Tassie Prep Flashcards
What is the Patho of ACS
Acute Coronary syndrome is a spectrum of illnessess.
1) Unstable Angina
- results when the blood flow is impeded to the myocardium. Most commonly, this block can be from plaque formation, thrombosis, vasospasm, and elevated blood pressure. Often, a combination of these is the provoking factor.
Non-ST elevation MI
- Non-ST-elevation myocardial infarction (NSTEMI) is a type of involving partial blockage of one of the coronary arteries, causing reduced flow of oxygen-rich blood to the heart muscle.
STEMI
-The pathogenic mechanism typically involves plaque rupture and thrombus formation within the coronary artery, though other processes may also lead to STEMI. This is when an artery is fully occluded starving a certain part of the heart of oxygen.
-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 is the Patho of Pulmonary Oedema
Cardiac Pulmonary Oedema
In acute cardiogenic pulmonary edema an increased left ventricular end-diastolic pressure causes the left atrium to pump against an increased load. The atrium becomes overwhelmed, and an increased hydrostatic pressure gradient is created. Eventually, the pulmonary interstitium becomes overloaded, and the pulmonary veins widen.
Backflow of fluid from the heart back into pulmonary circulation occurs.
Due to a increase in hydrostatic pressure and decrease in oncotic pressure, fluid shifts into interstitial spaces, pressure builds in these spaces and pushes fluid into the Alveoli, causing fluid on the lungs.
Patients most at risk are patients with LVF. The left ventricle no longer functions as well due to a change in physiology like e.g. hypertrophy.
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 0.05 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.
What is the Patho of Asthma
There are two phases of an asthma exacerbation, which include the early phase and the late phase.
Early Phase
The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. These antibodies respond to certain triggers in the environment.
IgE antibodies then bind to mast cells and basophils. When a pollutant or risk factor gets inhaled, the mast cells release cytokines and eventually de-granulate.
This causes mast cells to release histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening.
Late Phase
Within the next several hours, the late phase occurs, in which eosinophils, basophils, neutrophils, and helper and memory T-cells all localize to the lungs as well, which perform bronchoconstriction and cause inflammation. Mast cells also play an essential role in bringing the late-phase reactants to the inflamed sites.
Patients may also have increased activity with goblet cells leading to hypersecretion of mucus in the airway leading to mucus plugging
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 the definitions of COPD (Emphysema and chronic bronchitis)
COPD is a term that includes 2 or more of the following 3 conditions
1. Asthma
2. Emphysema
3. Chronic Bronchitis
These 3 conditions all impact the airways and lungs, generally speaking cause wide spread inflammation.
These conditions lead to long term structural changes in the airway.
What is the Patho of Emphysema.
Emphysema
Definition
- Emphysema is defined as an abnormal permanent enlargement of air spaces, accompanied by the destruction of alveolar walls and without obvious fibrosis. This process leads to reduced gas exchange, changes in airway dynamics that impair expiratory airflow, and progressive air trapping. This could be due to Genetics, Smoking chemical inhalation and more.
Patho
Pathophysiology of Emphysema:
Alveolar Wall Destruction:
- The hallmark of emphysema is the destruction of the walls between the alveoli (the small air sacs in the lungs where gas exchange occurs). This leads to the enlargement of the air spaces.
Normally, the alveolar walls provide surface area for gas exchange and maintain the structure of the lung. In emphysema, the breakdown of these walls reduces the surface area for oxygen exchange, leading to decreased oxygenation of the blood.
Loss of Elastic Recoil:
-The destruction of alveolar walls and the loss of elastic fibers result in a decrease in lung elasticity (or “recoil”).
The elastic recoil of the lungs is important for expelling air during exhalation. When this recoil is lost, the airways and alveoli collapse during exhalation, causing air trapping and difficulty in fully exhaling.
This leads to hyperinflation of the lungs.
What is the Patho of Chronic bronchitis.
Chronic bronchitis is characterized by chronic inflammation of the airways (bronchi), which leads to increased mucus production, airflow limitation, and difficulty with breathing. It is defined clinically as a productive cough (mucus production) for at least 3 months per year for two consecutive years or more.
Patho
Chronic Inflammation:
- Chronic exposure to irritants (primarily cigarette smoke, but also air pollutants, occupational dust, and fumes) leads to persistent inflammation in the lower respiratory tract, especially the bronchi. inflammatory mediators are released contributing to airway injury and remodeling. The inflammation leads to increase in mucus and increase in hypertrophy. This will lead to further obstruction of airways.
Mucus Hypersecretion:
The thick mucus leads to chronic productive cough, a key feature of chronic bronchitis. The cough is worse in the mornings and is often associated with sputum (mucus) production.
Due to damaged Cilia, patient often have issues clearing mucus. This means a build up of mucus and a build up of Bacteria are breeding grounds for further infections.
Inflammation and mucus buildup lead to narrowing of the bronchi, making it difficult for air to flow in and out of the lungs.
Chronic inflammation also causes remodeling of the airway wall, with fibrosis (scarring) and thickening of the airway walls, further contributing to airflow obstruction.
Bronchial Smooth Muscle Constriction:
Chronic bronchitis is often associated with bronchospasm (constriction of the bronchial smooth muscle), which further narrows the airways and increases resistance to airflow.
Decreased Gas Exchange:
The chronic narrowing and inflammation of the airways result in ventilation-perfusion mismatch. While air may enter the lungs, it cannot reach all areas of the alveoli effectively due to blocked or narrowed airways, reducing oxygen uptake and carbon dioxide clearance.
Over time, this leads to hypoxemia (low oxygen levels in the blood) and hypercapnia (increased carbon dioxide levels), especially in advanced disease.
Air Trapping and Hyperinflation:
In patients with chronic bronchitis, the collapse of small airways during exhalation leads to air trapping—the retention of air in the lungs after expiration. This causes lung hyperinflation,
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.
What is the Patho of Anaphylaxis
Anaphylaxis is a severe, life-threatening allergic reaction that occurs rapidly after exposure to an allergen. It involves multiple organ systems.
The pathophysiology of anaphylaxis is primarily driven by often IgE-mediated response, which leads to widespread vasodilation, smooth muscle contraction, and airway obstruction.
Flow Chart
Immune system mistakenly recognizes the allergen as harmful. In response, B cells produce IgE antibodies specific to that allergen.
These IgE antibodies bind to mast cells and basophils, which are abundant in tissues like the skin, lungs, gastrointestinal tract, and blood vessels. These cells are considered “primed” for future allergic reactions.
When an individual who has been sensitized to an allergen is exposed again, the allergen binds to the IgE on mast cells and basophils, triggering their activation.
Once the individual is exposed again to the allergen, the allergen will bind to IgE causing a response. This in turn causes
Degranulation:
Mast cells and basophils undergo degranulation, releasing histamine, leukotrienes, prostaglandins, cytokines, and other inflammatory mediators into the bloodstream.
Histamine is one of the most potent mediators released during anaphylaxis, causing widespread vasodilation, increased vascular permeability, and smooth muscle contraction.
Breakdown of systems
Vasodilation and Hypotension:
- Histamine and prostaglandins cause vasodilation and increase the permeability of the blood vessels. This results in fluid leakage from the bloodstream into the tissues, leading to edema (swelling) and a drop in blood volume. This can also lead to angio-oedema in the airway.
Hypotension develops due to both the fluid loss and vasodilation, contributing to shock if untreated. This reduced perfusion leads to inadequate oxygen delivery to tissues, including vital organs such as the heart and brain.
Bronchoconstriction
-Leukotrienes and histamine cause bronchoconstriction leading to wheezing, shortness of breath, and respiratory distress.
Cutaneous Symptoms:
Histamine and other mediators cause itching, urticaria (hives), and angioedema (swelling of the skin and deeper tissues), which are often seen in the skin.
Gastrointestinal Symptoms:
-Histamine, leukotrienes, and other mediators can affect the gastrointestinal tract, leading to symptoms such as nausea, vomiting, and abdominal cramps.
These symptoms may be accompanied by diarrhea in some cases.
Cardiovascular Effects:
-Anaphylaxis can lead to cardiovascular collapse due to decreased cardiac output (due to hypotension and vasodilation) and dysrhythmias (irregular heart rhythms).
Arrhythmias can occur due to the profound circulatory changes and hypoxia (low oxygen levels in the blood).
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.
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
