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Rebeka Wright Recognition and Treatment of the Critically Unwell Patient Rebeka Wright PA-R, BSc (Hons), PgDip (Physician Associate studies), PGCert (Critical Care) Physician Associate Critical Care – Guys and St Thomas’ Hospital NHS Foundation Trust No conflict of interests Introduction History of critical care Correcting abnormal physiology in first instance Recognising the unwell diagnostic considerations patient second Respiratory failure Many simple interventions to correct abnormal Shock physiology can occur in ward setting Renal Failure Critical Care “care for patients who have potentially recoverable conditions who can benefit from more detailed observation ( with or without invasive treatments) then can be provided safely in an ordinary ward”. Intensive Care Society Level 2 – single organ failure, post op, stepdown from higher levels Level 3 – advanced respiratory support alone of monitoring or support two or more organ systems History of Critical Care Florence Nightingale in her observation of recovery areas near the operating theatre 1923 – Johns Hopkins Hospital USA – post op neurosurgical patients WWII and Korean and Vietnam wars Modern concept after Poli epidemic in 1952 Copenhagen positive pressure ventilation from ‘iron lung’ Further expansion in 1960s 1992 First formation of advisory committee for intensive care medicine 2001 First ICM training programme launched 2010 Faculty of ICM training Very heterogeneous – variable care nationwide Recognising the Unwell Patient Essential to recognise to Airway initiate immediate action to Airway obstruction correct abnormal physiology Impaired airway protection Breathing Anticipation of at risk patients Respiratory arrest RR<8 or >25 e.g. post op SaO2 <90%/paO2 <8Kpa on 50% FiO2 ABCDE approach pCO2 >6.5 or pH <7.3 NEWS2 >5 review by clinician HR <40 or >130 with critical care experience, Lactate >2 BE >-4 >7 MET call/peri-arrest UOP <0.5ml/kg/hr GCS <12 or drop >2 Prolonged siezures NEWS2 NEWS2 NEWS2 Monitoring Other equipment Respiratory Failure Key Concepts Causes Oxygen therapy HFNC CPAP NIV Invasive Ventilation VV- ECMO Key Concepts SaO2 indicator of oxygenation NOT ventilation. Average person at rest 1L/min TV supply metabolic demands – we breathe more for CO2 clearance Minute Ventilation = Tidal Volume (TV) x RR – pCO2 is inversely proportional to MV Simplified alveolar gas equation PAO2 = FiO2 (Patm –pH2O) – PACO2/R~0.8 • simply the more CO2 there is the less space there is for O2 . Dead space – 2ml/Kg – part of each breath that does not take part in gas exchange – anatomical and alveolar VA (alveolar volume) = RR x (TV – dead space) V/Q matching – West Zones Optimal V/Q = 1 PPV increases zone 2 V/Q 0.36 Causes respiratory Failure 1. Acute Hypoxaemic – Type 1 pO2 <8 normal or low pCO2 V/Q mismatching – Pneumonia, PE, pulmonary oedema, ARDS . 2. Ventilatory – Type 2 raised pCO2 >6.5-7 CNS depression, respiratory muscle weakness . 3. Post – Op – atelectasis and reduction FRV . 4. Type IV respiratory failure – hypoperfusion or shock. DO2 = CO x CaO2 = [(Hb x SaO2 x k) + (PaO2 x 0.023) Oxygen therapy Nasal specs, venturi Oxygen therapy in hypercapnia o Causes pulmonary vasodilatation increases shunt fraction o Haldane effect – deoxygenated Hb high affinity for O2 o Hypoxic drive HFNC CPAP – improved oxygenation PEEP prevents alveolar collapse improving recruitment thus improvement of V/Q mismatching Decrease in venous return – leading to decrease in preload and decreased work load NIV NIV mask NIV BTS guidelines NIV - non invasive ventilation Indications – acute hypercapnic respiratory failure pH <7.25 pCO2>6.5 RR >23 if persisting after bronchodilators and O2 COPD, NM disease/chest wall deformity, OSA/OHS Contraindications Absolute – severe facial deformity/burn/upper airway obstruction Relative pH <7.15 or pH <7.25 + (GCS <8, confused, agitated cognitive impairment ICU referral – impending resp arrest, NIV failing to reduce pCO2, SaO2<85% on NIV, need for sedation to tolerate, pH <7.25 or RR >25 on optimal setting – if fail NIV then ventilated mortality is increased Asthma/pneumonia – poor outcomes Complications – pressure ulcer, gastric distension, PTX 4. IPAP – inspiratory positive airway pressure aid inspiratory 5. EPAP – expiratory positive airway pressure to increase inspiratory pressure – improves PaO2 and pressure stents upper airways and recruits CO2 – 15 (20 if pH <7.25) max 30 underventilated lung – improves PaO2 – 3 unless OSA known or suspected max 8 3. Set Ti 0.8-1.2 (PC only 2. Set BUR 16-20 1. Set PC/PS NIV trouble shooting Elevated PaCO2 = increase IPAP or decrease EPAP – IPAP – EPAP = TV and MV is TV xRR Low PaO2 = increase EPAP/IPAP/both – not home NIV (max FIO2 0.5) ABG after 30-60mins Use 24/7 then taper 72hrs Invasive Ventilation Invasive ventilation Indications – RR>35 PaO2 <8 Set up on FiO2 0.5% PaCo2 >7.5 pH <7.25 GCS <8, poor sputum 1. FiO2 clearance, exhaustion, failure to improve on NIV 2. Mode- Full or partial/ volume or pressure RSI – sedative, opiate, neuromuscular blocker – 3. Full support – RR TV (6ml/Kg) or Pinsp preoxygenate-sedative- (to target TV) NMB-cricoid pressure- 4. PEEP intubation 5. I:E Cardiovascular response- Reduces RV preload, LV Increase pO2 increase FiO2/PEEP afterload Decrease pCo2 Increase MV (TV xRR) VV-ECMO Large bore cannulae venous system through oxygenator Allows lungs time to heal Not haemodynamic support Rescue method – refractory hypoxaemic respiratory faliure Potentially reversible aetiology Shock Clinical syndrome when acute circulatory failure with an inadequate or inappropriately distributed perfusion results in failure to meet tissue metabolic demands causing generalized cellular hypoxia Signs and Symptoms: Confusion, Tachypnoeia, Hypotension, Cold or cyanosed or warm and flushed, Decreased UOP Key concepts Types Management Monitoring Key Concepts - preload MAP = CO (SV x HR) x SVR SV determined by preload, afterload, myocardial contractility Preload – myocardial sarcomere length prior to contraction – EDV (echo)or EDP ( CVC/PAC) • Venous return • Ventricular compliance • Pericardial compliance • Valvular disease • Atrial kick • Ventricular wall thickness • Intrathoracic pressure Key concepts - Afterload MAP = CO (SV x HR) x SVR Afterload – sum of the forces opposing ventricular ejection = Ventricular wall stress Ventricular wall stress directly proportional to P x r/ T P = ventricular transmural pressure (ITP – Ventricular cavity pressure during ejection) r = ventricular chamber radius (increased with EDV) T = Ventricular wall thickness Key concepts - Contractility MAP = CO (SV x HR) x SVR Contractility – factors other than HR, preload and afterload responsible for changes in myocardial performance. Primarily dependent on intracellular Ca2+ • Drugs • Disease – Ischaemia, HF • Autonomic tone • Increased HR • Increased afterload Obstructive Types • Massive PE Cardiogenic • Atrial thrombus • MI and complications • Cardiac tamponade • Myocarditis • Abdominal compartment syndrome • Myocardial contusion • Tension pneumothorax • Takotsubo • Dynamic hyperinflation – asthma • Septic . Hypovolaemic • Drugs • Haemorrhage • Cardiomyopathy • Fluid loss • Dysrhythmias . Distributive • Severe AR, AS or MS • Neurogenic • LVOT obstruction • Liver failure . Endocrine/metabolic • Septic • Adrenal insufficiency • Anaphylaxis • Hypo/hyperthyroid • DKA • Severe electrolyte disturbance e.g. low Ca2+ Types of Shock High Low CVP/JVP Peripheries Cold Warm Warm Cold Low High High Low Pulse volume Cardiogenic/obstructive Sepsis/ CO2 retention Haemorrhage/ Sepsis/anaphylaxis Diagnosis Septic Fluid overload Fluid loss anaphylaxis Neurogenic, endocrine Management Shock Identify aetiology is key Correct hypoxaemia Dependent on aetiology – treat underlying cause Optimise preload Minimise Afterload Increase contractility Volume resus – optimise preload . Bleeding – blood products . Colloid e.g. albumin . Crystalloid – physiologically balanced . Assessing fluid responsiveness – straight leg raise Increase SVR MAP = CO (SV x HR) x SVR Vasopressors Alpha receptors = peripheral vasoconstriction • Noradrenaline = alpha Beta1 receptors = (beta 1) chronotrophy and inotropy Beta 2 receptors • Phenylephrine pure alpha vaso/bronchodilatation agonist • Metaraminol = alpha (beta 1+2) • Vasopressin V1 Iinocostrictors • Adrenaline = alpha and Beta 1 (beta2) Increase contractility . Inodilator • Dobutamine = beta 1, 2 (alpha) MAP = CO (SV x HR) x SVR • Levosimensan and milrinone (PDE) . Inoconstrictor • Adrenaline alpha and Beta 1 • Dopamine – low dose D1 vasodilation, intermediate B agonism, high dose Alpha agonism CO monitoring Sepsis – life threatening organ dysfunction due to dysregulated host response to infection SOFA or qSOFA (SBP <100, RR>22 GCS <15) score >2 (mortality 10%) Septic shock – MAP <65 + Lac>2 despite adequate fluid resuscitation (mortality >40%) Management – begin immediately 30ml/Kg crystalloid in 3hrs Regular review of CO (dynamic over static variables) MAP>65 if req vasopressors Fluid resus to normalise lactate Cultures Abx – broad- spectrum (within 1hr of recognition), rationalised once organism identified. Not in inflammatory conditions, duration 7-10/7, short duration, PCT Identification of source and source control Noradrenaline (need art line), dobutamine Hb>70, Plt>10 or >20 if risk of bleeding, >50 if bleeding or needing proceedure Renal Replacement Threapy Indications o Fluid overload (refractory to medical treatment) o Refractory hyperkalaemia o Uraemic pericarditis/ encephalopathy o Refractory metabolic acidosis pH<7.3 o Raised Cr Types CRRT, PIRRT, IHD CRRT – haeamodynamic instability Access HD – dialysis via diffusion HF – filtration mix Anticoagulant Exchange rate L/min – Ur/Cr, K Fluid removal / fluid balance Questions ?.
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