Coronary Artery Disease
Anatomy and Physiology: Blood vessels work to direct and transport blood flowing from the heart to the body and from the body to the heart. They carry blood full of nutrients and oxygen that allows tissue to function normally. Blood vessels also help to remove waste from tissue that result as a product of metabolism. There are three types of blood vessels, arteries, veins and capillaries. Both arteries and veins are comprised of three main layers, the tunica intima, the tunica media and the tunica externa.
The capillaries however, are only comprised of one layer of endothelial tissue, one cell thick (Marieb, 2007). The layers of blood vessels Tunica Externa: This is the outer most layer of blood vessels. It helps provide structure for the vessel as a whole, being made of large collagen fibres, and helps to keep blood vessels in place by anchoring them to surrounding organs and tissue. It is also where nerves and lymphatic vessels (in the venous system) connect to the vascular system (Marieb, 2007). Tunica Media:
The middle layer of blood vessels is constructed primarily from smooth muscle and sheets of elastin. This gives blood vessels their ability to stretch and contract. Vasoconstriction is when the smooth muscle of the tunica media contracts making the lumen of the vessel smaller. Vasodilatation is a relaxing of the smooth muscle allowing the lumen of the vessel to dilate (Marieb, 2007). Tunica Intima: This is the innermost layer of blood vessels. The intima is made up of the endothelium and, in larger blood vessels, the subendothelial layer.
The endothelium is constructed of a simple squamous epithelium. It is this thin, tightly packed layer of cells that provide a slick surface for the blood that travels within and minimises friction between blood cell and vessel wall (Marieb, 2007). Blood vessels Arteries: These blood vessels carry blood away from the heart and move from the largest diameter vessel, the aorta, to the smallest diameter vessels, arterioles, before becoming part of the capillary network. Arteries have a smaller lumen and larger smooth muscle layer, the tunica media, when compared with veins (see diagram 1).
This allows them to maintain a high-pressure environment, which is essential to facilitate the movement of oxygen, wastes and nutrients between tissue and the blood. It also allows blood to move rapidly (Martini, 2004). Veins: These blood vessels, as apposed to arteries, carry blood towards the heart and move from the smallest diameter vessels, venules that begin at the capillary bed, to the largest vein, the vena cava, which ends at the right atrium of the heart. Veins have a wide lumen meaning they can accommodate a larger volume of blood then arteries.
At any given time in an average adult, the veins hold up to 65% of the total blood volume (Marieb, 2007). Because veins hold a large volume of blood but are only under a fraction of the pressure of arteries they rely on gravity and the movement of muscles external to the veins themselves to propel blood. Small valves located at regular intervals on the tunica intima help prevent back flow of blood (Martini, 2004). Capillaries: Capillaries connect the arterial and venous systems. The capillary bed is a system of inter woven capillaries that start as arteriole and gradually fade in to venules (see diagram 1).
The interwoven capillaries lay with their one-celled walls next to tissues and organs and allow oxygen to pass through the cell wall into the tissue and for wastes to be transported into the blood for removal (Martini, 2004). Coronary circulation: Coronary circulation deals with the blood vessels involved with transporting blood to the tissue of the heart. The heart like all muscles requires blood flow to provide oxygen for the production of adenosine triphosphate (ATP) which fuels metabolic processes and provides cells with energy.
There are two main arteries that provide blood to the heart, the left coronary artery and the right coronary artery. The left coronary artery branches of into the, anterior interventricular artery also known as the left anterior descending artery providing blood to the anterior walls of both ventricles and the interventricular septum, and the circumflex artery, which provides blood to the left atrium and the posterior wall of the left ventricle (see diagram 2 a).
The right coronary artery branches into the marginal artery, providing blood flow to both anterior and posterior walls of the right ventricle and the posterior interventricular artery suppling both posterior ventricular walls (see diagram 2 a). Both the anterior and posterior interventricular arteries meet at the apex of the heart (see diagram 1. 3 a) There is also the, small, middle and great cardiac veins that carry blood away from the heart via the coronary sinus (see diagram 2 b) (Marieb, 2007; Porth, 2005). Aetiology/Causes: Mrs. X’s CAD is a result of atherosclerosis of her right coronary artery and her anterior descending artery.
Atherosclerosis is a thickening of artery walls caused by the presents of plaques or lesions and results in decreased blood flow. The majority of the people in the world have fatty lesions in their arteries from a young age (Marieb, 2007). The exact cause of why some of these fatty lesions grow to be atherosclerotic plaques and others do not is unknown but is believed to be a result of the inflammatory response resulting from damage of endothelial tissue of the tunica intima accompanied by an increase in cholesterol in the blood (Libby & Theroux, 2005; Cassar, Holmes, Rihal, & Gersh, 2009). Risk Factors:
Risk factors that have been related to CAD are, * Being a male over the age of 45, or being a female over the age of 55 * Having a family history of premature coronary heart disease * Being a current cigarette smoker * Increased Low-density lipoprotein (LDL) * Low high-density lipoprotein (HDL) * Hypertension of over 140/90mmHg or currently taking antihypertensive * Diabetes mellitus (Porth, 2005). Mrs. X is a female, 72 years old and is currently taking antihypertensive medication. Epidemiology: The World Health Organisation (2011) identifies cardiovascular disease as the leading cause of death globally, accounting for 17. million deaths in 2008. According to The Ministry of Health (2011) ischemic heart disease, secondary to coronary artery disease, was the second leading cause of death in New Zealand in 2008 with 5554 deaths in total, males making up 53% of the total. The majority of deaths associated with ischemic heart disease where of those over the age of 65. However, statistics show a disproportionate number of Maori deaths related to ischemic heart disease between the ages of 45-64 when compared with non-Maori in the same age group.
Non-Maori females have the lowest numbers of deaths compared with all other groups (Ministry of Health, 2011). Pathophisiology: The process of atherosclerosis begins with several factors that work to undermine the normal function of the endothelial cells in the tunica intima of arteries, namely to convey oxygenated blood to tissue with minimal friction and maximum efficacy. First of these factors is the presences of increased amounts of LDL in the blood (Stage 1 in diagram 3). These cells are used to transport lipids within the body.
The LDL’s small size means that when there is an abundance of them in the blood stream, or when they are accompanied by risk factors such as hypertension, hyperglycaemia or toxins associated with cigarette smoke, and respiratory infections, all of which undermine the integrity of the endothelium, they begin to penetrate the endothelial lining of the arteries and enter the subendothelium (see stage A on diagram 4), (DiSabatino, & Butcher, 2008; Marieb, 2007; Fuster, Libby, Beckman, Hiatt, Thompson, (…) Loscalzo, 2004).
After the LDL’s have compromised the endothelium the inflammatory response begins. Macrophages work to break down the LDL’s through oxidization and begin the process of phagocytosis (see stage 2-3 in diagram 3). The oxidized LDL’s initiate cytokines and growth factors to be sent out attracting Monocytes into cell tissue to assist phagocytosis (Libby, & Theroux, 2005).
They also cause an increase the production of vascular adhesion molecules, integrin and selectin, which assist in maintaining monocytes in the desired area of the endothelium (see stage 4-5 in diagram 3). Foam cells develop from the macrophages as they ingest the oxidized LDL’s. As the foam cells proliferate and increase in size, they begin to damage endothelial cells which cause platelet aggregation around the foam cells. This accompanied with the increase in the adhesion of the endothelium causes cells to clump together in a concentrated area.
The addition of platelets stimulates smooth muscle cells to migrate from the tunica media into the tunica intima to assist in the breakdown of lipids as the plaque grows it forms a protective fibrous cap, to contain the ever growing cells, this is called a stable atheroma or fibrous plaque (see stage 6-7 in diagram 3 & stage B in diagram 4) (Libby, & Theroux, 2005; Fuster, Libby, Beckman, Hiatt, Thompson, (…) Loscalzo, 2004). Over time the atheroma grows. As it grows the artery around it expands to accommodate the encroachment on the lumen.
But, the blood vessel can only accommodate a certain amount and eventually, as the atheroma continues to collect, platelets, smooth muscle cell, macrophages and lipids, it begins to affect the lumen of the vessel and the flow of blood (see B on diagram 4)( DiSabatino, & Butcher, 2008; Libby, & Theroux, 2005). As the fibrous plaque continues to grow, the fibrous cap beings to thin as a result of enzymes and the risk of rupture increases, this is called a complicated lesion (see stage C on diagram 4).
When a rupture occurs it results in a drastic increase in platelet action, which in turn results in the formation of a thrombus. The thrombus increases the size of the plaque and results in either partial or complete occlusion of the affected vessel. The affected vessel in turn affects the tissue being supplied by that vessel. In Mrs. X’s case the affected vessels are coronary arteries and the tissue affected is the myocardium. A decrease in the oxygen supplied to the myocardium is called ischemia.
If the occlusion continues or completely inhibits all blood flow the myocardial tissue will be injured. If the injured tissue is not reoxygenated then the cells die, this is called a myocardial infarction (DiSabatino, & Butcher, 2008; Libby, & Theroux, 2005; Cassar, Holmes, Rihal, & Gersh, 2009). Signs and symptoms: CAD is predominantly asymptomatic in the early stages. It is not until the occlusion of the coronary arteries inhibits the oxygen supply to the myocardial tissue that symptoms begin. The most common symptom of CAD is angina pectoris or chest pain.
This can be a chronic stable pain that is predictable in both severity and duration and is usually associated with increases in oxygen demand, for example, during exercise, and is quickly resolved with treatment. Unstable angina is associated with more acute CAD. It also involves chest pain but the pain experienced is more frequent less predictable in terms of severity and duration, is often not associated with exercise, for example; during the night when sufferer is in bed and, is not easily resolved with treatment.
Mrs. X has experienced chronic stable angina for the last 18 months and is undergoing intervention before it escalates into an acute unstable condition (DiSabatino, & Butcher, 2008; Libby, & Theroux, 2005; Cassar, Holmes, Rihal, & Gersh, 2009). Laboratory and Diagnostic tests: * Exercise stress testing/ Electrocardiogram: This test was performed on Mrs X as part of the diagnosis of her CAD. It assesses changes in her electrocardiogram (ECG) as a result of increased oxygen demand.
Mrs X tested positive for CAD and her ECG would have looked similar to diagram 6. Note the abnormal depression of the ST segment characteristic of ischemia (see diagram 6). As compared with the normal ECG in diagram 5 (Jones, 2005; DiSabatino, & Butcher, 2008; Cassar, Holmes, Rihal, & Gersh, 2009). * Cardiac Catheterisation/ Arteriogram: This test is done to ascertain the level of atherosclerotic build up within the coronary arteries. Normal results show appropriate blood flow within cardiac arteries, the absences of deformities or lesions.
Mrs X’s results were abnormal. They revealed minimal plaque build-up on all of the coronary arteries with 80% occlusion of the right coronary artery and 60% occlusion of the anterior descending artery (DiSabatino, & Butcher, 2008; Cassar, Holmes, Rihal, & Gersh, 2009). Surgical Treatment: Mrs X underwent a coronary artery bypass graft (CABG) in an effort to improve the blood flow to the myocardium by attaching new blood vessels to bypass the occluded ones. The first step is the harvesting of replacement blood vessels.
Mrs X had her saphenous vein harvested from her right leg (see A on diagram 7). The next step in CABG surgery is a sternotomy. This opens the chest cavity by cutting through the sternum to allow the surgeon to access the heart. The redirection of Mrs X left internal mammary artery would be done after the opening of the chest cavity (see B on diagram 7) (Miller, 2010; DiSabatino, & Butcher, 2008; Suri, Kathuria, & Molinari, 2010; Cassar, Holmes, Rihal, & Gersh, 2009). Once all the replacement blood vessels are ready the bypass begins.
In an on pump CABG it would be at this time that cardiopulmonary bypass pump would be connected to the vena cava and the aorta to allow circulation while the heart is stopped. Mrs X, however, underwent an off pump CABG meaning that her heart continued to beat throughout the procedure but the tissue being operated on was held in place with an Octopus, a suction device used to stabilise the heart during surgery. At this stage the saphenous vein graft is attached to the aorta and then attached at a space free from occlusion on the right coronary artery (see C on diagram 7).
Attachment of the LIMA to the anterior descending artery follows a similar process but instead of having to connect the graft to the aorta it remains connected to the internal mammary artery and is just relocated in the chest cavity to reach the heart (see D on diagram 7). Once all the grafts are firmly stitched in place the surgeons begin to close up the chest cavity. They put chest drains in place around the pericardium and the plural cavity to ensure any excess fluid is drained out. A pacing wire is also put in place.
A pericardial ventricular pacing wire was put in place for Mrs X; this allowed for controlled pacing of her heart if cardiac output is compromised. As a result of the surgery Mrs X had a 23cm wound on her right left, from the saphenous vein graft and a 12cm wound on her sternum from the sternotomy. Post-operative care of patients having undergone CABG is centred around maintenance of cardiac output and minimisation of stress on the new grafts (Miller, 2010; DiSabatino, & Butcher, 2008; Suri, Kathuria, & Molinari, 2010; Cassar, Holmes, Rihal, & Gersh, 2009).
Pharmacological treatment: * Deltaparin sodium: was prescribed to Mrs X to prevent the formation of thrombi post operatively. Deltaparin sodium works to inhibit the clotting cascade and prolong clotting time. Its effectiveness is evaluated by an activated partial throboplastin time (APTT) maintained within the ranges of 25-30 seconds. Mrs X is reacting well to the Deltaparin and her APTT is being maintained at 27 seconds within the therapeutic range. Mrs X is currently receiving 2500units in 0. 2ml subcutaneously twice a day. Major dverse reactions to Deltaparin include increased risk of haematoma, increased risk of haemorrhage, thrombocytopenia and elevated liver functions tests (Medsafe, 2011). * Simvastatin: Mrs X has been taking simvastatin for several years to assist in the management of her cholesterol. Simvastatin is used to reduce hypercholesterolemia. It does this by inhibiting HMG-CoA reductase the enzyme responsible for the production of cholesterol within the body. It is used in conjunction with lifestyle changes to reduce the advancement of CAD. Mrs X is currently taking 40mg orally once daily, usually at night.
The predominant adverse reaction experienced from simvastatin is gastrointestinal upset (Medsafe, 2011). * Metoprolol: Mrs X has been taking Metoprolol- for several months as a prophylaxis against angina. Metoprolol works as a ?? blocker meaning that it inhibits the effect of catecholamines which are released by the body during mental and physical stress and cause an increase in cardiac function. Metoprolol works to decrease the oxygen demand of cardiac muscle and therefore reduce the incidents of angina. Mrs X is currently taking 47. 5mg orally once a day.