Clinical Flashcards
Definition of acute pulmonary oedema
Rapid buildup of fluid in the alveoli and interstitium that has extravasated out of the pulmonary circulation, imparing gas exchange and lung compliance
Primary survey acute pulmonary oedema
Look at pt and assess if sick patient - sweaty, nauseated, anxious. Ask for obs and any nursing investigations already done, e.g. urine dip and ecg. Consider calling for help.
A - nil
B
-LOOK:
severely breathless
dry or pink, frothy cough
sitting upright/several pillows [Paroxysmal nocturnal dyspnoea or orthopnoea]
cyanosis
-FEEL
nil
-LISTEN:
Fine crackles- widespread or basal
-MEASURE
Sats <90% room air
Tachypnoea
ABG
CXR
-DO
15L high flow oxygen through a non rebreathe mask
C
-LOOK
Congested neck veins
Raised JVP
-FEEL
Weak pulse
-LISTEN
Gallop rhythm (3rd heart sound)
-MEASURE
Hypotensive (or hypertensive if SNS), tachycardic
ECG
Catheterise (oliguric)
Bloods: FBC, renal function, electrolytes, glucose, cardiac enzymes, LFTs, clotting, BNP, TFTs
-DO
Obtain intravenous access and give
Nitrates if SBP>90 (2spray GTN or 1-3mg isosorbide dinitrate)
Diuretic: 20-40mg slow I.V furosemide (transient venodilation)
Thromboembolic prophylaxis
D - nil
E - hepatomegaly, peripheral oedema
Causes of acute pulmonary oedema
Cardiogenic:
- Left ventricular failure (ACS, arrythmia, pericarditis, endocarditis, myocarditis, valve dysfunction)
- Increased intravascular volume (fluid overload, renal failure)
- Pulmonary venous outflow obstruction (mitral valve stenosis)
Non-cardiogenic
- High output (sepsis, anaemia, thyrotoxicosis)
- Vascular permeability (pancreatitis, eclampsia, DIC, burns)
- Environment (High altitude, downing)
- Other (head injury, drugs, PE)
Definition of acute heart failure
Acute decompensated heart failure is a life-threatening condition on a background of chronic heart failure where the heart function suddenly and severely deteriorates. Both pulmonary and systemic congestion are common findings.
Heart failure is when the heart fails to maintain blood flow to meet metabolic demand.
30-day mortality is 15% in those with NT-proBNP>5000ng/L and 5% in those with NT-proBNP<5000ng/L
Can rule out HF if NT-proBNP<300 (BNP<100)
Patients with heart failure should generally be discharged from hospital only when their clinical condition is stable and the management plan is optimised.
Primary survey acute heart failure
Look at pt for a sense of whether this is a sick patient. Ask for obs and any nursing investigations already done, e.g. urine dip and ecg. Consider calling for help - if cardiogenic shock, may require continuous heart monitoring (classically HDU).
A - nil
B
-LOOK:
severely breathless
dry or pink, frothy cough
sitting upright/several pillows [Paroxysmal nocturnal dyspnoea or orthopnoea]
cyanosis
-FEEL
nil
-LISTEN:
Fine crackles- widespread or basal
-MEASURE
Sats <90% room air
Tachypnoea
ABG
CXR
-DO
15L high flow oxygen through a non rebreathe mask
Cardiogenic pulmonary oedema + severe dyspnoea + acidaemia is an indication to call for senior to provide CPAP
C
-LOOK
Congested neck veins
Raised JVP
-FEEL
Weak pulse
-LISTEN
Gallop rhythm (3rd heart sound)
-MEASURE
Hypotensive (or hypertensive if SNS), tachycardic
ECG
Catheterise (oliguric)
Bloods: FBC, renal function, electrolytes, glucose, cardiac enzymes, LFTs, clotting, BNP, TFTs
-DO
Obtain intravenous access and give
Nitrates if SBP>90 and in hospital (2spray GTN or 1-3mg isosorbide dinitrate sublingual)
Diuretic: 40mg slow I.V furosemide (transient venodilation)
Thromboembolic prophylaxis
D - nil
E - hepatomegaly, peripheral oedema
When pt is stabilised, will need medications:
ACEI - reduce peripheral vascular resistance, myocardial remodelling
Beta blocker - slow heart rate to improve perfusion and increase end diastolic volume
Spironolactone - aldosterone antagonist (RALES study)
Diuretic -symptomatic
Consider surgical treatment of some precipitants e.g. severe aortic stenosis
SBAR handover for pulmonary oedema/ Acute decompensated heart failure
Situation: name of nurse, name of patient, ward, age, concern
Background: reason for admission, comorbidities including heart disease, renal failure, thyroid disease, treatment in hospital (including recent i.v. fluids and drugs taking), most recent obs and trend
Assessment: what is nurse’s main concern
Recommendation: does the nurse have a sense of how urgent? reassure that I am on the way, if pt deteriorates call 2222 for periarrest, retake obs, catheter and urine dip, ECG. Have notes and drug chart at bedside. Stop CCB and NSAIDs (removing beta blockers is assoc. with increased mortality - propensity dependent?)
Cause of acute decompensated heart failure
Chronic HF + Infection (e.g. IECOPD), MI, non compliance with medications, uncontrolled HTN, arrhythmia, renal failure, DM, anaemia, CCBs
No HF + Cardiac disease (MI, arrhythmias, valvular disease, cardiomyopathy), vascular (HTN)
Definition of coma
Unrousable unresponsiveness
Causes of coma
Metabolic: toxins (CO, ETOH, TCA), glucose dysregulation, hypoxia, co2 narcosis, septicaemia, hypothermia, myxoedema, addisonian crisis, hepatic/uraemic encephalopathy
Neurological: trauma, infection, vascular (clot or bleed), epilepsy
Primary assessment for coma
Find nurse, ask for all obs and ECG, tell me when done
D - remove any dangers
R - assess response by AVPU (pain by sternal rub)
2222 CRASH CALL
Lay bed flat, stabilise C-spine if hx of trauma
A
-LOOK
look inside mouth for obstructions and suction if found
-FEEL
for air on cheek, simultaneously look for chest rise
-LISTEN
stridor, snoring, gurgling
-MANAGE
with need for c-spine stabilisation, oropharyngeal and nasopharyngeal airways may give least displacement (guedel)
B
-LOOK:
airway central? cyanosis, chest rises/spontaneous breathing
-FEEL
for expansion
-LISTEN:
for symmetrical breath sounds
-MEASURE
Sats <90% room air
RR
ABG
-DO
15L high flow oxygen through a non rebreathe mask if spontaneous breathing and put in recovery position, if no RR begin 30:2 chest compressions and bag valve mask ventilation + adrenaline every 3-5 mins. If enough people, assess rhythm and consider defibrillator for VT/VF
C
-LOOK
Colour, fluid volume status whilst...
-FEEL
Pulse
-LISTEN
Heart sounds
-MEASURE
BP
HR
ECG
Bloods: FBC, renal function, liver function, clotting, glucose, blood culture
-DO
Obtain intravenous access and give
I.V pabrinex
I.V glucose
i.V naloxone or flumazenil if likely to be toxic
D - pupils, glucose consider CT head
E - expose and collect ID, medical jewellery
Reversible causes cardiac arrest
Hypoxia
Hypovolaemia
Hypothermia
Hypo/hyperkalaemia
Tension pneumothorax
Thrombosis (PE)
Tamponade
Toxins
Diagnosis anaphylaxis
A - airway angioedema, stridor
B - wheeze
C - tachycardia, hypotension, clammy and pale
D - anxiety, confusion, sense of doom, decreased conciousness
E - urticaria, itching, swelling, watering eyes, abdominal cramps, nausea, vomiting, diarrhoea
Anaphylaxis is likely when the following 3 are present
- sudden onset, rapid progression
- life threatening A, B or C problem
- Skin or mucosal changes
Blood tests for anaphlaxis
Timed mast cell tryptase (preferably at 2hrs, none at 4hrs fom symptom onset)
What is in a renal profile?
Urea Creatine Sodium Potasisum Chloride Bicarbonate
From this, various limits can be worked out:
eGFR (less accurate in high and low GFR states)
Urea-creatine ratio
Anion gap
Causes of a raised urea
Pre-renal:
Increased hepatic production
high protein diet
gastro-intestinal haemorrhage - “protein meal”
Increased protein breakdown
trauma, major surgery, extreme starvation with muscle breakdown
Increased renal reabsorption
Reduced renal perfusion (congestive cardiac failure, shock, severe diarrhoea)
Iatrogenic
Urea infusion for it’s diuretic action, drug therapy leading to an increased production e.g. tetracyclines, corticosteroid
Renal:
any cause of acute or chronic renal failure
Post-renal:
any cause of urinary outflow obstruction
Causes of a raised creatine
There is considerable variation in the excretion of creatinine based on individual patient factors, time, and method of testing.
Is a way of measuring glomerular filtration but actually measures:
creatine production (varies on gender and race)
glomerular filtration
tubular secretion
Raised creatine may indicate renal failure
What is in a liver function test?
Alanine aminotransferase (ALT) Aspartarte aminotransferase (AST) Alkaline phosphatase (ALP) Gamma glutamyl transferase (GGT or ‘Gamma GT’)
Bilirubin
Albumin
Clotting studies, i.e. prothrombin time (PT) or international normalised ratio (INR)
Anion gap equation
= ([Na+] + [K+]) − ([Cl−] + [HCO−
3]) = 3-11 mEq/L
Raised in KULT Ketones Urea Lactate Toxins e.g. alcohol and aspirin
Arterial alveolar gradient
A-a= FiO2(Patm-Ph2o) - 1.25PaCO2 - PaO2
Room air = 150 - 1.25PaCO2 - PaO2
Medication for anaphlaxis
Adrenaline 500 micrograms 1:1000
Chloramphenamine 10 mg slow I.V
Hydrocortisone 200mg slow I.V
Don’t forget O2 and fluids
Observation for at least 6 hrs - biphasic reaction
Definition acute asthma attack
Moderate:
increasing symptoms
PEF >50–75% best or predicted
Severe - any one of: PEF 33–50% best or predicted respiratory rate ≥25/min heart rate ≥110/min inability to complete sentences in one breath
Life threatening - any one of: PEF <33% best or predicted SpO2 <92% PaO2 <8 kPa normal PaCO2 (4.6–6.0 kPa) silent chest cyanosis poor respiratory effort arrhythmia exhaustion altered conscious level hypotension
Near fatal:
Raised PaCO2 and/or requiring mechanical
ventilation with raised inflation pressures
Bloods in acute asthma attack
ABG - look at blood gases, potassium, glucose
FBC
CRP
If hypotensive, U&Es
Serum theophylline (where aminophylline is used for more than 24 hours)
Medications for asthma attack (adult doses)
Salbutamol 5 mg nebulised (remember cannot give this through non-rebreathe mask)
Ipratropium bromide 500micrograms nebulised
Oral prednisolone 50mg or I.V hydrocortisone 100mg
Consult with senior staff: Life threatening asthma - I.V magnesium sulphate 2 mg
When to do a CXR in acute asthma
- suspected pneumomediastinum or pneumothorax
- suspected consolidation
- life-threatening asthma
- failure to respond to treatment satisfactorily
- requirement for ventilation
Reasons for ITU
- deteriorating PEF
- persisting or worsening hypoxia
- hypercapnia
- ABG analysis showing pH or H+
- exhaustion, feeble respiration
- drowsiness, confusion, altered conscious state
- respiratory arrest.
Airway
LOOK
- at patient- alert, talking
- in mouth - tongue, vomitus, secretions, foreign body
FEEL
- breath on cheek, also use opportunity to look for chest rise
LISTEN
- stridor, gargling, gurgling
MEASURE
- O2 (if airway compromise, need to be aware of this during interventions)
DO
- recovery position
- head tilt, chin lift
- nasopharyngeal unless basal skull fracture or coagulopathy
- oropharyngeal (guedel) adjuncts unless gag reflex present
- bag valve mask may help to keep airway patent esp if also no spontaneous breathing (two person technique)
- Laryngeal mask airway - senior support
- Secure airway (by someone else): trachea
and bronchial tree are protected from aspiration
of gastric contents or secretions by
the presence of a cuffed endotracheal tube
(or a tracheostomy
“An anaphylaxis pack normally contains two ampoules of adrenaline
(epinephrine) 1:1000, four 23G needles and four graduated 1 ml
syringes, and Laerdal or equivalent masks suitable for children and
adults. “
Breathing
LOOK
- at patient- colour, position, work of breathing
- at obs: RR and O2 sats + trend
FEEL
- symmetrical lung expansion
LISTEN
- without stethoscope - audible wheeze
- with stethoscope - crackles, wheeze, rhonchi
MEASURE
- peak flow
- ABG
- ambulatory oxygen saturations
- consider CXR request if someone around
DO
- high flow 15L oxygen through a non rebreathe mask
- nebulisers through a simple face mask - options are mucolytics (3-7% saline nebs, carbocysteine 750mg oral ), salbutamol (5mg), ipratropium bromide (500 micrograms)
- Green venturi masks (60%)/ high flow with titration according to sats for COPD
- Non invasive - CPAP or BiPAP (will need senior support) IF decompensating type 2 resp failure
- Invasive (will need anesthetist)
Circulation
LOOK
- at patient- colour, clinical hydration status (skin turgor, sunken eyes, dry mucous membranes, odema, raised JVP)
- at obvious sites of haemorrhage
- at obs: Heart rate, blood pressure
- at fluid balance chart
FEEL
- Pulse character, rate, rhythm, volume
- CRT
- Temperature of peripheries
LISTEN
- Heart sounds, murmurs, additional sounds
- If suspicion of stroke: carotids
MEASURE
- Lying and standing blood pressure
- ECG
- Bloods (so many)
- May need VBG
- ABPI
DO
- I.V access - 2 wide bore cannulae in antecubital fossae
- 250-500ml 0.9% saline I.V stat (use pressure bag, consider warming)
- Catheterise + monitor urine output
- May need O negative blood
- May need to activate major haemorrhage protocol and ask for pack 1
- May need resuscitation trolley +/- defibrillator
Disability
Pupillary reflexes
AVPU
Glucose measurement
Exposure
LOOK
- rashes, medical jewellery, superficial infection sites
Causes of AKI
Pre-renal
- Any type of shock
- Renal artery stenosis
- Renal vein thrombosis
Renal
- Tubular disease
Ischaemic
Toxic - aminoglycosides, radio-contrast, NSAIDs, rhabdomyolysis
- Interstitial disease
Acute interstitial nephritis (usually due to a drug induced allergic reaction, e.g. penicillins, NSAIDs)
Infiltrative disease: sarcoidosis, lymphoma
SLE
- Glomerulonephritis
Post renal
- Stones
- Strictures
- BPH
- Prostate cancer
Tumour lysis syndrome
High potassium, high phosphate, low calcium, low uric acid, high lactate
Investigations for glomerulonephritis
Urine MC&S
Blood:
ASLO, ANCA, Anti-GBM, Complement levels, Antinuclear antibodies
Renal biopsy
Acute tubular necrosis
Toxic: statins, myoglobin, aminoglycosides, cisplatin
Ischaemic - hypoperfusion
Investigations for AKI
Urea, creatinine, and electrolytes—to determine the stage of AKI and identify any associated electrolyte abnormalities.
• FBC—to diagnose any associated anaemia or elevated WCC suggesting infection.
• Arterial blood gas—to identify any acidosis.
• ECG—to identify any abnormalities secondary to electrolyte derangement.
• Urinalysis and microscopy—to identify any proteinuria, haematuria, or red cell casts.
• Urine culture—if infection is suspected.
• Blood culture—if infection is suspected.
• Renal ultrasound—if obstruction suspected.
Diagnosis of AKI
One from:
• serum creatinine rises by ≥ 26 µmol/L from the baseline value within 48 hours; or
• serum creatinine rises ≥1.5-fold from the baseline value that is known, or presumed to have occurred, within 1 week; or
• urine output is ‹0.5 ml/kg/hour for ›6 consecutive hours.
Management of AKI
- Adequate volume replacement
- treatment of the underlying medical condition (e.g. sepsis, haemorrhage), 3. relief of any renal tract obstruction (e.g. urinary catheterization)
- avoidance of nephrotoxic medications
Indications for dialysis
A - intractable acidosis
E - electrolyte distrubances
I - intoxicants (methanol ethylene glycol, Li, ASA)
O - intractable fluid overload
U - uremic symptoms (nausea, seizure, pericarditis)
Causes of raised sodium
Hypovolaemia
- Diuretics
- N and V
Euvolaemic
- DI
Hypervolaemic
- Iatrogenic (hypertonic saline)
- Mineralocorticoid excess e.g. Conns
- Excess intake (psychogenic or paediatric)
Causes of low sodium
Hypovolaemia
- Diarrhoea and vomiting
Euvolaemic
- SIADH
- Addison’s
- Hypothyroid
Hypervolaemic
- Heart failure
- Liver failure
- Renal failure
Causes of hyperkalaemia
Pseudo-hyperkalaemia
• Sample haemolysis
• Tourniquet use
• Sample taken from limb with IV fluids containing K+
Intra- to extracellular shift • Acidosis (e.g. DKA) • Heavy exercise • Insulin deficiency • Drugs (e.g. β-blockers, suxamethonium, digoxin toxicity)
Potassium load • Potassium supplements (orally or IV) • Crush injury/rhabdomyolysis • Burns • Tumour cell necrosis • Massive or incompatible blood transfusion • GI bleed
Decreased potassium excretion
• Acute kidney injury
• Chronic renal failure patients subjected to a K+ load
• Pre-dialysis
• Drugs e.g. NSAIDs, ACEI, K+ sparing diuretics (amiloride, spironolactone), β-blockers
• Aldosterone deficiency (e.g. Addison’s disease)
Causes of hypokalaemia
Barters/Conns syndrome(hyperaldosteronism) Alkalosis Diuretics Laxative abuse Other causes: insulin overdose Acute glucose load Diarrhoea
Treatment for stroke
300mg aspirin asap - if swallowing difficulty, can give rectally
CT head or MRI if posterior cerebral artery affected (dizziness, dyplopia, dysphasia, dysarthria)
Thrombolysis with alteplase (dosing based on weight - 0.6mg/kg) IF: bleeding risk low (including INR, HTN, clinical suspicion subarachnoid haemorrhage), within 4.5 hrs
Control blood pressure if for thrombolysis or hypertensive crisis (encephalopathy, nephropathy, cardiac failure) - remember cerebral compensation post ischaemia
Glasgow-Blatchford
Likelihood of GI bleed
Blood Pressure Pulse Melena Syncope Hepatic disease Cardiac failure Urea Haemoglobin
Rockall score predicts prognosis
Upper GI bleed medications
Pack 1 (Blood group O-) if hb<80 or massive bleed
I.V omeprazole 80mg
I.V terlipressin 2mg
Correct coagulopathy: vitamin K, FFP, platelets, octaplex
Urgent endoscopy - adrenaline, sclerotherapy, laser coag, banding
Warfarin reversal
No active bleed:
Stop warfarin (2-4days)
Vitamin K phytomenadione (4-6 hrs, 0.5mg halves INR from 5 to 2.5)
Octaplex (immediate effect for up to 6 hrs - prothrombin complex)
Active bleed:
Stop warfarin
Vitamin K and Octaplex (25-50units)
Surgery immediately:
Stop warfarin
0.5mg phytomenadione, slow i.v. injection
Acute asthma medications
Salbutamol 5mg nebs
Ipratropium 0.5mg nebs
Hydrocortisone 100mg I.V. or 60mg prednisolone oral
MgSO4 2g I.V
Consider:
amophylline 5mg/kg over 20 mins
I.V. salbutamol 2g
PE medications
Morphine 10mg, metoclopramide 10mg (unless young female - then give ondansetron 8mg)
Enoxaparin 1.5mg/kg s.c.
USS legs if clincial suspicion
Senior support:
If critically ill with a massive PE - consider thombolysis (alteplase 50mg bolus stat)
If non-resuscitatable systolic BP <90, consider ionotropic support
Pneumothorax management
No well accepted management strategy
Tension: large bore cannula in 2nd intercostal space, midclavicular line above rib
Primary: <50yrs, symptomatic, >2cm - Aspirate
using wide bore cannula
Secondary: >50 years/smoking/lung disease, >2cm - Chest drain Size 8–14Fr Admit
Secondary and >1cm, observe for 24hrs
DKA management
Adult: Fluid resuscitate according to clinical picture, then fluid replace as below. Add KCL 20mmol/L into second bag. Insulin infusion, 0.1u/kg/h actrarapid. Start 10% dextrose at BM 14
DKA - suggests need for HDU/ITU
• Blood ketones over 6 mmol/L
• Bicarbonate level below 5 mmol/L
• Venous/arterial pH below 7.1
• Hypokalaemia on admission (under 3.5 mmol/L)
• GCS less than 12 or abnormal AVPU scale
• Oxygen saturation below 92% on air (assuming
normal baseline respiratory function)
• Systolic BP below 90 mmHg
• Pulse over 100 or below 60 bpm
• Anion gap above16 [Anion Gap = (Na+ + K+) –
(Cl- + HCO3-) ]
DDX Collapse
Reflex
- Vasovagal
- Hypersensitivity (carotid sinus, situational e.g. micturition)
Cardiovascular
- Arrythmias
- Valve pathology - aortic stenosis, HOCM
- Massive pulmonary embolism
- Aortic dissection
Orthostatic
- Dehydration
- Drugs e.g. antihypertensives
- Autonomic instability (diabetes, Parkinson’s)
Neuro
- Stroke
- Epilepsy
- Head trauma
Metabolic
- Hypoglycaemia
- Toxins: alcohol, sedatives, opioids
DDx Confusion
Chronic
- Dementia
Acute
- Pain
- Sepsis
- Meningitis/encephalitis
- Stroke/ Myocardial infarction
- Brain tumour
- Post ictal state
- Hypoxia/Hypercapnia
- Hypoglycaemia/ Hyperglycaemia
- Renal failure/UTI/urinary obstruction
- Constipation
- Medication- or illicit drug-related/ alcoholic ketoacidosis/ hepatic encephalopathy
- Hypernatraemia/Hyponatraemia/Hypercalcaemia
- Dehydration (volume depletion)
Hypernatraemia management
Rehydration
Causes are mainly fluid losses [dehydration, burns, DandV] and DI
Hyponatraemia management
Hypervolamic: fluid restrict
Euvolaemic: correct cause
Hypovolaemic: 0.9% saline
Glasgow score for pancreatitis
PO2 <8kpa Age >55 Neutrophils/WBC >15 Ca >2 Renal function urea>16 Enzymes LDH > 600, AST> 200 Albumin >32 Sugar >10
Indications for CT head after head trauma
GCS less than 13 on initial assessment in the emergency department.
GCS less than 15 at 2 hours after the injury on assessment in the emergency department.
Suspected open or depressed skull fracture.
Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
Post-traumatic seizure.
Focal neurological deficit.
More than 1 episode of vomiting.
C-spine assessments
NEXUS
Canadian
Causes of raised ICP
Abscess Tumour CSF blockage Venous sinus thrombosis Cerebral odema Idiopathic intracranial hypertension
Clinical picture for raised ICP
Raised ICP headache, vomiting, altered mental state, papilloedema
Principles of HONK management
Ng tube - risk of aspiration if GCS<8
Rehydrate over 48 hours
Consider including 20mmol/L potassium as necessary
Consider insulin after 1hr, start with low amounts to avoid rapidly changing the osmolality - can be calculated based on blood sugar 0.1u/kg/hr is standard
LMWH - enoxaparin e.g. 40mg sc
Prevent pressure sores e.g. spenco boots for heels
HONK diagnosis
Osmolality> 320
Glucose >28
Hypovolaemia
Bloods for HONK
ABG - also gives PE indication
FBC (WCC for nurse) UandEs Clotting LFTs Glucose
Nurse instructions for HONK
Stop metformin Obs ECG (MI can ppt HONK) Fluid balance chart Catheterise Pressure sore prophylaxis
Thyroid storm meds
Fluid resuscitate
Propanolol 5mg
Carbimazole - senior input for dose
Hydrocortisone 100mg
Lugols iodine 4 hrs later
Treat precipitant: MI, infection, trauma, recent thyroid surgery
