QLD CPG Review Flashcards
Symptoms of cardiac chest pain?
- Retrosternal chest pain
- Decribed as burning, pressure or tightness
- Referred pain (eg. arms or jaw/teeth)
- Dyspnoea
- Diaphorisis
- Nausea and vommiting
- Feeling of impending doom.
Treatment options for ACS?
After any IV medication = 100 ml flush.
Standard interventions:
- GTN: 400 mcg spray sublingual
- Oxygen
- Aspirin: 1 x 300 mg tablet orally
Pain Relief:
- Fentanyl: comes in 100 mcg in 2 ml. Mix with 8 ml of saline to get 10 ml dilution. Thus you will have 10 mcg
of Fentanyl per 1 ml.
IV Dose: 25-50 mcg increments up to a max of 100 mcg.
In patients over 70, Fentanyl should be given in 25 mcg increments up to a max of 100 mcg.
Nausea:
- Comes in 4 mg in 2 ml. Dose is 4mg IV or IM.
- Paediatric dose in above 5 yrs old = 2 mg
- Paediatric dose above 3 years old 100 mcg per kilo . One possible dilution for this is take your 4 mg in 2ml. Draw up 1 ml and discard remainder. Add your 2mg in 1ml with 9 ml of saline. You now have 2000 mcg in 10 ml. Dividing 2000 by 10 you move decimal place one to the left….so 200 mcg per 1 ml.
Symptoms of bradycardia?
- HR < 60 bpm
- Hypoxia is a common cause of bradycardia. Check effectiveness of breathing/auscultation
- Hypotension (< 90 mmHg systolic)
- Syncope
- Dysponea
- Diaphoresis
- Nausea
Treatment for bradycardia?
Non-Cardiac bradycardia: Always focus on reversible causes.
Cardiac Bradycardia:
- Atropine: Comes in 1.2 mg / 1ml. dose for bradycardia is 600 mcg IV. Repeat after 2 minutes. Maximum total dose is 1.2 mg - Call for ICP support.
- Transcutaneous Pacing - Call for ICP support.
- Adrenaline - Call for ICP support.
- Isoprenaline - Call for ICP support. This drug is a synthetic amine similar to adrenaline. Except highly selective acting exclusively on B1 adrenergic receptors increasing chronotrope, inotrope and dromotrope (conduction speed).
Explain Atropine?
Class: Anticholinergic
Molecular target: Muscarinic acetylcholine receptor
Type of interaction: Reversible, competitive antagonist
Atropine in a competitive antagonist of muscarinic Ach receptors and exerts an anti-cholinergic effect. The ideal dosing for atropine is unknown and thankfully, the risk of toxicity is extremely low. It is thought that delay in reaching therapeutic atropinisation has negative consequences for morbidity and thus aggressive dosing is recommended in organophosphate poisoning.
acetylcholine is regulated by acetylcholinesterase, which is responsible for breaking it down.
What occurs in organophosphate poisoning?
acetylcholine (ACH) is regulated by acetylcholinesterase, which is responsible for breaking it down. Organosphosphates attach to acetylcholinesterase binding sites, preventing it from attaching to acetylcholine and downregulating hydrolysis. Thus ACH becomes excessive.
Two key types of ACH receptors exist, muscarinic and nicotinic. Nicontinic are fast acting, and exist throughout the body including at the neuromuscular junction. They are ion channels that bind with ACH, allow Na+ influx and thus depolarisation and muscle contraction.
With two much ACH, nicotinic receptors are overwhelmed and muscle twitching occurs in the patient.
Muscarinic receptors are also found within smooth muscle, the cardiac conduction system and exocrine glands. Muscarinic receptor type 2 (M2) is found extensively throughout the myocardial tissue, and binding of AcH to M2 receptors which are secondary activates a G-protein coupled response (secondary messenger response). This influences the SA node, decreasing its firing rate and slowing electrical conduction. This mechanism explains the bradycardia seen in these patients.
ECH features of SVT? Caused by?
- 140-280 bpm and is regular in nature. It may cease spontaneously (and abruptly) or continue indefinitely until medical treatment is sought.
- QRS complexes usually narrow (< 120 ms)
- P waves are typically buried in the QRS complex
Re-entry mechanism triggered by:
- Increase in sympathetic activation
- Stimulants (drugs, coffee, alcohol, energy drinks)
- Electrolyte or acid base disorders
- Hyperventilation
- Stress (wolf-parkinson white syndrome)
Symptoms of SVT?
- Well tolerated and rarely life threatening
- A narrow complex tachycardia RARELY requires cardio-version.
- AF patients with greater than 24 hour history, are at risk of thrombus. Therefore a delayed approach to cardioversion should be considered.
- Palpitations
- Chest pain or discomfort - burning, tightness, pressure
- Dysponea
- ALOC
- Haemodynamic instability
Treatment for narrow complex tachycardia?
If there is haemodynamic compromise:
- oxygen
- Aspirin (If myocardial ischemia is suspected)
- IV Fluids
- Cardioversion required
No Haemodynamic compromise:
- Oxygen
- Aspirin (If myocardial ischemia is suspected)
- Modified Valsalva manoevre:
- Blow into a 10 ml syringe for 15 seconds whilst semi recumbent. Then place patient immediately supine with leg raise for 45 seconds.
Cardiogenic Shock treatment?
- Oxygen
- CPAP
- Aspirin
- Adrenaline (ICP skill)
- IV fluid (titrate to physiological response to fluid, reassessing obs)
What are symptoms for broad complex tachycardia?
- Defined as heart rate >100bpm and QRS >.12 seconds.
- The most important clinical feature in BCT is the haemodynamic status. Those with haemodynamic instability require immediate cardioversion. Delay may result in cardiac arrest.
Differentials may include:
- VT
- SVT with abberant conduction such as pre-existing BBB
- Pre-excitation (eg Wolff-Parkinson white syndrome)
Treatment for broad complex tachy?
No pulse? - treat as per cardiac arrest
Haemodynamically compromised?
- Cardioversion ( call for ICP )
Not yet Haemodynamically compromised?
- Call ICP for amiodarone and magnesium sulfate
What are the temperature ranges for heat exhaustion vs heat stroke?
Heat exhaustion ( 37 degrees - 40 degrees) Characterised by loss of fluid and electrolytes. Can progress rapidly to heat stroke left untreated.
Heat stroke ( > 40 degrees) A potentially life-threatening condition that leads to death/multi-organ failure
What are non environmental causes of hyperthermia ?
It is called intrinsic hyperthermia
- Infection
- Seratonin Syndrome
- Status epilepticus
- CVA involving the hypothalamus
- Drug withdrawl
What are key considerations in hyperthermia?
- Patients can become hypothermic when cooled too rapidly. If the patient shivers, is cool to the touch or peripherally shut down then discontinue cooling.
- The degree and duration of hyperthermia is a key predictor of outcome.
Symptoms of hyperthermia in heat exhaustion and heat stroke?
Heat exhaustion:
- Severe headache/dizziness
- Diaphorisis (sweaty), neusea and vomiting
- Tachyponea, tachycardia, hypotension
- Muscle pain/cramps
Heat stroke:
- Dry skin and hot (no sweat)
- CNS dysfunction such as siezures, ALOC and extreme fatigue)
- Dysrythmias
- Hypotension
- Hypoglycemia and hyperkalaemia
Treatment for hyperthermia (both types almost the same)
Unconcious Yes?
- Remove patient from heat source
- Exposure
- Prioritise breathing via:
Oxygen
IPPV
LMA
Then progress to regular conscious treatment protocol
- Remove patient from heat source
- Exposure
- Strip - Spray - Fan - Ice (ultimate technique). Ice in maxilla, groin, neck. ICE is ONLY in heat stroke (>40 degrees). Otherwise ‘gentle’ cooling is used.
- Cooled IV fluid - titrate to patient response/BP
- Ondansatron. Come in: 4 mg in 2 ml Dose: 4mg IM
- Analgesia
- Paracetamol if infectious cause suspected.
What are the temperature ranges for hypothermia
Also list symptoms for each
Mild (35 - 32 Degrees)
- Vasoconstriction
- lethargy
- Ataxia (poor movement coordination)
- Tachycardia
- Normotensive
Moderate (32 - 28 degrees)
- Confusion / Delerium
- ALOC
- Hypotension
- BRADYCARDIA
- Muscle regidity
Severe (<28 degrees)
- Coma
- DILATED PUPILS
- Dysrythmias
- Slow AF
- VF
Are Sats accurate in hypothermia?
Not entirely, as there is a shift left in the oxygen/haemoglobin dissassociation curve. Thus oxygen is bound tight the Haemoglobin…and sats read high. Despite this, the delivery of oxygen to tissue is reduced and tissue may be in fact hypoxic despite good sats.
What is the treatment for hypothermia in patients with no signs of life?
Resuscitation but with some special considerations:
- They arent dead until they are WARM and dead. Signs of life are unreliable whilst the patient is hypothermic.
- WITHOLD adrenaline and all other resus drugs such as amiodarone until the patient temp is higher than 30 degrees.
- Once above 30 degrees the standard drug interval should be doubled. So adrenaline after every round (2 minutes) instead of 4.
- As body temperature DECREASES, Bradycardia leads into AF….then into VF…then aystole.
What is the treatment for patients with hypothermia who HAVE signs of life?
- Minimise patient movement - Cardiac irritability is enhanced, as is the potential for clotting.
- Prevent further heat loss. Remove wet clothing. Blanket -> space blanket -> blanket.
- Minimal IV Fluid - Permissive hypotension only.
- Oxygen: ensure adequate
- 12 lead ECG: As body temperature DECREASES, Bradycardia leads into AF….then into VF…then aystole.
- Serial temperature monitoring
- BGL - how long have the been there?
How should you define an anaphylactic reaction in the field?
Any acute onset of illness with typical skin features such as uticarial rash, erythema/flushing and/or angiooedema.
PLUS
Involvement and/or cardiovascular and/or severe gastro symptoms
OR Any acute onsent of hypotension OR bronchospasm where anaphylaxis is considered possible EVEN IF skin features are not present.
Signs and symptoms of moderate reaction vs anaphylaxis?
Moderate:
- lip swelling, face, eyes
- Hives
- Tingling mouth
- Abdo pain
Anaphylaxis:
- Stridor, noisy breathing
- Tongue swelling
- Throat tightness or difficulty swallowing
- Wheeze or cough
- Dizziness or collapse
- Pale and floppy (Young children)
Key risk assessment items for anaphylaxis?
- very reaction is different. Some only react with hypotension and dizziness.
- Uticaria and angiooedema may be transient or overlooked. 1 in 6 anaphylactic deaths occurs without skin reaction - whilst cardio or respiratory symptoms occured.
- If uncertain if asthma…treat with adrenaline first, prior to salbutamol.
