Page 569 - ACCCN's Critical Care Nursing

546 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

TABLE 20.6 Adverse reactions to blood products

Symptom Possible diagnosis Investigation Action
Fever >1°C over baseline or Bacterial contamination Blood and Bag cultures Stop transfusion Supportive care IV antibiotics
>38°C Chills, rigors Febrile Non-Haemolytic Exclude other causes Anti-pyretics
Use leucodeplete products
Rash, hives, wheeze, Allergy Nil Slow transfusion Antihistamine
dyspnoea, hypotension Anaphylaxis Patient IgA level ABC resuscitation
Anti-IgA antibodies Adrenaline and steroid IgA deficient or
washed cells in future
Chills, hypotension, back ABO incompatibility Check ABO type DAT IAT Stop transfusion
pain, haemoglobinuria, Emergency (code or MET) call
ooze from IV sites Haemolysis EUC, Coag, Hb Haemolysis Tests Maintain BP and renal function
Bacterial contamination Blood and Bag cultures IV antibiotics if sepsis possible
Dyspnoea, productive TRALI* occurs within 6 HLA granulocyte antibody tests Stop transfusion, supportive care Notify ARCBS
cough, pink frothy hours of transfusion
sputum, pulmonary
oedema, hypotension
with TRALI
*TRALI – Transfusion related acute lung injury.

congestive cardiac failure, 53,54 trauma and obstruction or to reduce pain, improve coronary perfusion and reduce
inhibition of left ventricular ejection (referred to as oxygen demand. Treatment of the underlying cause is
obstructive shock e.g. pulmonary emboli, dissecting again critical; this may include surgery to repair obstruc-
aneurysm, tamponade) 37,53 (see Chapter 10). Myocardial tion to flow or percutaneous resolution of a coronary
depression from non-cardiac causes such as sepsis, acido- artery blockage.
sis, myocardial depressant factor, hypocalcaemia or drug
55
impact may be so severe as to present as cardiogenic
shock. CLINICAL MANIFESTATIONS
The clinical features of cardiogenic shock are reflective of
Incidence has been estimated at 3% of patients present- congestive cardiac failure, although with greater
56
ing with AMI, and mortality remains high (50–80%), severity: 50,51,58
given death from AMI overall is 7%. This is despite
treatment advances including emergency revascularisa- ● low cardiac output and hypotension
tion. 57,58 Wider distribution of interventional cardiac ● poor peripheral perfusion: pale, cool, clammy
revascularisation services has likely improved outcome peripheries
for patients who present early in the course of their ● oliguria
acute disease. ● altered mentation, restlessness and anxiety
● tachycardia and arrhythmias
Clinical signs include poor peripheral perfusion, tachy- ● pulmonary congestion with widespread inspiratory
cardia and other signs of organ dysfunction such as con- crackles and hypoxaemia (perhaps with frank pulmo-
fusion, agitation, oliguria, cool extremities, dyspnoea, nary oedema)
49
many of which are present in hypovolaemic shock. ● dyspnoea and tachypnoea
Compensatory mechanisms are conflicting for a patient ● respiratory alkalosis (hyperventilation) or acidosis
with cardiogenic shock, as cardiac workload is increased (respiratory fatigue)
on an already-failing heart yet cardiac muscle oxygen ● lactic acidosis
delivery may be compromised. A careful but rapid ● distended neck veins, elevated jugular venous
54
assessment of the clinical history is helpful in differentiat- pressure.
ing the precipitant cause of this shock.
Features consistent with the cause of the cardiogenic
Managing patients with heart failure as a result of cardio- shock may also be present, including chest pain and ST
genic shock can be challenging and is often undertaken segment changes, murmurs, features of pericardial tam-
simultaneously with preparation for definitive treatment. ponade and arrhythmias.
Maintaining perfusion is difficult, as compensatory
mechanisms usually cause further harm to the heart. In the absence of invasive monitoring, the profile of
While judicious administration of fluid is considered hypotension, peripheral hypoperfusion, and severe pul-
in terms of optimising remaining cardiac function monary and venous congestion are evident although this
(Starling’s Principle), administration of pharmacological ‘classic’ profile is not universal. On initial examination,
agents that reduce cardiac workload and improve func- 30% of patients with shock of left ventricular aetiology
tion is paramount: dobutamine for inotropic and had no pulmonary congestion and 9% had no
afterload-reducing effects via vasodilation; and morphine hypoperfusion. 59