Filtered Unit 8: Responses to Altered Cardiovascular Function PDF

UNIT 8 Responses to altered cardiovascular function Chapter 28 A person-centred approach to assessing the cardiovascular and lymphatic systems...

UNIT 8 Responses to altered cardiovascular function Chapter 28 A person-centred approach to assessing the cardiovascular and lymphatic systems Chapter 29 nursing care of people with coronary heart disease Chapter 30 nursing care of people with cardiac disorders Chapter 31 Nursing care of people with vascular and lymphatic disorders Chapter 32 Nursing care of people with haematoloGICaL disorders Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  Chapter 28 A person-centred approach to assessing the cardiovascular and lymphatic systems Penny Paliadelis Learning outcomes KEY TERMS Describe the anatomy and physiology of the cardiovascular and lymphatic systems. Examine investigations and observations important for assessing a person’s cardiovascular and afterload 942 lymphatic system function. apical impulse 967 Accurately interpret normal and aberrant data gained from assessment of a person’s arrhythmia 970 cardiovascular and lymphatic system. blood flow 946 Discuss manifestations of impaired cardiovascular and lymphatic systems. blood pressure 946 cardiac index (CI) 942 cardiac output (CO) 940 Clinical competencies cardiac reserve 940 Assess an ECG strip and identify normal cardiac function and abnormal rhythm. contractility 941 Conduct and document a health history for people having or at risk of alterations in the structure ejection fraction 940 and function of the cardiovascular, haematological or lymphatic systems. erythropoiesis 947 Conduct and document a physical assessment of cardiovascular, haematological and lymphatic haemolysis 947 status. ischaemic 940 Monitor the results of diagnostic tests and report abnormal findings. Korotkoff’s sounds 971 leucocytosis 950 Equipment needed leucopenia 950 Stethoscope with diaphragm and bell lymphadenopathy 977 Blood pressure cuff lymphoedema 973 mean arterial pressure Tape measure (MAP) 946 Metric ruler murmur 954 Doppler ultrasound device (if needed) and transducer gel orthostatic hypotension 972 peripheral vascular resistance (PVR) 946 preload 942 pulse 943 pulse pressure 973 stem cell 947 stroke volume (SV) 940 thrill 969 Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 937 The cardiovascular system is comprised of the heart (the lungs. Two-thirds of the heart mass lies to the left of the ster- system’s pump), the peripheral vascular system (a network num; the upper base lies beneath the second rib, and the pointed of arteries, veins and capillaries) and the haematological apex is approximate with the fifth intercostal space, midpoint to system (blood and blood components). The lymphatic sys- the clavicle (see Figure 28.1). tem (the lymph, lymph nodes and spleen) is a special vas- The heart is covered by the pericardium, a double layer of cular system that helps maintain sufficient blood volume in fibroserous membrane (see Figure 28.2). The pericardium en- the cardiovascular system by picking up excess tissue fluid cases the heart and anchors it to surrounding structures, form- and returning it to the bloodstream. The heart, a muscular ing the pericardial sac. The snug fit of the pericardium prevents pump, beats an average of 70 times per minute, or once every the heart from overfilling with blood. The outermost layer is 0.86 seconds, every minute of a person’s life. This contin- the parietal pericardium, and the visceral pericardium (or epi- uous pumping moves blood through the body, nourishing cardium) adheres to the heart surface. The small space between tissue cells and removing wastes. Deficits in the structure the visceral and parietal layers of the pericardium is called the or function of the heart affect all body tissues. Changes in pericardial cavity. A serous lubricating fluid produced in this cardiac rate, rhythm or output may limit almost all human space cushions the heart as it beats. functions, including self-care, mobility, and the ability to The heart wall consists of three layers of tissue: the maintain tissue perfusion, fluid volume status, respirations epicardium, the myocardium and the endocardium (see ­ and comfort. Cardiac changes may also affect self-concept, Figure 28.2). The epicardium covers the entire heart and great sexuality and role performance. vessels and then folds over to form the parietal layer that lines the pericardium and adheres to the heart surface. The myocar- dium, which is the middle layer of the heart wall, consists of Structure and function of specialised cardiac muscle cells (myofibrils) that provide the the cardiovascular system bulk of contractile heart muscle. The endocardium, which is The heart is a hollow, cone-shaped organ approximately the the innermost layer, is a thin membrane composed of three lay- size of an adult’s fist, weighing less than 500 grams. It is lo- ers; the innermost layer is made up of smooth endothelial cells cated in the mediastinum of the thoracic cavity, between the that line the inside of the heart’s chambers, the great vessels vertebral column and the sternum and is flanked laterally by the and the valves. Midsternal line Superior vena cava Second rib Left lung Aorta Diaphragm Parietal pleura (cut) Apical impulse Pulmonary A trunk Pericardium (cut) Right lung Apex of heart Heart Diaphragm B Anterior C Figure 28.1 Location of the heart in the mediastinum of the thorax. A, Relationship of the heart to the sternum, ribs and diaphragm. B, Cross-sectional view showing relative position of the heart in the thorax. C, Relationship of the heart and great vessels to the lungs Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 938 UNIT 8 Responses to altered cardiovascular function Fibrous pericardium Parietal layer of serous pericardium Pericardial cavity Visceral layer of serous pericardium (epicardium) Heart Myocardium wall Endocardium Figure 28.2 Coverings and layers of the heart Chambers and valves of the heart d­ evoid of all oxygen—i.e. ‘deoxygenated’—even at the tissues.) The heart has four hollow chambers, two upper atria and two The superior vena cava returns blood from the body area above lower ventricles. They are separated longitudinally by the inter- the diaphragm, the inferior vena cava returns blood from the ventricular septum (see Figure 28.3). body below the diaphragm, and the coronary sinus drains blood The right atrium receives oxygen-poor blood from the veins from the heart. The left atrium receives freshly oxygenated blood of the body. (Note that the terms ‘deoxygenated’ and ‘oxygen- from the lungs through the pulmonary veins. poor’ are often used interchangeably; however, ‘oxygen-poor’ is The right ventricle receives oxygen-poor blood from the more technically correct. Haemoglobin will never become fully right atrium and pumps it through the pulmonary artery to Superior vena cava Aorta Right pulmonary artery Left pulmonary artery Pulmonary trunk Left atrium Right atrium Left pulmonary veins Right pulmonary veins Pulmonary valve Aortic valve Bicuspid (mitral) valve Fossa ovalis Left ventricle Tricuspid valve Papillary muscle Chordae tendineae Interventricular septum Right ventricle Endocardium Myocardium Inferior vena cava Pericardium Figure 28.3  The internal anatomy of the heart, frontal section Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 939 (diastole) produces the second heart sound, or S2 (characterised Main Right Right pulmonary Lungs Pulmonary by the syllable ‘dub’). atrium ventricle veins artery Systemic, pulmonary and coronary Left atrium circulation Superior Because each side of the heart both receives and ejects blood, the vena cava heart is often described as a double pump. Blood enters the right Body Aorta Left atrium and moves to the pulmonary bed at almost the exact same ventricle Inferior time that blood is entering the left atrium. The circulatory system vena cava has two parts: the pulmonary circulation (moving blood through the capillary bed surrounding the lungs to link with the gas ex- Figure 28.4 Blood flow around the systemic circuit change system of the lungs) and the systemic circulation, which supplies blood to all other body tissues. In addition, the heart muscle itself is supplied with blood via the coronary circulation. the pulmonary capillary bed for oxygenation. The newly Systemic circulation oxygenated blood then travels through the pulmonary veins The systemic circulation consists of the left side of the heart, to the left atrium. Blood enters the left atrium and crosses the aorta and its branches, the capillaries that supply the brain the mitral (bicuspid) valve into the left ventricle. Blood is and peripheral tissues, the systemic venous system and the vena then pumped out of the aorta to the arterial circulation (see cavae. The systemic system, which must move blood to periph- Figure 28.4). eral areas of the body, is a high-pressure system. The chambers of the heart are separated by valves that al- low unidirectional blood flow to the next chamber or great Pulmonary circulation vessel. The atria are separated from the ventricles by the two The pulmonary circulation consists of the right side of the heart, atrioventricular (AV) valves; the tricuspid valve is on the right the pulmonary artery, the pulmonary capillaries and the pulmo- side and the bicuspid (or mitral) valve is on the left. The flaps nary veins. Because it is located in the thorax near the heart, of each of these valves are anchored to the papillary muscles the pulmonary circulation is a low-pressure system. Pulmonary of the ventricles by the chordae tendineae. These structures circulation begins with the right side of the heart. Oxygen-poor control the movement of the AV valves to prevent backflow of blood from the venous system enters the right atrium through two blood. The ventricles are connected to their great vessels by large veins, the superior and inferior venae cavae, and is trans- the semilunar valves. On the right, the pulmonary (pulmonic) ported to the lungs via the pulmonary artery and its branches (see valve joins the right ventricle with the pulmonary artery. On Figure 28.6). After oxygen and carbon dioxide are exchanged in the left, the aortic valve joins the left ventricle to the aorta (see the pulmonary capillaries, oxygen-rich blood returns to the left Figure 28.5). atrium through several pulmonary veins. Blood is then pumped Closure of the AV valves at the onset of contraction (systole) out of the left ventricle through the aorta and its major branches produces the first heart sound, or S1 (characterised by the syllable to supply all body tissues. This second circuit of blood flow is ‘lub’); closure of the semilunar valves at the onset of relaxation called the systemic circulation. Heart Left side Right side Chambers Valves Major vessels Chambers Valves Major vessels Left atria Left ventricle To heart From heart Right atria Right ventricle To heart From heart Pulmonary Pulmonary Aorta Vena cava vein artery Atrioventricular Semilunar Atrioventricular Semilunar Mitral Aortic Tricuspid Pulmonary Figure 28.5 Summary of key components of the heart Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 940 UNIT 8 Responses to altered cardiovascular function contraction ­delivers blood through the pulmonary circulation Capillary beds and the systemic circulation, it is during ventricular relaxation of lungs where gas exchange that the coronary arteries fill with oxygen-rich blood. After the occurs blood perfuses the heart muscle, the cardiac veins drain the blood into the coronary sinus, which empties into the right atri- um of the heart (see Figure 28.7B). Blood flow through the coronary arteries is regulated by sev- eral factors. Aortic pressure is the primary factor. Other factors Pulmonary circuit include the heart rate (most flow occurs during diastole, when the muscle is relaxed), metabolic activity of the heart and blood Pulmonary Pulmonary vessel tone (constriction). arteries veins The cardiac cycle and cardiac output Aorta and The contraction and relaxation of the heart constitutes one Venae branches heartbeat and is called the cardiac cycle (see Figure 28.8). cavae ­Ventricular filling is followed by ventricular systole, a phase during which the ventricles contract and eject blood into the Left pulmonary and systemic circuits. Systole is followed by a atrium ­relaxation phase known as diastole, during which the ventri- cles refill, the atria contract and the myocardium is perfused. Left ­Normally, the complete cardiac cycle occurs about 70 to 80 Right atrium ventricle times per minute, measured as the heart rate (HR). During diastole the volume in the ventricles is increased Right to about 120 mL (the end-diastolic volume), and at the end of ventricle systole about 40 mL of blood remains in the ventricles (the end-systolic volume). The difference between the end-diastol- Systemic circuit ic volume and the end-systolic volume is called the stroke ­volume (SV) (see Figure 28.9). Stroke volume ranges from 60 to 100 mL/beat and averages about 80 mL/beat in an adult. The cardiac output (CO) is the amount of blood pumped by the ventricles into the pulmonary and systemic circulations in 1 minute. Multiplying the stroke volume (SV) by the heart rate Capillary beds (HR) determines the cardiac output: CO = SV × HR. The ejec- of all body tissues where tion fraction is the stroke volume divided by the end-diastolic gas exchange volume and represents the fraction or percentage of the diastolic occurs volume that is ejected from the heart during systole (Mohrman & Heller, 2010). For example, an end-diastolic volume of 120 mL divided by a stroke volume of 80 mL equals an ejection fraction of 66% (see Figure 28.9). The normal ejection fraction ranges Oxygen-poor, Oxygen-rich, CO2-rich blood CO2-poor blood from 50% to 70%. The average person’s cardiac output ranges from 4 to 8 L/min. Figure 28.6  Pulmonary and systemic circulation Cardiac output is an indicator of how well the heart is functioning as a pump. If the heart cannot pump effectively, cardiac out- put and tissue perfusion are decreased. Body tissues that do Coronary circulation not receive enough blood and oxygen (carried in the blood The heart muscle itself is supplied by its own network of ves- on haemoglobin) become ischaemic (deprived of oxygen). If sels through the coronary circulation. The left and right coro- the tissues do not receive enough blood flow to maintain the nary arteries originate at the base of the aorta and branch out ­functions of the cells, the cells die. (Cellular death results in to encircle the myocardium (see Figure 28.7A), supplying necrosis or infarction.) blood, oxygen and nutrients to the myocardium. The left main Activity level, metabolic rate, physiological and psycholog- coronary artery divides to form the anterior descending and ical stress responses, age and body size all influence cardiac circumflex arteries. The anterior descending artery supplies the output. In addition, cardiac output is determined by the inter- anterior interventricular septum and the left ventricle. The cir- action of four main factors: heart rate, preload, afterload and cumflex branch supplies the left lateral wall of the left ventricle. contractility. Changes in each of these variables influence car- The right coronary artery supplies the right ventricle and forms diac output intrinsically and each can also be manipulated to af- the posterior descending artery. The posterior descending artery fect cardiac output. The heart’s ability to respond to the body’s supplies the posterior portion of the heart. While ventricular changing need for cardiac output is called cardiac reserve. Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 941 Aorta Superior Right vena cava coronary Left artery coronary artery Anterior cardiac Great veins cardiac vein Circumflex artery Coronary Small Right cardiac sinus atrium vein Anterior descending artery Middle Marginal cardiac artery Posterior vein interventricular A artery B Figure 28.7  Coronary circulation. A, Coronary arteries; B, coronary veins Left atrium Right atrium Left ventricle Right ventricle Passive Atrial AV valves Semilunar valves Isovolumetric filling contraction close open; ventricles relaxation eject blood 1 2 3 Mid-to-late diastole Ventricular systole Early diastole (ventricular filling) (atria in diastole) Figure 28.8  The cardiac cycle has three events: (1) ventricular filling in mid-to-late diastole, (2) ventricular systole, and (3) isovolumetric relaxation in early diastole Heart rate v­entricular filling during diastole. Cardiac output then falls Heart rate is affected by both direct and indirect autonomic ­because decreased filling time decreases stroke volume. Cor- nervous system stimulation. Direct stimulation is accomplished onary artery perfusion also decreases because the coronary through the innervation of the heart muscle by sympathetic and ­arteries fill primarily during diastole. Cardiac output decreases parasympathetic nerves. The sympathetic nervous system in- during bradycardia if stroke volume stays the same because the creases the heart rate, whereas the parasympathetic vagal tone number of cardiac cycles is decreased. slows the heart rate. Reflex regulation of the heart rate in re- sponse to systemic blood pressure also occurs through activa- Contractility tion of sensory receptors known as baroreceptors or pressure Contractility is the inherent capability of the cardiac mus- receptors located in the carotid sinus, aortic arch, venae cavae cle fibres to shorten. Poor contractility of the heart muscle and pulmonary veins. reduces the forward flow of blood from the heart, increases If heart rate increases, cardiac output increases (up to a the ventricular pressures from accumulation of blood vol- point) even if there is no change in stroke volume. However, ume and reduces cardiac output. Increased contractility may rapid heart rates decrease the amount of time available for stress the heart. Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 942 UNIT 8 Responses to altered cardiovascular function 120 mL 40 mL 120 mL 40 mL End-diastole End-systole Figure 28.9 Stroke volume is end-diastole volume minus end-systole volume; ejection fraction is stroke volume divided by end-diastole volume, expressed as a percentage Preload (e.g. through vasoconstriction), PVR and/or SVR increases Preload is the amount of cardiac muscle fibre tension or stretch and the work of the ventricles increases. As workload increas- that exists at the end of diastole, just before contraction of the es, consumption of myocardial oxygen also increases. A com- ventricles. Preload is influenced by venous return and the com- promised heart cannot effectively meet this increased oxygen pliance of the ventricles. It is related to the total volume of demand and a vicious cycle ensues. By contrast, a very low blood in the ventricles: the greater the volume, the greater the afterload decreases the forward flow of blood into the systemic stretch of the cardiac muscle fibres and the greater the force circulation and the coronary arteries. with which the fibres contract to accomplish emptying. This principle is called Starling’s law of the heart. Clinical indicators of cardiac output This mechanism has a physiological limit. Just as contin- For many people who are critically ill, invasive haemodynam- uous overstretching of a rubber band causes the band to relax ic monitoring catheters are used to measure cardiac ­output in and lose its ability to recoil, overstretching of the ­cardiac quantifiable numbers. However, advanced technology is not the muscle fibres eventually results in ineffective contraction. only way to identify and assess compromised blood flow. Be- Disorders such as kidney disease and congestive heart failure cause cardiac output perfuses the body’s tissues, clinical indi- result in sodium and water retention and i­ncreased preload. cators of low cardiac output may be manifested by changes in Vasoconstriction also increases venous return and preload. organ function that result from compromised blood flow. For Too little circulating blood volume results in a decreased example, a decrease in blood flow to the brain presents as a ­venous return and therefore a decreased preload. A decreased pre- change in level of consciousness. Other manifestations of de- load reduces stroke volume and thus cardiac output. Decreased creased cardiac output are discussed in ­Chapters 9 and 29. preload may result from haemorrhage or maldistribution of blood Cardiac index (CI) is the cardiac output adjusted for volume, as occurs in ‘third spacing’ (see Chapter 9). the person’s body size, also called the person’s body sur- face area (BSA). Because it takes into account the person’s Afterload BSA, the cardiac index provides more meaningful data Afterload is the force the ventricles must overcome to eject about the heart’s ability to perfuse the tissues and there- their blood volume. It is the pressure in the arterial system fore is a more accurate indicator of the effectiveness of the ahead of the ventricles. The right ventricle must generate circulation. enough tension to open the pulmonary valve and eject its vol- BSA is stated in square metres (m2), and cardiac index ume into the low-pressure pulmonary arteries. Right ventricle is calculated as CO divided by BSA. Cardiac measurements afterload is measured as peripheral vascular resistance (PVR). are considered adequate when they fall within the range of The left ventricle, in contrast, ejects its load by overcoming the 2.5 to 4.2 L/min/m2. For example, two people are deter- pressure behind the aortic valve. Afterload of the left ­ventricle mined to have a cardiac output of 4 L/min. This parameter is is measured as systemic vascular resistance (SVR). Arterial within normal limits. However, one person is 157 cm tall and pressures are much higher than pulmonary pressures; thus, the weighs 54.5 kg, with a BSA of 1.54 m2. This person’s car- left ventricle has to work much harder than the right ventricle. diac index is 4 4 1.54, or 2.6 L/min/m2. The second person Alterations in vascular tone affect afterload and ventricular is 188 cm tall and weighs 81.7 kg, with a BSA of 2.52 m2. work. As the pulmonary or arterial blood pressure increases This person’s cardiac index is 4 4 2.52, or 1.6 L/min/m2. Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 943 Sinoatrial node (pacemaker) Internodal pathways Atrioventricular node Atrioventricular bundle (bundle of His) Right bundle branch Left bundle branch Purkinje fibres Figure 28.10  The intrinsic conduction system of the heart The cardiac index results show that the same cardiac output illustrated in Figure 28.11. These major arteries branch into of 4 L/min is adequate for the first person but grossly inade- successively smaller arteries, which in turn subdivide into the quate for the second person. smallest of the arterial vessels, called arterioles. The smallest arterioles feed into beds of hair-like capillaries in the body’s The conduction system of the heart organs and tissues. The cardiac cycle is perpetuated by a complex electrical cir- In the capillary beds, oxygen and nutrients are exchanged cuit commonly known as the intrinsic conduction system of the for metabolic wastes, and deoxygenated blood begins its jour- heart. Cardiac muscle cells possess an inherent characteristic of ney back to the heart through venules, the smallest vessels of self-excitation, which enables them to initiate and transmit im- the venous network. Venules join the smallest of veins, which pulses independent of a stimulus. However, specialised areas of in turn join larger and larger veins. The blood transported by the myocardial cells typically exert a controlling influence in this veins empties into the superior and inferior venae cavae enter- electrical pathway. ing the right side of the heart. The major veins of the systemic One of these specialised areas is the sinoatrial (SA) node, circulation are shown in Figure 28.12. ­located at the junction of the superior vena cava and right atrium (see Figure 28.10). The SA node acts as the normal ‘pacemaker’ of the heart, usually generating an impulse 60 to Structure of blood vessels The structure of blood vessels reflects their different functions 100 times per minute. This impulse travels across the atria via within the circulatory system (see Figure 28.13). Except for the internodal pathways to the atrioventricular (AV) node, in the tiniest vessels, blood vessel walls have three layers: the tunica floor of the interatrial septum. The very small junctional fibres intima, the tunica media and the tunica adventitia. The tunica of the AV node slow the impulse, slightly delaying its transmis- intima, the innermost layer, is made of simple squamous epithe- sion to the ventricles. It then passes through the bundle of His lium (the endothelium); this provides a slick surface to facilitate at the atrioventricular junction and continues down the inter- the flow of blood. In arteries the middle layer, or tunica media, ventricular septum through the right and left bundle branches is made of smooth muscle and is thicker than the tunica media of and out to the Purkinje fibres in the ventricular muscle walls veins. This makes arteries more elastic than veins and allows the (Mohrman & Heller, 2010). arteries to alternately expand and recoil as the heart contracts and relaxes with each beat, producing a pressure wave, which The Peripheral Vascular System can be felt as a pulse over an artery. The smaller arterioles are The two main components of the peripheral vascular system less elastic than arteries but contain more smooth muscle, which are the arterial network and the venous network. The arteri- promotes their constriction (narrowing) and dilation (widening). al network begins with the major arteries that branch from In fact, arterioles exert the major control over arterial blood the aorta. The major arteries of the systemic circulation are pressure. The tunica adventitia, or outermost layer, is made of Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 944 UNIT 8 Responses to altered cardiovascular function Internal carotid artery External carotid artery Vertebral artery Common carotid arteries Subclavian artery Brachiocephalic artery Aortic arch Axillary artery Coronary artery Ascending aorta Thoracic aorta Branches of coeliac trunk: Brachial artery Left gastric artery Common hepatic artery Abdominal aorta Splenic artery Superior mesenteric artery Renal artery Gonadal artery Radial artery Inferior mesenteric artery Ulnar artery Common iliac artery External iliac artery Internal iliac artery Deep palmar arch Superficial palmar arch Digital arteries Femoral artery Popliteal artery Anterior tibial artery Posterior tibial artery Dorsalis pedis artery Arterial arch Figure 28.11 Major arteries of the systemic circulation Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 945 Dural sinuses External jugular vein Vertebral vein Internal jugular vein Subclavian vein Superior vena cava Right and left brachiocephalic veins Axillary vein Cephalic vein Great cardiac vein Brachial vein Hepatic veins Basilic vein Splenic vein Hepatic portal vein Superior mesenteric vein Median cubital vein Renal vein Inferior vena cava Ulnar vein Inferior mesenteric vein Radial vein Common iliac vein External iliac vein Internal iliac vein Digital veins Femoral vein Great saphenous vein Popliteal vein Posterior tibial vein Anterior tibial vein Peroneal vein Dorsal venous arch Dorsal digital veins Figure 28.12 Major veins of the systemic circulation Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 946 UNIT 8 Responses to altered cardiovascular function Capillary network Valve Lumen Tunica intima: Endothelium Subendothelial layer Internal elastic lamina Tunica media Tunica adventitia Artery Vein Figure 28.13 Structure of arteries, veins and capillaries. Capillaries are composed of only a fine tunica intima. Notice that the tunica media is thicker in arteries than in veins connective tissue and serves to protect and anchor the vessel. 3. Diameter of the vessel: the smaller the diameter of a ves- Veins have a thicker tunica adventitia than do arteries. sel, the greater the friction against the walls of the vessel Blood in the veins travels at a much lower pressure than and, thus, the greater the impedance to blood flow. blood in the arteries. Veins have thinner walls, a larger lumen Blood pressure is the force exerted against the walls of the and greater capacity, and many are supplied with valves that arteries by the blood as it is pumped from the heart. It is most help blood flow against gravity back to the heart. The ‘milk- accurately referred to as mean arterial pressure (MAP). The ing’ action of skeletal muscle contraction (called the muscular highest pressure exerted against the arterial walls at the peak pump) also supports venous return. When skeletal muscles con- of ventricular contraction (systole) is called the systolic blood tract against veins, the valves proximal to the contraction open pressure. The lowest pressure exerted during ventricular relax- and blood is propelled towards the heart. The abdominal and ation (diastole) is the diastolic blood pressure. thoracic pressure changes that occur with breathing (called the Mean arterial blood pressure is regulated mainly by cardiac respiratory pump) also propel blood towards the heart. output (CO) and peripheral vascular resistance (PVR), as rep- The tiny capillaries that connect the arterioles and venules resented in this formula: MAP 5 CO 3 PVR. For ­clinical use, contain only one thin layer of tunica intima, which is permeable the MAP may be estimated by calculating the diastolic blood to the gases and molecules exchanged between blood and tissue pressure plus one-third of the pulse ­pressure (the difference be- cells. Capillaries typically are found in interwoven networks. tween the systolic and diastolic blood pressure). They filter and shunt blood from precapillary arterioles to post- capillary venules. Factors influencing arterial blood pressure Blood flow, peripheral vascular resistance and blood pressure, which influence arterial circulation, are in turn influenced by Physiology of arterial circulation various factors, as follows: The factors that affect arterial circulation are blood flow, pe- The sympathetic and parasympathetic nervous systems are ripheral vascular resistance and blood pressure. Blood flow re- the primary mechanisms that regulate blood pressure. Stim- fers to the volume of blood transported in a vessel, in an organ ulation of the sympathetic nervous system exerts a major or throughout the entire circulation over a given period of time. effect on peripheral resistance by causing vasoconstriction It is commonly expressed as litres or millilitres per minute or of the arterioles, thereby increasing blood pressure. Para- cubic centimetres per second. sympathetic stimulation causes vasodilation of the arteri- Peripheral vascular resistance (PVR) refers to the oppos- oles, lowering blood pressure. ing forces or impedance to blood flow as the arterial channels Baroreceptors and chemoreceptors in the aortic arch, become more and more distant from the heart. Peripheral vas- carotid sinus and other large vessels are sensitive to pres- cular resistance is determined by three factors: sure and chemical changes and cause reflex sympathetic 1. Blood viscosity: the greater the viscosity, or thickness, of stimulation, resulting in vasoconstriction, increased heart the blood, the greater its resistance to moving and flowing. rate and increased blood pressure. 2. Length of the vessel: the longer the vessel, the greater the The kidneys help maintain blood pressure by excreting or resistance to blood flow. conserving sodium and water. When blood pressure Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 947 decreases, the kidneys initiate the renin–angiotensin mech- content or structure can adversely affect health. Anaemia, the anism. This stimulates vasoconstriction, resulting in the most common RBC disorder, is an abnormally low RBC count release of the hormone aldosterone from the adrenal cortex, or reduced haemoglobin content. Polycythaemia is an abnor- increasing sodium ion reabsorption and water retention. In mally high RBC count. addition, pituitary release of antidiuretic hormone (ADH) The red blood cell is shaped like a biconcave disk (see promotes renal reabsorption of water. The net result is an ­Figure 28.15). This unique shape increases the surface area of increase in blood volume and a consequent increase in the cell and allows the cell to pass through very small capillar- ­cardiac output and blood pressure. ies without disrupting the cell membrane. RBCs are the most Temperatures may also affect peripheral resistance: cold common type of blood cell. causes vasoconstriction, whereas warmth produces vasodi- Haemoglobin is the oxygen-carrying protein within RBCs. lation. Many chemicals, hormones and drugs influence It consists of the haem molecule and globin, a protein mole- blood pressure by affecting CO and/or PVR. For example, cule. Globin is made of four polypeptide chains—two alpha epinephrine causes vasoconstriction and increased heart chains and two beta chains (see Figure 28.16). Each of the four rate; prostaglandins dilate blood vessel diameter (by relax- polypeptide chains contains a haem unit containing an iron ing vascular smooth muscle); endothelin, a chemical atom. The iron atom binds reversibly with oxygen, allowing released by the inner lining of vessels, is a potent vasocon- it to transport oxygen as oxyhaemoglobin to the cells. Haemo- strictor; nicotine causes vasoconstriction; and alcohol and globin is synthesised within the RBCs. The rate of synthesis histamine cause vasodilation. depends on the availability of iron (Bullock & Hales, 2012). Dietary factors, such as intake of salt, saturated fats and Normal adult laboratory values for red blood cells are defined cholesterol, elevate blood pressure by affecting blood and identified in Table 28.1. The size, colour and shape of stained ­volume and vessel diameter. RBCs also may be analysed. RBCs may be normocytic (normal Race, gender, age, weight, time of day, position, exercise size), smaller than normal (microcytic) or larger than normal and emotional state may also affect blood pressure. These (macrocytic). Their colour may be normal (normochromic) or factors influence the arterial pressure. Systemic venous diminished (hypochromic). pressure, though it is much lower, is also influenced by such factors as blood volume, venous tone and right atrial Red blood cell production and regulation pressure. In adults, RBC production (erythropoiesis) (see Figure 28.17) begins in red bone marrow of the vertebrae, sternum, ribs and Structure and Function pelvis, and is completed in the blood or spleen. Erythroblasts begin forming haemoglobin while they are in the bone mar- of Blood row, a process that continues throughout the RBC lifespan. Blood is an exchange medium between the external environ- Erythroblasts differentiate into normoblasts. As these slightly ment and the body’s cells. Blood consists of plasma, solutes smaller cells mature, their nucleus and most organelles are (e.g. proteins, electrolytes and organic constituents), red blood ejected, eventually causing normoblasts to collapse inward and cells, white blood cells and platelets (which are fragments of assume the characteristic biconcave shape of RBCs. The cells cells). The haematopoietic (blood-forming) system includes enter the circulation as reticulocytes, which fully mature in the bone marrow (myeloid) tissues, where blood cells form, about 48 hours. The complete sequence from stem cell to RBC and the lymphoid tissues of the lymph nodes, where white takes 3 to 5 days. blood cells mature and circulate. All blood cells originate from The stimulus for RBC production is tissue hypoxia. The cells in the bone marrow called stem cells or haemocytoblasts. hormone erythropoietin is released by the kidneys in response The origin of the cellular components of blood is illustrated in to hypoxia. It stimulates the bone marrow to produce RBCs. Figure 28.14. However, the process of RBC production takes about 5 days Regulatory mechanisms cause stem cells to differentiate to maximise. During periods of increased RBC production, into families of parent cells, each of which gives rise to one the percentage of reticulocytes (immature RBCs) in the blood of the formed elements of the blood (red blood cells, platelets exceeds that of mature cells. and white blood cells). The functions of blood include trans- porting oxygen, nutrients, hormones and metabolic wastes; Red blood cell destruction protecting against invasion of pathogens; maintaining blood RBCs have a life span of about 120 days. Old or damaged RBCs coagulation; and regulating fluids, electrolytes, acids, bases are lysed (destroyed) by phagocytes in the spleen, liver, bone and body temperature. marrow and lymph nodes. The process of RBC destruction is called haemolysis. Phagocytes save and reuse amino acids and Red blood cells iron from haem units in the lysed RBCs. Most of the haem Red blood cells (RBCs, erythrocytes) and the haemoglobin unit is converted to bilirubin, an orange-yellow pigment that is molecules they contain are required to transport oxygen to removed from the blood by the liver and excreted in the bile. body tissues. Haemoglobin also binds with some carbon diox- During disease processes causing increased haemolysis or im- ide, carrying it to the lungs for excretion. Abnormal numbers of paired liver function, bilirubin accumulates in the serum, caus- RBCs, changes in their size and shape, or altered haemoglobin ing a yellowish appearance of the skin and sclera (jaundice). Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 948 UNIT 8 Responses to altered cardiovascular function Erythroblast Rubricyte Erythrocyte Red cells Megakaryoblast Metamegakaryocyte Thrombocytes (platelets) Platelets Stem cell (haemocytoblast) Eosinophils Myeloblast Promyelocyte Neutrophils Basophils Monoblast Monocyte Macrophage White cells B cell lymphocyte Plasma cell Lymphoblast T helper T-cytotoxic lymphocyte lymphocyte T suppressor Figure 28.14 Blood cell formation from stem cells. Regulatory factors control the differentiation of stem cells into blasts. Each of the five kinds of blasts is committed to producing one type of mature blood cell. Erythroblasts, for example, can differen- tiate only into RBCs; megakaryoblasts can differentiate only into platelets Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 949 β1 β2 Top view α2 Polypeptide chain α1 Side view Haem group containing iron atom Figure 28.15  Top and side view of a red blood cell (eryth- rocyte). Note the distinctive biconcave shape Figure 28.16  The haemoglobin molecule includes globin (a protein) and haem, which contains iron. Globin is made of four subunits, two alpha and two beta polypeptide chains. A haem disk containing an iron atom (red dot) nests within the folds of each protein subunit. The iron atoms combine reversi- bly with oxygen, transporting it to the cells TABLE 28.1 Full blood count (FBC) Component Purpose Normal values Haemoglobin (Hb) Measures the capacity of the haemoglobin to carry gases Women: 12–17.5 g/dL Men: 13.6–17.5 g/dL Haematocrit (HCT) The haematocrit represents the percentage of whole blood volume Women: 35–45% composed of erythrocytes Men: 39–49% Total RBC count Counts number of circulating RBCs Women: 4–5 3 106 /μL Men: 4.5–6 3 106 /μL Red cell indices: MCV Determines relative size of MCV (mean corpuscular volume) 76–96 fL MCH Mean corpuscular haemoglobin 27–33 pg MCHC Evaluates RBC saturation with Hb (MCHC = mean corpuscular 32–36% haemoglobin concentration) WBC count Measures total number of leucocytes (total count) and whether each Total WBC count: 4300–10 800/ μL (leucocytes) kind of WBC is present in proper proportion (differential) (4.3–10.8 3 109 /L) WBC differential: Neutrophils: 50–70% Eosinophils: 2–4% Basophils: 0–2% Lymphocytes: 20–40% Monocytes: 4–8% Platelets Measures number of platelets available to maintain clotting functions 150 000–400 000 /μL (150–400 3 109/L) Bone marrow Bloodstream Stem cell Committed cell Haemocytoblast Erythroblasts Normoblasts Reticulocyte Erythrocytes Figure 28.17  Erythropoiesis. RBCs begin as erythroblasts within the bone marrow, maturing into normoblasts, which eventually eject their nucleus and organelles to become reticulocytes. Reticulocytes mature within the blood or spleen to become erythrocytes Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 950 UNIT 8 Responses to altered cardiovascular function White blood cells Platelets White blood cells (WBCs, leucocytes) are a part of the body’s Platelets (thrombocytes) are cell fragments that have no defence against microorganisms. On average, there are 5000 nucleus and cannot replicate. They are metabolically active, to 10 000 WBCs per microlitre of blood, accounting for about however, producing ATP and releasing mediators required for 1% of total blood volume. Leucocytosis is a higher than nor- clotting. Platelets are formed in the bone marrow as pinched- mal WBC count; leucopenia is a WBC count that is lower off portions of large megakaryocytes (see Figure 28.14). than normal. Platelet production is controlled by thrombopoietin, a pro- WBCs originate from haemopoietic stem cells in the bone tein produced by the liver, kidney, smooth muscle and bone marrow. These stem cells differentiate into the various types of marrow. The number of circulating platelets controls white blood cells (see Figure 28.14). thrombopoietin release. Once released from the bone mar- The two basic types of WBCs are granular leucocytes (or row, platelets remain in the spleen for about 8 hours before granulocytes) and non-granular leucocytes. Granulocytes entering the circulation. Platelets live up to 10 days in circu- have horseshoe-shaped nuclei and contain large granules lation. There are about 250 000 to 400 000 platelets in each in the cytoplasm. Stimulated by granulocyte-macrophage microlitre of blood. An excess of platelets is thrombocytosis. colony-stimulating factor (GM-CSF) and granulocyte colony- A deficit of platelets is thrombocytopenia. stimulating factor (G-CSF), granulocytes mature fully in the bone marrow before being released into the bloodstream. Haemostasis The three types of granulocytes are as follows: Platelet and coagulation disorders affect haemostasis, the con- Neutrophils (also called polymorphonuclear (PMN) or trol of bleeding. Haemostasis is a series of complex interac- segmented (segs) leucocytes) comprise 60–70% of the tions between platelets and clotting mechanisms that maintains total circulating WBCs. Their nuclei are divided into three a relatively steady state of blood volume, blood pressure and to five lobes. Neutrophils are active phagocytes, the first blood flow through injured vessels. The five stages of haemo- cells to arrive at a site of injury. Their numbers increase stasis are (1) vessel spasm, (2) formation of the platelet plug, during inflammation. Immature forms of neutrophils (3) development of an insoluble fibrin clot, (4) clot retraction, (bands) are released during inflammation or infections and and (5) clot dissolution. are referred to as having a shift to the left (so named Vessel spasm because immature cell frequencies appear on the left side of the graph) on a differential blood count. Neutrophils When a blood vessel is damaged, thromboxane A2 (TXA2) is have a lifespan of only about 10 hours and are constantly released from platelets and cells, causing vessel spasm. This being replaced. spasm constricts the damaged vessel for about 1 minute, reduc- Eosinophils comprise 1–3% of circulating WBCs, but are ing blood flow. found in large numbers in the mucosa of the intestines and Formation of the platelet plug lungs. Their numbers increase during allergic reactions and Platelets attracted to the damaged vessel wall change from parasitic infestations. smooth disks to spiny spheres. Receptors on the activated Basophils, which comprise less than 1% of the WBC count, platelets bind with von Willebrand’s factor, a protein mole- contain histamine, heparin and other inflammatory media- cule and exposed collagen fibres at the site of injury to form tors. Basophils increase in number during allergic and the platelet plug (see Figure 28.18). The platelets release inflammatory reactions. adenosine diphosphate (ADP) and TXA2 to activate nearby Non-granular WBCs (agranulocytes) include the mono- platelets, adhering them to the developing plug. Activation cytes and lymphocytes. They enter the bloodstream before of the clotting pathway on the platelet surface converts fi- final maturation. brinogen to fibrin. Fibrin, in turn, forms a meshwork that Monocytes are the largest of the WBCs. They comprise binds the platelets and other blood cells to form a stable plug approximately 3–8% of the total WBC count. Monocytes (see Figure 28.19). contain powerful bactericidal substances and proteolytic enzymes. They are phagocytic cells that mature into macro­ Development of the fibrin clot phages. Macrophages dispose of foreign and waste materi­al, The process of coagulation creates a meshwork of fibrin strands especially in inflammation. They are an active part of the that cements the blood components to form an insoluble clot. immune response. Coagulation requires many interactive reactions and two clot- Lymphocytes comprise 20–30% of the WBC count. Lym- ting pathways (see Figure 28.20). The slower intrinsic path- phocytes mature in lymphoid tissue into B cells and T cells. way is activated when blood contacts collagen in the injured B cells are involved in the humoral immune response and vessel wall; the faster extrinsic pathway is activated when antibody formation, whereas T cells take part in the blood is exposed to tissues. The final outcome of both path- cell-mediated immunity process (see Chapter 12). Plasma ways is fibrin clot formation. Each procoagulation substance is cells (which arise from B cells) are lymphoid cells found in activated in sequence; the activation of one coagulation factor bone marrow and connective tissue; they also are involved activates another in turn. Table 28.2 lists known factors, their in immune reactions. origin and their function or pathway. A deficiency of one or Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 951 Injury to vessel lining exposes Fibrin clot collagen fibres; Platelet with trapped platelets adhere plug forms red blood cells Collagen Platelets Fibrin fibres Chemical release increases platelet adhesion Figure 28.19 Scanning electron micrograph of an RBC trapped in a fibrin mesh Mediating factors Calcium from platelets and and other Source: Micro Discovery/Corbis. thromboplastin + clotting from damaged factors cells in blood repair. Like coagulation, fibrinolysis requires a sequence of plasma interactions between activator and inhibitor substances. Plas- minogen, an enzyme that promotes fibrinolysis, is converted Coagulation into plasmin, its active form, by chemical mediators released from vessel walls and the liver. Plasmin dissolves the clot’s Prothrombin fibrin strands and certain coagulation factors. Stimuli such as 1 activator exercise, fever and vasoactive drugs promote plasminogen ac- tivator release. The liver and endothelium also produce fibri- nolytic inhibitors. 2 Prothrombin Thrombin Structure and Function of the Lymphatic System The structures of the lymphatic system include the lymphat- Fibrinogen Fibrin ic vessels and several lymphoid organs (see Figure 28.21). 3 (soluble) (insoluble) The organs of the lymphatic system are the lymph nodes, the spleen, the thymus, the tonsils and the Peyer’s patches of the Figure 28.18  Platelet plug formation and blood clotting. small intestine. Lymph nodes are small aggregates of special- The flow diagram summarises the events leading to fibrin clot ised cells that assist the immune system by removing foreign formation material, infectious organisms and tumour cells from lymph. Lymph nodes are distributed along the lymphatic vessels, forming clusters in certain body regions, such as the neck, more factors or inappropriate inactivation of any factor alters axilla and groin (see Figure 28.21). The spleen, the largest normal coagulation. lymphoid organ, is in the upper left quadrant of the abdomen Clot retraction under the thorax. The main function of the spleen is to fil- After the clot is stabilised (within about 30 minutes), trapped ter the blood by breaking down old red blood cells and stor- platelets contract, much like muscle cells. Platelet contraction ing or releasing to the liver their by-products (such as iron). squeezes the fibrin strands, pulling the broken portions of the The spleen also synthesises lymphocytes, stores platelets for ruptured blood vessel closer together. Growth factors released blood clotting and serves as a reservoir of blood. The thymus by the platelets stimulate cell division and tissue repair of the gland is in the lower throat and is most active in childhood, damaged vessel. producing hormones (such as thymosin) that facilitate the im- mune action of lymphocytes. The tonsils of the pharynx and Clot dissolution Peyer’s patches of the small intestine are lymphoid organs Fibrinolysis, the process of clot dissolution, begins shortly a­ fter that protect the upper respiratory and digestive tracts from the clot has formed, restoring blood flow and promoting tissue foreign pathogens. Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 952 UNIT 8 Responses to altered cardiovascular function Intrinsic pathway (slow) Blood is exposed to collagen in wall of damaged vessel XII Activated XII Extrinsic pathway (rapid) XI Activated XI Blood is exposed to IX extravascular tissue Activated IX Mediating factors from Thromboplastin III aggregated released platelets Ca2+ Ca2+ V VII VIII complex VII complex X Activated X Ca2+ V Common pathway Prothrombin activator Prothrombin II Ca2+ Thrombin Fibrinogen I XIII Fibrin Activated XIII Cross-linked fibrin clot Figure 28.20  Clot formation. Both the slower intrinsic pathway and the more rapid extrinsic pathway activate factor X. Factor X then combines with other factors to form prothrombin activator. Prothrombin activator transforms prothrombin into thrombin, which then transforms fibrinogen into long fibrin strands. Thrombin also activates factor XIII, which draws the fibrin strands together into a dense meshwork. The complete process of clot formation occurs within 3 to 6 minutes after blood vessel damage The lymphatic vessels, or lymphatics, form a network around and veins that eventually drain into the right lymphatic duct and the arterial and venous channels and interweave at the capillary left thoracic duct, both of which empty into their respective sub- beds. They collect and drain excess tissue fluid, called lymph, clavian veins. Lymphatics are a low-pressure system without a that ‘leaks’ from the cardiovascular system and accumulates at pump; their fluid transport depends on the rhythmic contraction the venous end of the capillary bed. The lymphatics return this of their smooth muscle and the muscular and respiratory pumps fluid to the heart through a one-way system of lymphatic venules that assist venous circulation. Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e  CHAPTER 28 A person-centred approach to assessing the cardiovascular and lymphatic systems 953 TABLE 28.2 Blood coagulation factors Factor Name Function or pathway I Fibrinogen Converted to fibrin strands II Prothrombin Converted to thrombin III Thromboplastin Catalyses conversion of thrombin IV Calcium ions Needed for all steps of coagulation V Proaccelerin Extrinsic/intrinsic pathways VI Derived from proaccelerin A hypothetical agent said to be derived from proaccelerin VII Serum prothrombin conversion accelerator Extrinsic pathway VIII Antihaemophilic factor Intrinsic pathway IX Plasma prothrombin component Intrinsic pathway X Stuart factor Extrinsic/intrinsic pathways XI Plasma prothrombin antecedent Intrinsic pathway XII Hageman factor Intrinsic pathway XIII Fibrin stabilising factor Cross-links fibrin strands to form insoluble clot Regional lymph nodes Right Cervical lymphatic nodes duct Internal jugular vein Axillary Entrance of thoracic duct nodes into left subclavian vein Thoracic duct Aorta Cisterna chyli Lymphatic collecting vessels Inguinal nodes Figure 28.21  The lymphatic system Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2017—9781488611766—LeMone/Medical–Surgical Nursing Vol 2 3e 954 UNIT 8 Responses to altered cardiovascular function Health assessment and precipitating and relieving factors, and any associated symp- documentation toms, noting the timing and circumstances. For example, ask the person: Cardiovascular, haematological and lymphatic function is What is the location of the chest pain you experienced? Did assessed by findings from a health assessment interview to col- it move up to your jaw or into your left arm? lect subjective data, a physical assessment to collect objective Describe the type of activity that brings on your chest pain. data and diagnostic tests. Consideration of all the data which Have you noticed any changes in your energy level? contributes to understanding a person’s absolute cardiovascular Have you felt light-headed during the times your heart is disease risk (CVD) should be considered. The National Vascular racing? Disease Prevention Alliance has produced comprehensive Have you noticed any glands that are sore and swollen? guidelines to assist clinicians with assessment of CVD risk. Sam- What do you think causes this? ple documentation of an assessment of cardiovascular function The interview begins by exploring the person’s chief com- is included in the boxes below. plaint (e.g. chest pain, palpitations or fatigue). Describe the person’s chest or leg pain in terms of location, quality or char- Health assessment interview acter, timing, setting or precipitating factors, severity, aggra- A health assessment interview to determine problems with the vating and relieving factors, and associated symptoms (see structure and functions of the cardiovascular and/or lymphatic Table 28.3). systems may be conducted during a health screening, may focus Explore the person’s history for heart disorders such as on a chief complaint (such as chest pain, fatigue and bleeding) angina, heart attack, congestive heart failure (CHF), hyper- or may be part of a total health assessment. tension (HTN) and valvular disease. Ask the person about If the person has a problem with cardiovascular or lymphat- previous heart surgery or illnesses, such as rheumatic fever, ic function, analyse its onset, characteristics, course, severity, scarlet fever or recurrent streptococcal throat infections. Also ask about the presence and treatment of other chronic illnesses such as diabetes mellitus, bleeding disorders or endocrine dis- Sample documentation orders. Review the person’s family history for coronary artery Assessment of altered cardiac function disease (CAD), HTN, stroke, hyperlipidaemia, diabetes, con- 28/2/2016 56-year-old male admitted to a coronary genital heart disease or sudden death. Nursing care unit from ED to rule out myocardial Ask the person about past or present occurrence of various entry infarction. He states he has pain in the cardiac symptoms, such as chest pain, shortness of breath, 1000 hrs middle of his chest that is ‘like a heavy difficulty breathing, cough, palpitations, fatigue, light head- pressure’; 6 on a 10-point scale. Skin edness or dizziness, fainting, heart murmur, blood clots or cool, slightly moist. BP 190/94 right arm and 186/92 left arm (both reclining). swelling. Because cardiac function affects all other body sys- Apical pulse 92, regular and strong