/ modest Tn elevation• Absence of myocarditis or phaeoPrasad Am Heart J 2008

Tako-tsubo: Mechanisms• Myocardial stunning: ? due to catecholamineor ischaemia-mediated multivessel,epicardial or microvascular spasm, abortedMI, or focal myocarditis• Why selective apical LV dysfunction isunknown; possibly increased responsivenessof apical myocardium to SNS stimulation

Tako-tsubo• Symptoms: ACS or ACPO• Minimal ST elevation in precordial leads• Small Tn elevation (peak < 24h), low forthe extensive wall motion abnormalities:Ramaraj Exp Clin Cardiol 2009Sharkey Am J Cardiol 2008

Tako-tsubo: Systole: No contraction inapical region and apical ballooningZeb Postgrad Med J 2011

ACPO: Diuretics• ACPO without pre-existent systemiccongestion generally causes intravascularvolume depletion• Diuretics may cause further dehydrationand exacerbate renal failure

ACPO: Conditions where diureticsmay not be valuable• Hypertensive heart failure• Acute ischaemia/MI• HFPEF• Tako Tsubo• HOCM• Negaitive pressure pulmonary oedema

Therapy: Oxygen• Recommended as early as possible toachieve saturation ≥ 95% (less in COPD)

NIV: Haemodynamic Response• RV preload reduced by IPPV•RV afterload determined by effect on PVR•Alveolar vessels: degree of alveolaroverdistension•Extra alveolar interstitial vessels:atelectasis or recruitmentMagder: ICM 1998Pinsky: JAP 1984; Crit Care Clin 1990Marini: ARRD 1987

LV preloadInfluenced by• RV preload• RV afterload• Ventricular interdependence

LV AfterloadDetermined by:• Ventricular work: SVR and BP• Cavity size Tension ∞ radius (Laplace)• Transmural pressure (tension)IPPV reduces: cavity size andtransmural tension

HemodynamicsPreloadCavity sizeSVRStrokevolumeBPContractilityMuscleshorteningAfterloadHRC.O.±ITP

LV Afterload: Transmural TensionIPPV increases ITP reducing transmural tensionMean Arterial Pressure 60ITPT TT TMean Airway Pressure +20T T =Transmural tension = 60-20 +20=80 = 40

Afterload: Negative PressurePulmonary Oedema• Markedly negative swings in ITP fromspontaneous ventilation increasesafterload and may precipitate ACPOparticularly with LV dysfunction• This can also occur in well compensatedpatients. Young fit malesStalcup: NEJM 1977Sofer: Chest 1984Beach: CCM 1973

Therapy: NIV with PEEP• Consider as early as possible with ACPO• Improves clinical parameters and LVfunction by reducing LV afterload• 3 meta-analyses showed reduced intubationand short-term mortalityMasip Heart Fail Rev 2007 &JAMA 2005Peter Lancet 2006

Clinical Effects of NIV• 30 extubated low risk patients:• 4 intervals: spontaneous ventilation, NIV,spontaneous, NIV• CI & S mv O 2 increased significantly with NIV• UO increased significantlyHoffman Thorac Cardiovasc Surg 2003

CPAP vs. Conventional therapy• 5 trials: significant improvement in gasexchange and intubation ratesRasanen Am J Cardiol 1985Lin J Formosan Med Assoc 1991Bersten NEJM 1991Lin Chest 1995L’Her ICM 2004• The latter demonstrated a reduction inmortality with CPAP

CPAP vs. BiPAP80 patients conventional therapy; CPAP11cm H 2 O vs BiPAP 17/11• CPAP/BiPAP significantly improveddyspnoea, vital signs, P/F ratios• Study stopped due to significant intubationdifference 42 vs 7% CPAP & BiPAP• 15day mortality higher with O 2 alone p< .05• Mortality hospital discharge not differentPark CCM 2004

CPAP: Practicalities• 5– 7.5cmH 2 O titrated to 10cmH 2 O• FiO 2 >0.4• Contraindications• Poor cooperation• Immediate need for intubation• Caution with ++ secretions

Measure Fluid Status: SVV

Fluid Status: SVV/PPVMeta-analysis of 29 studies during MV:• >12% predicted fluid responsiveness• Sensitivity, specificity: PPV: 0.89 and 0.88SVV: 0.82 and 0.86PPV more accurate (direct vs. derived)Reliable only if TV ≥8 mL/kg and nospontaneous breathingDe Backer ICM 2005Marik CCM 2009

Thermodilution TechniqueCold bolusinjectionMeasurementof thermodilution

Thermodilution Decay CurveITTV = CO * MTtPTV = CO * DStMTt: : Mean transit timeDSt: : Downslope timeBelda FJ 26 th ISICEM Brussels 2006

CO x MTt= Vd of cold indicator=IT Thermal VolumeCO x DSt= Cold indicator mixing chamberP Thermal VolumeCO x (MTt- DSt)=GEDVITBV (PBV)= 1,25 x GEDVEVLW = ITTV- ITBVMichard Crit Care Med 2007

Fluid Status: GEDV/ITBV• Lower values indicate volume-depletion• Confirmatory evidence of fluid depletion espatrial fib, spontaneous ventilation• Fluid responsive CI corresponds with anincrease in GEDVI and ITBVI• But increased CI from inotropes leavesGEDVI/ITBVI unchangedBerkenstadt Anesth Analg 2001

Fluid Status: EVLW• >EVLWI associated with more severeARDS/LIS and higher mortality• No consensus on normals or indexingparameters• Predicted BW may be superior to predictmortality, MOF and diagnose ARDS• Valuable confirmatory evidence of fluiddepletionChew Crit Care 2012Chung PLoS One 2010Effros Am J Physiol Lung Cell Mol Physiol 2008Maharaj Cardiol Res Pract 2012Camporota Critical Care 2012

“Normal Values”• CI 3.0 – 5.0 l/min/m 2• GEDVI 680 – 800 ml/m 2• ITBI(PBV) 850- 1000ml/m 2• SVV 10 %• ELWI 3.0 – 7.0ml/kg (Oedema: >10mL/kg)

Interface

Case Study CVP 8Male 56: Post extubationdypspneaPink frothy sputumConfusedPost extubation Pulm oedema:∆∆- LV dysfunction/MI- Negative pressurepulmonary oedemaIntervention: Fluids: if responseinadequate, dobutamineMAP 70PEEP 12P/F 68CI 1.6SVV 22SVRI 2800EVLW 18ml/kgGEDV 400ml/m 2