ACC Flashcards
What is the trimodal distribution of trauma death?
FIRST: at time of injury (secs to mins)
SECOND: mins to hrs post injury
THIRD: days to weeks post injury
How is major trauma defined?
Patients with injury severity score (ISS) >15
What is the ABCDE approach when there is life threatening injury?
A: Airway management with cervical spine protection
B: Breathing and ventilation
C: Circulation with hemorrhage control (stop bleeding)
D: Disability and neurological status (GCS)
E: Exposure and environment (don’t let people become cold)
What are the main features of an airway assessment?
1) ADEQUACY: assess for signs of obstruction
2) INJURIES: compromising airways?
3) MANAGE INADEQUATE AIRWAY IMMEDIATELY
4) DEFINITIVE AIRWAY
What are the signs of obstructed airway?
- absent breath sounds
- snoring/ stridor/ gurgling
- hoarse voice
- obtundation (reduced conscious level)
- cyanosis
- paradoxical movements/intercostal recession/ accessory muscles
- tracheal deviation
- laryngeal crepitus
What are examples of injuries that could compromise the airway?
- facial fractures
- facial burns
- neck wounds
- epistaxis/vomiting
- head injury with low GCS
What is the immediate management for an airway?
- head tilt/chin lift
- jaw thrust
- oropharyngeal airway (Guedel airway)
- nasopharyngeal airway
- laryngeal mask airway
What are examples of definitive airways?
ET intubation
SURGICAL AIRWAYS
- emergency cricothyroidotomy
- tracheostomy
What can be done to protect the cervical spine in acute injury?
- hard collar, tape and blocks applied
- manual in-line stabilization
What are the signs of ventilatory compromise?
- inadequate or asymmetrical chest rise and fall
- labored breathing
- decreased or absent air entry
- low oxygen sats
What are the injuries that could compromise ventilation (ATOM FC)?
ATOM FC
A- airway obstruction
T- tension pneumothorax
O- open chest wound
M- massive haemothorax (>1500ml blood)
F- flail chest
C- cardiac tamponade
OTHERS INCLUDE
- simple pneumothorax
- blunt cardiac injury
- traumatic aortic disruption
- trachaeobronchial tree injury
- pulmonary contusion
- esophageal rupture
- diaphragmatic injury
- haemothorax
What are the signs suggestive of thoracic injury?
- Abnormal oxygen sats or respiratory rate
- Abnormal chest movement
- Chest wall bruising, wounds, surgical emphysema
- Rib, clavicular, scapular or sternal fractures
- Tracheal deviation
- Abnormal air entry
How is inadequate ventilation managed?
- Optimise oxygenation (15L NRBM)
- Needle/tube thoracocentesis
- Pericardiocentesis (for cardiac tamponade)
- Consider need for intubation
How is shock defined?
A clinical syndrome caused by INADEQUATE TISSUE PERFUSION and OXYGENATION LEADING TO ABNORMAL METABOLIC FUNCTION
What are the causes of shock in trauma?
- haemorrhagic (hypovolemic)
- obstructive
- cardiogenic
- neurogenic
What is involved in the assessment for shock (HEP B)?
H- hands: temp, sweating, cap refill
E- End organ perfusion: conscious levels, UO
P- Pulse: rate, regularity, quality
B- Blood pressure: hypotension (late sign- stage 3 haemorrhagic shock)
Check for blood loss
- external wounds
- chest cavity
- abdo cavity (+ retroperitoneal)
- pelvic cavity
- long bone fractures
What is done in a circulation assessment?
Assess for signs of shock
Any injuries which could or WILL cause shock?
How is inadequate circulation managed immediately?
- Optimise oxygenation (15L NRBM)
- Splints/tourniquet/ direct pressure for active haemorrhage
- 2x large bore IV access in anterior cubital fossa
- fluid resuscitation: warm crystalloid, blood
- IV tranexamic acid if haemorrhaging
- Consider activation of massive transfusion protocol
- Definitive haemostasis
What is the TRAUMA TRIAD OF DEATH?
1) HYPOTHERMIA
2) COAGULOPATHY
3) ACIDOSIS
How does acidosis occur in trauma?
Haemorrhage leads to REDUCED OXYGEN DELIVERY which leads to ACIDOSIS due to INCREASED LACTATE
What causes hypothermia in trauma?
HYPOPERFUSION and DECREASED HEAT GENERATION-
can induce coagulopathy, arrhythmias, increases SVR, reduces CO and left shift to Hb curve
What causes coagulopathy in trauma?
induced by activation of fibrinolytic system and haemodilution from fluids
What is reviewed in the disability portion of ABCDE approach?
- Review ABC, check not hypoxic or hypotenisve
- Check drug chat
- Examine pupils
- GCS and AVPU
- Check lateralising signs
- Capillary glucose
- Airway protection
What is reviewed in the examination portion of ABCDE approach?
- Examine the patient
- eFAST: beside US to look for pneumothorax, haemothorax, pericardial effusion + intraperitoneal haemorrhage. Fluid is black on the scan. Peri-hepatic, splenic, pelvic, pericardial and anterior thoracic views.
- Check temperature
- Take a history and reassess
What is the main goal in management for head trauma in hospital?
To prevent secondary brain injury caused by:
- inadequate oxygenation
- hypoperfusion
- hyperglycemia
What are the severity scores for GCS assessment?
MINOR: GCS 13-15
MODERATE: GCS 9-12
SEVERE: GCS 3-8
GCS <8 = coma
What are the eye opening scores for GCS?
4 spontaneous
3 to voice
2 pain
1 none
What are the verbal response scores for GCS?
5 orientated 4 confused 3 inappropriate words 2 sounds 1 none
What are the best motor response scores for GCS?
6 obeys commands 5 localises to pain 4 normal flexion 3 abnormal flexion 2 extension 1 none
What is involved in a disability assessment following head trauma?
check for signs of head injury:
- facial/scalp bruising or hematoma
- scalp or facial lacerations
- pupil size and reaction
- capillary glucose
- GCS (if <8 early involvement of anaesthetist)
- Manage neurodisability
What are the steps for managing neurodisability?
- Optimise oxygenation
- Maintain cerebral perfusion (BP>90/>65)
- Avoid hyperglycemia
- Avoid pyrexia
- manage pain effectively- can lead to rise in ICP
- Definitive imaging and treatment
What is the NICE criteria for performing a CT head within 1 hour?
1) GCS <13 on initial assessment in ED
2) GCS <15 at 2hrs after injury on assessment in ED
3) Suspected open or depressed skull fracture
4) post traumatic seizure
5) Sign of basal skull fracture
6) Focal neurological deficit
7) >1 episode of vomiting
What is the NICE criteria for CT head within 8 hours of injury?
1) >65 years old
2) >30mins retrograde amnesia of events immediately before head injury
3) any history of bleeding/clotting disorders/ on warfarin
4) dangerous mechanism of injury
What are the signs of basal skull fracture?
- haemotympanum
- ‘panda eyes’
- CSF leakage from ear or nose
- Battle’s sign (bruising over mastoid process)
What is cerebral perfusion pressure defined as?
CPP = MAP - ICP
mean arterial pressure- intracranial pressure
What is the Monro-Kellie hypothesis?
The cranial compartment is incompressible and the volume inside the cranium is fixed
Cranium and its constituents (blood, CSF, brain) are therefore in a state of equilibrium.
An increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another
What is the pathophysiology of traumatic brain injury?
- As ICP increases, CPP decreases
- The response to this is to RAISE systemic blood pressure and DILATE CEREBRAL BLOOD VESSELS
- But, this ACCELERATES INTRACRANIAL HAEMORRHAGE and INCREASES ICP due to increased cerebral blood volume, lowering CPP further
- Cushing response is a pre-terminal sign
What is Cushing response?
- hypertension
- bradycardia
- irregular respiration
What are the lateralising signs associated with raised ICP?
- dilated pupil, sluggish then fixed
- aphasia
What is the most common injured spinal area?
CERVICAL (55%)
How are spinal injuries classified?
Split into COMPLETE and INCOMPLETE injury, 1 week post injury.
What is the sign on incomplete spinal injury?
SACRAL SPARING- perianal sensation
How is spinal injury clinically diagnosed?
- Presence of neurological deficit
- Presence of pain or tenderness along the spine
- No distracting injury should be present
- Patient should not be intoxicated
What is the log roll?
Manoeuvre used to move trauma patient and allows posterior to be examined without active movement.
How many people are required to perform log roll manoeuvre?
FIVE
1- to stabilise neck
3- to roll
1- to examine back/spine and perform DRE
What are the various spinal cord syndromes?
1) central cord syndrome
2) anterior cord syndrome
3) brown-sequard syndrome
4) complete spinal cord syndrome
What is central cord syndrome?
- incomplete injury to cervical cord leads to more extensive motor weakness in upper limbs than lower.
- the mechanism of injury for central cord syndrome is a hyperextension injury with pre-existent cervical spondylosis- without damage to the vertebral column.
There is a variable degree of sensory loss below level of injury in combination with bladder dysfunction and urinary retention.
What is anterior cord syndrome?
- interrupted blood supply to the anterior portion of spinal cord.
- characterized by loss of motor function below level of injury
- loss of sensations carried by spinothalamic tracts (pain and temp.)
- preservation of sensation carried by posterior columns (fine touch and proprioception)
- may have: areflexia, flaccid anal sphincter, urinary retention, intestinal obstruction
What is brown-sequard syndrome?
- lateral hemisection of spinal cord
- ipsilateral loss of motor function
- ipsilateral loss of vibration sense
- ipsilateral loss of fine touch and proprioception
- contralateral loss of pain and temperature
What is complete spinal cord syndrome?
- complete loss of sensory and motor function usually only clear 6-8 weeks after injury
What are the signs of spinal injury?
- diaphragmatic breathing
- evidence of neurogenic shock (low BP+ bradycardia)
- responds to pain only above clavicles
- priapism (prolonged erection)
- flexed posture of upper limbs or flaccid areflexia
- patient complains of loss of sensation or function
- spinal tenderness, bruising or swelling on log roll
How is spinal injury managed immediately?
- optimise oxygenation
- ensure adequate ventilation
- maintain spinal cord perfusion- avoid hypotension
- maintain immobilisation
- document thorough spinal cord examination
- urinary catheterization and NG tube
- definitive imaging
- early specialist advice
What constitutes most MSK trauma?
- pelvic fractures
- limb injuries
What are the signs of MSK trauma?
- limb deformity or amputation
- patient localising pain to limb/body part
- soft tissue injury or wounds
- splinting applied pre-hospitally
- pelvic instability- do not spring pelvis
- neuromuscular compromise
How is MSK injury managed immediately?
- optimise oxygenation
- maintain tissue perfusion (avoid hypotension)
- apply splints (reduce blood loss, pain and improve alignment)
- analgesia
- IV antibiotics
- Monitor complications: compartment syndrome, skin necrosis, nerve compression
What are commonly used trauma scores?
- AIS (abbreviated injury scale)
- ISS (injury severity scale)
- RTS (revised trauma score)
- TRISS (trauma score- injury severity score)
What are the general principles of the RRAPID
Initial assessment:
- If patient not breathing and has no pulse- COMMENCE CPR and CALL FOR HELP
- Airway
- Breathing
- Circulation
- Disability
- Exposure
INFORM SENIORS (med reg, critical care outreach)
What are the principles of airway management in RRAPID?
- talking = patent airway
- look, listen and feel for breathing
- signs of partial airway obstruction: paradoxical chest and abdominal movements, grunting/gurgling, foreign bodies
- full obstructed airway = silent
- cyanosis/ hypoxia is a late sign
- if airway obstructed- CALL FOR HELP
- head tilt chin lift- jaw help
- oropharyngeal or nasopharyngeal airway
- suction of secretions (yankauer)
- oxygen
- call anesthetist
What are the principles of breathing in RRAPID?
- respiratory rate
- oxygen saturation
- ABG (include lactate if risk of sepsis)
What are the principles of circulation in RRAPID?
- hands-temp
- cap refill (<2 secs)
- pulse- character and HP obs
- BP
- JVP
- cannulate- bloods (blood culture, FBC, U+Es, CRP), cross match, group and save, fluid challenge
- urine output
What are principles of disability in RRAPID?
- AVPU faster than GCS
- Pupillary light reflex- equal and reactive
- blood glucose
What are principles of exposure in RRAPID?
- expose patient for examination and source of illness
- abdo exam (flatten patient)
- check legs (oedema and rashes)
- check back with assistants
- temperature
What are the 12 steps of management for the unconscious patient?
1) ABCDE assessment
2) Consider intubation if GCS <8
3) 15L O2 non-rebreathe
4) IV access- fluids if clinically indicated
5) Blood glucose and glucose for hypoglycemia
6) Control any seizures
7) IV thiamine (Pabrinex) if diagnosis unclear and wernicke’s encephalopathy possible
8) Trial of naloxone/ flumazenil- easy and rapid response
9) Antibiotics (IV cefotaxime) if any signs of infection
10) Head CT if any suspicion of stroke
11) Routine biochemistry, hematology, thick films, blood cultures. blood ethanol. drug screen
12) Raised ICP- may require mannitol infusion
What are the causes of an unconscious patient?
COMA
- Cerebral
- Overdose
- Metabolic
- Any other
What are the cerebral causes of an unconscious patient?
Cerebral
- haemorrhage
- infarction
- tumour
- infection
- trauma
What are the overdose causes of an unconscious patient?
Overdose
- alcohol
- alcohol withdrawal
- drugs (sedative, narcotics, psychotropics)
- poisons (CN, CO)
- venom
What are the metabolic causes of an unconscious patient?
Metabolic
- endocrine
- hypoglycaemia
- hyperglycaemia
- environmental- hypo/hyperthermia
- organ failure
- electrolytes
- acid-base disorders
- vitamin deficiencies
- sepsis
What are the A- causes of an unconscious patient?
- arrhythmias
- asphyxia
- Anaemia
- AMI/PE
- Any cause of shock
What are the different types of shock?
- Septic shock
- Hypovolemic shock
- Anaphylactic shock
- Neurogenic shock
- Cardiogenic shock
What is the general assessment for shock?
- ECG: check the rate, rhythm, ischemia
- cold, clammy suggests cardiogenic shock or fluid loss, check for signs of anaemia or dehydration
- warm and well perfused with bounding pulse indicates septic shock
- features of anaphylaxis: history, urticaria, angiooedema, wheeze
- if JVP is raised, cardiogenic shock is likely
How is septic shock defined?
Severe sepsis with hypotension (systolic BP<90 or decrease of >40 from baseline)
OR
The requirement for vasoactive drugs- despite adequate fluid resuscitation
What is the response for septic shock?
A. Complete BUFALO within 1 hr
B. 15L/min O2 via reservoir bag
C. Fluid challenge of 500ml-1000ml Hartmann’s bolus
D. Blood cultures- before antibiotics
E. Lactate and Hb via ABG or VBG
F. Administer start broad spectrum antibiotics
G. Insert urinary catheter and monitor hourly UO
How is hypovolemic shock defined?
Usual symptoms of shock will be present but also faintness on standing, cyanosis, dyspnoea, LoC and symptoms relating to bleeding site.
What are the causes of hypovolemic shock?
- Blood loss
- Burns
- Dehydration
What is the classification of hypovolemic shock?
CLASS 1: 10-15% blood loss, physiological compensation, and no clinical changes appear
CLASS 2: 15-30% blood loss, postural hypotension, generalized vasoconstriction and reduction in urine output to 20-20ml/hr
CLASS 3: 30-40% blood loss, hypotension, tachycardia over 120, tachypnoea, urine output under 20ml/hour and the patient is confused
CLASS 4: 40% blood loss, marked hypotension, tachycardia and tachypnoea. No urine output and the patient is comatose
What are the investigations for hypovolemic shock?
- Check Hb, U+Es, LFTs and do group+ save and cross match
- Coagulation screen
- ABGs: metabolic acidosis with raised lactate
- Urine output
- US and imaging to assess site of bleeding
- CVP if evidence of shock
What is the management for hypovolemic shock?
- 15L O2 via NRBM and get IV access
- Fluid resuscitation and bloods
- SURGERY is the definitive treatment if actively bleeding
- Prevent multi organ failure
- Inotropes and vasopressors can be given in critical care setting
What is the pathophysiology of anaphylactic shock?
- Immediate type hypersensitivity reactions due to interaction of antigens with specific IgE antibodies bound to mast cells and basophils.
- Mast cells and basophils respond by releasing vasoactive and bronchoconstructive substances including histamine, leukotrienes and ECF-A.
How do we recognize anaphylactic shock?
- rash
- urticaria
- laryngeal oedema (choking, coughing, stridor)
- angio-oedema
- severe bronchospasm
- hypotension
- shock
- nausea
- vomiting or diarrhea
- rhinitis
- tachycardia
What is the response for anaphylactic shock?
1) ABCDE assessment
2) Secure airway and call an anaesthetist (imminent intubate + ventilate, in an emergency, cricothyoidectomy)
3) O2 15L/min NRBM
4) Call an anaesthetist
5) IV access and bloods: FBC, U+Es, LFTs, calcium and glucose
6) Raise legs to restore circulation (lie flat and head down tilt)
7) Adrenaline 0.5ml of 1:1000 IM (0.5mg)
8) Repeat adrenaline as necessary every 5 mins (by monitoring BP and pulse)
9) May use small IV boluses of adrenaline if have access and experience
10) Chlorphenamine 10mg slow IV (or IM)
11) Hydrocortisone 200mg slow IV (or IM)
12) Fluid bolus- 500ml 1L of warmed Hartmann’s solution over 10mins
13) if audible wheeze, treat for asthma
14) ICU for inotropes
What is the triad of symptoms for acute severe symptoms?
- WHEEZE
- SoB
- COUGH
What are the signs and symptoms of moderate acute asthma?
- Increasing symptoms
- PEF >50-75% best or predicted
- No features of acute severe asthma
What are the signs and symptoms of acute severe asthma?
- PEF 33-50% best or predicted
- RR >25/min
- HR >110/min
- Inability to complete sentences in one breath
What are the signs and symptoms of life-threatening asthma?
- PEF <33% best or predicted
- SpO2 <92%
- PaO2 <8kPa
- Normal PaCO2 (4.6-6kPa)
- Silent chest
- Cyanosis
- Poor respiratory effort
- Arrhythmia
- Exhaustion
- Altered conscious level
- Hypotension
What are the signs and symptoms of near-fatal asthma?
- Raised PaCO2
- Requiring mechanical ventilation with raised inflation pressures
What is the response for acute severe asthma?
- ABCDE assessment
- Sit patient up
- Give O2 15L via reservoir mask
- ABG
- IV access and bloods: FBC, U+Es, glucose
- Consider CRP, blood and sputum cultures if sepsis suspected
- Salbutamol 5mg nebulised with O2
- Ipratropium bromide 0.5mg nebulised with O2 (4-6hrly)
- Hydrocortisone 200mg stat + 100mg IV or prednisolone 40mg orally QDS for at least 5 days post attack
- Magnesium sulphate 1.2-2g IV over 20mins if life threatening
- CXR to exclude infection and pneumothorax
- ECG- assess right heart strain
- Monitor PEFR, ABG, K+
What is the action of salbutamol?
Smooth muscle relaxation leads to dilation of bronchial passages
What is the action of ipratropium bromide?
- Antimuscarinic leads to dilation of bronchi
- Inhibits mucus secretion
What is the action of hydrocortisone?
- Glucocorticoid
- Activates anti-stress and anti-inflammatory pathways
- 40-50mg prednisolone daily for at least 5 days after admission
What is the action of magnesium sulphate?
- Inhibits smooth muscle contraction
- Decreases histamine release from mast cells
- Inhibits acetylcholine release
What are the causes of community acquired pneumonia?
- Strep pneumoniae = 40%
- H. influenzae
- Influenza A+B
- Staph. aureus
- Moraxella catarrhalis
What are the causes of atypical pneumonia?
- Mycoplasma
- Legionella pneumoniphilia
Chlamydia pneumonia
What is the presentation for pneumonia?
- Cough (productive or non-productive)
- SoB
- fever
- pleuritic chest pain
- prodromal coryzal symptoms
- Respiratory distress
What are the investigations for pneumonia?
- CXR
- FBC
- U+E
- LFT
- CRP
- ABG
- blood and sputum cultures
- urine for legionella antigen
What is CURB-65?
C- CONFUSION?
U- UREA>7mmol/L
R- RR> 30
B- BP <90 systolic or <60 diastolic
65- >65years old
What is the management for pneumonia?
- ABCDE
- Venous access- assess fluid status and manage accordingly
- O2 at least 35% if hypoxic on ABG
- Ventilation if hypercapnia or hypoxia not corrected with max inspired O2
- Analgesia
- Start empirical antibiotics after cultures have been taken usually 5-7 days, 10 days in high risk patients
- Salbutamol neb if asthma/COPD for bronchospasm + mucocilliary action
- Fluids
What is the medical management for pneumonia?
MILD TO MODERATE- Amoxicillin or doxycycline
SEVERE CAP- Co-amoxiclav TDS 1.2g + clarithromycin 500mg BD or. cefotaxime/cefuroxime + clarithromycin
HAP- cefotaxime and metronidazole
ASPIRATION PNEUMONIA- Cefuroxime + metronidazole or benzylpenicillin + gentamicin + metronidazole
What are the signs/symptoms of acute exacerbation of COPD?
- Increasing dyspnoea +cough
- reduced exercise tolerance
- use of accessory muscles
- tachypnoea
- cyanosis
- wheeze
- increased sputum purulence
- UR symptoms
What are the causes of acute exacerbation of COPD?
- Strep pneumonia
- Haemophilus influenza
- Moraxella catarrhalis
What is the response for acute exacerbation of COPD?
- ABCDE approach
- Sit patient up
- controlled O2 therapy with venturi mask- but always treat hypoxia with increasing O2
- ABG- decreased PaO2 and raised bicarb in chronic disease
- IV access and bloods: blood cultures, FBC, U+Es, glucose
- SALBUTAMOL 5mg neubliser 4hrly
- IPRATROPIUM BROMIDE 500mg nebuliser 6hrly
- HYDROCORTISONE 100mcg nebulizer 6hrly
- ECG evidence of for pulmonate
- Antibiotics if evidence of infection
- CXR to exclude infection and pneumothorax
- Sputum sample and chest physio
When should non invasive ventilation be considered?
- COPD with a respiratory acidosis
- Hypercapnic respiratory failure secondary to chest wall deformity or neuromuscular diseases
- cardiogenic pulmonary oedema unresponsive to CPAP
- weaning from tracheal intubation
When is NIV not indicated in?
- impaired consciousness
- severe hypoxaemia
- patients with copious respiratory secretions
- consider intubation and ventilation if appropriate
What is cardiogenic acute pulmonary oedema?
- Due to elevated capillary pressure from left sided heart failure.
- Valve disease
- Ischaemia
- Arrythmia
What is non-cardiogenic acute pulmonary oedema?
- Minimal elevation of pulmonary capillary pressure
- Caused by altered alveolar-capillary membrane permeability- ARDS or lymphatic insufficiency
- Neurogenic e.g. status epilepticus, head injury
- Hypoalbuminaemia- liver failure, sepsis, dilution
What are the causes of acute pulmonary oedema?
- High-output heart failure
- Heart disease
- acute PE
- cardiac tamponade
- cardiomyopathy
- fluid overload
- liver failure
- acute/chronic airway obstruction
What are the features of acute pulmonary oedema?
- dyspnoea
- orthopnoea
- cough pin frothy sputum
- inspiratory crackles
- wheeze
- collapse
- cardiac arrest
- shock
What are the findings of acute pulmonary oedema?
CXR: cardiomegaly, fluffy bilateral shadowing with peripheral sparing, kersey B lines, pleural effusions. Exclude pneumothorax and consolidation
ECG: IHD, arrhythmias
ABG: O2 down, CO2 up/normal/down
What is the response to acute pulmonary oedema?
- ABCDE assessment
- Sit patient up
- O2 15L/min NRBM
- IV access and bloods: FBC, U+Es, LFTs, glucose
- Monitor BP and O2 sats
- Treat any arrhythmias
- DIAMORPHINE 2.5mg-5mg IV
- FUROSEMIDE 40-120mg IV slowly
- METOCLOPRAMIDE 10mg IV
- GTN 2 sprays of 500mcg sublingual if BP>90
- GTN infusion 50mg in 50ml
What is the action of diamorphine?
- Opiate
- To relieve anxiety and distress associated with dyspnoea
What is the action of furosemide?
- Loop diuretic
- Improves breathlessness and relieves congestion
What are the features of pneumothorax?
- sudden onset dyspnoea
- pleuritic chest pain/dull central chest pain
- unilateral reduced chest expansion
- unilateral decreased breath sounds
- unilateral hyper resonance to percussion
- CXR confirmation
Who is likely to suffer from pneumothorax?
- Ventilation patients
- Trauma patients
- Patients who’ve had CPR (tension)
- Lung disease especially acute exacerbations of asthma or COPD
- Infection
- Blocked, clamped or displaced chest drains
- Patients receiving NIV
- Patients undergoing hyperbaric O2 treatment
- post-thoracic procedures e.g. subclavian vein cannulation
- primary- tall, young, male smoker
What are the margins of large pneumothorax?
- 50% of lung volume lost- lung margin is >2cm from chest margin on CXR
What are the margins of small pneumothorax?
lung margin <2cm from chest wall on CXR
What is the response for normal pneumothorax?
- ABCDE
- O2 increases rate of resorption and reduces hypoxia >35%
- CXR
- Small primary pneumothorax- discharge and safeguarding and follow up
- Chest aspiration in primary and small secondary if <50yrs and asymptomatic- 2nd intercostal space mid clavicular line
- intercostal chest tube drainage in all others- 5th intercostal space mid-axillary line
What is the response for tension pneumothorax?
- ABCDE approach
- O2 15L/min via reservoir mask
- do not delay in management by waiting for CXR
- needle decompression- large bore needle (14-16G) 2nd intercostal space mid clavicular line with syringe filled with 0.9% saline
- insertion of chest drain (5th intercostal space mid-axillary line)
What is the surgical response for pneumothorax?
- pleuredesis
- pneumothorax if large defect in chest wall
What are the risk factors for pulmonary embolism?
- malignancy
- post surgery
- immobility
- OCP
- pregnancy
- previous DVT/PE
- increasing age
- obesity
- smoking
- infection
- dehydration
- inherited thrombophilias
- right heart failure/ pulmonary hypertension
What are the features of pulmonary embolism?
- sudden onset dyspnoea
- pleuritic chest pain
- haemoptysis
- syncope
- CVS collapse
- raised JVP
- hypoxia
- postural hypotension
- Massive PE
- cyanosis
What investigations are done in pulmonary embolism?
CXR is often normal
CT angiogram confirms
ECG: S1Q3T3, right axis deviation and RBBB
WELLS SCORE
What is the criteria for ruling out PE?
HAD CLOTS
H- hormone use
A- age >50yrs
D- DVT/PE history
C- Coughing up blood L- unilateral Leg swelling O- Oxygen sats T- tachycardia>100 S- surgery or trauma
can rule out id NONE of the above criteria are satisfied AND the Wells score is <3 and there is no clinical suspicion
What is the response for PE?
1) ABCDE assessment
2) sit patient up
3) O2 15L/min reservoir mask
4) Consider if respiratory support required
5) ABG
6) IV access and bloods: FBC, U+Es, glucose
7) Attach cardiac monitor
8) Treat hypotension with fluid bolus
9) Give NSAIDs and if no repose then 10mg IV morphine and antiemetic
10) if high risk anticoagulant with LMWH
11) Once diagnosis is confirmed start warfarin for up to 6 months- INR 2-3
12) Can use IVC filter if confirmed DVT
What is the definition of AKI?
RISE IN SERUM CREATININE
- > 26umol/L within 48hrs
- 1.5x baseline value within 1 week
OR
URINE OUTPUT <0.5ml/kg/hr for 6hrs
What is Stage 1 of AKIN staging?
- rise in serum creatinine >26umol/L within 48 hrs
- rise in serum creatinine 1.5-1.9x baseline value within 1 week
- urine output >0.5ml/kg/hr for 6 hrs
What is Stage 2 of AKIN staging?
- rise in serum creatinine 2-2.9x baseline value within 1 week
- urine output >0.5ml/kg/hr for 12 hrs
What is Stage 3 of AKIN staging?
- rise of serum creatinine >354umol/L
- rise in serum creatinine >3x baseline value within 1 week
- commenced renal replacement therapy
- urine output <0.3ml/kg/hr for 24 hrs
- anuric of 12hrs
What are the risk factors for AKI?
- age >65
- CKD
- cardiac failure
- liver disease
- PVD
- DM
- nephrotoxins
- hypovolaemia
- sepsis
- ethnicity (black)
- surgery
What are the pre-renal causes of AKI?
- dehydration
- hypotension
- shock
- sepsis
- cardiac failure
- renal artery stenosis
What are the intrinsic renal causes of AKI?
- prolonged hypo-perfusion
- nephrotoxins
- glomerulonephritis
- vasculitis
- interstitial nephritis
- hemolytic uraemic syndrome
- acute tubular necrosis
- eclampsia
- rhabdomyalsis
What are the post-renal causes of AKI?
OBSTRUCTION
- renal stones
- retro-peritoneal fibrosis
- thrombosis
- bladder cancer
- pelvic mass
- enlarged prostate
What are the clinical features of AKI?
- hypovolaemia
- palpable bladder
- signs of vasculitis
- bruits (renal artery stenosis)
- malaise, confusion, coma
- nausea/vomiting
- backache
- haematuria
- fluid overload
- pericardial rub
What investigations should be done in AKI?
- volume assessment
- septic screen
- USS
- urinalysis and microscopy
- FBCs, U+Es, bicarb, LFTs, calcium, phosphate, glucose, ANAs
- ECG (K+, arrhythmias)
- ABG
- CXR- HF with pulmonary oedema
- Nephrotoxic drugs
What is the response for AKI?
- ABCDE assessment
- IV access and bloods
- treat underlying cause
- optimise fluid balance
- treat overload with nitrates, furosemide and O2
- treat complications- hyperkalaemia, acidosis, pulmonary oedema, bleeding
- review drug chart (STOP nephrotoxic drugs)
- renal replacement therapy
What are the two types of urinary tract infection?
- LOWER: cystitis
- UPPER: pyelonephritis
What are the causes of urinary tract infections?
- E.coli
- proteus
- klebsiella
- s. faecalis
- pseudomonas (mostly inpatients/catheterised)
What is the presentation for cystitis?
- dysuria
- frequency
- haematuria
- suprapubic discomfort
- urgency
What is the presentation for pyelonephritis?
- systemic features
- loin/back pain
- vomiting
- rigors
- preceding cystitis
- shock/sepsis
What are the investigations for UTI?
URINALYSIS
- haematuria
- proteinuria
- leucocytes
- nitrites
MCS
- leucocytes
- WBCs
- U+E
- FBC
- cultures and USS for upper UTI
What is the management for cystitis?
3-6 DAYS
- trimethoprim/nitrofurantoin
men require a 2 week course
for catheterized patients: ciprofloxacin/ co amoxiclav for 7 days
What is the management for pyelonephritis?
- ABCDE
- IV antibiotics- gentamicin bolus
- Cefuroxime 750mg TDS 7-14 days
- await cultures
- monitor UO- high fluid balance
- opioids
What are the causes of male urinary retention?
- BPH/ cancer
- phimosis
- meatal stenosis
- UTI
What are the causes of female urinary retention?
- prolapse
- pelvic mass
- retroverted gravid uterus
- vaginitis
- lichen planus
- UTI
- post partum
What are the causes of urinary retention in males and females?
- drugs
- calculi
- cancer
- faecal impaction
- strictures
- neurological
- post surgery
- trauma
What are the presentations of urinary retention?
- inability to pass urine and bladder discomfort
- O/E: tender enlarged bladder, dull to percussion.
- Check for prolapsed disc/cord compression
What are the investigations for urinary retention?
- routine bloods
- urine MC+S
- US
- CT
- cystoscopy
- lower limb PNS and PR for anal tone
What is the management for urinary retention?
- Urethral catherization
- suprapubic catheterization if urethral is contraindicated
- Alpha blocker in men
- treat underlying cause
What are renal calculi?
They occur when urine is saturated with minerals such as calcium oxalate, struvite, uric acid or cysteine
Vary in size from gavel to large staghorn calculi
What is the most common type of renal calculi?
calcium oxalate (75%)
What are the risk factors for renal calculi?
- hyperparathyroidism
- prolonged immobility
- primary renal disease
- dehydration
- diuretics/steroids
- recurrent UTIs
- renal abnormalities
- FHx
What is the presentation for renal colic/stones?
PAIN
- dull loin ache= stone in renal pelvis
- severe colicky loin-groin pain, sudden onset= ureteric stone
- suprapubic/perineal/ testicular ache= bladder stone
HAEMATURIA
FEVER/RIGORS
SWEATY, NAUSEA, DISTRESS, PALE
ABDO TENDERNESS
What are the investigations for renal colic/stones?
- CT imaging of choice
- U+E
- glucose
- FBC
- HB and WCC
- calcium
- urine dipstick and MCS
- USS, AXR
What is the management for renal colic/stones?
- Diclofenac (IM/PR)
- antiemetics
- high fluid intake
- treat associated infection
- small stones will pass spontaneously
- large stones may need extracorporeal shock
- when discharged, encourage high fluid intake, reduced salt, oxalate and urate levels
What is testicular torsion?
twisting of spermatic cord causing compromised blood supply. Peak age range 7-14 years old bit also occurs commonly in the first 10 days of life.
What is the presentation of testicular torsion?
- acute swelling of scrotum with severe pain
- vomiting
- O/E red, tender, swollen testes, Angell’s sign
- reducing pain may indicate necrosis?
What is Angell’s sign?
- opposite testes horizontal position
What are the differentials for testicular torsion?
- epididymitis
- orchitis
- hydrocele
- hernia
- tumour
What is the management for testicular torsion?
- US integrated with color Doppler gold standard
- possible to reduce manually by specialist
- refer for: exploration, detorsion, orchidoplexy
How is hyperkalaemia recognized?
- serum K+ >5mmol
What are the ECG changes for hyperkalaemia?
- tall tented T waves
- small P waves
- wide QRS complexes
- VF
What are the signs and symptoms of hyperkalaemia?
- fast, irregular pulse
- chest pain
- weakness
- palpitations
- light-headedness
What are the causes of hyperkalaemia?
- oliguric AKI
- potassium sparing diuretics
- drugs (ACEi)
- rhabdomyolysis
- metabolic acidosis
- iatrogenic
- addisons disease
- massive blood transfusion
- artefact
What are the complications of hyperkalaemia?
- cardiac arrhythmia
- sudden death
What is the response for hyperkalaemia?
- ABCD assessment
- IV access and bloods (FBC, U+Es, LFTs, glucose)
- attach to cardiac monitor
- monitor BP and O2 sats
- IMMEDIATE TREATMENT IF K>6mmol/L with ECG changes or potassium>6.5mmol/L regardless of ECG changes
What are the medical management options for hyperkalaemia?
- CALCIUM GLUCONATE
- INSULIN AND GLUCOSE
- SALBUTAMOL NEBULISER
- CALCIUM RESONIUM and LACTULOSE
What are the doses for administering calcium gluconate for hyperkalaemia management?
- 10% calcium gluconate 10mls IV over 2 mins
OR
- 10% calcium chloride 10mls over 10 mins
- Repeat dose after 5-10mins if ECG improvement
- Provides cardio-protection- no change in serum potassium level
What are the doses of insulin and glucose for hyperkalaemia management?
- short acting insulin 10U in 50mls of 50% glucose IV over 5-10mins
- insulin shifts potassium into cells temporarily
- monitor blood sugar levels regularly
What are the doses of salbutamol nebulizer for hyperkalaemia management?
- salbutamol 5mg nebuliser
- shifts potassium into cells temporarily
What are the doses of calcium resonium and lactulose for hyperkalaemia management?
- 15mg orally every 6-8hrs
- removes potassium from GI tract
What are the life threatening causes of chest pain?
- Acute MI
- Angina/ACS
- Aortic dissection
- Tension pneumothorax
- PE
- Oesophageal rupture
What are the non-life threatening causes of chest pain?
- pneumonia
- chest wall pain: muscular, rib, bony mets, chostochondritis
- GOR
- Pleurisy
- Empyema
- Pericarditis
- Oesophageal spasm
- Herpes zoster
- Cervical spondylitis
- Intra-abdo: cholecystitis, peptic ulcer, pancreatitis
- sickle cell crisis
What are types of ACS chest pain?
- dull retrosternal
- left sided pain
- tight/crushing heavy
- radiate to left arm, shoulder and jaw
What are the signs of cardiac ischemia?
- exacerbated by exercise/stress
- relieved by rest/nitrates/O2
What are the autonomic symptoms associated with chest pain?
- nausea
- anxiety
- sweating
What are the symptoms associated with pleuritic irritation?
- sharp
- well localized pain
- exacerbated by breathing/coughing
What is the management for patients with acute chest pain?
- ABCDE assessment
- O2 if indicated- keep sats > 96%
- Analgesia
- Aspirin and GTN if cardiac is suspected
- ECG
- IV access and bloods- FBC, U+Es, troponin, D-dimer
- CXR (erect PA)
- further management dependent on most likely cause
What is aortic dissection?
- disruption of the medial layer of the wall of the aorta caused by intramural bleeding.
- leads to formation of a true and a false lumen
What are the risk factors of aortic dissection?
- genetic (Marfan’s, Turner’s, Ehler’s Danlos)
- HTN
- previous cardiac surgery
- aortic coarctation
- pregnancy
What are the presentations of aortic dissection?
Presents in two phases:
- after first event with severe pain and pulse loss
- second event starts when pressure exceeds limit and rupture occurs into pericardium or pleural space leading to cardiac tamponade
O/E: aortic regurgitation
- different BP>20mmHg
- pleural rub
- haemothorax
- altered consciousness
- oliguria
What are the complications of aortic dissection?
- angina
- paraplegia
- limb ischaemia
What are the investigations for aortic dissection?
- ECG: signs of acute MI with ST changes
- CXR: widened mediastinum, abnormal aortic contour, tracheal shift, pleural effusion
- ECHOCARDIOGRAM- transoesophageal
- CT
What is the management for aortic dissection?
- ABCDE ICU
- Manage HTN with beta blockers
- Ascending type A- control of BP
- Descending type B- control of BP
What are acute coronary syndromes?
- Medical emergency classified on ECG and troponin levels.
- Classified into ST-ACS or NST-ACS
- Most ST-ACS will develop into STEMI
What are the features of NST-ACS?
- T wave inversion or ST depression
- NST-ACS further divided into
- unstable angina
- NSTEMI (which will show a rise in troponin level)
What are the risk factors for acute coronary syndrome?
- increasing age
- male
- family history of IHD
- smoking
- hypertension
- DM
- hyperlipidaemia
- obesity
- sedentary lifestyle
What is the general presentation of acute coronary syndrome?
- chest pain at rest>20mins
- tight, heavy, crushing, radiating to jaw and L arm
- history of angina
- shortness of breath
- sweating
- nausea
- palpitations
- signs of heart failure
- ECG changes
- troponin rise (12 hrs)
- CXR may show pulmonary oedema/cardiomegaly
What investigations are done in acute coronary syndrome?
- essential to exclude STEMI for which immediate thrombolysis is indicated
- routine bloods
- ECG
- troponin: peak at 12hrs
- echocardiography
- CXR
- angiography
What is the immediate management for general ACS?
- ABCDE assessment
- 15L O2 NRBM to maintain 94-98% oxygen saturations
- IV access and bloods: FBC, U+Es, calcium, magnesium, glucose and troponin
- serial ECGs
- Analgesia: morphine 2.5mg-10mg slow IV bolus
- antiemetic: 50mg cyclizing OR 10mg metoclopramide
- GTN spray x2 puffs
- aspirin 300mg oral loading dose
- clopidogrel 300mg for 12 months
What is the additional management for NSTEMI?
- refer to cardiology
- fondaparinux 2/5mg subcutaneously after discussion with cardiology
- assess need for revascularisation
What is the additional management for STEMI?
- refer to cardiology
- Primary PCI if within 12hrs of onset
- Thrombolysis if PCI not available
What are the long term medical management options in ACS?
- ACE inhibitors
- Statins
What is myocardial infarction?
A condition which is included in the spectrum of acute coronary syndromes. Caused by necrosis of myocardium due to ischemia.
Most are anterior or inferior
CHD is the most common cause of death
What is the criteria or diagnosis in myocardial infarction?
RISE IN TROPONIN together with:
1) SYMPTOMS
2) ECG CHANGES
3) PATHOLOGICAL Q WAVES
4) IMAGING SHOWING DEATH OF MYOCARDIUM
What are the risk factors for MI?
- age
- male
- family history
- smoking
- DM
- HTN
- obesity
- south asian ethnicity
What is the presentation for MI?
CHEST PAIN
- central.epigastric crushing pain radiating to the arms, shoulders, neck or jaw
- radiation to the left arm or neck is common
- Associated with sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations
SHORTNESS OF BREATH
ABDOMINAL DISCOMFORT/JAW PAIN
What can be seen on examination in an MI?
- low grade fever, pale and cool and clammy skin
- hypotension or hypertension
- dyskinetic cardiac impulse (in anterior wall MI)
- 3rd and 4th heart sound, systolic murmur if mitral regurgitation or VSD develops, pericardial rub
- signs of congestive heart failure
What are the investigations for MI?
- routine bloods
- repeated troponin levels
- ECGs
- CXR, echocardiogram, SPECT scan
- monitor vital signs
- myocardial perfusion imaging and exercise ECG to assess risk before discharge
What is the management for MI?
- ABCDE assessment
- 15L O2 NRBM
- GTN spray
- morphine IV 5mg
- aspirin 300mg and clopidogrel 75mg
- beta blocker
- PCI within 90 mins
- if no PCI then fibrinolysis with alteplase IC
- CABG if failed PCI, cardiogenic shock or multi vessel disease
- ACE inhibitor
- Statin
What is stable angina?
- chest pain or discomfort caused by ischemia. Usually occurs because there is narrowing of the coronary arteries.
- Can also because by valvular disease
- occurs when the pain is precipitated by predictable factors (usually exercise)
What is the presentation for angina?
- Chest pain (if unresolved by GTN- treat as ACS)
Anginal pain is: - constricting discomfort in chest, neck, shoulders, jaw, arm
- precipitated by exertion
- relieved by rest or GTN in 5 mins
What is a differential of anginal pain?
PRINZMETALS- which occurs at rest with circadian pattern
What are the investigations for angina?
- ECG: pathological Q waves, LBBB, ST depression, T wave inversion
- routine bloods
- baseline LFTs before beginning statins
- TFTs
- troponin
- echocardiography
- refer to secondary pain if pain at rest or rapidly progression
- refer to rapid access chest pain clinic if suspected angina
What is the management for angina?
- modify CV risk factors
advise that when an angina attack occurs: - stop and rest
- use GTN
- take a second dose after 5 mins if not eased
- take a third dose after another 5 mins if still not eased
- call 999 if another 5 mins pass without ease
What additional medical management should be considered for angina?
BETA BLOCKER/CCB AS FIRST LINE TREATMENT If ineffective, consider adding: 1. a long acting nitrate 2. Ivabradine 3. Ranolazine
ASPIRIN (75-300mg) or CLOPIDOGREL
ACE INHIBITOR
STATIN
How is cardiac arrest recognized?
The patient will be unresponsive and not breathing
- perform airway manouevers and use adjuncts as appropriate
What is the management of cardiac arrest?
- establish IV access when possible
- call 222
- begin CPR at rate 30:2
- rate 100-120/min
- rescue breaths to last 1 sec with ventilation bag
- attach defibrillates and other monitoring equipment
- assess rhythm
What is the management of cardiac arrest in VF/pulseless VT?
- SHOCK
- return to chest compressions for 2 mins
- then assess pulse and rhythm
- Give 1mg IV adrenaline every 3-5 mins
- After 3rd shock give: 300mg IV amiodarone
What is the management of cardiac arrest in pulseless electrical activity (PEA)/asystole?
- NOT SHOCKABLE
- 1 mg IV adrenaline as soon as venous access
- Give 1mg IV adrenaline every 3-5mins
- After 3rd shock give: 300mg IV amiodarone
- Continue CPR
What are the reversible causes of cardiac arrest?
- hypoxia
- hypovolaemia
- hypothermia
- hyperkalaemia
- tension pneumothorax
- tamponade
- toxins
- thromboembolism
What is the action of adrenaline?
- vasoconstriction to increase myocardial and cerebral perfusion pressure.
- higher coronary blood flow increases frequency and amplitude of VF waveform.
- Improves short term survival
- can cause post cardiac arrest myocardial dysfunction and impairs microcirculation
What is the action of amiodarone?
- membrane stabilizing anti-arrythmic
- increases duration of action potential
- increases refractory period in atrial and ventricular myocardium. Slows atrioventricular conduction
- give IV bolus 300mg flushed with 20ml 0.9% NaCl or 5% dextrose
- further dose of 150mg may be given for recurrent/refractory VF/VT
What is pericarditis?
Acute inflammation of outer fibrous and inner serous membranes of the heart
What are the causes of pericarditis?
- MI
- viral (coxsackie, mumps, EBV, CMV, HIV)
- bacterial
- TB
- locally invasive carcinoma
- rheumatic fever
- uraemia
- post cardiac surgery
- collagen vascular disease (SLE)
What is the presentation of pericarditis?
CHEST PAIN
- central
- sharp
- retrosternal
- relieved by sitting forward
- SOB
- worse on exercise
- radiating to neck
PERICARDIAL FRICTION RUB
- intermittent
- positional
- louder during inspiration
- scratchy sound heard in midline
fever, cough, SOB, arthralgia, rash
pericardial effusion may develop- rise in venous pressure
What is Becks triad in cardiac tamponade?
1) hypotension
2) increased venous pressure
3) muffled HS
What are the investigations for pericarditis?
- ECG- 10% normal, sinus tachycardia, AF/flutter/atrial ectotropics, concave/saddle-shaped ST elevation in limb leads or all chest leads, prominent peaked T-waves
- pericardial effusion
- no pathological Q waves- unlike MI
- CXR heart size, pulmonary oedema, infection
- Bloods: FBC, ESR, CRP, U+E, troponin, cultures.
- Echo: if cardiac tamponade/ pericardial effusion suspected
What is the management for pericarditis?
- ABCDE
- Analgesia- NSAIDs- naproxen 250mg TDS increases coronary flow + PPI
- opioids may be needed
- steroids (prednisolone 60mg PO OD for 2 weeks)
- Colchicine analgesia 1mg/day
- pericardiocentesis for pericardial effusion
- stop anticoagulants in case of haemopericardium
What causes supraventricular tachycardia (Narrow QRS complexes)?
- Abnormalities of impulse conduction
2. Disorders of impulse initiation causing narrow complex tachycardias
What are the risk factors of SVT?
- MI
- mitral valve prolapse
- pericarditis
- pneumonia
- chronic alcohol
- digoxin toxicity
What is the presentation of SVT?
- palpitations
- dizziness
- fatigue
- chest pain
- dyspnoea
- syncope
What can be seen on examination for SVT?
- tachycardia (140-250bpm)
- resulting HF may lead to tachypnoea
- hypotension
- fluid overload
What are the investigations for SVT?
- routine bloods
- ECG: acute, 24hr ambulatory, exercise
- cardiac enzymes
- electrolytes
- CXR
- echocardiogram
What is the management for SVT?
- Address precipitating factors: caffeine, alcohol, digoxin, drugs, hyperthyroidism
- DC cardio version is most effective means or terminating unstable tachycardia
- If stable then vagal manoeuvres (Valsalva, carotid massage)
What is the management for sinus tachycardia?
BETA BLOCKER
NO DIHYDROPYRIDINE CCB e.g. diltiazem, verapamil
What is the management for sinus node re-entry tachycardia?
BETA BLOCKER
DILTIAZEM, VERAPAMIL
What is the management of focal atrial tachycardia?
- CCBs
- BETA BLOCKER
- Flecainide
- Sotalol
- Amiodarone
When is radio frequency catheter ablation indicated for supra ventricular tachycardia?
- First line therapy as a curative option
- If the SVT is refractory to antiarrythmic drug therapy
- If the person is intolerant of anti arrhythmic drug therapy
- If antiarrhythmic drug therapy is contraindicated
When should urgent referral be made in conjunction with SVT?
- syncope with palpitations on exertion
- broad complex tachycardia
- pre-excitation (delta wave) on a 12 lead ECG
- structural heart disease
- severe symptoms
What are the complications associated with SVT?
- haemodynamic collapse
- HF
- DVT
- tamponade
- MI
- cardiomyopathy
What is ventricular tachycardia?
- Broad complex tachycardia defined as >3 ventricular extrasystoles in succession at rate of >120bpm
- Can be monomorphic VT is regular rhythm from a single focus
- Can be polymorphic VT which is irregular with beat to beat variations in QRS
What are the different types of VT?
FASICULAR TACHYCARDIA
- originates from the LBB
- produces QRS complexes of relatively short duration
RIGHT VENTRICULAR OUTFLOW TRACT TACHYCARDIA
- originates from right ventricular outflow tract
- ECG typically shows right axis deviation with LBBB pattern
- usually responds to drugs such as alpha-blocker or calcium antagonists
TORSADES DE POINTES TACHYCARDIA
POLYMORPHIC VENTRICULAR TACHYCARDIA
What is the presentation of ventricular tachycardia?
- Symptoms of IHD or hemodynamic compromise
- Chest pain, palpitations, dyspnoea, dizziness, syncope, fluid overload
What are the clinical signs of ventricular tachycardia?
- degree of haemodynamic instability
- respiratory distress
- basal fine lung
- crepitations
- raised JVP
- hypotension
- anxiety
- agitation
- lethargy
- coma
What are the investigations for VT?
ECG
- rate greater than 100bpm
- wide QRS complexes
- presence of AV dissociation
- fusion beats
ELECTROLYTES: hypokalaemia, hypomagnesaemia, hypocalcaemia
LEVELS OF DRUGS
TROPONIN
CXR: CHF signs
What is the management for pulseless VT?
- ABCDE
- VF or pulseless VT is treated by unsynchronized defibrillation
- Defibrilation is followed by airway management if required
- supplemental oxygen
- vascular access
- amiodarone
What is the management for stable VT?
- lidocaine
- cardioversion
What is ventricular fibrillation?
When the ventricle contracts randomly causing complete failure of cardiac function. Most commonly identified arrhythmia in cardiac arrest.
What are the risk factors for ventricular fibrillation?
- coronary artery disease
- acute MI
