3007 Exam Revision PDF

Airway Anatomy and physiology Airway assessment Look: Inspection/Observation Observe the overall appearance of your patient: Are they alert, orientated, active/hyperactive/drowsy, irritable? Colour (centrally and peripherally): Are they pink, flushed, pale, mottled or cyanosed?...

Airway Anatomy and physiology Airway assessment Look: Inspection/Observation Observe the overall appearance of your patient: Are they alert, orientated, active/hyperactive/drowsy, irritable? Colour (centrally and peripherally): Are they pink, flushed, pale, mottled or cyanosed? Respiratory rate (watching the rise and fall of the chest): What is the rhythm and depth (shallow, normal or deep)? Respiratory effort (work of breathing [WOB]): Is it mild, moderate, severe? Are they show signs of shortness of breath? Use of accessory muscles: intercostal/subcostal/suprasternal/su praclavicular/substernal retractions, head bob, nasal flaring Symmetry and shape of chest Tracheal position and tracheal tug Monitor for oxygen saturation Listen: Auscultation Listen for absence /equality of breath sounds Auscultate lung fields for bilateral adventitious noises e.g.: wheeze, crackles etc. Audible sounds: vocalisation, wheeze, stridor, grunt, cough - productive/paroxysmal Feel: Palpation Bilateral symmetry of chest expansion Skin condition – temperature, turgor and moisture Capillary refill (central/peripheral) Fremitus (tactile) Airway obstructions including types and causes Types of airway obstructions Upper airway obstructions. Lower airway obstructions Partial airway obstructions Complete airway obstructions Acute airway obstructions Chronic airway obstructions ○ Growths or tumours Causes of airway obstruction Foreign object (e.g. food, small toys etc.) Aspiration of bodily fluids (e.g. vomitus/gastric contents, blood, sputum plug) Swelling due to an immune response, anaphylaxis. Trauma (e.g. haematoma in the neck) Tumour (cancerous or non-cancerous growth near airway structures) Drug induced (decreased LOC) Poison and toxic exposure Laryngospasm Tongue obstruction: most common in unconscious patients Indications for airway management Apnea Airway obstruction Reduced LOC (particularly if GCS 90% Is there anyone else who needs to be here? ○ ?TBI → neurosurg Do we need to notify anyone else? Determine “Plan A” based on likely injuries ○ Plan B/C/D Equipment and drugs ○ ?PAN scan On pt arrival Write up MIST On the trolley ○ Everyone pays attention to the pt once they are there ○ Handover may be missed Mechanism of injury Injury sustained Signs at the scene ○ A-G Treatment initiated TRAUMA CALL Compulsory Multidisciplinary ○ Intensive care ○ Surgical ○ Anaesthetics ○ Radiology  Early attendance Organised systematic approach Blood transfusions Equipment required for blood transfusion Blood administration sets Must have 170-200 micron filter to remove clots and debris Lines must be changed when transfusion is complete or every 12 hours Bloods should not be piggybacked into other lines Compatible IV solutions Red cells ○ 0.9% N/S ○ 4% Albumin Platelets and FFP ○ 0.9% N/S Pumps/ Syringe driver Used when gravity flow is unreliable or controlled rates are required Rapid infusion devices Used to warm and administer blood rapidly in critical bleeding/ massive transfusion Different blood products e.g. Red cells Red cell transfusions ↑ O2-carrying capacity by ↑ the red cell count. Conditions include anaemia caused by ○ Chemotherapy treatment ○ Blood loss due to trauma/surgery ○ Inherited or acquired haematological disorders Platelets Prevent or stop bleeding by forming a plug that is held in place by clotting proteins. Patients may require platelet transfusions if they have a low platelet count or non-functioning platelets FFP Liquid part of blood and contains antibodies, clotting proteins and albumin. It is processed to make fresh frozen plasma (FFP) Patients may require a FFP transfusion to replace clotting factors. Signs and symptoms of transfusion reaction Fever Dyspnoea Urticaria Nurses’ responsibilities in blood administration Initial set of observations Temp HR RR BP Any existing rashes Legal responsibilities Informed consent occurred and documented Valid prescription Pt ID band attached and correct Blood product has correct pt identification and product details Two nurses must check the product Complete documentation ○ Start and finish dates and times ○ Batch number ○ Observations and outcomes in patient records Ongoing monitoring Monitored closely for the first 15 mins At least hourly throughout Escalating /what to do if the patient has a transfusion reaction Asymptomatic ≥ 38°C + rise ≥ 1°C from baseline within 4 hours of starting ○ Antipyretic ○ Continue to monitor ○ Escalate if worsening Symptomatic ≥ 38°C and rise ≥ 1°C from baseline within 15 minutes of starting or ≥ 39°C ○ Stop transfusion ○ Escalate ○ Sepsis work-up Dyspnoea ○ Stop transfusion and do not restart ○ Escalate Urticaria or rash ○ Asymptomatic less than ⅔ of the body 2–3 hours after starting Give antihistamine Continue to monitor Escalate if worsening and do not restart transfusion ○ Asymptomatic or symptomatic more than ⅔ of body early Stop transfusion Give antihistamine + corticosteroid if asymptomatic and monitor Escalate if worsening  Do not restart transfusion Implement BLS if symptomatic (Anaphylaxis) Airway obstruction Hypotension Nausea vomiting Escalate Do not restart transfusion Sepsis Sepsis pathophysiology, signs and symptoms Pathophys Infection WBC recruitment WBC release inflammatory markers (cytokines, TNF, interleukins) and other molecules to fight source of infection causing localised: ↑ Vascular dilation + ↑ Vascular permeability (leakiness) → localised ↓ Systemic Vascular Resistance (SVR) ○ In sepsis this occurs systemically as infection is all around the body: i. ↓ SVR → Low BP → low oxygenation ii. ↑ Permeability → fluid leaking into tissue instead of cells → low oxygenation + swelling iii. WBC attempt to damage infectious cells → also damage vessel walls → clotting factors release to fix damage to vessel → rate of damage to walls > rate of coagulation → bleeding out of blood vessels + coagulation blocking small blood vessel → low oxygenation iv. Highly vascularised lungs are damaged by WBC trying to fight infection → unable to oxygenate blood v. CO ↑ to improve BP → WBC damages heart cells → ↓ CO (myocardial depression) vi. ↑ anaerobic ATP production → lactic acid buildup + ineffective ATP production → metabolic acidosis + Cellular dysfunction → cellular death vii. Prostaglandins → fever ○ Hypoperfusion to organs → MODS Signs and symptoms Hypotension (early sign) Tachypnoea Hyper/ hypothermia (‘cold sepsis’) Tachycardia Low SpO2 Altered GCS Acidosis Urine dysfunction  Raised lactate, WCC or CRP Looks unwell Common sources of infection Abdomen – bowel perforation, appendix, surgical wound Lungs – pneumonia Skin – wound (open wound, drain sites, IDC etc), burn, cellulitis, Central Venous Access Device (CVAD) Urinary tract – very common any basic procedure = potentially introducing microorganisms. Central nervous system – meningitis, brain abscess DO NOT delay treatment looking for a source → early assessment & management is vital we treat symptoms while we find the cause ○ Every 1 hour delay may 7% increase in mortality Sepsis risk factors Adults Aged ≥ 65 years Immunocompromised Indwelling medical device Recent surgery or invasive procedure History of fever or rigours Known infection ATSI Fall not related to mechanism of injury Paeds < 3 months old Re-presentation within 48hrs Immunocompromised Indwelling medical device Recent surgery or invasive procedure High level of parental concern Signs of toxicity in paediatrics ○ ↓ Alertness, arousal, or activity ○ Pale or mottled colour ○ Cool peripheries ○ Weak cry ○ Grunting ○ Rigors Non-blanching rash Sepsis management - Sepsis six Blood cultures ○ FBC, EUC, CRP/PCT, LFTs, coags, glucose, urine, swabs (infection screen), WBC Urine output ○ Catheterisation Fluids IV/ IO ○ Crystalloid fluids ○ SBP > 100mmHg Antibiotics ○ Broad spectrum Lactate measurement Oxygen ○ SpO2 ≥ 95% Nursing interventions and rationales Prevention - Knowledge to identify signs of deterioration Early recognition - Understand what is happening on a pathophysiological level Early intervention - Skill to implement interventions to prevent deterioration Process of escalation/sepsis pathway 1. Recognise any signs of infection 2. Recognise any risk factors 3. Escalate to: a. Blue i. One or less yellow zone criteria ii. Continue to monitor for other criteria and treat b. Yellow i. Two or more yellow zone criteria including Lactate ≥ 2 ii. Clinical review c. Red i. Any one of the following: 1. SBP < 90mmHg 2. Lactate ≥ 4 3. Base excess < -5.0 ii. Rapid Response 4. Adult Sepsis Pathway a. Assess and maintain airway b. BUFALO Arterial Blood Gas interpretation Normal values of an ABG pH 7.35 - 7.45 CO2 35 - 45 mmHg HCO3 22 - 26 mmol/L PaO2 80 - 100 mmHg SO2 96% - 98% Memorise the top 5 K+ 3.5 - 5.0 mmol/L Na+ 135 - 145 mmol/L Lactate 0.5 - 1.0 mmol (keep < 2) Hb Dependent on pt Ca++ 2.1 - 2.6 mmol/L pH = H+ ion concentration in the ECF Acidemia = low pH Alkalemia = high pH Acid = chemical compound that can give up a free H+ ion Respiratory acid - CO2 Metabolic acid - keto acids, lactic acids No insulin = breakdown of fat stores and proteins = ketone production Base = compound that can accept a free H+ ion Bicarbonate (HCO3) main Proteins, phosphate and ammonia Respiratory acidosis Cause ↑ CO2 retention COPD Pulmonary oedema Severe pneumonia Pathophys ↑ CO2 retention from hypoventilation Compensatory response is ↑ HCO3 retention by kidney Respiratory alkalosis Cause ↑ CO2 clearing Hyperventilation Liver failure Pathophys ↑ CO2 excretion from hyperventilation Compensatory response is ↑ HCO3 excretion by kidney Metabolic acidosis Cause DKA Lactic cause (Sepsis) Shock Renal failure Pathophys Gain of fixed acid, inability to excrete acid or loss of base Compensatory response is ↑ CO2 excretion by lungs Metabolic alkalosis Cause Vomiting NG suctioning Diuretic use Hypokalaemia Pathophys Loss of strong acid or gain of base Compensatory response is ↑ CO2 retention by lungs Burns Management Anatomy & function of skin Thermoregulation – can get hypothermic Fluid and electrolyte imbalance – fluid loss, hypovolemic shock Immune response – loss of layer of skin protecting body Protection from bacterial invasion Neurosensory interface – loss of nerve endings (depends on the depth of the burn) Pathophysiology of burns including burn depths Zone of Coagulation (Necrosis) This part of tissue is damaged and unable to be fixed immediately Zone of Stasis (Damage) Can be saved with nursing care Zone of Hyperaemia (Survival) Will survive no matter what Systemic responses Burns ≥ 20% → systemic response  Release of inflammatory mediators (histamine, prostaglandins) + neural stimulation → ↑ vascular permeability → systemic swelling + hypovolaemia → hypovolaemic shock Mass movement of albumin into interstitial space → swelling + hypovolaemia Release of cortisol due to stress → adrenaline released → vasoconstriction shunting blood to core organs → ↓ perfusion to kidneys → AKI → impact to electrolyte and fluid balance Adrenaline release → ↑ HR → ↑↑↑ metabolic demand → immunosuppression + ↑ protein breakdown Inflammatory response → ↑ vascular permeability → ↑ fluid in lungs → pulmonary oedema → acute respiratory distress syndrome (ARDS) Causes Flame → Fire Scald → Steam Contact → Hot metal Chemical → Acid Friction → Vehicle Radiant heat → Heater Electrical → Lightning Reverse thermal → Frostbite Nursing management of burns in the: Pre-hospital care (First aid) Stop burning process Remove all clothing 20min Cool running water Effective within 3hrs of injury Emergent phase (First 72 hours Resuscitative): Airway ○ Early intubation ○ Secure C-spine if necessary ○ ?airway swelling ○ ?Inhalation burns Breathing ○ Ventilation ○ O2 therapy ○ Burns to torso can cause swelling and inelasticity → ↓ ability to ventilate properly Consider escharotomy Circulation ○ Fluid resuscitation ○ Establish IV access ○ Insert IDC ○ Bloods  Disability ○ GCS ○ Pupils ○ other factors e.g. D & A ○ Prevent secondary injury ○ Analgesia Exposure ○ Keep warm → prevent hypothermia ○ Remove jewellery ○ Assess how much the total body surface area is burned Secondary assessment including head-to-toe or systems-based assessment once patient is more stable. Remember to check electrolytes! Patient history including: ○ A – Allergies ○ M – Medications ○ P – Past Illnesses ○ L – Last Meal ○ E – Events/Environment related to injury Psychosocial assessment Gather following information: ○ Date & time of burn injury → important because fluid management is from time of injury ○ Date & time of first presentation ○ Source of injury & length of contact time ○ Clothing worn ○ Activities at time of burn injury ○ Adequacy of first aid (what first aid action + how long) Ice causes vasoconstriction Acute phase (Wound healing) Mobilisation of extracellular fluid + subsequent diuresis Main aims of care: ○ Wound care REMOVE Exudate Serocrusts Pus Debris Slough Necrotic tissue Loose macerated skin Haematomas  Foreign Bodies REDUCE Odour Bioburden Excessive moisture PREPARE Wound bed for visualisation and dressing application PROMOTE Epithelialisation Wound contracture Moisturising of healed areas Twice weekly skin care ○ Excision and grafting ○ Pain management ○ Physical and occupational therapy ○ Nutritional therapy TBSA assessment (rule of nines) – consider differences between adults and paediatrics Fluid resuscitation/ urine output goals (Modified parkland formula) In burns ≥ 20% For first 24 hours: 2–4 mL Hartmann's × patient's weight in kg × %TBSA burn ○ ½ given in first 8 hours  ○ ¼ given in the second 8 hours ○ ¼ given in the third 8 hours In paeds ≥ 10% Circumferential Burns Implications Circumferential burn → swelling → compresses muscles, blood vessels, etc. → insufficient blood supply → ischaemic → pain Swelling → ↓ ability to breathe Nursing responsibilities Escharotomy Monitor circulation of peripheries Triage Understanding of background/ rationale for triage The purpose of triage is to ensure emergency care is delivered according to clinical urgency and patient need. Australasian triage scale categories and definitions 1 – Immediate 2 – Emergency /Imminent threat to life (