(2) Approach to Shock Flashcards
Definition of shock
Circulatory shock: an abnormality of the circulatory system that results in reduced organ perfusion and tissue oxygenation
causes of shock are broadly caused by
- reduced cardiac output e.g. hypovolaemic, cardiogenic, obstructive
- reduced systemic vascular resistance e.g. septic shock, anaphylactic shock
summary of 4 main types of shock
CHOD
Cardiogenic
Hypovolaemic
Obstructive
Distributive
causes of hypovolaemic shock
- haemorrhage
- vomiting
- diarrhoea
- diuresis e.g. post catheter
- burns
- third spacing e.g. pancreatitis, severe sepsis, anaphylaxis)
causes of cardiogenic shock
- Myocardial infarction
- Cardiomyopathy
- Cardiac arrhythmia
- Tachy or brady
- Negatively inotropic drug overdose (e.g. beta blockers or CCB)
cause sof Obstructive shock
- Tension pneumothorax
- Massive PE
- Cardiac tamponade
causes of Reduced systemic vascular resistance (SVR):
- Septic shock
- Anaphylactic shock
- Neurogenic shock
why treat shock as early as possible
- Effects of shock are initially reversible, but rapidly become irreversible, resulting in multiorgan failure and death
- Initiate treatment early
Features of shock
- Hypotension
- Tachycardia
- Oliguria
- Abnormal mental state
- Tachypnoea
- Cool, clammy, cyanotic skin]
- Metabolic acidosis
- Hyperlactatemia
- Others
o Chest pain and ECG changes e.g. anterior wall MI
o Fever and cough or history of ongoing UTI
o RTA and patient has head and spinal cord injuries, quadriparesis and paraplegia
o History of insect bite, lip swelling and rash
o Central abdominal pain, patient unresponsive
o Abdominal pain, vomiting and diarrhoea since 3 days
o History of AF, presented with HR 180, sweating and SOB
blood pressure is related to
BP = CO x SVR
c
cardiac output
CO is the volume of blood pumped by the heart per minute and is in turn related to heart rate (HR) and stroke volume (SV) as follows:
CO = HR x SV
stroke volume
is the volume of blood pumped by the heart per contraction and is determined by
* Preload
* Myocardial contractility
* Afterload
Preload
- Preload is the ventricular wall tension at the end of diastole and reflects the degree of myocardial muscle fibre stretch; it is determined by volume status, venous capacitance and the difference between mean venous pressure and right atrial pressure
- Preload is related to SV by the Frank-Starling mechanism; increased fibre length initially leads to an increased SV but above a certain point, the fibres become overstretched and further filling results in a decreased SV, as is the case in cardiac failure
Myocardial contractility
is the intrinsic ability of the heart to work independently of preload and afterload; positive inotropes increase the contractility, shifting the Frank-Starling curve upwards
afterload
Afterload is the pressure that the heart must work against to eject blood during systole.
why does shock cause lactic acidosis
- Regardless of the cause of shock, inadequate organ perfusion and tissue oxygenation results in cells switching from aerobic to anaerobic metabolism
- This generates a lactic acidosis that disrupts the cellular environment and causes myocardial depression
History in a shocked patient
Assessment of severity
* Dyspnoea
* Confusion
* Light-headedness
* Drowsiness
* Oliguria/anuria
Symptoms of the cause
approach to shock
a to e
Airway
- May be compromised by reduced conscious level
Breathing
- Hypoxia
- Tachypnoea
- Kussmaul’s breathing: hyperventilation to compensate for metabolic acidosis manifesting as ‘air hunger’
Circulation
- Cold, pale peripheries
- Prolonged capillary refill times (CRT >2 s)
- Tachycardia
- Hypotension
- Oliguria
- Anuria
Disability
- Confusion
- Drowsiness
- Unconsciousness
Investigation of shock
- Bloods including blood gas to check pH and lactate
- Electrocardiogram (ECG)
- Chest radiograph (CXR)
- Echocardiography
In trauma
* Pelvic XR
* CT chest/abdo/pelvis as indicated
* FAST
initial management of shock
- Assess the patient from an ABCDE perspective
- Maintain a patent airway
- Use manoeuvres, adjuncts, supraglottic or definitive airways as indicated and suction any sputum or secretions
- Deliver high flow oxygen 15L/min via reservoir mask to keep sats over 94%
- Attach monitoring
- Pulse oximetry and non-invasive blood pressure
- Three-lead cardiac monitoring
- Request 12 lead ECG and portable CXR
- Obtain large-bore intravenous (IV) access and take bloods including blood gas to check pH and lactate
- Fluid resuscitation IV
- Urethral catheterisation and fluid balance monitoring aiming for a urine output >0.5 ml/kg/hour
If BP fails to respond consider referral to HDU/ICU for
* Central line insertion with central venous pressure (CVP) and central venous oxygen saturation (ScvO2) monitoring
* Arterial line insertion and invasive arterial BP monitoring
* Vasopressor and/or inotrope infusion
further management of shock: haemorrhagic
Identify the source(s) of bleeding and achieve haemorrhage control e.g. direct compression, pelvic binder, splinting of long bone fractures, surgical ligation of bleeding vessels
Restoration of adequate circulating volume:
- Cross-match blood and activate the major haemorrhage protocol
- Transfuse O negative blood initially, followed by type-specific and fully cross-matched blood as soon as it is available; aim for permissive hypotension
- Correct coagulopathy by transfusion of platelets, fresh frozen plasma and cryoprecipitate as appropriate
further management: septic shock
broad spec antibiotics such as meropenem
further management: anaphylactic shock
Adrenaline 0.5 mg intramuscular (IM) for anaphylactic shock
further management: tension pneumothorax
Needle thoracocentesis and intercostal chest drain insertion for tension pneumothorax
further management: cardiac tamponade
Pericardiocentesis and thoracotomy
further management: massive PE
Thrombolysis
further mangeemnt: unstable tachyarrythmias
Synchronised direct current (DC) cardioversion
further mangement: unstable bradyarrhythmias
pacing
