Definition
Systolic BP < 90 mm Hg, or 30 mm Hg below baseline for at least 30 mins,
evidence of poor tissue perfusion and persistence of shock after correction of
non-myocardial factors (eg hypovolaemia, hypoxia, acidosis, arrhythmias)
Aetiology
Pathophysiology
Compensatory mechanisms such as salt & water retention and peripheral
vasoconstriction tend to exacerbate LV dysfunction. Also decreased perfusion
pressure, especially in the presence of multi-vessel coronary disease leads to
further depression of myocardial contractility.
Investigations
Echo for all patients to exclude surgically correctable lesion and tamponade
and to look for RV infarction
ECG: normal ECG virtually excludes possibility of cardiogenic shock caused
by MI
Treatment
optimize preload and afterload. Vasodilators should be given with extreme
caution. Nitroprusside may cause coronary steal. Vasodilators particularly
important when mitral regurgitation is a major contributing factor
inotropes. Dobutamine or
levosimendan unless shock is profound in which case drugs with
vasoconstrictor actions preferable. Phosphodiesterase inhibitors should be
reserved for those in whom catecholamines have failed to improve cardiac
performance or those in whom arrhythmia or ischaemia limits catecholamine dose
intra-aortic balloon pump. Only of value if subsequent revascularization is
possible
thrombolysis. No definite evidence that this alters prognosis. May be less
effective in patients with cardiogenic shock because of poor coronary blood
flow. Combination of thrombolysis and IABP may be more effective. Mortality
higher in those treated with t-PA compared to those treated with streptokinase
PTCA. Probably treatment of choice in cases due to IHD. Both PTCA and CABG
need to be performed within first few hours (ideally within 2-4 h) of onset of
symptoms. Result in improved survival at 6 months and 1 year although not at
30 days
CABG. May be of benefit if facilities immediately available. Operative
mortality is high
Patients with RV infarction leading to cardiogenic shock particularly
sensitive to volume depletion and prone to deterioration from bradycardia and
loss of AV synchrony due to advanced heart block. Focus of therapy should be
immediate restoration of adequate LV filling pressure, maintenance of sinus
rhythm or synchronized pacing and use of dobutamine to stimulate RV systolic
function
HOCM
usual methods used to treat cardiogenic shock exacerbate obstruction
plasma volume expansion and IV titration of beta-blockers reduce ventricular
outflow obstruction and improve cardiac output
Prognosis
poor
only about 1/3 of patients actively treated survive initial episode and many
of the survivors have continuing angina, CCF and decreased exercise tolerance
approximately 1/2 with a surgically correctable lesion leave hospital
RV function usually returns to normal in survivors of cardiogenic shock
associated with RV infarction
50% of patients who require maximal therapy and IABP to come off bypass die.
If ventricular assist device also required then only 35-45% survive.
Functional prognosis for these survivors quite good
Mortality without aggressive highly technical care is 70-90%. Hospitals
without the facilities for IABP or high-risk angioplasty and surgical
intervention should begin initial resuscitative measures and then make a rapid
decision about transfer to a hospital with the necessary resources
Myocardial stunning and hibernation
Myocardial stunning
Mechanical dysfunction of myocardium which persists despite absence of
irreversible damage and restoration of normal or near-normal coronary flow and
which recovers spontaneously.
Clinically important in 3 settings:
- after MI (especially after thrombolysis or primary angioplasty)
- after complicated coronary interventions (when myocardium may be ischaemic
for long periods, particularly if there is pre-existing LV dysfunction)
- after cardiac surgery
Mechanical circulatory support may be preferable to inotropes for patients
with stunned myocardium as inotropes may adversely influence recovery of
potentially ischaemic segments
Hibernating myocardium
Myocardium with impaired function that is persistently impaired at rest due
to decreased coronary blood flow but which demonstrates improved function when
balance between oxygen supply and demand is improved.
Dobutamine echocardiography can be used to differentiate between stunned
myocardium with a patent artery ( function that
persists during infusion) from stunned myocardium with a stenosed artery or
hibernation (initial followed by deterioration).
© Charles Gomersall July 1999, March 2006
| 
