This essay is a cardiac case study for a patient ‘John Jones’ written for the bridging module of the Paramedic Science course. A case study aims to examine complex phenomena to increase understanding of them (Yin, 2003). With this in mind, this essay will explore the location, structure and function of the heart, describe the blood flow through the heart, and examine the complications when a disruption occurs in that blood flow. It will then analyze the risk factors associated with this patient and describe a management and treatment plan from an Emergency Medical Technician (EMT) prospective.
The cardiovascular system is very complex and unique. It’s main functions are to transport oxygen and nutrients to the body’s tissues, whilst removing waste products such as carbon dioxide, urea and creatine. It is responsible for hormonal control, regulation of temperature and acts as a host defense, this is all maintained by homeostasis (Pilbery & Lethbridge, 2016). It consists of the heart, blood, arteries, veins and capillaries (Walker & Parker, 2019).
The heart is a muscular, hollow, cone-shaped organ, which sits within the mediastinum, a region within the thoracic cavity that extends from the sternum to the vertebral column. It sits medial to the lungs and posterior to the sternum. The human heart weighs between 225 and 310 grams and lies in an oblique position, with two-thirds to the left of the body’s midline (Waugh & Grant, 2018). The hearts apex is located on the midclavicular line at the level of the fifth intercostal space (Caroline, 2008).
The heart has 3 layers, all of which have different functions. The epicardium is the outer most layer of the heart wall. Its thin serous membrane secretes serous fluid to lubricate the heart, preventing friction during contractions (Siegfried, 2002). The myocardium is the middle layer of the heart, which is made of cardiac muscle tissue. It’s responsible for pumping blood around the body under involuntary control (Pilbery & Lethbridge, 2016). The endocardium is the smooth, innermost layer of the heart, made of endothelial cells, which line the chambers and valves of the heart. The smooth surface helps to prevent blood from sticking and allowing normal blood flow through the heart (Siegfried, 2002).
The heart is divided into four chambers. The right side of the heart is divided from the left side by the septum (Walker & Parker, 2019). The heart has two superior chambers, atria, which are responsible for receiving blood from the veins and two inferior chambers, ventricles, which are responsible for pumping blood into the aorta and pulmonary artery (Walker & Parker, 2019).
The atria and ventricles are divided by atrioventricular (AV) valves. The right AV valve has three cusps (tricuspid valve) and the left AV valve (mitral valve) has two cusps (Waugh & Grant, 2018). Semilunar valves are located between the right ventricle and pulmonary artery (pulmonary valve) and the left ventricle and the aorta (aortic valve). These valves prevent backflow of blood during cardiac contraction (Waugh & Grant, 2018).
Each cardiac contraction is achieved by a sequence of electrical activity, causing the muscles within the four chambers to contract. The sinoatrial node is the pacemaker of the heart, and is located at the top of the right atrium. Here impulses are initiated causing the atrial muscle to contract. The impulse travels to the atrioventricular node, through the bundle of his, down both left and right bundle branch, through the purkinje fibers, causing the ventricles to contract (Walker & Parker, 2019).
As your heart contracts, deoxygenated blood from the systemic circulation enters the right atrium through the superior and inferior vena cava. As the right atrium contracts, blood passes through the right AV valve, into the right ventricle (Caroline, 2008). The cusps of the valves have fibrous cords called chordae tendinea, which connect to the papillary muscle, which are located within the ventricles of the heart, this prevents the valves from inverting during contraction (Siegfried, 2002). As the right ventricle contracts, it closes the right AV valve and blood is forced through the pulmonary semilunar valve, into the pulmonary circulation, through the pulmonary trunk. The semilunar valve prevents back flow in to the right ventricle. The pulmonary trunk splits into the left and right pulmonary artery, where deoxygenated blood is pushed into the lungs. Interexchange of gases takes place, where the carbon dioxide is removed and oxygen is reabsorbed (Caroline, 2008). The pulmonary arteries are the only arteries within the body to carry deoxygenated blood (Pilbery & Lethbridge, 2016). Oxygenated blood is returned into the systemic circulation through the four pulmonary veins into the left atrium. Blood passes through the left AV valve and enters the left ventricle (Siegfried, 2002). The left ventricle has a much thicker myocardium wall as it comes under extreme pressure whilst pumping blood around the body. Blood exits the left ventricle via the aortic semilunar valve into the aorta (Walker & Parker, 2019). Oxygen rich blood is pumped around the body, delivering oxygen and nutrients to the body’s cells, through the arteries, arterioles and capillaries (VanPutte et al., 2016). Once the body’s tissues have received it’s oxygen and nutrients, the capillaries pick up waste products and carbon dioxide, which travel back via the venules and veins to the heart through the superior and inferior vena cava. Skeletal muscle contraction and one way valves within the veins helps to achieve venous return (Siegfried, 2002).
The heart itself requires its own blood supply in order to function and survive, this is achieved by the right and left coronary arteries (Walker & Parker, 2019). The right and left coronary arteries branch off at the base of the ascending aorta and provide blood to both sides of the heart. Most of the venous blood is collected into several small veins that join to form the coronary sinus, a large vein at the back of the heart, which empties into the right atrium (Waugh & Grant, 2018).
As described above the blood supply and functions of the heart are very complex, but vital for life. One of the major issues that disrupts the main function of the heart is when the blood flow to the hearts arteries is reduced, preventing efficient oxygen and nutrient supply. This is known as a Myocardial Infarction or Heart attack (VanPutte et al., 2016). Lack of oxygen causes part of the tissue to die. The infarction can also disrupt the conduction system of the heart. Most commonly, the cause of artery narrowing is atherosclerosis (Siegfried, 2002). Atherosclerosis is the build up of fatty deposits within the walls of the arteries, which cause them to become thick, hard and lose elasticity (Walker & Parker, 2019).
There are a number of things that can increase your likelihood of having an MI. These are known as modifiable and non-modifiable risk factors. Modifiable risk factors can be changed, whereas non-modifiable risk factors can’t, but they can be controlled and their effect reduced by lifestyle changes (Heart.org). In the case of patient John Jones, there are a number of modifiable risk factors mentioned in his past medical history and social history, which suggest he has an increased risk of suffering an MI. Such as: -
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Obesity
Obesity is characterized as excessive accumulation of body fat, with a body mass index greater than 30 being deemed obese (Walker & Parker, 2019). Obesity increases cardiac workload because the heart has to work harder to pump blood to all the additional tissues. This causes enlargement of the heart. Increased pressure in the vessels results in high blood pressure (hypertension). Hypertension causes arteries to lose their elasticity, causing narrowing, which decreases blood flow to the heart (Waugh & Grant, 2018).
Ischaemic Heart Disease (IHD)
IHD is the narrowing of the coronary arteries, caused by a build up of atherosclerosis, which develop slowly over time. Eventually, the arteries become so narrow, less blood and oxygen reaches the heart muscle (British Heart Foundation, 2020). There are several risk factors that can increase the risk of developing IHD, obesity, diabetes, smoking, all of which the patient has in his history. If the plaque breaks off, the artery can become occluded, causing an MI (Pilbery & Lethbridge, 2016).
Smoking
Smoking has a considerable effect on your cardiovascular system. Chemicals found in cigarettes damage the blood vessels and cause a build up of atherosclerosis, increases your risk of MI (British Heart Foundation, 2020).
Alcohol
Mr Jones is a heavy drinker who consumes 10 units per day. This amount over a long period of time increases the risk of heart disease, by weakening the heart, affecting its ability to pump blood around the body (alcohol.org).
Diabetes
Diabetes is caused by deficiency or absence in insulin, a peptide hormone produced by the beta cells within the pancreas. Mr Jones is type ii diabetic, a very common condition on obese patients (Pilbery & Lethbridge, 2016). The body’s inability to respond to insulin leads to chronic high glucose levels, this causes damage and narrowing to the blood vessels, reducing blood flow to the heart (Walker & Parker, 2019).
Evidence shows that the best possible outcome for a patient suffering ST-Elevation myocardial infarction (STEMI) would be direct admission to the Primary Percutaneous Coronary Intervention (PPCI) department through the STEMI pathway (Brown et al., 2019). As an EMT, I do not have direct access to this pathway. Delays in getting the patient to the most appropriate care could be detrimental to the patient’s outcome. Restoring coronary blood flow as soon as possible is essential (Brown et al., 2019). Evidence states STEMI patients would benefit from the following treatment.
In my current scope of practice as an EMT, I would be wearing appropriate personal protective equipment. I would make sure that the patient receives constant reassurance because he is showing sign of anxiousness. I would use distraction techniques and make sure that I explain exactly what I am doing and why. Once I have established the patient’s condition and findings, I would administer a single does of 300 milligram aspirin as soon as possible for the patient to chew, unless there are any known allergies (National Institute for Health and Care Excellence (NICE), 2020). I would also make sure the patient has not taken aspirin prior to our arrival (Pilbery & Lethbridge, 2016).
The patient complains of pain score of 8/10. It is important to do what I can within my scope of practice, to help relieve the pain. Paracetamol is not recommended for patients suffering chest pains (Brown et al., 2019). I would be able to offer the patient entonox, as per JRCALC guidelines (book of guidelines used by ambulance personnel). Entonox is used to treat moderate to severe pains (Brown et al., 2019). I would continue to closely monitor patient’s condition carrying out further observations, checking patient’s temperature and blood glucose levels (Pilbery & Lethbridge, 2016). I would update Clinical Contact Centre of patient’s condition, asking them to let me know if Paramedic back up becomes available.
The patient would be assisted to the Ambulance with limited movement, using a carry chair, the patient would also be assisted onto the stretcher. This will help reduce further strain on the heart. I would continue to reassure the patient, monitor patient’s vital signs, monitoring any changes to patient’s electrocardiogram (ECG), and continuously assess patient’s condition, also re assessing patient’s pain score. Defibrillator pads would be placed on the patient’s chest as two thirds of patients suffer a cardiac arrest before they reach hospital (Brown et al., 2019). I would closely monitor the patient’s oxygen levels, aiming for 94% or above. I would only administer oxygen if patient becomes hypoxaemic (Brown et al., 2019).
It is essential to undertake a time critical transfer to the nearest, most appropriate hospital, within my scope of practice. I would contact the emergency department (ED) with a pre alert using the ASHICE acronym. The patient would be driven as smoothly as possible under emergency conditions. I would continuously reassure and reassess patient’s condition on route and record patient’s details and vital signs on the patients clinical record (PCR). On arrival to the ED, I would give a full detailed handover to the receiving staff.
IHD is a serious condition caused by the build up fatty deposits within the coronary arteries, reducing blood supply to the heart. Mr Jones has many modifiable and non-modifiable risks, which have resulted in the patient suffering an MI. An adjustment to his lifestyle would help prevent a possible reoccurrence in the future.
References
- Brown, S. N., Kumar, D. S., James, C., & Mark, J. (Eds.). (2019). JRCALC clinical guidelines 2019. Class Professional.
- Caroline, N. L. (2008). Nancy Caroline’s emergency care in the streets (6th ed.). Jones and Barlett.
- Pilbery, R., & Lethbridge, K. (2016). Ambulance care practice. Class Professional.
- Siegfried, D. R. (2002). Anatomy and physiology for dummies. Wiley. VanPutte, C., Regan, J., & Russo, A. (2016). Seeley’s essentials of anatomy and physiology (9th ed.). McGraw-Hill Education.
- Walker, R., & Parker, S. (2019). The human body book: An illustrated guide to it’s structure, function, and disorders. Dorling Kindersley.
- Waugh A., & Grant, A. (2018). Ross and Wilson anatomy and physiology in Health and illness (13th ed.). Elsevier.
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