JC C WCS 9
LOW BP/FAST PULSE & NO BP/NO PULSE
Dr Michael Irwin
Anaesthesiology
Thu 31-10-02
OBJECTIVES
- Concept of O2 delivery and its determinants
- Understand the classification of the causes of shock and their Mx
- Understand the Principles of BLS
INTRODUCTION
DETERMINANTS OF O2 DELIVERY
Oxygen content of blood (CaO2)
Ability to delivery oxygenated blood around the body (CO)
SHOCK
- Inadequate O2 delivery to meet cellular metabolic demands
- May be caused by a failure of one or more factors
- Impaired O2 delivery
- Hypoxia
- Anaerobic metabolism (inefficient)
- Acidosis (build-up lactic acid)
- Viscous cycle (as pH drops, further deterioration in cell function)
- Cell Death
- Less highly metabolic cells (eg. Fat, muscle) tolerate periods of low oxygen than other tissues (eg. Brain)
- Eg. Can apply tourniquet to a limb for up to 2hr during orthopaedic surgery
DO2 = CO x CaO2
Ie. DO2 = (HR x SV) x (Hb x SaO2 x 1/100 x 1.34) + (pO2 x 0.027)
1.34 of O2 carried per gram fully saturated Hb
0.027 ml O2 dissolved in plasma for each kPa of pO2 (partial pressure of oxygen)
Main determinant of O2 carriage is Hb
- Eg. CarboxyHb in chronic cigarette smokers (CO in Hb and inactivates it). Body compensates by increasing Hb (polycythaemia). But O2-carrying capacity is decreased, as Hb increases, viscosity of blood increases, therefore more difficult to pump blood to where it is required
- Optimal 10-13g (>13-14 oxygen delivery will decrease because CO affected)
CLASSIFICATION OF SHOCK
- Hypovolaemic - eg. Following haemorrhage (decreased fluid and Hb), burns (fluid loss), dehydration (acute GI illness)
- Cardiogenic
("pump failure") - eg. Following MI, arrhythmia
- Septic
shock - VD and myocardial depression (relative hypovolaemia), total blood vol is normal, normal 80-85% is in venous capacitance, if that is increased, has major effect on blood amount in arterial system) (may also have VD in arteries, which results in inability to maintain adequate pressure to perfuse along concentration gradient, usu occurs along with cardiogenic problem - eg. Septic shock has direct myocardial depression, therefore combination of septic shock and cardiogenic shock)
- Others
- eg. Anaphylaxis (medicines, snake bites), adrenocortical insufficiency, neurogenic (SC injury - flaccid paralysis, loss of vasomotor tone)
TREATMENT OF SHOCK
- ID the cause
- Tx appropriately
- Restore O2 delivery
- BLS: ABC
- Hypovolaemic - IV fluids and/or blood
- Cardiogenic - VD and/or inotropes (VD to remove resistance b/c heart may be shifted across)
- Septic - as above + eradication of infective focus, ABX (adrenaline commonly used)
BLS
INTRODUCTION
Initial assessment
Aw maintenance
EAV
Chest compression
BLS = no equipment
+ Aw/facemask = BLS with aw adjunct
OBJECTIVES
- Maintain adequate ventilation and circulation until means can be obtained to reverse the underlying cause of the arrest
- Eg. VF = cardiac arrest, cardiogenic shock (BLS maintains some part of O2 delivery until definitive Tx like defibrillation, which will not be any use after 10 minutes)
- "Holding operation"
- May itself reverse the cause (eg. Aw obstruction)
- Rapid deployment is essential
(irreversible cerebral damage in 3-4 mins)
- Assessment + aw
- Breathing
- Circulation
RECOGNITION OF CARDIAC ARREST
- The Dx of cardiac arrest is clinical
- LOC
- Absence of major pulse (carotid, femoral)
Note: do not feel for radial pulse in emergency (hypotensive, difficult to feel)
Lay people do not bother to check pulse in emergency situation (b/c they are not good at detecting pulse)
IS PT RESPONSIVE - YES
- Check of injuries
- Reassess
- Obtain help
IS PT RESPONSIVE - NO
- Should for help
- Open aw
- Check breathing
- Check pulse
- SLIDE: carotid pulse medial to SCM, fingers slide laterally from tracheal cartilage. Use broad part of fingers (wide SA) - more likely to palpate pulse if one is present
- SLIDE: head tilt, chin lift. If suspected cervical spine injury, careful
OPENING THE AW
("Sniffing the morning air", "Drinking a pint of beer")
- Head tilt
- Chin lift
- Jaw thrust
- Note: ¯ tone of aw with decreased consciousness. Tendency of fibromuscular larynx to collapse (but brain subconsciously increases tonic action of those m's) - LOC, those reflexes lost, walls sucked together -> stridor -> hypoxia -> cell death
- Therefore, open aw by pulling jaw forward
IS PT BREATHING - YES
- Use recovery position
- Call for help
- Recovery position: logroll Pt onto side, can be done by one rescuer. Pt's aw pushed fwd, unconscious person at risk of regurgitation and asphyxiation (cannot close larynx)
- RECOVERY POSITION ONLY USED FOR UNCONSCIOUS BREATHING PT's
IS PT BREATHING - NO?
(Pulse present)
- Ventilate (2 breaths)
- Call for help
- Continue ventilation
EXPIRED AIR VENTILATION
- Blow steadily (2 sec) into casualty's mouth and watch chest rise
- Expired air has 14% O2
- Maintain chin lift, remove mouth allow chest to fall
- Repeat Laerdal mask
- Self-inflating mask
- Hosp: bag and mask (risk of infection)
IS PT BREATHING - NO
(Pulse absent)
- Call for help
- Perform CPR
CHEST COMPRESSION
- Firm flat surface
- ID site of compression
- Apply vertical pressure with arms straight
- Depress sternum 4-5cm and release
- Repeat at 80/min
- Note: special resuscitation boards available in hospital (can slide under Pt)
CPR
- 1 pax = 15 compression : 2 ventilation
- 2 pax = 15 compression : 2 ventilations
(NOT 5:1)
SCENARIOS
SCENARIO 1
25/M motorcyclist collision with lamppost
INITIAL FINDINGS
- LOC (GCS 7/15)
- Weak, rapid pulse
- Signs of aw obstruction (stridor)
WHAT TO DO?
- A = aw (neck stabilisation and intubate)
- This Pt trauma victim - likely to have cervical spine injury
- Pt probably will not need anaesthesia for intubation (b/c unconscious), may need m relaxant. Intubation to be done by an expert
- B = breathing
- Ventilate (Ambu bag, high conc oxygen)
- C = circulation
- 14G IV cannula x 2 (L arm, L saphenous vein)
- 10ml blood for X-M (cross-match)
- Fluid b/c this Pt likely to be hypovolaemic pulse (weak pulse)
- Once Hb falls below 8 (6 in young person) - have to give blood transfusion
REASSESS
- BP 60/40
- P 150
- GCS 7/15
- # R femur
- ? # Pelvis
- R chest injury
WHY IS PT HYPOTENSIVE & TACHYCARDIC
- ? Cardiogenic problem - heart unlikely to pump blood (not likely that this young Pt has had MI)
- ? Preload problem - heart does not have anything to pump
TREATMENT
- IV crystalloid or colloid
- Warm reassess repeat
INITIAL IMPROVEMENT BUT DETERIORATION
- Decreased SaO2
- Increased aw pressure
- Decreased air entry R side
DIFFERENTIAL Dx
- Further bleeding
- Tension pneumothorax
- Cardiac tamponade
OUTCOME
- Pneumothorax on R side
- Drained
- Improvement
- Note; # ribs tear visceral pleura (every time you sqeeze bag, air forced through tear into pleural space (usu only potential space), and pressure builds in pleural space and compresses lung
- Not time to do X-ray in these Pt's
- Normally do needle thoracocentesis first
SCENARIO 2
69/M 48hr after surgery for aortic anerysectomy. Epidural local anaesthetic function - good analgesia
PRE-OP COMORBIDITIES
- Stable angina
- HT - well-controlled
- Smoker - mild COPD
FOUND
- Pale
- Sweaty
- Conscious but slightly confused
- P 130/irregular
- BP 90/50
- Note: BP relative - eg. 90/50 not normal in elderly HT male
MANAGEMENT
- A - aw (clear)
- Even if clear, always document that you have checked and that it is clear
- B - breathing (slightly tachpnoeic, O2-therapy given by mask)
- O2 is simple intervention, recommended for all critically ill Pt's (regardless of type 1 or type 2 resp failure)
- Type 1 - oxygenation failure (hypoxaemia ± hypercarbia) ® PaO2 < 8 kPa on inspired O2 of > 60%
- Type 2 - ventilatory failure (hypercarbia predominance ± hypoxaemia) ® PaCO2 > 6 kPa
- C - circulation (IV cannula inserted)
- Resuscitation trolley sent for (plan ahead)
DIFFERENTIAL Dx
- Arrhythmia (pulse fast, irregular) - ECG monitor shows atrial fibrillation (common in elderly population)
- ? Secondary to MI (peak time for post-op incidence) or ischaemia
- Peak time for post-op MI is 2-3d (as in this Pt)
- Hypotension (could be secondary to arrhythmia or excessive sympathetic block from epidural (usu not tachycardic) or surgical bleeding)
- SNS arises from T12-L2
- Less likely that he has secondary surgical bleeding b/ 2d post-op
- LA toxicity (too much, epidural catheter migrated into epidural BV, negative inotropic effect on heart because blocks channels) - usu causes bradyarrhythmia
DIAGNOSIS
- Cardiogenic shock (pump failure)
PATHOPHYSIOLOGY
- Loss of atrial contraction (AF)
- Fast HR in presence of ischaemic heart disease
- Myocardial supply demand imbalance
- Exacerbation of ischaemia
- Decreased myocardial contractility
TREATMENT
- Unstable haemodynamics - cardioversion (restoration of normal rhythm of the heart by electrical shock)
- Stable - antiarrhythmic drugs
- Many require inotropic support
- Excessive IV fluids will exacerbate this Pt's condition
- Fluid challenge - give 200ml of crystalloid/ colloid solution (if worse - no more fluid; if better - give more fluid)
Q: GLUCOSE FOR RESUSCITATION?
Do not give glucose fluids for resuscitation in these Pt's
- This shock - hyponatraemia
- Hyperglycaemic is assoc. with worse urological outcome in these Pt's
- Must be crystalloid/ colloid (also controversial which to use)
- Crystalloids largely better than colloids
- Albumin is the worst thing you can give for resuscitation
- Crystalloid (Hartmans, Ringers lactate, normal saline) - give more than you need to give for colloid
- Blood loss for surgery - give 4x estimated blood loss of crystalloid for resuscitation (b/c moves out of intravascular space into interstitial space - Pt's become oedematous, but no harm done)
- When do you give dextrose?
- Dextrose and glucose interchangeable (both CHO)
- Given for chronic maintenance fluid therapy (one dextrose 5% solution, then saline, then dextrose etc)