# Definition - A clinical syndrome where tissue perfusion, and hence oxygenation, is inadequate to maintain normal metabolic function of the cells and organs # Stages of shock - Compensated shock - Compensation by - Increased cardiac output - by tachycardia and increased contractility - Increased peripheral vascular resistance - to maintain BP and shunt blood to vital organs - This is caused by neurohumoral stimulation leading to increased circulating - catecholamine - angiotensin (RAA system) - aldosterone - vasopressin - Clinical manifestation - Anxiety - Thirst - Restlessness - Tachycardia - Cold and clammy extremities (peripheries) - Reduced urine output and urinary sodium - Decompensated shock - Progressive shock - develops when normal compensatory mechanisms cannot cope with the ongoing cardiovascular insult - Refractory (irreversible) shock - without intervention, progressive shock goes into irreversible shock and the cerebral and cardiac function are so compromised that no intervention will be able to restore normal cardiovascular function # Classifications of shock ### Classification based on the mechanism - Hypovolaemic shock - [[Cardiogenic shock]] - Septic shock [[Sepsis & septic shock]] - Neurogenic or anaphylactic shock ### Classification based on physiology - Reduced return to heart (reduced preload/hypovolaemia/tank) - Reduced total peripheral resistance (reduced afterload/distributive/pipe) - Obstruction to filling (obstructive/pipe) - Pump dysfunction (cardiogenic/pump) #### 1) Reduced venous return to heart a.k.a. hypovolaemic shock - Intravascular compartment - Blood loss - external bleeding - trauma - GI bleeding - internal (concealed bleeding) - haemothorax - haemoperitoneum (ruptured AAA, ruptured ectopic) - retroperitoneum (ruptured AAA, pelvic trauma) - Plasma loss - burns - sweating/dehydration - pancreatitis - ascites (peritonitis, liver disease) - toxic epidermal necrolysis (TEN), erythroderma, pemphigus - Extravascular loss - GI loss - vomiting - diarrhoea - bowel obstruction - Renal tract - adrenal insufficiency (aldosterone deficiency) - DM (polyuria) - DI (polyuria) - Diuretics - Polyuric intrinsic renal disease #### 2) Reduced total peripheral resistance a.k.a. distributive shock - Arterial vasodilatation - Altered venous capacitance - Causes - septic shock - anaphylactic shock - neurogenic shock - vasoactive drugs (vasodilator, sedatives or toxins) - adrenal insufficiency (cortisol deficiency) - thyrotoxicosis/thyroid storm - liver failure - systemic inflammatory response features (e.g. pancreatitis, trauma, burns) - prolonged shock from any cause (decompensated shock) #### 3) Obstruction to filling a.k.a. obstructive shock - tension pneumothorax - pericardial tamponade - large pulmonary embolism/pulmonary hypertension - atrial myxoma/left atrial mural thrombus #### 4) Pump dysfunction a.k.a. cardiogenic shock - reduced contractility - systolic dysfunction - ischaemia (AMI) - myocarditis (infectious, hypersensitivity) - myocardial contusion - cardiomyopathy - toxins/drugs (CCB,doxorubicin) - impaired relaxation - diastolic dysfunction - RV infarct - arrhythmia - VT - AF (when cardiac output is dependent on atrial pumping) - bradycardia (heart block, drugs) - forward flow failure - ruptured ventricular septum or free wall - chordae tendineae rupture or papillary muscle dysfunction (Post-MI) - critical mitral or aortic stenosis - mitral or aortic regurgitation - prosthetic valve thrombus/dysfunction # Pathophysiology of shock - perfusion depends on MAP and CVP - MAP = CO x TPR - MAP falls when either of the two reduces (or both) - CO = SV x HR - MAP = SV x HR x TPR - Therefore, MAP or perfusion pressure depends on - Stroke volume - Heart rate - TPR - SV in term depends on preload (EDV), afterload (TPR), and contractility. - Hence, MAP depends on - Preload (tank) - Contractility (pump) - Heart rate (pump) - TPR (pipe) - This is the four thing that you need to review for possible fix when tackling shock. - ![[Pasted image 20260512100328.png]] # Clinical features - Initial stage: - Evidence of hypovolaemia - Thirst - Presyncopal symptoms - nausea, yawning, preferring to lie down - Compensatory mechanisms (increased CO, increased TPR) - Tachycardia (may be masked by age, drugs) - Cold and clammy extremities - reduced cap refill - difficult cannulation due to venous collapse - note: warm peripheries in distributive/neurogenic shock - Reduced urine output - When compensatory mechanisms start to fail: - hypotension - SBP <90mmHg, or - reduction of more than 30mmHg in a previously hypertensive patient - Evidence of end-organ perfusion - CNS - anxiety, agitation, drowsiness, coma - raising lactate # Management of shock ### Assessment of shock - See & Treat is the way to go - Primary survey - A - assess and support - B - high-flow oxygen to compensate for reduced delivery - consider intubation and mechanical ventilation to increased controlled variables and for respiratory support (e.g. to facilitate management of acidosis etc) - consider filling the tank first before starting PPV - C - Prevent leak - Haemorrhage control - Fill tank - IV access - Replace volume - crystalloid or blood depends on context - Crystalloid - Normal Saline vs CSL - Blood - immediately available blood products warmed by a catridge-warming device - Fix pump and pipe - inotropes/vasopressors (check below section) - Secondary survey - Chest XR - ECG - US - FELS - RUSh - IDC - Investigations - VBG/ABG - FBC, EUC, Troponin, CMP, LFT, CRP, Coags, G&H - Consider invasive BP monitoring with an art line especially if the patient is needing vasoactive drugs - Systolic pressure variation or swing of the arterial waveform baseline during respiration (usually with mechanical ventilation) is at least as sensitive as CVP or pulmonary artery wedge pressure as marker of the need for more fluid ### Interventions in shock #### Fluid therapy - What to give - =='Replace that which is lost, at the rate at which it is lost'== - Physiologic crystalloid - either NS or CSL - Albumin has no benefit compared to crystalloids ([^1]SAFE study) - Colloids cause more harm than crystalloids - Replace blood if it is lost - How to give - intravenous if possible - wide-bore IVCs at antecubital, saphenous and femoral veins - Boluses of 10-40ml/kg stat - Smaller boluses if overloaded or low EF - Important to observe whether patient is fluid responsive or not - Complications - Hypothermia - Dilutional coagulopathy - Hyperchloraemic acidosis (clinical insignificant; change to CSL) - Pulmonary oedema - Don't be afraid of pulmonary oedema in fluid therapy. - Can be due to fluid or can be due to other process - Treat with furosemide and/or PPV - Respiratory failure or the requirement for ventilation does not influence mortality in most ICU outcome studies. - Conversely, renal failure and infarction of the myocardium, brain and gut are all major risk factors for death. #### [[Inotropes and vasopressors]] - **Always fill the tank before fixing the pump and pipe** (remember Frank-Starling curve) - Noradrenaline can never go wrong as initial agent - Otherwise, choose according to possible pathophysiology - Adrenaline for cardiac output and some pressor action - Dobutamine/Milrinone for RV contractility/CO (use together with NA to prevent hypotension) - Vasopressin to increase TPR - Metaraminol to increase TPR mainly - minimal direct effect on contractility - Secondary effect increases NA -> mild NA effect - Tachyphylaxis - Dopexamine, levosimendan and the older phosphodiesterase inhibitors are rarely used in regular ED practice - How to give - Dosage - follow local guidelines - Peripherally - Norad, Metaraminol - All preferably via central access - How to titrate - 'titrate to desired effect and monitor for undesired effect' - Complications - Excessive tachycardia, hypertension, tremor, anxiety, raised ICP - Adrenaline causes metabolic effects - hyperglycaemia, hypokalaemia, lactic acidosis - myocardial ischaemia due to increased consumption - splanchnic or myocardial ischaemia (more likely to be due to inadequate resuscitation rather than vasoconstriction) - Remember, don't give 'too large, too concentrated or too rapid' #### Corticosteroids - should be reserved for adrenal insufficiency (or if patient is already on steroid) # Causes of 'unresponsive shock' (shock not responding to fluid) 1. Adrenal crisis 2. Neurogenic shock 3. Toxicological ![[Pasted image 20260510182608.png]] ![[Pasted image 20260510182259.png]] [^1]: Saline vs. Albumin Fluid Evaluation Study