Cardiogenic Shock



Cardiogenic Shock


David V. Daniels

Todd J. Brinton

Randall Vagelos



BACKGROUND

Cardiogenic shock is a state of inadequate tissue perfusion and dysoxia due to primary cardiac dysfunction clinically manifest by systemic hypotension and end-organ compromise.



  • Historical mortality approaches 80% without revascularization1


  • Current era mortality remains as high as 60%2


  • Complicates 7%-9% of all acute myocardial infarctions (AMI)3,4


  • Shock criteria often absent on admission (<10% of patients) but usually develops early in the hospitalization (mean time MI to onset 5.5 hours in the SHOCK trial registry)


  • Multifactorial etiologies (LV failure – 79%, Severe MR – 7%, acute ventricular septal defect (VSD) – 4%, isolated right ventricular (RV) failure – 2%, tamponade – 1.4%2)


  • Majority of cases secondary to AMI present with ST segment elevation myocardial infarct (STEMI)


FEATURES OF CARDIOGENIC SHOCK5



  • Persistent systemic hypotension: systolic blood pressure (SBP) <90mm Hg or mean arterial pressure (MAP) >30 mm Hg below baseline


  • Cardiac index <1.8 liters/min/m2 or inotrope dependence to maintain cardiac output and blood pressure (BP)


  • Pulmonary artery wedge pressure (PAWP) >18 mm Hg


  • Signs of systemic hypoperfusion (cool extremities, oliguria, lactic acidosis)


HISTORY



  • Rapid diagnosis essential: history and physical exam should be focused and brief with simultaneous initial resuscitation


  • Inquire about time course of symptoms, new or changing angina, shortness of breath (SOB), paroxysmal nocturnal dyspnea (PND), orthopnea, edema, weight changes, or fatigue



  • History of MI, heart failure (HF), or valvular disease


  • Recent changes in medication dose or type


PHYSICAL EXAM

Look for the following:



  • Absolute or relative hypotension (SBP >30 mm Hg below baseline)


  • Check bilateral blood pressures if hypotension suspected as unilateral subclavian or axillary stenosis may falsely classify patients as centrally hypotensive.


  • Narrow pulse pressure (pulse pressure <25% of the SBP has a sensitivity and specificity of 91% and 83% for a cardiac index of <2.2 L/min/m2)4


  • Cool underperfused extremities, altered mental status, low urine output


  • Pulmonary edema and respiratory distress


  • Signs of HF: Elevated JVP, S3, S4, tachycardia, hypoxia, crackles


  • Peripheral edema suggests some component of chronic HF and can be absent with acute HF


  • New systolic murmur suggests acute mitral regurgitation (MR) or VSD, assess for a thrill


  • Listen with patient leaning forward to detect the diastolic murmur of AI


  • Asymmetric pulses and a focal neurologic exam (aortic dissection)


LABORATORY EXAMS AND IMAGING


Labs



  • Complete blood count (CBC) w/ diff, comprehensive metabolic panel (CMP), cardiac enzymes, APTT/PT, BNP


  • Serial lactate measurements and ABGs useful in following tissue perfusion and response to therapy


ECG



  • Rapid assessment of potential acute coronary syndrome (ACS), arrhythmia, or heart block


  • Although most ACS associated with cardiogenic shock presents as a STEMI, significant ST depression or other signs of ischemia should prompt consideration of early angiography in the setting of shock


  • Inferior ST elevation should prompt R sided leads to assess for RV injury or infarct


  • Isolated anterior ST depression should prompt posterior leads to assess for true posterior STEMI


Chest X-ray



  • Assess mediastinum and always consider aortic dissection



  • Pulmonary edema (1/3 of patients without pulmonary edema in the SHOCK trial)


  • Clear lungs with hypotension +/− hypoxia, consider massive PE


Echo



  • An extremely useful test for systolic function, regional WMAs, RV infarct, mechanical complications of MI, tamponade, and valvular lesions


  • Transesophageal echocardiography (TEE) may be necessary for technically suboptimal transthoracic echocardiogram (TTE), on ventilator, or to evaluate for aortic dissection (especially in unstable patients who can’t go to computed tomography (CT))


Helical CT of the Chest



  • Useful to assess for proximal pulmonary embollism (PE) and aortic dissection (sensitivity only 83% for proximal dissection in one study)


  • Sensitivity and specificity probably institutional and reader dependent


  • Even if patient is in acute renal failure (ARF) the benefits of IV contrast likely outweigh the risks in this patient population and may need to consider dialysis


  • Different phase of contrast needed for optimal PE and aortic dissection evaluations









TABLE 4-1 Etiology of cardiogenic shock































































































































































































Etiology


Findings


Acute severe LV failure (most common cause of cardiogenic shock)



Often from massive anterior infarct



ST elevation often seen



Consider in aggressive titration of HF meds → decompensation


Mechanical complications of AMI


Papillary muscle rupture or dysfunction w/ severe MR



Classically 2-7 days post-MI




More common with inferior/posterior infarct because of single blood supply to posterior papillary muscle via the RCA




Often with an early systolic murmur vs. classic holosystolic murmur because of early systolic equalization of LV → LA pressure




Echo with severe MR, +/− flail leaflet



Acute ventricular septal defect (vsd)




Higher risk with “wrap around LAD” should be alerted to this complication when anterior STEMI presents with concomitant inferior lead ST elevation (OR 17)8




Anterior MI → apical VSD




Inferior MI → basal VSD




Holosystolic murmur radiating to R sternal border often with a thrill




PO2 step-up from RA to RV/PA (use the swan that’s in!)




Echo dx by color Doppler



cardiac tamponade (free wall rupture or hemorrhagic effusion)




Beck’s triad: hypotension, distant heart sounds, JVD




Pulsus paradoxus




Echo support of dx by effusion + RA/RV diastolic collapse, PW Doppler




Swan: Equalization of diastolic pressures – RA = RVD = PAD Can see as an early complication of PCI (coronary rupture)


RV infarct



Seen most often with concomitant inferior wall MI




Check R sided leads




JVD, + Kussmaul’s sign, hypotensive response to NTG and diuretics, responds to fluids, generally clear lungs




May see bradycardia, heart block, GI symptoms from RCA ACS




Echo will show RV dilation, hypokinesis




Swan: RA pressure >10 mm Hg and RA:PCWP >0.8


Stress cardiomyopathy (Tako tsubo) Or “broken heart syndrome”



Consider as a cause of cardiogenic shock in ST elevation with normal epicardial coronary arteries



Preponderance of post menopausal females, often significant “life stressor” is identifiable




Look for apical or more rarely basal ballooning




Consider acute LVOT obstruction as an etiology of shock; if present, trial of phenylephrine


RV failure secondary to massive PE



Signs and symptoms of acute RV failure in the absence of AMI



Echo with dilated RV




Diagnosis by Helical CT angiography


Proximal aortic dissection



Pulse deficits and focal neuro exam



Suspect with widened mediastinum on CXR




Severe AI with extension to the root on Echo




Cardiac tamponade




May see inferior STEMI because the RCA is most often compromised by dissection


Tachyarrhythmias



AF/Atrial flutter w/ RVR, VT


Bradyarrhythmias



Anterior infarct → Mobitz II or CHB with slow ventricular escape




Inferior infarct → sinus bradycardia, Mobitz I → CHB usually with junctional escape


Myocarditis



Acute LV dysfunction, positive enzymes, +/− fever and viral prodrome


Endocarditis



Acute valvular regurgitation in the setting of septic picture and vegetations




Positive blood cultures


Hemorrhagic shock



Either as a primary presentation or as a complication of thrombolytics and anticoagulants




Shock with low filling pressures


Septic shock



Can see LV dysfunction in severe sepsis




Can see positive cardiac enzymes


LV, left ventricular; LAD, left anterior descending; LVOT, left ventricular outfloor tract.

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Jul 16, 2016 | Posted by in CARDIOLOGY | Comments Off on Cardiogenic Shock

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