Page 573 - ACCCN's Critical Care Nursing

550 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

output. Vasoconstriction also further increases myocar- Respiratory support
dial work and myocardial oxygen demand, and may Varying degrees of pulmonary oedema accompany car-
worsen ischaemia. 74
diogenic shock, causing hypoxaemia due to intrapulmo-
Dobutamine has traditionally been the inodilator of nary shunt, decreased compliance and increased work
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choice, although accumulating evidence for levosimen- of breathing (WOB). Hyperventilation with respiratory
dan, a calcium-sensitising agent, suggests improved out- alkalosis may initially compensate for hypoxaemia and
comes. 71,73 However, the slow onset of action time of lactic acidosis, but fatigue during this increased WOB
levosimendan (hours) makes it a less suitable drug for may cause patient progression to hypoventilation and
acute resuscitation; other inotropes are therefore cur- respiratory acidosis. Oxygen is administered for hypox-
rently used initially and if required, levosimendan is then aemia, but responses may be limited as the primary gas
introduced. The long half-life (>5 days) of levosimendan exchange defect is an intrapulmonary shunt. Non-
confers a lasting impact on contractility after cessation of invasive ventilatory approaches may be sufficient, but a
the infusion. Milrinone is also an effective inodilator, wary eye for the need to intubate and mechanically ven-
70
but excessive vasodilation may contribute to significant tilate should be maintained in the acute phase of treat-
hypotension; in practice a concurrent vasoconstrictor ment. CPAP at conventional levels of 5–15 cmH 2 O is
(e.g. noradrenaline) may be administered. Close manage- well established as a support for the spontaneously
79
ment of intravascular fluid volume is critical when using breathing patient with pulmonary oedema. CPAP
these agents. improves hypoxaemia, lessens WOB, reduces left ven-
tricular afterload and provides additional benefit by
Dopamine and adrenaline are the major agents in the impeding venous return, an effect that may lessen pul-
inoconstrictor class, and are more effective at raising monary congestion. These benefits are weighed against
blood pressure than inodilators. Both agents also increase the potential for hypotension.
cardiac output, but when there is significant impairment
of contractility the increase in afterload may cause cardiac If hypoventilation and dyspnoea continue despite the use
output to suffer. Importantly, inoconstrictors increase of CPAP, non-invasive bi-level positive airway pressure
myocardial work and oxygen demands, raise heart rate, (BiPAP) is considered. Additional pressure support is
and increase the risk of tachyarrhythmias; these impacts applied during inspiration, above existing CPAP, improv-
are stronger with adrenaline than for dopamine. ing inspiratory efficiency, with increased tidal volume and
less work of breathing. 66,80 Endotracheal intubation and
Afterload control ventilation should be undertaken when neither CPAP nor
Specific management of afterload, independent of BiPAP result in improvement, or when the patient con-
contractility, is sometimes necessary, although caution is tinues to deteriorate or tire. Many clinicians prefer to
needed as the maintenance of blood pressure often intubate and ventilate early, even in the absence of a
provides little scope for further afterload reduction. Arte- specific respiratory need, to decrease the cardiovascular
riodilators such as sodium nitroprusside reduce afterload demands of the greater ventilatory effort. However this
and increase cardiac output, although with limitations approach is controversial as mechanical ventilation is
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due to hypotension. The introduction of oral angiotensin- associated with poorer patient outcomes and disturbs
76
converting enzyme (ACE) inhibitors as soon as possible cardiovascular balance as it exerts changes to intratho-
after stabilisation of the patient with infarct-related car- racic pressures, particularly at inspiratory initiation.
diogenic shock is strongly recommended. 77,78 Ventilation strategies largely reflect those for other com-
pliance disorders (e.g. ARDS), and are described in more
Adjunctive therapies detail in Chapter 15. Initially, full mechanical ventilation
A range of adjunctive therapies are available for refractory with little or no contribution from the patient is appro-
shock, when first-line treatments are not effective, and priate to correct arterial blood gases and lessen the
can include insertion of an intraaortic balloon pump, cardiovascular demands of the ventilatory burden. Sub-
initiation of mechanical ventilation and correction of sequent reduction of ventilatory support, as the patient’s
metabolic disturbances. These strategies are discussed respiratory ability improves, follows conventional
below in relation to cardiogenic shock. processes.
Intra-aortic balloon pumping Biochemical normalisation
Frequent biochemistry measurement is necessary to
Low cardiac output, pulmonary congestion, reduced detect and monitor the following aspects of care:
MAP, and myocardial ischaemia from cardiogenic shock
may all be improved by the introduction of intra-aortic ● arterial blood gases to identify the adequacy of venti-
balloon pump (IABP) therapy (see Chapter 12). Balloon lation and oxygenation and the presence of metabolic
inflation during diastole raises MAP and promotes coro- acidosis
nary and systemic blood flow, while balloon deflation in ● lactic acid measurement to assess the level of shock
advance of systole reduces afterload. This afterload reduc- and changes in patient response to treatment
tion improves cardiac output and reduces left ventricular ● hypokalaemia or hypomagnesaemia due to aggressive
systolic pressure, lessening the oxygen demands of the diuretic use
ischaemic ventricle by reducing the necessary contractile ● hyperkalaemia due to severe acidosis, especially in the
force of the left ventricle. presence of renal failure