Acute Care and Trauma Flashcards
What is acute kidney injury (AKI)?
An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output
What is the aetiology of acute kidney injury (AKI)?
AKI may be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction, or intrinsic kidney disease
What are the risk factors of acute kidney injury (AKI)?
Advanced age
Underlying kidney disease
Diabetes Mellitus
Sepsis- may result in acute tubular necrosis, infectious glomerulonephritis, pre-kidney AKI from hypotension, or drug-induced injury from medications
Nephrotoxins e.g. aminoglycosides, NSAIDs, vancomycin
What are the pre-renal causes of an AKI?
Reduced renal perfusion:
Shock (hypovolaemic, septic, cardiogenic)
hepatorenal syndrome (liver failure)
What are the renal causes of an AKI?
Acute tubular necrosis- ischaemia, drugs and toxins
Acute glomerulonephritis
Acute interstitial nephritis- NSAIDs, penicillins, sulphonamides
Vessel obstruction- Renal artery/vein thrombosis, cholesterol emboli, vasculitis
Other causes:
myeloma, haemolysis, nephropathy
What are the post renal causes of an AKI?
Stone
Tumour (pelvic, prostate, bladder)
Blood clots
Retroperitoneal fibrosis
What is the epidemiology of AKI?
Incidence of 1800 per million
What are the presenting symptoms of AKI?
Usually asymptomatic Lower urinary tract symptoms- urgency, frequency or hesitancy Low urine output (oliguria) Malaise Anorexia Nausea and vomiting Pruritus (itching) Drowsiness Convulsions, coma (caused by uraemia)
What are the signs of acute kidney injury (AKI) on physical examination?
Oedema
What are the appropriate investigations for AKI and interpret the results?
1st line:
Basic metabolic profile- an acutely rising creatinine may be the only sign. Acutely elevated serum creatinine, high serum potassium, metabolic acidosis.
Serum potassium- elevated in hyperkalaemia
LFTs will be deranged in hepatorenal syndrome
FBC- leukocytosis may suggest an infection
CRP- elevated in infection and vasculitis
Blood culture- Positive for bacterial pathogen
Urinalysis- RBCs, WBCs, cellular casts (glomerulonephritis), proteinuria, positive nitrite, and leukocyte esterase
CXR- signs of infection or fluid
ECG- changes associated with hyperkalaemia (tented T waves)
Others:
Renal ultrasound- check for an obstructive cause
What is the management plan for acute kidney injury?
1.Assess hydration and fluid balance:
Pulse rate, lying and standing BP, JVP, skin turgor, chest auscultation, peripheral oedema, central venous pressure, fluid and weight charts. ECG monitoring (hyperkalaemia)
- If hypovolaemic (+ hyperkalaemia)
- fluid resuscitation
- review medications and stop nephrotoxins
- identify and treat underlying cause
others:
-vasoactive drug
-blood transfusion - If hypervolaemic (+ pulmonary oedema and hyperkalaemia)
- loop diuretic (under specialist supervision) and sodium restriction
- identify and treat underlying cause
consider: renal replacement therapy
Metabolic acidosis (if pH < 7.2): 50–100 mL of 8.4% bicarbonate via central line over 15–30 min
What medications can cause an AKI?
Acute tubular necrosis (ATN): paracetamol, aminoglycosides, amphotericin B (anti-fungal), NSAIDs, ACE-inhibtors, lithium
Acute interstitial nephritis: NSAIDs, penicillins, sulphonamides
Others: opioids, other antibiotics e.g. trimethoprim, vancomycin
What is the treatment for acute pulmonary oedema?
P- positioning (sit up)
O- oxygen
D- diuretic (furosemide) and fluid restriction
M- (dia)morphine
A- anti-emetics
N- nitrates (GTN infusion if SBP >110, or 2 puffs GTN spray if SBP >90)
What are the possible complications of acute kidney injury (AKI)?
Common and life-threatening: Hyperkalaemia Sepsis Metabolic acidosis Pulmonary oedema Hypertension. Less common: Gastric ulceration, bleeding (platelet dysfunction), muscle wasting (hypercatabolic state), uraemic pericarditis, uraemic encephalopathy, acute cortical necrosis
What is the prognosis for patients with acute kidney injury (AKI)?
Acute tubular necrosis has biphasic recovery starting with oliguria then leading to polyuria (resulting from regeneration of the tubular cells).
Prognosis depends on the number of other organs involved, e.g. heart, lung.
Many of those with ATN recover.
Acute cortical necrosis may cause hypertension and chronic renal failure.
What is acute respiratory distress syndrome?
A syndrome of acute and persistent lung inflammation with increased vascular permeability
What are the causes of acute respiratory distress syndrome?
(TOAST) Transfusion Overdose of drugs Aspiration Sepsis Transplantation (PIP) Pneumonia Injury/burns Pancreatitis
What is ARDS characterised by?
A - Absence of raised capillary wedge pressure
R - Reduced blood oxygen (hypoxaemia)
D - Double-sided infiltrates (bilateral infiltrates)
S - sudden onset (acute- within 1 week)
What is the aetiology of acute respiratory distress syndrome?
Severe insult to lungs
Inflammatory mediators released
Capillary permeability increases
Results in pulmonary oedema, reduced gas exchange and reduced lung compliance
(Injury, inflammation, increased permeability)
What is the epidemiology of acute respiratory distress syndrome?
Annual UK incidence 1 in 6000
What are the pathological stages of ARDS?
Exudative
Proliferative
Fibrotic
What are the presenting symptoms of ARDS?
Rapid deterioration of respiratory function
Dyspnoea
Cough
Symptoms of cause
What are the signs of ARDS on physical examination?
Think SMURF: fast, blue, noisy: Cyanosis Tachypnoea Tachycardia Widespread crepitations Hypoxia refractory to oxygen treatment (Usually bilateral but may be asymmetrical in early stages)
What are the appropriate investigations for ARDS? Interpret the results
1st line:
CXR- bilateral infiltrates
ABG- low partial oxygen pressure
Sputum/ blood/ urine cultures- positive if underlying infection
Amylase- elevated in cases of acute pancreatitis
Others:
BNP- <100 nanograms/L make HF less likely, so ARDS more likely
Pulmonary artery catheterisation- Pulmonary artery occlusion pressure (PAOP) ≤18 mmHg suggests ARDS
What is adrenal insufficiency?
Deficiency of adrenal cortical hormones (mineralocorticoids, glucocorticoids and androgens)
What is the aetiology / risk factors of adrenal insufficiency?
Primary (Addisons disease): Autoimmune (>70%)
Secondary: Pituitary or hypothalamic disease.
Surgical: After bilateral adrenalectomy.
Medical: (iatrogenic) sudden cessation of long-term steroid therapy
4Is:
- Infections: Tuberculosis, meningococcal septicaemia (Waterhouse–Friderichsen syndrome), Cytomegalovirus (HIV patients)
- Infiltration: Metastasis (lung, breast, melanoma), lymphomas, amyloidosis
- Infarction: Secondary to thrombophilia
- Inherited: Adrenoleukodystrophy 1, ACTH receptor mutation
What is the epidemiology of adrenal insufficiency?
Most common cause is iatrogenic. Primary causes are rare
What are the presenting symptoms of adrenal insufficiency?
Chronic presentation:
Non-specific vague symptoms such as dizziness, anorexia, weight loss, diarrhoea, vomiting, abdominal pain, lethargy, weakness, depression
Acute presentation: (Addisonian crisis)
Acute adrenal insufficiency with major haemody-
namic collapse often precipitated by stress (e.g. infection or surgery)
What are the signs of adrenal insufficiency on physical examination?
Postural hypotension
Increased pigmentation: Generalised but more noticeable on buccal mucosa, scars, skin creases, nails, pressure points (resulting from melanocytes being stimulated by increased ACTH levels)
Loss of body hair in women (androgen deficiency)
Associated autoimmune conditions: e.g. vitiligo
Addisonian crisis: Hypotensive shock, tachycardia, pale, cold, clammy, oliguria
What are the appropriate investigations for adrenal insufficiency? Interpret the results
Confirm the diagnosis:
9a. m. serum cortisol <100nmol/L is diagnostic of adrenal insufficiency.
- If 9 a.m. cortisol > 550 nmol/L: adrenal insufficiency is unlikely.
- Patients with 9 a.m. cortisol of between 100 and 550 nmol/L should have a short ACTH stimulation test (short SynACTHen test)
- Serum cortisol <550 nmol/L at 30 min indicates adrenal failure (primary)
Addisonian crisis:
Bloods- Haematology (FBC for neutrophilic, ESR for infection), Biochemistry (U&Es for raised urea and potassium, low sodium, CRP for infection), Microbiology (blood cultures)
Urine- MCS
What is the management for addisonian crisis?
- Rapid IV fluid rehydration (0.9% saline, 1 L over 30–60 min, 2–4 L in 12–24 h)
- 50ml of 50 % dextrose to correct hypoglycaemia.
- IV 200 mg hydrocortisone bolus followed by 100 mg 6 hourly (until BP is stable).
- Treat the precipitating cause (e.g. antibiotics for infection)
- Monitor temperature, pulse, respiratory rate, BP, sat O2 and urine output.
What is the management plan for adrenal insufficiency?
Chronic:
Replacement of glucocorticoids with hydrocortisone (three times/day) and mineralocorticoids with fludrocortisone
Hydrocortisone dosage needs to be increased during acute illness or stress
If associated with hypothyroidism, give hydrocortisone before thyroxine (to avoid precipitating an Addisonian crisis)
Advice: Steroid warning card, Medic-alert bracelet, emergency hydrocortisone ampoule, patient education
What are the possible complications of adrenal insufficiency?
Hyperkalaemia
Death during an Addisonian crisis
What is the prognosis for patients with adrenal insufficiency?
Adrenal function rarely recovers, but normal life expectancy can be expected if treated
What is alcohol withdrawal?
A patient who is alcohol dependent and has stopped or reduced their alcohol intake within hours or days of presentation
What does alcohol dependence mean?
Characterized by three or more of:
. Withdrawal on cessation of alcohol
. Tolerance
. Compulsion to drink, difficulty controlling termination or the levels of use
. Persistent desire to cut down or control use
. Time is spent obtaining, using, or recovering from alcohol
. Neglect of other interests (social, occupational, or recreational)
. Continued use despite physical and psychological problems
What are the risk factors of alcohol withdrawal?
History of alcohol withdrawal syndrome
Abrupt withdrawal of alcohol
What is the aetiology of alcohol withdrawal?
- Alcohol enhances inhibitory GABA activity and inhibits excitatory glutamate neurotransmission.
- Chronic alcohol exposure results in a compensatory reduction in GABA receptor function and upregulation of the glutamate NMDA receptors.
- Abrupt alcohol cessation leads to overactivation of the excitatory NMDA system relative to the GABA system
What is the epidemiology of alcohol withdrawal?
WHO estimates that 43% of the world population consumes alcohol, with 18.2% of drinkers aged over 15 years engaging in heavy episodic alcohol consumption
Up to 25% of people in alcohol withdrawal experience hallucinations, while seizures occur in 10% of patients.
If alcohol withdrawal is not treated or is inadequately treated, 5% of patients will progress to delirium tremens, typically 48 to 72 hours after the last drink
What is delirium tremens?
An acute confusional state caused by the withdrawal of alcohol (48–72h after cessation) Features include: -Sweating -Hallucinations/ delusions/ confusion -Coarse tremor - Agitation - Fever -Tachycardia
What are the presenting symptoms of alcohol withdrawal?
HAD A PINT
Headache
Anxiety/ agitation
Depression
Anorexia
Palpitations
Insomnia
Nausea
Tremor
others: visual hallucinations, confusion, seizures
What are the signs of alcohol withdrawal?
Signs suggestive of chronic alcohol misuse: Dupuytrens contracture Palmar erythema Bruising Spider naevi Telangiectasia- widened venules cause threadlike red lines or patterns on the skin Bilateral parotid enlargement Gynaecomastia Smell of alcohol
What are the appropriate investigations for alcohol withdrawal? Interpret the results
1st line:
VBG- respiratory alkalosis with delirium tremens
Bloods:
- FBC for thrombocytopenia, increased MCV
-Blood glucose for hypoglycaemia
-U&Es for electrolytes deficiencies e.g. hypomagnesaemia, hypokalaemia, hypophosphataemia
-LFTs for elevated liver enzymes (AST, ALT, and GGT)
- bone profile for hypocalcaemia
- coagulation studies for chronic liver disease (prolonged INR and prothrombin time)
Others:
Toxic screen- barbiturates, paracetamol
What is the management plan for a patient with alcohol withdrawal?
*ABCDE* Amobarbital (hypnotic and anxiolytic) (IV) B1 vitamin (thiamine) Chloro- Diaz- Epoxide
*chlorodiazepoxide is a benzodiazepine
What are the possible complications of alcohol withdrawal?
Seizures, delirium tremens Chronic complications include: Cerebral atrophy and dementia Cerebellar degeneration Optic atrophy Peripheral neuropathy Myopathy.
Indirect effects include hepatic encephalopathy, thiamine deficiency, causing Wernickes encephalopathy or Korsakoffs psychosis
What is the prognosis for patients with alcohol withdrawal?
Depends on complications.
Alcoholic fatty liver is reversible on abstinence from alcohol. In general, 5-year survival rates in those with alcoholic cirrhosis who stop drinking are 60–75%, but < 40% in those who continue
What is the reason for fatality in alcohol withdrawal?
Seizures (generalised tonic-clonic)
What is anaphylaxis?
Acute life-threatening multisystem hypersensivity syndrome caused by sudden release of mast cell- and basophil-derived mediators into the circulation
What is anaphylaxis characterised by?
Rapidly developing life-threatening airway and/or breathing and/or circulation problems
Usually associated with skin and mucosal changes
What is the aetiology of anaphylaxis?
Immunologic: IgE-mediated or immune complex/complement-mediated
Non-immunologic: mast cell or basophil degranulation without the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)
Inflammatory mediators such as histamine cause bronchospasm, increased capillary permeability and
reduced vascular tone, resulting in tissue oedema
What are the common allergens?
PILFERS
Peanuts Insect stings Latex Fish Egg Radiological contrast agents Shellfish
What is the epidemiology of anaphylaxis?
Relatively common
What are the presenting symptoms of anaphylaxis?
Acute onset of symptoms on exposure to allergen (SOB):
Skin (rash, pruritis)
Oedema (lips, face)
Breathing (short of breath, wheezing)
Biphasic reactions occur 1–72 h after the first reaction in up to 20% of patients
What are the signs of anaphylaxis on physical examination?
URTICARIA: Urticaria Reduced BP Tachypnoea Infected conjunctiva and swollen eyes Cyanosis Audible wheeze Rhinitis Increased heart rate Airway swelling
What are the appropriate investigations for anaphylaxis? Interpret the results
The diagnosis of anaphylaxis is made clinically.
1st line:
Serum (mast cell) tryptase (measured within 15 min–3 h after onset of symptoms)= elevated
Histamine levels (measured preferably within 30 min after symptom onset)
Urinary metabolites of histamine (which may remain elevated for several hours after symptom onset)
ABG: elevated lactate
ECG: Non-specific ST ECG changes are common post-adrenaline
What is the management plan for a patient with anaphylaxis?
Oxygen Can Help Anaphylaxis: Oxygen (100%) Chloropheniramine (10mg) Hydrocortisone (100mg) Adrenaline (IM)- 0.5 mL of 1:1,000, can be repeated every 10mins according to response of pulse and BP
Advice: Educate on use of adrenaline pen for IM administration. Provide Medicalert bracelet
What are the possible complications of anaphylaxis?
(RDS)
Respiratory failure
Death
Shock
What is the prognosis for patients with anaphylaxis?
Good if prompt treatment given
What is an arterial blood gas (ABG)?
A procedure to measure the acidity (pH) and the levels of oxygen and carbon dioxide in the blood from an artery
What are the indications for an arterial blood gas?
Respiratory failure - in acute and chronic states.
Any severe illness which may lead to a metabolic acidosis:
Cardiac failure
Liver failure
Renal failure
Hyperglycaemic states associated with diabetes mellitus
Multiorgan failure
Sepsis
Burns
Poisons/toxins
PLUS Ventilated patients
What are the possible complications of an arterial blood gas?
Local hematoma Arterial vasospasm Arterial occlusion Air or thrombus embolism Local anesthetic anaphylactic reaction Infection at the puncture site
What is aspirin overdose?
Excessive ingestion of aspirin (salicylates) causing toxicity
What are the risk factors of aspirin overdose?
Overdose can occur as a result of: Deliberate self-harm Suicidal intent By accident (e.g. in children) Ingestion of 10–20 g can cause moderate-to-severe toxicity in adults.
What is the aetiology of aspirin overdose?
- Aspirin (acetylsalicylate) increases respiratory rate and depth by stimulating the CNS respiratory centre.
- This hyperventilation produces respiratory alkalosis in the early phase.
- The body then compensates by increasing urinary bicarbonate and K+ excretion, causing dehydration and hypokalaemia.
- Loss of bicarbonate together with the uncoupling of mitochondrial oxidative phosphorylation by salicylic acid and build up of lactic acid can lead to metabolic acidosis.
What is the epidemiology of aspirin overdose?
One of the most common drug overdoses
What are the presenting symptoms of aspirin overdose?
The patient may be asymptomatic initially.
Early symptoms: Flushed appearance, fever, sweating, hyperventilation, dizziness, tinnitus, deafness.
Late symptoms: Lethargy, confusion, convulsions, drowsiness, respiratory depression, coma
OVERDOSE Over- Ventillation Ears ringing (tinnitus) Red-faced (flushed appearance) Dizziness Overtired Sweating (fever) Epileptic-looking (convulsions)
What are the signs of aspirin overdose on physical examination?
Fever
Tachycardia
Hyperventillation
Epigastric tenderness
What are the appropriate investigations for aspirin overdose. Interpret the results
ABG: initially respiratory alkalosis; later concomitant metabolic acidosis
Salicylate levels: (500–750mg/L is a moderate overdose; >750mg/L is a severe overdose)
Bloods:
-Serum electrolytes: hypokalaemia, hypocalcaemia, and/or hypomagnesaemia
-FBC: WBC may be elevated
-LFTs: AST and ALT may be elevated
ECG: May show signs of hypokalaemia – small T waves, U waves
What is asthma?
Chronic inflammatory airway disease characterized by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
What are the risk factors of asthma?
Genetic factors:
Family Hx
Atopy (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens)- eczema, atopic dermatitis, allergic rhinitis is strongly associated
Environmental factors: House dust mite Pollen, Pets (e.g. urinary proteins, furs) Cigarette smoke Viral respiratory tract infection Aspergillus fumigatus spores
What is the pathogenesis of asthma?
Early phase (up to 1 h): Exposure to inhaled allergens results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.
Late phase (after 6–12h): Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness.
Airway remodelling: the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts from cytokines and proliferative growth factors
What is the epidemiology of asthma?
Affects 10% of children and 5% of adults
Acute asthma is a very common medical emergency and still responsible for 1000–2000 deaths/year in the UK
What are the presenting symptoms of asthma?
Episodes of wheeze Breathlessness Cough Worse in the morning and at night Interfering with exercise, sleeping, school/ work
What are the exacerbating factors of asthma?
Cold Viral infections Drugs (b-blockers, NSAIDs) Exercise Emotions
What are the signs of asthma on physical examination?
Tachypnoea Use of accessory muscles Prolonged expiratory phase Polyphonic wheeze* on expiration Hyper inflated chest
What are the signs of a severe asthma attack?
PEFR < 50% predicted
HR > 110/min (tachycardia)
RR > 25/min
Inability to complete sentences
What are the signs of a life threatening asthma attack?
PEFR<33% Silent chest Bradycardia Hypotension Confusion Coma Cyanosis
What are the appropriate investigations for asthma? Interpret the results
1st line:
- FEV1/FVC: <70% of predicted
- Peak flow
- CXR: hyper inflated lungs
- FBC: Eosinophilia
What is the acute management of asthma?
O SHIT ME
Oxygen (high flow)
Salbutamol- 2.5-5mg NEB
Hydrocortisone- 100mg IV (or prednisolone 40mg PO)
Ipratropium- 500mcg NEB
Theophylline*: aminophylline infusion- 1g in 1L saline 0.5ml/kg/h
Magnesium sulphate- 2g IV over 20mins Escalate care (intubation and ventilation)
*smooth muscle relaxation (bronchodilation) and suppression of the response of the airways to stimuli
What is the chronic management for asthma? (Stepwise)
Step 1: Inhaled short acting B2 agonist as needed (if used >1 / day move to 2)
Step 2: Step 1 + regular inhaled lose dose steroids (400mcg/day)
Step 3: Step 2 + long acting B2 agonist (if inadequate control increase steroid dose to 800mcg/day)
Step 4: Step 3 + increase inhaled steroid dose to 2000mcg/day and add 4th drug (leukotriene receptor antagonist or B2 agonist tablet)
Step 5: Step 4 + addition of regular oral steroids (maintain high dose inhaled steroids) and refer to specialist
review every 3-6 months
1: SABA
2: SABA + inhaled steroid
3: SABA + inhaled steroid (high dose if needed) + LABA
4: SABA + LABA + high dose inhaled steroids + leukotriene receptor antagonist
5: SABA + LABA + high dose inhaled steroids + leukotriene receptor antagonist + regular oral steroids and refer to specialist
What are the complications of asthma?
Growth retardation
Pectus carinatum (pigeon chest)
Recurrent infections
Pneumothorax
What is the prognosis for patients with asthma?
Children: many improve as they grow
Adults: adult onset is usually chronic
What is a burns injury?
A very common injury predominantly to skin and superficial tissues caused by heat from hot liquids, flame or contact with hot objects
How is the severity of burns injuries assessed?
- Burn size (% of total body surface area)
- Depth ( first to fourth degree)
What symptoms and signs would be seen on physical examination for burns injuries?
Erythema Dry/ wet and painful Dry and lacking of physical sensation (insensate) Cellulitis If face affected- clouded cornea
What are the risk factors for burn injuries?
Young children
Age > 60 years
What are the investigations for burn injuries?
FBC: Hb, Platelets, WCC, CRP, ESR
ABG: assessment of lungs/ inhalation injury
Wound biopsy and histology
What is the management for a burns injury?
Initial treatment: wound cooling, cleaning and dressing
Then: topical antibiotic prophylaxis, tetanus immunisation and opioid analgesia
What is the prognosis for a burns injury?
*depends on the severity of the burn
Associated injuries e.g. inhalation injury/ trauma adversely affect the prognosis
What are the three severities of burns injuries and the approximate healing time for each of them?
- Superficial - 7 days
- Deep - 21 days
- Full thickness - requires skin graft
What is cardiac arrest?
Acute cessation of cardiac function
What are the reversible causes for a cardiac arrest?
4 Hs and 4Ts: Hypokalaemia Hypothermia Hypovolaemia Hypoxia
Tamponade
Tension pneumothorax
Thromboembolism
Toxins
What signs would be seen on physical examination for a a patient in cardiac arrest?
Unconscious
Patient is not breathing
Absent carotid pulses
What are the 4 cardiac rhythm disturbances?
Ventricular fibrillation (VF)
Pulseless ventricular tachycardia (VT)
Pulseless electrical activity
Asystole
What are the appropriate investigations for a cardiac arrest?
Cardiac monitor: Classification of the rhythm directs management
Bloods: ABG, U&Es, FBC, cross-match, clotting, toxicology screen, glucose.
What is the management for a cardiac arrest?
Safety: approach with caution, defibrillators and oxygen are hazards- call for help
A: Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift.
B: Assess breathing by look, listen and feel.
If not breathing, give two effective breaths immediately.
C: Assess circulation at carotid pulse for 10 s.
If absent, give 30 chest compressions at rate of 100/min. Continue cycles of 30 compressions for every two breaths.
Proceed to advanced life support as soon as possible.
What is the advanced life support for a cardiac arrest?
- Attach cardiac monitor and defibrillator
2. Assess the rhythm
What cardiac rhythms are shockable?
Ventricular tachycardia
Ventricular fibrillation
What is the management for shockable cardiac rhythms?
- Defibrillate once
- Resume CPR immediately for 2 min, and then defibrillate
- Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
- If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus
(anti-arrhythmic)
What cardiac rhythms are non-shockable?
Pulseless electrical activity
Asystole
What drug is given in asystole or PEA cardiac arrests?
Atropine (3 mg IV, once only) if asystole or PEA with rate <60/min
What is the management for non- shockable cardiac rhythms?
- CPR for 2 min, and then return to assessing rhythm
- Administer adrenaline (1 mg IV) every 3–5 min.
- Atropine (3 mg IV, once only) if asystole or PEA with rate <60/min
What is the treatment for the reversible causes of cardiac arrest?
Hypothermia: Warm slowly
Hypo- or hyperkalaemia: Correction of electrolytes
Hypovolaemia: IV colloids, crystalloids or blood products
Hypoxia: oxygen
Tamponade: Pericardiocentesis under xiphisternum up and leftwards
Tension pneumothorax: Needle into second intercostal space, mid-clavicular line
Thromboembolism: management for PE, MI
Toxins: antidotes
What are the complications of a cardiac arrest?
Irreversible hypoxic brain damage, death
What is the prognosis for patients with a cardiac arrest?
Resuscitation is less successful in the arrests that occur outside hospital.
Duration of inadequate effective cardiac output is associated with poor prognosis.
What is Blood product transfusion?
A lifesaving procedure to treat hemorrhages and to improve oxygen delivery to tissues
What are the indications for Blood product transfusion (red cell)?
Symptomatic anemia (causing shortness of breath, dizziness, congestive heart failure, and decreased exercise tolerance)
Acute sickle cell crisis
Acute blood loss of more than 30 percent of blood volume
What are the indications for Blood product transfusion (fresh frozen plasma)?
Can be used for reversal of anticoagulant effects
What are the indications for Blood product transfusion (Platelet transfusion)?
To prevent haemorrhage in patients with thrombocytopenia or platelet function defects
What are the indications for Blood product transfusion (Cryoprecipitate)?
Used in cases of hypofibrinogenemia, which most often occurs in the setting of massive hemorrhage or consumptive coagulopathy
What are the possible complications of Blood product transfusion?
Acute complications occur within minutes to 24 hours of the transfusion, whereas delayed complications may develop days, months, or even years later
*Infections are less common because of advances in the blood screening process
Non-infectious complications (acute): -Acute haemolytic reaction -Allergic/Anaphylactic reaction -Coagulation problems in massive transfusion -Metabolic derangements -Septic or bacterial contamination -Transfusion-associated circulatory overload Non-infectious complications (delayed): -Delayed haemolytic reaction -Iron overload -Post-transfusion purpura
Infectious complications:
- Hepatitis B virus
- Hepatitis C virus
- Human T-lymphotropic virus 1 or 2
- Human immunodeficiency virus
