Tassie Prep Flashcards
-What leads would you see elevation in with a inferior STEMI
- what artery is affected?
- How can you confirm RCA occlusion?
Leads II, III and AVF
The main artery affected would be the right coronary artery.
Less commonly the Left circumflex.
You can confirm RCA occlusion by moving V4 from L) side to right side (in same position) if there’s elevation this will confirm RCA occlusion.
Will All patients present with pain during a STEMI event?
Not all patients will present with pain during a STEMI event, some pt for example, Diabetic, Elderly and atypical presentations may not present with pain.
What is AT standard treatment for ACS
300mg Aspirin
400mcg of GTN at 5min intervals (if BP >100)
Pain relief
- Morphine 0.05mg/kg (max 5mg) per dose, total (max 20mg)
OR
Fentanyl 0.5mcg/kg (Max 50mcg) per dose. total (200mcg).
What are the criteria for SVT
Regular
Narrow QRS complex (<120ms)
Rate >100 (generally >140bpm)
Buried or Absent P waves
How does AT manage AVNRT and AVRT SVT?
Either Asymptomatic or symptomatic manage as per Abdominal modified Valsalva maneuver
ICP may give Adenosine, if ineffective and pt deteriorating then they may Sync Cardioversion.
What is the criteria for VT
Wide QRS > 120 ms (Generally >160ms)
Regular
> 100bpm
No P Waves
What are some unstable signs of VT
- Congestive cardiac failure
- BP <80
- GCS <13
Rapidly deteriorating
What are some signs of Severe Cardiogenic Pulmonary Oedema?
- Hypertension > 160 systolic
- Decreasing GCS
- Dyspnea
- Coarse Crackles on lungs
- Formulating
- Coughing
- Irritability
- Patient may also have pitting Oedema in legs (fluid overload), not all patients with this will be severe APO.
Why do patients respond to GTN with APO
GTN causes
- Venodilation which allows for venous pooling and reduces venous return (reduces preload)
- Ateriodilation reduces systemic vascular resistance and arterial pressure (reduces afterload).
These reduces the pressure in the heart, causing veneo and aterio- dilation, thus reducing hydrostatic pressure which allows for oncotic pressure to push fluid back out of interstitial spaces.
Why do patients with APO respond to CPAP?
CPAP works on both Cardiac and respiratory systems. CPAP increases intrathoracic pressure, which reduces preload by decreasing venous return.
CPAP lowers afterload by increasing the pressure gradient between the left ventricle and the extra-thoracic arteries.
Decrease the systemic venous return and the left ventricular (LV) afterload, thus reducing LV filling pressure and limiting pulmonary edema.
Essentially it causes cardiac vasodilatation, reducing pressure in the heart, this also causes a reduction in hydrostatic pressure (allowing for oncotic pressure to overcome and push fluid out of the interstitial spaces.
Due to CPAP increasing pressure in the lungs it also assists in pushing fluid back out of the alveoli.
What is Tassie Ambulance Management for APO (basal/ Midzone Crackles)
Firstline
- Posture: sit patient upright
- If BP >100 systolic: GTN 400mcg at 5/60 intervals (no max)
Note: if nil improvement treat as per Full field crackles.
What is Tassie Ambulance Management for APO (full field Crackles)
Manage same as Basal/ Midzone crackles
- Provide positioning
- GTN at 400mcg if BP >100 systolic
- Call for ICP backup
ICP
- CPAP
- Potential GTN Infusion.
- Potential administration of frusemide.
Pain Management.
What are the specific indication to give Fentanyl over Morphine.
- Contraindication to Morphine
- Short Duration desirable.
- Hypotension
- Nausea and/ or vomiting.
Notes
Fentanyl should be a drug of choice for trauma pt who have inadequate perfusion.
What is the dosage of Morphine and Fentanyl in the pain management guideline.
Morphine IM or Subcut
- Up to 0.1mg/kg (max single dose 10mg) repeated once after 20 minutes if required.
Morphine IV/IO
- Up to 0.05mg/kg (max 5mg) to a total of 20mg.
Fentanyl IM or Subcut
- Up to 1mcg/kg (max single dose 100mcg) Repeated once after 20 minutes if required
Fentanyl IV/IO
- Up to 0.5 mcg (max of 50mcg/kg), repeat at 5/60 to a total of (200mcg) if required.
Consider reducing narcotic doses for what patient who
- > 65 years old
- Shocked patients
- Frail patients
- Cardiovascular compromised patients
- Underlying lung disease
- Metabolism disorders e.g (kidney or liver)
- Clinical decision making from paramedics.
How do Ambulance Tasmania clinically define Asthma
A combination of variable respiratory symptoms including
1. Wheezing
2 Shortness of breathe
3. Coughing
4. Chest tightness
Asthma is acute and reversible.
How does Ambulance Tasmania treat Mild to Moderate Asthma
Salbutamol pMDI with spacer
- Deliver 12 puffs at 20/60 intervals until resolution.
Or
Nebulize
Salbutamol 5mg in 2.5ml, repeat at 5/60 intervals if required.
How does Ambulance Tasmania treat Severe Asthma
Salbutamol pMDI with spacer
- Deliver 12 puffs at 5-10/60 intervals until resolution.
Ipratromium bromide pMDI with Spacer
- Deliver 8 doses at 20/60 (max 3 repeats)
If pMDI Spacer Unavailable
Salbutamol Nebulized
- 10mg in 5ml
with
Atrovent
- 500mcg in 1ml
Repeat salbutamol
- 5mg in 2.5ml at 5/60 as required
Repeat Atrovent at
- 500mcg at 20/60 intervals (max 3 doses)
Dexamethasone
8mg in 2ml IV, IM or oral.
How does Ambulance Tasmania treat life threatening Asthma
Adrenaline IM
- 500mcg IM at 5/60 as required.
Salbutamol Nebulized
- 10mg in 5ml
with
Atrovent
- 500mcg in 1ml
Repeat salbutamol
- 5mg in 2.5ml at 5/60 as required
Repeat Atrovent at
- 500mcg at 20/60 intervals (max 3 doses)
Dexamethasone
- 8mg in 2ml IV, IM or oral.
Normal Saline
- 20mls/kg
What is Ambulance Tasmania treatment for COPD
Salbutamol pMDI with spacer
- Deliver 8 puffs with 4 breaths repeat 10/60 as required
Ipratropium bromide pMDI with Spacer
- Deliver 4 doses and 4 breathes per dose at 10/60 as required
Or
Nebulize
Salbutamol 5mg in 2.5ml, repeat at 5/60 intervals if required.
If pMDI spacer unavaible or unable to tolerate
Salbutamol Nebulized
- 10mg in 5ml
with
Atrovent
- 500mcg in 1ml
Repeat at 10 minute intervals as required
Dexamethasone
- 8mg in 2ml IV, IM or oral.
Oxygen therapy (nasal prongs)
- titrate to 88-92
If pt deteriorates
- Ventilate at 5-8 ventilations per minute at 7ml/kg.
-Allow for prolonged expiratory phase.
-Gentle lateral chest pressure if required.
Why do we give bronchodilators to patients in Resp distress
Bronchodilators primarily function by relaxing the smooth muscle surrounding the airways, which allows the airways to dilate (widen) and reduce resistance to airflow.
Beta-2 Adrenergic Agonists: Salbutamol
Mechanism: They activate beta-2 adrenergic receptors (beta-2 receptors) located on the smooth muscle cells of the bronchi.
When these receptors are activated by the drug, they stimulate adenylyl cyclase, an enzyme that increases the production of cyclic AMP (cAMP) within the smooth muscle cells.
The increased levels of cAMP activate protein kinase A which then lead to the relaxation of bronchial smooth muscle. This process ultimately dilates the airways and reduces airway resistance.
Atrovent
Mechanism: block the action of acetylcholine (ACh), a neurotransmitter released from parasympathetic nerve endings that typically stimulates muscarinic receptors (M1, M2, M3) on bronchial smooth muscle cells.
When acetylcholine binds to these receptors, it causes the smooth muscle to contract (bronchoconstriction).
By blocking muscarinic receptors, anticholinergics inhibit this bronchoconstrictor effect and promote bronchodilation.
How does Adrenaline Assist with life threatening airway presentations e.g Asthma
Beta-2 Adrenergic Receptor Stimulation:
Adrenaline primarily acts on beta-2 adrenergic receptors located on the smooth muscle cells of the bronchi and bronchioles.
When adrenaline binds to these receptors, it activates a cascade of events that leads to the relaxation of bronchial smooth muscle, causing bronchodilation (widening of the airways).
Vasoconstriction (Alpha-1 Receptor Activation):
-Adrenaline also stimulates alpha-1 adrenergic receptors, which are located on smooth muscle cells in blood vessels.
When these receptors are activated, it causes vasoconstriction, or the narrowing of blood vessels.
This effect is particularly helpful in reducing airway edema (swelling) that can occur during an asthma attack, as vasoconstriction decreases the permeability of blood vessels and limits the leakage of fluid into the tissues, which can worsen inflammation.
Inhibition of Inflammatory Mediators:
-Adrenaline has an indirect effect on inflammatory cells (such as mast cells, eosinophils, and neutrophils) in the airways. It can decrease the release of histamine and other pro-inflammatory mediators that contribute to airway inflammation and bronchoconstriction.
By reducing the release of these inflammatory substances, adrenaline helps to diminish the inflammatory response in the lungs.
Improvement of Mucociliary Clearance:
-Adrenaline can also enhance the function of the mucociliary escalator, the system that clears mucus from the airways. This helps remove excess mucus and reduces obstruction.
Whats the difference between coarse and fine crackles when listening to patients chests.
Fine Crackles:
Typically occur in rapid bursts or intermittent popping sounds during inspiration.
Timing:
Fine crackles are heard late in inspiration (end of the inspiratory phase).
Underlying Causes:
Fine crackles are usually a sign of fluid or inflammation in the alveoli and small airways.
They are often associated with conditions that involve interstitial lung disease, pulmonary fibrosis, or congestive heart failure (especially when there is fluid in the alveoli).
Other conditions include pneumonia, acute respiratory distress syndrome (ARDS), and atelectasis.
Clinical Significance:
- Coarse Crackles:
They have a bubbling, gurgling, or rattling quality.
Coarse crackles can be heard in both inspiration and expiration.
Timing:
Coarse crackles are typically heard early in inspiration but may also be audible during expiration, especially in more severe cases.
Underlying Causes:
Coarse crackles are commonly associated with the larger airways or bronchi and suggest more significant secretions in the airways or larger bronchi.
Common causes include bronchitis, pneumonia, chronic obstructive pulmonary disease (COPD), emphysema, and bronchiectasis.
They can also occur with severe pulmonary edema, where larger airways become filled with fluid.
Why is Glucagon used in Anaphylaxis for patient unresponsive to Adrenaline.
Glucagon can be used in the treatment of anaphylaxis when there is a severe or refractory case of hypotension (low blood pressure) that does not respond to adrenaline. Glucagon may be necessary in certain situations due to some patients taking beta-blockers
- Epinephrine Resistance in Beta-Blocked Patients
Beta-blockers (such as atenolol, metoprolol, or propranolol) are medications that block beta-1 and beta-2 adrenergic receptors, preventing the action of epinephrine and other catecholamines on the heart and smooth muscle. This can blunt the effectiveness of Adrenaline during anaphylaxis, especially in terms of its cardiovascular effects (e.g., increasing heart rate and blood pressure).
In such cases, glucagon becomes useful because it increases heart rate and cardiac output through beta-receptor-independent mechanisms. Specifically, glucagon activates the glucagon receptor, leading to an increase in cyclic AMP (cAMP) inside the cells, which stimulates the heart (positive inotropic and chronotropic effects) and improves vasoconstriction and blood pressure.
Glucagon’s Mechanism of Action in Anaphylaxis
-Glucagon acts on the glucagon receptor, which is distinct from the beta-adrenergic receptors that are typically targeted by adrenaline. This means that glucagon can work even in the presence of beta-blockers or when epinephrine’s effects are diminished or resistant.
Why do patients who have had an anaphylactic attack require transport to hospital and how long are they required to be monitored.
Patients are required to be monitored for at least 4 hours. This is due to patients re-presenting with signs and symptoms once adrenaline and other therapies wear off.
What is Ambulance Tasmania’s Treatment for Anaphylaxis.
Adrenaline
- 500mcg IM (repeat at 5/60) as required.
Consider Nebulized adrenaline as per Upper airway obstruction.
5mg Adrenaline Nebulized.
Further Mx as per Asthma
Salbutamol Nebulized
- 10mg in 5ml
with
Atrovent
- 500mcg in 1ml
Repeat salbutamol
- 5mg in 2.5ml at 5/60 as required
Repeat Atrovent at
- 500mcg at 20/60 intervals (max 3 doses)
Dexamethasone
8mg in 2ml IV, IM or oral.
What does the RASH Criteria stand for?
How does the criteria work?
R- Respiratory Distress
- Short of breathe, Wheeze, cough or stridor
A- Abdominal
- Nausea, vomiting Diarrhea, abdominal pain or cramping
S- Skin
- Hives, rash, flushing, welts, angio-oedema, swollen lips or tounge.
H- Hypotension
- Hypotension or altered conscious state.
Pt needs to meet two or more of these symptoms with or without confirmed antigen exposure.
OR
Isolated hypotension <90mmhg, or isolated bronchospasm or isolated upper airway obstruction following likely exposure to antigen
OR
Any symptom of RASH in patient with known exposure to antigen with previous history of Anaphylaxis or severe allergic reactions to the same antigen.
What are the ECG Parameters including….
- What does small box represent
- What does one large box represent.
- PR interval
- QRS
- T waves
1 Small box = 0.04ms
1 Large box = 0.2
PR Interval = Between 0.12 -0.2ms (3- small squares)
QRS <0.12 (narrow, Less than 33 small sqaures) or > 0.12 Broad
T waves = Upright, none peaky or Inverted (not including V1 or lead III) for inverted.
What a normal PH range?
Which is acidosis and which is alkalosis.
PH ranges from 0-14
A normal blood PH range for a person is between 7.35-7.45
Acidosis is below 7.35
Alkalosis is above 7.45
Explain blood gas regulation through Bicarb and Respiratory regulation.
Blood Gas Regulation (Respiratory and Renal Systems)
The human body maintains its pH balance primarily through the bicarbonate buffer system and respiratory regulation:
Note: Hydrogen Ions are Acidic and come as a by product of metabolic waste.
During anaerobic respiration, when oxygen is scarce (e.g., during intense exercise), glucose is converted into lactic acid (lactate), which dissociates to release hydrogen ions.
Bicarbonate buffer system:
- In the blood, carbonic acid (H₂CO₃) dissociates into hydrogen ions (H⁺) and bicarbonate ions (HCO₃⁻). This helps buffer changes in pH. If the blood becomes too acidic, the kidneys can excrete excess hydrogen ions and retain bicarbonate ions to restore balance. If the blood becomes too alkaline, the kidneys can do the opposite.
Respiratory regulation:
The respiratory system helps control blood pH by adjusting the levels of carbon dioxide (CO₂). When CO₂ dissolves in the blood, it forms carbonic acid, which dissociates into hydrogen ions. Breathing rate can increase or decrease to help regulate CO₂ levels in the blood, and therefore control pH. Rapid breathing can help reduce CO₂ and raise pH (make the blood less acidic), while slow breathing can retain CO₂ and lower pH (make the blood more acidic).
The kidneys
play a critical role in maintaining long-term pH balance by excreting or retaining hydrogen ions and bicarbonate. The kidneys adjust the pH of the blood through a few key processes:
Excretion of Hydrogen Ions: The kidneys filter blood and remove hydrogen ions (H⁺) from the bloodstream, which are then excreted in urine. This process helps to lower blood acidity when there is an excess of hydrogen ions.
Reabsorption of Bicarbonate: The kidneys also reabsorb bicarbonate (HCO₃⁻) from the urine back into the blood. Bicarbonate acts as a buffer to neutralize excess hydrogen ions and raise the blood pH.
Ammonium Production: The kidneys also generate ammonium (NH₄⁺) from ammonia (NH₃), which helps to excrete excess hydrogen ions and further regulate pH.
CO2 +H2O↔H2CO3↔H+ + HCO3−
What is ETCO2 and how do paramedic utilize it in practice?
ETCO₂ stands for End-Tidal Carbon Dioxide, which is the concentration of carbon dioxide (CO₂) in the exhaled breath at the end of expiration. It is measured in millimeters of mercury (mmHg) or as a percentage.
Normal ETCO₂ levels range from 35–45 mmHg
Higher than 45 can indicate Respiratory acidosis. The higher the reading this indicates that there are high levels of Co2 during exhalation indicate acidosis.
Paramedic Practice.
Airway Management
- Confirmation of Endotracheal Tube (ETT) Placement:
After intubation, paramedics use ETCO₂ to confirm that the ETT is in the trachea and not the esophagus. A sustained ETCO₂ waveform indicates correct placement.
Continuous Monitoring: Ensures the tube remains in place during transport.
- Cardiac Arrest and CPR
- Effectiveness of Chest Compressions:
ETCO₂ levels reflect the quality of CPR. An ETCO₂ reading above 10 mmHg suggests effective chest compressions, while lower values indicate the need for improvement.
- Indicator of ROSC (Return of Spontaneous Circulation):
A sudden rise in ETCO₂ may signal that the heart has started beating again. - Respiratory Emergencies
- Assessing Ventilation:
Helps paramedics gauge the severity of conditions like asthma, COPD, or respiratory distress.
Rising ETCO₂ may indicate hypoventilation, while low levels suggest hyperventilation.
- Adjusting Ventilator Settings:
If a patient is on mechanical ventilation, ETCO₂ helps fine-tune the ventilator to maintain appropriate CO₂ levels. - Shock and Trauma
- Monitoring Perfusion:
Low ETCO₂ can indicate poor perfusion, which might occur in cases of shock or significant blood loss. - Sedation and Pain Management
- Monitoring Sedation Levels:
During procedural sedation, paramedics use ETCO₂ to monitor for respiratory depression and ensure patient safety.
What are some CPAP contraindications
(please note that CPAP isn’t currently available for use in AT guidelines, however could be utilized on consult)
Due to this, these are sourced from AV
- Cardiac Arrest
- Patient agitated or intolerance
- Nil improvement after 1 hour
- HR <50
- SBP <90
- GCS <13
- Decreasing SPO2
- Loss of airway control
- Copious airway secretions
- Active vomiting
- Paramedic judgement
What is the Patho of croup?
Croup, also known as laryngotracheobronchitis, is a common respiratory illness in children characterized by inflammation and narrowing of the upper airway, particularly the larynx, trachea, and bronchi. This condition typically results in a distinctive barking cough, stridor, and hoarseness.
Most commonly effecting ages 6 months to 6 years old.
Inflammation:
- The infection triggers inflammation of the respiratory epithelium, leading to:
Oedema and swelling of the subglottic region (below the vocal cords).
Increased mucus production.
Airway Obstruction:
-The subglottic space is naturally narrow, especially in young children.
Inflammation and swelling in this region cause significant airway narrowing, leading to increased airway resistance.
Severity:
Mild: Barking cough without stridor at rest.
Moderate: Stridor at rest with mild to moderate respiratory distress.
Severe: Significant stridor, severe respiratory distress, lethargy, or hypoxia.
What is Ambulance Tasmania Management of Mild, Moderate and severe Croup
Mild Croup
- Dexamethasone 0.15mg/kg (max 12mg) PO
- Review exclusion criteria and red flags
- Treat and refer, safety netting and GP appointment.
Moderate croup
- Dexamethasone 0.15mg/kg (max 12mg)
- Transport to ED
Severe Croup
- Consider ICP
- Dexamethasone 0.6mg/kg (max 12mg) PO, IM, IV.
- Adrenaline 5mg in 5ml Nebulized.
- Transport.
What are some clinical signs of Croup
- Fever with signs of systemic illness
- Irritability
- Inspiratory stridor (at rest or exertion)
- Feeling worse at night
- Barking cough and/ or Hoarse voice
- Total duration 3-7 days
Precipitated by URTI 1-2days prior to barking cough
How does Adrenaline and Dexamethasone help croup.
Adrenaline
- Adrenaline stimulates alpha-adrenergic receptors, leading to vasoconstriction in the subglottic mucosa. This reduces mucosal swelling and edema, quickly widening the airway.
Also stimulates beta-adrenergic receptors in the lungs:
Bronchodilation: Helps to improve airflow, although croup primarily involves the upper airway.
Dexamethasone
Corticosteroid: Dexamethasone works by reducing inflammation through inhibition of cytokine production and suppression of the inflammatory response.
Decreases subglottic Oedema and mucus production over time.
Unlike adrenaline, it addresses the underlying inflammatory process, providing more sustained relief.
What is the Patho Hypoglycemia
Hypoglycemia occurs when blood glucose levels drop too low, typically below 3.9 mmol/L
What Happens in Hypoglycemia:
Insufficient Glucose for Cells:
- The body doesn’t have enough glucose to use as energy.
- When glucose drops, the body releases counter-regulatory hormones:
Glucagon (from the pancreas) signals the liver to release stored glucose (glycogen) and assist with the transfer into glucose.
What is the Patho of Hyperglycemia
Hyperglycemia occurs when blood glucose levels are too high, typically above 7.0 mmol/L (fasting) or 11.1 mmol/L (post-meal).
What Happens in Hyperglycemia:
Insufficient Insulin or Insulin Resistance:
- Type 1 Diabetes: The body doesn’t produce enough (or any) insulin, which is needed to help glucose enter cells.
-Type 2 Diabetes: The body becomes resistant to insulin, so glucose cannot enter cells effectively, even if insulin is present.
Glucose Accumulates in the Blood:
Insulin is a gate keeper for cells and allows cells to uptake glucose to use as energy. Since glucose can’t enter cells properly, it builds up in the bloodstream.
Cells are starved of energy, so the liver produces even more glucose, worsening the problem.
Osmotic Effects:
-High glucose levels pull water out of cells into the bloodstream, leading to dehydration and excessive urination (polyuria).
This can cause increased thirst (polydipsia).
Metabolic Imbalance:
In the absence of insulin, fat breakdown increases, leading to ketone production. This can result in diabetic ketoacidosis (DKA) in Type 1 diabetes.
In severe Type 2 diabetes, hyperosmolar hyperglycemic state (HHS) can develop, with very high blood sugar and severe dehydration.
What is Hyperosmolar Hyperglycemic State (HHS)
What is Diabetic Ketoacidosis (DKA)
Insulin Insufficiency
Glucagon, adrenaline, cortisol, and growth hormone are released to compensate.
These hormones promote glucose production by the liver (gluconeogenesis) and breakdown of glycogen (glycogenolysis), worsening hyperglycemia.
Fat break down leads to fatty acid production, these are then converted to Ketones.
Ketones are acidic, causing metabolic acidosis.
The body attempts to compensate by increasing breathing rate (Kussmaul respirations) to blow off CO₂ and reduce acidosis.
Electrolyte Imbalances:
Hyperglycemia causes osmotic diuresis, leading to loss of water, sodium, and potassium in the urine.
Dehydration and Hypovolemia:
Osmotic diuresis leads to severe dehydration and loss of circulating blood volume (hypovolemia), which can cause hypotension and reduced tissue perfusion.
How do Paramedics treat Hypoglycemia under Ambulance Tasmania Adult Guidelines.
If BGL <4 and responds to commands
- Glucose paste 15g
Inadequate response?
- Repeat dose of glucose paste.
- Glucagon.
Note
- If adequate response, insure patient eats substantial food within 30/60
Does not respond to commands or nil improvement from above
- IV Cannula (large vein) + confirm patency.
- Glucose 10% 15g in 150ml initial dose. (normal saline 10ml flush)
- If IV not attainable then Glucagon 1mg in 1ml
If inadequate response
- Repeat Glucose 10% 10g in 100ml IV
- Repeat this every 5 minutes until BGL >4.
How do Paramedics treat Hyperglycemia under Ambulance Tasmania Adult Guidelines.
ketones < 0.6
- Assess signs of dehydration.
- If nil Dehydration then consider referral pathway.
- If dehydration present treat as per below.
Ketones >0.06
- Transport to hospital for ongoing management.
If patient dehydrated (Tachycardic or hypotensive (HR >100 or BP <100))
- Manage as per Fluid guideline
- Normal saline 20ml/kg, Nil repeat.
Consider consult for further fluid if nil ICP Available and long transport times.
What is the normal range of ketones?
What are the different ranges and risk levels.
Normal range: <0.06
Mild to Mod: 0.06-3
Severe: >3
What are some exclusion criteria for Hyperglycemia when assessing referral pathways?
- Post hypoglycemia event and alone.
- Unable/ unwilling to eat.
- Pregnancy
- Moderate to Severe dehydration
- Nil pHx of Diabetes
- Steroids
- Chronic Alcoholics
- Ketones >0.06
What is Euglycemic Ketoacidosis and how is it relevant in Prehospital care?
Euglycemic ketoacidosis (EKA) is a rare form of diabetic ketoacidosis (DKA) where blood glucose levels remain normal or only mildly elevated (typically <11 mmol/L, but significant ketosis and metabolic acidosis still occur. This condition is most commonly associated with:
- Sodium-Glucose Co-Transporter-2 (SGLT-2) Inhibitors: ( canagliflozin, dapagliflozin, and empagliflozin)
- Alcoholics
- Prolonged fasting/ Starvation
- Acute illness or stress
- Pregnancy
What is the patho of a Seizure
Seizures occur when neurons in the brain fire excessively or synchronously.
This abnormal firing disrupts the balance between excitatory (e.g., glutamate) and inhibitory (e.g., GABA) neurotransmitters.
Hyperexcitable Neurons:
In seizure-prone areas, neurons have a lower threshold for firing due to changes in:
Ion channels (e.g., sodium, calcium, and potassium channels).
Neurotransmitter systems (reduced GABA or increased glutamate).
Seizures can be focal (originating in one area)
or
generalized (involving both hemispheres of the brain).
Causes
- Certain conditions can predispose the brain to seizures, including:
Structural damage (stroke, trauma, tumors).
- Electrolyte imbalances (e.g., low sodium or calcium).
- Infections (e.g., meningitis, encephalitis).
- Genetic mutations affecting ion channels or receptors.
- Withdrawal from alcohol or sedatives.
How does Ambulance Tasmania treat Seizures?
Continuous or Recurrent seizures.
(More than one (without full recovery) or longer than 5 minutes)).
Age <60
- Midazolam 0.1mg/kg IM (Max 10mg) per dose.
Age >60
- Midazolam 0.05mg/kg (max 10mg) per dose
If nil improvement after 10/60
- Repeat Midazolam IM dose once only (Max 20mg total).
How do Benzodiazepines treat seizures?
They work by enhancing the activity of the gamma-aminobutyric acid (GABA) neurotransmitter in the brain.
GABA-A Receptor Modulation:
- Benzodiazepines bind to the GABA-A receptors in the central nervous system (CNS).
GABA is the brain’s primary inhibitory neurotransmitter, which reduces neuronal excitability.
When benzodiazepines bind to these receptors, they enhance the effect of GABA by increasing the frequency of chloride ion channel opening.
Hyperpolarization of Neurons:
The increased influx of chloride ions into neurons makes the inside of the cell more negative (hyperpolarized).
This reduces the likelihood that the neuron will fire (send an electrical signal), calming excessive brain activity during a seizure.
As per Ambulance Tasmania Seizure guideline, If a Patient has a pHx of Seizures and refuses transport to hospital, is this acceptable.
Yes, If a patient has a responsible third party present and able to watch the patient then they can be left at home. Crews should advise this person of actions to take if this event reoccurs and stress the importance of follow up with primary care physicians.
How does Ambulance Tasmania treat TCA OD
If patient has any of the following signs
1. Less than adequate perfusion
2. Positive R Wave (>3mm) in AVR
3. Progressively Widening QRS >0.12
4. QT Prolongation
5. QTc >500ms
Modified FAST Assessment Tool
ACT FAST Assessment tool
What is Wallace rule of 9s
