Shock Flashcards
Define shock:
Global tissue hypoxia secondary to impaired perfusion.
Don’t have to be hypotensive.
Targets when treating shock:
PHYSIOLOGICAL
SBP >90 (or baseline)
MAP >65
PR <100
Central cap refill <4
CVP 8-10
PERFUSION
Urine output >0.5ml/kg/hour (1 for child, 2 for infant)
Lactate <2 (10-20% clearance per 2 hours)
CLINICAL:
Improved mental state
Improved peripheral pulses
Reduced pressor requirement
SIRS definition:
2 or more of:
Temp >38 or <36
PR > 90
RR >20
WCC >12, <4 or >10% immature or bands
Role of sodi bic in shock:
Severe acidosis:
1- Depresses myocardium/ haemodynamics
2- Reduced sensitivity to endogenous catecholamines
However, in shock it can also:
- Increase lactate
- Worsen intracellular acidosis
- Impair tissue O2 offloading
(+more)
- HyPOkalaemia
ITS ROLE IS IN NAGMA (bicarb loss), NOT RAGMA (ie. shock)
—> but okay to try.
Consider for pH 7.1 or less.
Dose: 8.4% product (contains 1mmol/ml)
Give 1mmol/kg, then HALF again 10minutely
Aim pH > 7.2
POCUS findings in different shock states:
Fluid resuscitation in shock: fluid type, complications:
No fluid type is superior
Hypotonic/ glucose fluids detrimental in critically unwell
Hartmanns or 0.9% saline at 20ml/kg suitable.
Complications:
- Hypothermia
- Coagulopathy (FFP)
- APO
- Tissue oedema (irrelevant unless compartment Sx)
- Hyperchloraemic acidosis (irrelevant)
Role of steroids in shock:
- Not routine/ well evidenced
- Reserve for:
—> known or suspected adrenal insufficiency (including steroid use)
—> refractory septic shock (improve BP but not mortality)
—> bacterial meningitis (deaf sequelae)
—> spinal cord injury (methylpred)
Eg. Hydrocortisone IV 100mg BD
Features and management of NEUROGENIC shock:
Loss of sympathetic tone (unopposed parasympathetic tone by vagus)
Hypotension (distributive, loss of SVR)
Bradycardia
Hypothermia
Flaccid paralysis below level of injury
Priapism
Urinary retention
- Norad
- Atropine
Volume assessment in shock:
- Haemoconcentration
- POCUS: Excessive (»50%) IVC variability
-Response to fluid bolus (incl straight leg raise: 300ml equivalent)
—> physiological
—> CVP change (Of 7, sustained)
-Variation in stroke vol/ pulse pressure (if ventilated)
Features and management of OBSTRUCTIVE shock:
- Signs of: tension PTx, tamponade, PE
- Murmur
- Distal ischaemia
- Source of embolism (eg. Femur #)
- POCUS: paradoxical septal movement, dilated RV, cause (tamponade, thrombus, myxoma etc.)
- **Preserve tachycardia
- Optimise preload with volume
- Norad
- Relieve obstruction**
INOPRESSORS: what are they, when to use:
Adrenaline
Noradrenaline
(Dopamine)
Norad first line for MOST SHOCK states, (including cardiogenic, where inodilator may be added later).
Adrenaline for shock where BRADYCARDIA is present, or BRONCHODILATION is desired. Additionally, ANAPHYLAXIS and POST-ARREST.
INODILATORS: what are they, and when to use?
Dobutamine
Isoprenaline
Milrinone
Inodilators are used for CARDIOGENIC SHOCK/ low cardiac output states. To increase cardiac output, whilst reducing myocardial demand via afterload.
Often added after BP initially boosted with an inopressor/pressor.
Dobutamine mainly. Isoprenaline for severe bradycardia. Milrinone for CCF patient (downregulated B receptors so other meds not as useful).
PURE PRESSORS: what are they, and when to use?
Metaraminol
Vasopressin
(Ephedrine
Phenylephrine)
REFRACTORY distributive shock (ie. catecholamine resistant state)
Adrenaline (as inopressor):
B1 ++
B2
A
**improves coronary blood flow
Alpha effect increases with dose > 0.05 microg/kg/min
Dose:
6mg in 100ml 5% dextrose
1ml/hr = 1microg/min
Start at 1-5 and titrate to BP.
If getting to 20, consider catechol resistant state (add vasopressin)
Uses:
- Arrest/ post-arrest
- Asthma
- Anaphylaxis
Adverse:
- Myocardial O2 consumption
- Lactate, worsens acidosis
- Hyperglycaemia
- Distal ischaemia
- Arrythmogenic
- Extravasation necrosis
Noradrenaline:
B1 (higher doses)
Alpha ++
First line in septic, distributive shock. Usually first in cardiogenic shock (with inodilator added later)
Dose:
6mg in 100ml 5% dextrose
1ml/hr = 1microg/min
Start 1-5 and titrate to BP
If approaching 20-30, consider catecholamine resistant state (add vasopressin)
Adverse:
- Myocardial O2 consumption
- Reflex bradycardia
- Arrythmogenic
- Hyperglycaemia
- Extravasation necrosis
RUSH protocol for POCUS in shock:
Rapid Ultrasound in SHock
”RUSH is to medical what FAST is to trauma”
Pump/Tank/Pipes approach
Echo probe
’HIMAP ED’
______
HEART- PLAX
- Contractility
- R heart collapse
- RV dilation
- Pericardial effusion
IVC
- Plethora
- Collapse
MORRISON’S
- RUQ, LUQ, bladder
AORTA
PLEURA
Ectopic
DVT
