Carbon Monoxide

Case encountered: 80 something year old, BBQ smoke inhalation and overdose on multiple medications. Smoke exposure over 14 hours, short periods of it in a sealed room. On arrival patient outside their house, GCS 15 and oriented x3. Patients saturations, pulse, blood pressure, respirations and BM within normal range, peripherally cold with a temperature of 35.3ÂșC, no cyanosis. Small haematoma and scrape to parietal region. MSK x4, chest clear bilaterally, mobilises as normal, no visual disturbances, headache, dizziness, bogginess on head, vomiting, nausea, headache, chest pain or shortness of breath. Visible soot in nostrils and around lips, none visible in throat.

Carbon monoxide (CO) is produced when fuels such as gas, oil, coal and wood do not burn fully (NHS Choices, 2012) for example in an enclosed space such as a sealed room. The oxygen is slowly used up and replaced with carbon dioxide which prevents the fuel burning fully and produces carbon monoxide. It is colourless, odourless and tasteless.

Red blood cells contain haemoglobin which has four binding sites. Carbon monoxide will bind to these sites and increase oxygen affinity in the remaining sites - haemoglobin will retain this instead of delivering it around the body. This results in low circulating volumes of oxygen, causing cell hypoxia and shifts the oxygen dissociation curve to the left, as shown below:



British Paramedic Association (2009) describes the oxyheamoglobin dissociation curve as the relationship between oxygen saturation and the amount of oxygen dissolved in the plasma (pO2 ). Carbon monoxide poisoning will show normal or higher oxygen saturation as it is being retained by the haemoglobin.

Symptoms include; dyspnoea, confusion, drowsiness, unconsciousness, headache, dizziness, nausea, vomiting. Most commonly noted in fatalities is cherry red skin (Mosby 2005, British Paramedic Association 2009) which initially starts with flushing or cherry pink skin.

Treatment in the pre-hospital setting – if not immediately life threatening - is high flow oxygen to try and displace CO molecules from the haemoglobin (British Paramedic Association, 2009). Gregory, P, Ward, A (2010) note that the half-life of carbon monoxide in room air is about 4 hours, but reduces to 30-40minutes on 100% oxygen.


References
British Paramedic Association (2009), Nancy Caroline’s Emergency Care in the Streets, 6th Edition, Sudbury, MA, Jones and Bartlett Publishers Inc, p. 26.24, 33.21

Gregory, P, Ward, A (2010), Sander’s Paramedic Textbook, London, Elsevier Health Services, p.677.

Mosby (2005), Mosby’s Dictionary of Medicine, Nursing & Health Professionals, 7th UK Edition, St. Louis, MI, Elsevier Health Sciences, p.297.


01/01/2014 Leave a comment

Blue Light Aware



So I’ve just finished my four week driving course with the ambulance service. I’ve just come across this video and can’t tell you how much this would help all us folk on blue lights if everyone watches it. I’d like to emphasize the solid white line, bends and following at an appropriate speed behind us sections.

We have no legal exemption to overtake anyone on a solid white line – we abide by the highway code whether we’re on lights or driving at normal road speed.

Please, please, please do not stop on a bend. We don’t have x-ray eyes (as useful as that might be!) we cannot see through the shrubbery or buildings and will not overtake you no matter how good your intention may be.

Finally, my favorite. If we’re on blue lights, especially on motorways or duel carriageways, please don’t tailgate or sit on our bumper. If you cannot see our side mirrors we cannot see you. At night time your headlights give our vehicles back-end a flattering heavenly glow.

We all thank you for the helpful and safe driving you do often present to us when we stick those blue lights on.

16/12/2013 Leave a comment

Myocardial Infarction Reflective

Introduction
Using Willis (2010) reflective model, this account focuses on myocardial infarction. The case encountered involved an elderly gentleman suffering cardiac chest pain for an hour before our arrival.

Case Description
The call was to a private residence where a 77 year old male having been suffering from cardiac chest pain for approximately and hour. Prior to our arrival the patient had taken Gaviscon to no effect before dialling 999. On arrival he was sitting in a chair, GCS 15, pale, clammy with non-radiating central chest pain. The gentleman was tachycardic, complaining of feeling nauseas, scoring his pain at 8/10 and was short of breath. The 3-lead ECG showed ST elevation; the 12-lead ECG confirmed and inferior infarction, showing ST elevation in leads 2, 3 and AVF with reciprocal depression (see appendices 1.1 and 1.2).

The patient was administered 300mg aspirin, 400mcg GTN with 600mg of clopidgrel after contacting the coronary care unit (CCU) for advice – due to the guidance for paramedics noting that its administration is only for those under the age of 75 years old. An 18G cannula was inserted once the patient was on the ambulance for 10mg metoclopramide and morphine (titrated to response (2x 5mg doses) could be administered.
En route the primary percutaneous coronary intervention (PPCI) team rang us in relation to the 12-lead we transmitted to them. They accepted the patient for immediate stenting in the PPCI suite. The patient’s clinical form can be viewed in appendices 1.0a & b.

Areas for Investigation
This case presents many areas that I would like to investigate; however on this occasion I will be looking specifically at recognising the signs and symptoms as well as treatment for a myocardial infarction (MI).

What does the Literature Say
Mosby (2005) states that a myocardial infarction is the necrosis of a portion of cardiac muscle caused by an obstruction in a coronary artery. The four most common areas in which a blockage can occur are lateral, inferior, septal or anterior – as seen in appendices 1.3. Reimer KA et al (1977) note that nearly half of potentially salvageable myocardium is lost within 1 hour of the coronary artery being occluded, and two-thirds is lost within 3 hours which JRCALC (2013) acknowledges noting that PPCI referral should be sought when in attendance within 2 hours of onset of symptoms.

Atherosclerosis can advance from angina; partially obstructing blood flow due to a plaque build-up protruding into the coronary arteries, to blocking them completely, cutting off the oxygen supply and culminating in an MI. Another cause is a severe spasm of a coronary artery, mainly bought on by drug misuse or hypoxia, which will cut off blood flow to the heart muscle. Cocaine, amphetamines and methamphetamines are the main drugs that can cause blood pressure, heart rate and temperature to rise as blood vessels constrict (stenosis). Taking one of these drugs causes increased motor activity so the hearts oxygen demand increases, but the drugs also cause stenosis so there’s a reduced blood supply to the cardiac muscle. “Heart attacks due to the use of cocaine are one of the most common causes of sudden death in young people” (NHS Choices, 2010). “Hypoxia can be caused by levels of oxygen in the blood decreasing due to carbon monoxide poisoning or a loss of normal lung function,” NHS Choices (2010). This means that the heart will receive un-oxygenated blood which damages it and triggers a heart attack.
However, the most common reason for a myocardial infarction is when “the plaque may rupture causing injured tissue to be exposed to circulating platelets” (Gregory, P, Ward, A, 2010). The rupture releases substances that encourage the platelets to coagulate and form a blood clot – or thrombus – that will sit on top of the plaque and may or may not occlude the coronary artery. NHS choices (2010) warns that if it “is not treated, the heart muscles will experience irreversible damage” as a result of being starved of oxygen. Cardiac muscle will die - infarct - without an oxygen supply, “areas of cell death are repaired with no contractile scar tissue” (Marieb, E, Hoehn, K, 2007) effecting the hearts overall function which could eventually lead to heart failure.

Symptoms can include having crushing tight central chest pain, radiating pain or ‘heaviness’ to the arms, neck and jaw, diaphoresis, nausea and vomiting, looking ashen, and dyspnoea (Greaves, I, Porter, K, 2006). There is also a high emphasis on a feeling of impending doom which is supported by JRCALC (2013), British Paramedic Association (2009) and Gregory, P, Ward, A (2010) to name a few. It is important to note that women may present slightly differently to men, the British Paramedic Association (2009) write that they may experience epigastric burning, light headedness and an onset of sudden of weakness or unexplained tiredness.
However, pain is absent in up to 30% of patients with myocardial infarction, especially the elderly and those with diabetes mellitus (Douglas, G et al, 2009), a condition often referred to as a silent MI. Gregory, P, Ward, A (2010) note that these patients symptoms relate to a drop in cardiac output often accompanied by sudden development of dyspnoea, progressing rapidly to pulmonary oedema, confusion, a sudden loss of consciousness, and an unexplained drop in blood pressure. When an ECG is done there will be no ST elevation (NSTEMI), however the T wave will often be inverted as the infarction does not include the whole thickness of the ventricular wall (Hampton, J, 2008).

Clinically the resounding sign of an MI is ST elevation with reciprocal depression on an ECG. The ST segment of an ECG represents the initial stages of left and right ventricular repolarisation, necrosis of the cardiac muscle obstruct this process resulting in elevation above the isoelectric line in an ECG (as seen in appendices 1.4). This diagnosis can be difficult however if the patient has a left bundle branch block (LBBB) or left ventricular hypertrophy due to its morphology. JRCALC (2013) strongly recommends that advice should be sought with queries surrounding LBBB with suspected ST elevation MI as reperfusion treatment might still be indicated. Additionally, pericarditis presents with global ST elevation and should be considered. As discussed before, it is possible to have a silent MI or NSTEMI which will not produce the ST elevation morphology due to its pathophysiology. The definitive diagnosis for a heart attack is a blood test in order to check troponin levels which cannot be done in the pre-hospital setting of the ambulance service.
The Joint Royal Colleges Ambulance Liaison Committee (JRCALC, 2013) strongly highlights the rapid treatment of a suspected MI with aspirin and clopidgrel administration, which Greaves, I, Porter, K (2006) concur with, as well as glyceryl trinitrate. Supplemental oxygen can be given in accordance with JRCALC guidelines and analgesic, with additional antiemetic, should also be considered.
Aspirin has an anti-platelet action which reduces clot formation, effectively thinning the blood (JRCALC, 2013) and provides secondary prevention of cardiovascular disease (Joint Formulary Committee, 2013). It inhibits the production of a chemical that causes platelets to stick together and therefore reduces the risk of clot formation and occlusion of arteries. In the case of a myocardial infarction the JRCALC (2013) states a 300milligram dose of aspirin should be chewed as it is the quickest administration route into the blood stream. If the MI is thrombus based, aspirin will stop it growing larger and break it down, before GTN administration, so it is able to flow through the coronary arteries with no adverse effect. In turn the risk of a significant infarct in the cardiac muscle is reduced as the obstruction is removed allowing supplemental oxygen given to be most effective. Contraindications set out by JRCALC (2013) to be considered before administration.
Clopidgrel is a platelet aggregation inhibitor (Mosby, 2005), promoting thinning of the blood and prevention of further clot formation. In the case of myocardial infarction a 600milligram dose should be administered orally, in accordance with the patient group directive (PGD) indications and contraindications. Current PGD states that it is only indicated in patient younger than 75 years old with STEMI; this is because specific data about the clopidogrel response in elderly patients is lacking (Cuisset, T, 2011). However, if in consultation with CCU or PPCI and they are happy for it to be administered in the prehospital setting under their orders it can be given. Contraindications must be considered in all circumstance, JRCALC (2013).
GTN is a vasodilator drug which causes dilation of the coronary arteries and systemic veins resulting in lower pre-load and reduces blood pressure (JRCALC, 2013). This means that the supply of oxygen to the heart improves while the amount it actually needs reduces – due to the decrease in blood volume a heartbeat returns to the heart, requiring it to use less energy - overall making it easier for the cardiac muscle to pump blood around the body. The dose the JRCALC (2013) states is one to two 400microgram dose sprays which can be repeated every 5-10 minutes providing systolic blood pressure is above 90. GTN would be used for both suspected stable/unstable angina and an MI as in both conditions coronary arteries are constricted, reducing or preventing blood flow and oxygen supply to the cardiac muscle. Greaves, I, Porter, K (2006, p.328) note that side-effects from the administration of GTN can include a headache, flushing, dizziness, postural hypotension and tachycardia; which can all be explained by vessel dilation
Oxygen is essential for the cell metabolism; adequate tissue oxygenation is essential for normal physiological function, (JRCALC, 2013). During myocardial infarction the cardiac muscle experiences a lack of oxygen from a partially or fully occluded coronary artery which results in central chest pain and dyspnoea which can lead to decreased saturation levels. Supplemental oxygen, if below 94%, can help raise saturation levels within the blood and reduces the breathlessness while promoting reperfusion. It also helps prevent the cardiac muscle having to endure any, or prolonged, periods of anaerobic respiration that causes the chest pain associated with myocardial infarction. The vasodilation by GTN and blood thinning effect of aspirin and clopidogrel promote the effective circulation of oxygen in the blood to boost saturation levels.
Next Time
Following my review of the literature the importance of appropriate pharmacology is clear. Prehospital drug administration plays a critical role in initiating the appropriate care pathway for myocardial infarction; reducing the negative impact an infarct will have overall. On this job drugs were given appropriately and timely in accordance with guidelines for which I would not have changed the way in which it was done.
Highlighted in the text review is the time critical nature of a myocardial infarct. In this instance it took an hour from call time until arrival at the PPCI unit; which was good overall considering our location from the hospital. While in the house we could have used the family to our advantage and asked them to clear the way through the room to the door for egress with a carry chair, instead of doing this ourselves which could have slightly reduced our on scene time. However, overall the timeliness of helping the patient and securing him for conveyance was reasonable.

Ethical Implications
The Department of Health states that it is the right of the patient to determine what happens to their own bodies. During this call we kept the patient informed that we had a very high suspicion that he was suffering a heart attack and the treatment that he required. The patient had mental capacity and was not coerced into treatment he did not want; he gave verbal consent.

Conclusion
Following the literature review concerning the signs, symptoms and treatment of myocardial infarction it’s clear that the patient we treated had a huge amount of classic signs and symptoms of a myocardial infarction. I have refreshed my knowledge of silent and NSTEMI as well as learning that females may also present slightly differently to a male with the same condition. Following the appropriate care pathway is essential in this time critical situation for the patient to gain the most effective outcome.


For references and appendices please click 'Read more' below.





30/09/2013 Leave a comment

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