Anda di halaman 1dari 8

Cardiac patient assessment: putting the patient first

Curie Scott, )ulie D Macinnes Abstract


Nursing roles are expanding and there is a growing expectation that nurses, with appropriate education and experience, are able to perform assessments that were traditionally conducted by doctors. This article discusses patient history., vital signs and physical exainination related to the cardiac patient. This will enable practitioners to enhance their knowledge and understanding of this valuable assessment influencing patient care. Key words: Heart disorders: prevention and screening assessment Patient A comprehensive assessment may be based on a nursing model, for example that by Roper et al (1980) which encompasses the activities of daily living. This model incorporates the risk of pressure sore development and a niitritioTial, cultural and spiritual assessment. In contrast, patient assessment may be necessarily brief and .succinct in an acutely or critically ill patient, allowing for a more comprehensive assessment at a later stage. In this situation the adoption of a focused assessment using an 'AliC approach, where airway, breathing and circulation are priorities, is often utilized. An 'early warning sign' system uses this AUC approach to quickly identify those patients at risk of deterioration and who require immediate intervention (McArthur-Rouse, 20(11). This article utilizes a systematic approach to appraise selected aspects relevant tor a cardiac patient assessment. These include history taking, which encompasses symptom assessment, past medical history, assessment of risk factors, medication, family history and social history. Vital signs (or ntirsing observations) are exploreci in addition to physical examination. The latter section considers a variety of significant details that can be observed in the cardiac patient when assessing hohsticaily Underpinning anatomy and physiology will be integrated throughout the discussion.

ursing roles are expanding and there is a growing expectation that nurses, with appropriate education and experience, are able to perform assessments that were traditionally conducted by doctors (NHS Management Executive, 1991; United Kingdom Central Council of Nursing, Midwifery and Health Visitnig (UKCC) (1992). A comprehensive, systematic patient assessment is necessary in the management and care of a patient with cardiac disease. Assessment can be described as 'an orderly collection ot information concerning the patient's health status which aitns to identity the patient's current health status, actual and potential health problems and areas for health improvement' (Estes,2002 p7). Assessment requires a prohlem-solving approach and forms the first stage of the nursmg process, followed by nursing diagnosis, identification of problems, intervention and evaluation. Assessment consists of: Patient history Determination of vital signs or nursing observations Physical examination Diagnostic investigations. Traditionally, the nursing role in patient assessment would be restricted to elements of patient history and nursing observations. However, nurses performing advanced roles increasingly perform physical examination in addition to requesting and interpreting many diagnostic investigations.
C'urie Scott is Senior LectiiriT and Julie I) M.iclniics is Senior Lecturer in Cardiac ('are, Department of AcUilt Nursing Studies, tl^ncorbury C]hrist C^hiirch University, Qioterbury, Kent
Accepted for publication: March 2006

Cardiac patient history


I'atient history is frequently the first element in a systematic patient assessment. It includes an exploration of symptoms and the determination of past medical history, medications, family and social history together with an assessment of risk factors for cardiac disease. Much of the information about a potential diagnosis is ascertained by the history so that further findings from the actual examination and tests are to confirm the probable cause. Symptom assessment Patients' symptoms need to be scrutinized by the practitioner to determine if these relate to an underlying cardiac condition in order to influence appropriate management. Though chest pain is the most obvious and common cardiac symptom, breathlessness, oedema, palpitations, syncope and fatigue are also described (Gieadle, 2003;Jowett and Thompson, 2003). Table 1 gives examples of questions that practitioners may use.
Chest pain The National Service Framework for Coronary Heart Disease

(Department of Health (DH), 2000) advocates the rapid

502

icish Jouiiial ol"

K. 2IK)(,.Vol i5,No

CARDIAC ASSESSMENT
assessment of chest pain to exclude non-cardiac chest pain and to enable the prompt treatment of stable angina antl acute coronary syndrome (ACS). Rapid access chest pain clinics are now commonplace {Wood andTininiis, 2001) and were developed to facilitate the differential diagnosis of chest pain and instigate appropriate treatment. Stable angina may be defined as symptomatic myocardial ischaeniia with chest pain lasting less than 5 minutes. It is commonly precipitated by exercise or stress, occurring over a number of weeks without significant deterioration Qowett and Thompson, 2(>()3). In contrast, ACS can be divided into two groups differentiated by electrocardiogram (ECG) changes and cardiac markers assessed from a venous blood sample. The first group is ST elevation myocardial infarction (STEMI). and the second consists of unstable angina (UA) and nonST elevation MI (NSTEMI). STEMI presents as symptoms of niyocardial ischaeniia coupled with ST elevation or new bundle branch block (BBB) on the ECG. UA and NSTEMI are also characterized by symptoms of myocardial ischaeniia but without ST elevation. UA and NSTEMI caii be differentiated by cardiac markers. When heart muscle (myocardium) is deprived of ox^'gen as a result of insufficient blood supply, ischaemic pain is the consequence. This ischaeniia occurs when there is thickening and hardening of the vessel walls (arteriosclerosis) and deposition of'plaques' containing cholesterol, lipids and fibrin in the inner walls (atherosclerosis) (Hrashers, 2004). Although arteriosclerosis is a normal conseqtience of aging, hypertension, high cholesterol (hypercholesterolaemia), smoking and diabetes can aggravate both processes. Classically., ischaemic chest pain presents as central chest pain. radiating to one or both arms,jaw or back. It is often described as a pressure, heaviness or ache, although it may be atypical. It may be of gradual or sudden onset and can be precipitated by exertion, cold or anxiety. It may be reheved by rest or medication, for example, glyceryl trinitrate (GTN). In ACS, associated symptoms include tiausea, vomiting and sweating. In contrast, when the outer wall of the heart (pericardium) IS mflamed, a condition known as pericarditis, the pain differs. Here, it is often described as a sharp, central chest pain unrelated to exertion, aggravated by inspiration or coughing and relieved hy sitting forward. The mnemonic 'PQRST' (outlined in Taiyle 2) is frequently cited as a structured method m the differential diagnosis of chest pain (Estes. 2(HI2; Spriiighouse, 2()(t2) and its use is transferable to other symptoms. Other origins of non-cardiac chest pain include aortic dissection, pulmonary embolism, pneumothorax, pneumonia and chest infections, oesophageal disorders (including indigestion and reflux), musculoskeletal, anxiety and postoperative pain (Fallon and Roques. 1997). Hence, a thorough, foctised assessment of chest pain is vital as an adjunct to patient history aiid physical examination.
Dyspnoea

'clinical syndrome that results from an inahility of the heart to provide an adequate cardiac output'. Patients with dyspnoea have a heightened awareness ot uncomfortable, distressing or laboured breathing either at rest or after a low level of exertion (Beers and Berkow. 2005). The reasoning for dyspnoea is complex but is su^ested to be mainly as a result of dysfunction of the left ventricle. Normally, oxygenated blood moves from the lungs into the left side of the heart,flowingfrom the atrium into the ventricle {Hi^ure /); therefore, increased pressure in the left ventricle will eventually result in back-pressure in the lung capillaries. This high pressure causes fluid to be forced out of the blood into the tissue spaces (interstitial space) causing pulmonary congestion. Other factors include stiffening of the lung, respiratory muscle fatigue and acidosis (Timmis and Mills, 2002). It is important to note the type and extent of exertion that causes dyspnoea (e.g. shopping, climbing stairs or walking) and whether exercise tolerance has deteriorated. In advanced heart fliilure patients may have dyspnoea at rest. Pulmonary congestion related to heart disease gives rise to orthopnoea and paroxysmal nocturnal dyspnoea. Orthopnoea is when breathlessness causes patients to be unable to lie flat and therefore use extra pillows or sit in a chair to sleep. The patient with paroxysmal nocturnal dyspnoea will describe waking suddenly from sleep (often trom lying flat) with acute dyspnoea and a sense of impending doom that is rectified on standing (Timmis and Mills, 2002).

Pulmonary semilunar valve Right atrium Tricuspid valve Inferior vena cava > Oxygenated blood Deoxygenated blood

Left pulmonary veins Left atnum Mitral (bicuspid) valve

Venules 4 Systemic ^ capiUarie Pencardial fluid Pericardium

Dyspnoea, or shortness of breath, may occur as a result of ,1 respiratory condition but is a major symptom in patients with cardiac problems, especially in heart failure. Heart tailure is defined by Jowett and Thompson (2003, p254) as a

Figure 1. Anatomy of the heart and normal route of blood jlow.

l nf Nursing, 2U()6.Vol IS. No

503

Palpitations

Syncope

Patients may convey an awareness of their heartbeat hy using terms such as their heart races, flutters, pounds, skips or misses a beat. To demonstrate the regularity and rate, the patient can be asked to tap out the rhythm. Initiating factors should be queried and whether the palpitations started and stopped suddenly or gradually (Bickley and Szihiygi, 2003). Palpitations could occur as a result of an arrhythmia causing the heart to beat at an abnormal rate or irregularly or because the heart is beating more forcefully (Epstein et al, 2003).
Oedema In addition to pulmonary congestion, pressure may increase in the right atrium causing backpressure in the systemic venous system {Fiiiure 1). Fluid may then accumulate in the interstitial space and produce swelling of the feet with patients revealing that their shoes, rings or clothes have become tight. Gravity plays a role here as patients may note that their swollen feet are worse in the evening and better

The processes of arteriosclerosis and atherosclerosis described above may result in decreased blood flow to the brain. This may cause a temporary loss of consciousness, defined as syncope, but verbalized by patients as fainting or a blackout. If this has occurred, an additional description of the episode from an observer is useful (Hattoii and Blackwood, 2003).
Poor peripheral circulation

in the morning.

Cardiac patients may have poor blood flow to their peripheries and therefore have colder feet or hands which may appear paler in comparison to the surrounding areas. Additionally, they may experience intermittent claudication - this is pain experienced in one or both legs when walking and IS reheved by rest (Epstien et al, 2003). The situation is similar to that discussed above in relation to myocardial ischaemia, although instead of coronary artery narrowing it occurs in the arteries in the leg and heralds existence of peripheral vascular disease. The pain is aching in nature and presents in the calt, thigh or buttocks. Past medical history (PMH) and assessment of cardiac risk factors An analysis of a patient s previous and current illnesses can be obtained from an interview with the patient and taniily members and from medical notes. Establishing any previous acute or chronic cardiac disease is of value. This includes the presence of existing coronary heart disease (CHD) as evidenced by previous niyocardial infarction or angina in addition to any previous cardiac surgery or congenital cardiac abnormalities. The existence of other diseases or risk factors associated with CHD, such as hypertension, hypercholesterohiemia, cerebrovascular accidents (CVA) and diabetes niellitus (DM) should also be explored. The presence of childhood illness such as rheumatic fever should be sought as the heart valves may be damaged so patients are at higher risk for endocarditis. Endocarditis relates to infection of the heart valves and, if suspected, then investigation into possible portals of entry of microorganisms (such as recent dental work) should be discussed (Gieadle, 2003). Additionally, in patients with suspected STEMI, contraindications for thrombolysis need confirmation through history and physical examination. For example, recent surgery or trauma, stroke, bleeding disorders or aortic dissection are absolute or relative contraindications to thrombolysis (Jowett and Thompson, 2003), Medication Current medications, including prescription, over the counter and herbal medications, should be ascertained as they may affect cardiac function or interact with any new drugs that are prescribed. The use of recreational drugs must be addressed due to their potential effect on cardiac rhythm. Often, scrutiny of a patient's medications draws attention to a condition that has not been disclosed previously, for example, a patient may not mention hypertension as their blood pressure is now controlled by medication. It is usual, while enquiring about medication, to note if the patient has any allergies.

Table I. examples of question to analyse specific symptoms


Chest pain: Have you had any pain or pressure in your chest, neck or arm? If 'yes' _ the following questions are necessary: o Can you describe the pain? o Where exactly is the pain? o How often does it occur and how long does it last? o How severe is the pain? o What brings the pain on? o What makes the pain better or worse? o Does the pain radiate anywhere? o Have you had any other symptoms (e.g. nausea, vomiting, sweating)? Dyspnoea: Are you short of breath on exertion? o If yes' _ how much exertion is necessary to make you short of breath? Are you short of breath when you are not doing anything (i.e. at rest)? Can you lie flat without feeling breathless? o If 'no' _ how many pillows do you need to sleep? Do you sleep in a chair? Have you ever woken suddenly from sieep short of breath? Palpitations: Are you ever aware of your heart beating, for exampie, racing or beating irregularly? o If 'y^s' _ Couid you describe what this is like? o If "y^s' _ When does the sensation occur? Oedema: Have you noticed swelling of your ankles? Have you noticed that your shoes, rings or clothes feel restrictive, especiaily at the end of the day? Syncope: Have you ever felt light headed/ dizzy or fainted? If 'y^s" _ could you describe what happened? If 'y^s' _ did you have any warning signs If yes" _ did anyone witness this (get a statement of what was seen If possible) Poor peripheral circulation: Do you have cold or blue hands or feet? Do you have pain in your legs on exercise? o If yes' _ how much exertion is necessary to produce this pain? o If 'y^s' _ what helps the pain disappear?

504

British Journal ot Nursmg, 2(l()().Vol 15, No 9

CARDIAC ASSESSMENT
Family and social history
Family history is the report of the occurrences of familial or genetic diseases. In the cardiac patient, this might include CHD, DM, CVA, familial hypercholesterolaemia, hypertension, cardiomyopathy, congeiHtal heart disease or sudden death (Gieadle, 2003). Social history explores information about the patient's lifestyle that affects health. In the cardiac patient this might include an analysis of established modifiable risk behaviour for CHD including smokmg, a diet high in saturated fats, lack of exercise, excessive alcohol consumption and stress. The use of a risk calculator may be used to establish a patient's risk status using specific information such as gender, age, serum cholesterol levels and other risk factors (Foxton, 20(14). This not only indicates level of risk but also provides a mechanism for targeting and evaluating heaith promotmg strategies. Work and home environment, leisure activities and social role would also need to be assessed to determine continuing care needs. Vital signs Vital signs are of paramount importance in ascertaining the patients clinical condition and underpin physical examination. Those that directly relate to the cardiovasctilar system include the pulse and blood pressure. However, other signs that may be useful are the patient's respiratory rate, temperature and level of consciousness. Pulse Most commonly, the radial artery is used to assess the rate and rhythm of the pulse. Bradycardia (<6(J beats per minute) may be caused by beta-blockade, hypoxia or parasympathetic (vagal) stimulation. Tachycardia (>10() beats per minute) may be caused by pyrexia, hypovolaeniia, shock, anxiety or pain (Doherty, 2002). An irregular rhythm should prompt further investigation through a 12-lead ECG. Conduction disturbances, e.g. heart blocks and atrial fibrillation, are commonly associated with cardiac disease. In cases of atria! fibrillation the rate should be measured by listening with a stethoscope at the apex (Timmis and MiDs, 2002). The character of the pulse should also be assessed, although this is best assessed using the carotid artery. For example, a pulse may be described as thready in cardiogenic shock; bounding in aortic insufficiency; or have decreased force if there is atherosclerotic narrowing or occlusion.

Table 2. Exploration of symptoms


Factors The patient Is asked... p Provoking or Palliative What makes the symptom worse or better What the symptom feels/looks/ sounds like Q Quality or Quantity R Region and Radiation Where the symptom occurs and if it radiates anywhere S Severity How severe tfie symptom is (rating scaies can be used) Whetfier the symptom intensity has altered The effect on normal activities T Timing When the symptom began and if it was sudden or gradual The frequency of the symptom How long the symptom lasts

(Tininiis and Mills, 2002) or post-surgical infection. In the cardiac patient, hypoxia and CVA may both be evidenced by alteration in neurological status, therefore, neurological observations and scoring systems such as the Glasgow Coma Scale should be recorded. Physicai examination A comprehensive assessment includes the examination of all body systems. The term physical examination includes the interpretation of observable signs. A noteworthy point is that the abihty to perform a cardiovascular assessment and percussion/auscultation of the chest are skills practitioners have identified as being valuable (Rushworth et al, 1998). Overview of cardiac physical assessment The cardiovascular examination requires exposure of the patient's chest which may cause patients to be apprehensive about potential findings and possible pain. Therefore, it is imperative to be sensitive and to ensure surroundings are appropriate for the examination to maintain privacy and dignity (Epstein et al, 2003). Although the formal method of cardiac examination will be explored, several aspects will have been noted when the patient is first seen, during the history taking and from recording of vital signs. The four principles of assessment that can he applied in most system-based assessments are inspection, palpation, percussion and auscultation {Table 3) though percussion is not integral to cardiac assessment. As the effects of cardiac disease often have an impact on the whole body, it is vital to survey the whole patient rather than focus immediately on the chest. The initial inspection may include noting signs of distress (e.g. grimacing in pain).

Blood pressure
A systolic blood pressure of less than 9()mmHg is indicative of poor circulation (Resuscitation Council UK, 2000). However, the mean arterial pressure (MAP) gives a better indication of perfusion and a reading of 60 niniHg is needed to perfuse coronary arteries, the brain and kidneys. Though this value is frequently established by blood pressure machines, it can be approximated from the usual blood pressure reading by: diastohc BP + (systolic BP - diastolic BP)/3. The respiratory rate should be recorded as it isfrec^uentlyan early sign of deterioration in a patient's condition (Ryan et al, 2004). An increased temperature may indicate endocarditis or pericarditis and is also apparent after a myocardial infarction

Table 3. Principles of assessment


Descrintlon Observation of the person as a whole in addition to a particular area (e.g. hands, face and chest) Palpation Technique using touch to determine the texture, temperature, moisture and organ size Percussion Describes the transmission of sound elicited by the practitioner tapping a finger with short sharp strokes against another finger that is firmly positioned over a particular organ Auscultation Uses both the bell and the diaphragm of a stethoscope to listen to sounds that internal organs produce Inspection

i Juurriji of Nursing, 20116, Voi 15, No

505

breathlessness, an obvious skin colour cbange (paleness or cyanosis) and general physique {Bickley and Szilaytji, 2()()3). Sonic patients with easily observable conditions such as Downs Syndrome or Marfan Syndrome are at higher risk of cardiovascular problems. Chest wall deformities may compress and displace the heart and there may be obvious pulsations from ancurysms (Tiiimiis and Mills, 2002). Practitioners bave differing frameworks relating to the order in which they assess patients but it is important to be methodical and streamline the assessment to limit the number of physical positions changed for the patient (Bickley and Szilaygi, 2003). However, most practitioners will commence the cardiac examination at the patient's hands.

The face
Ceneral inspection

The tace can then be assessed by noting tbe person's general colour and that ot the conjunctiva which may indicate anaemia. Patients may have signs of hypercholestcrolaenu'a that result in a greyish ring at the periphery of the cornea (an arcus) and yellow lesions under the skin (xanthelasma) often around the eyes. However, these are suggested to be non-specific in those over the age of 50 years (White, 2002). Finally, evidence of blue discolouration of the mouths mucous membranes or tongue (central cyanosis) signifies reduced oxygenation of the blood and should be noted.
Jugular venous pressure

Hands
On inspection of the hands, signs of reduced peripheral perfusion such as peripheral cyanosis (blue discolouration) and reduced capillary refill time may be evident. Capillary refill is assessed by compressing the distal phalanx of the middle finger for 5 seconds; once the pressure is released it should take approximately 2 seconds for the colour to be regained, although this could be up to 4 seconds in tbe elderly (Epstein et al. 2003). Although reduced cardiac output may cause decreased peripheral pcrtusion, it is important to ensure the patient is not cold as the same sign is observed. Additionally, nicotine stains and nail clubbing may be obvious. Clubbing is distinguished by the oblkenition of the angle between the nail base and the adjacent skin, thickening ot tissue at the nail bed and the nail may be curved (Timmis and Mills, 2002). Tlic underlying cause of clubbing is unknown but is suggested to be related to increased vascularity and increased tissue fluid (Epstein et al, 2003) with cardiac causes being cyanotic heart disease and endocarditis. An additional sign tor the latter are splinter baeniorrhages noted as tiny splinter-like lesions in the nail bed.The radial pulse sbould be palpated tor the rate and rhythm as discussed above.

The estimation of the jugular venous pressure (|VP), though difficult to perform initially, is an assessment skill that is regularly used to estimate the patients blood volume state and cardiac function (Bickley and Szilaygi. 2003). The internal jugular vein is observed for a reflection of central venous pressure which relates to right atrial pressure. The technique is outlined in Fij^urc 2 and a normal JVP is 4 cm or lower. If, however, the JVP is too high to ascertain at a 45 angle, the patient may have to be assessed in a sitting position and this positional change must be documented. High JVP measurements can occur in congestive heart failure, tamponade (excessive fluid within the double sac of the pericardium), fluid overload, pulmonary embolism and superior vena cava obstruction (Tiiiiniis and Mills 2002).Tbose accustomed to evaluating the JVP gain further detailed information by scrutinizing the JVP's undulating character known as 'the waveform".
Carotid pulse

Top of the internal jugular vein ^^ / ^y Vertical height of JVP (<4cm) ' '/ .Sternal angle ^ Sternum

The pulse character is assessed by carotid artery palpation and retlects iett ventricular function. Bilateral carotid pulses must not be compressed simultaneously and care should be taken that the carotid sinus is not stimulated. These actions may result ill a reflex drop in pulse rate and blood pressure and decreased blood flow to the brain causing syncope. While palpating the carotid arteries, vibrations called 'tlirills' may be perceived and, when auscultated, these vascular, murnuir-likc sounds are termed 'bruits'.

The precordium
Tbe assessment continues with observation of the chest wall. Any chest shape abnormalities and unusual pulsations should be noted. Palpation to the left of the sternum will establish whether the hand is lifted by eacb heartbeat (heaves) or if heart murmurs are palpable (thrills). The mam purpose of palpation is to locate the apical impulse, or apex beat. Tliis is the most lateral site of impulse on the chest wall and, as this correlates to the contraction of the left ventricle, the assessment gives an indication o{ the condition of this chamber. In adults the apex beat is usually found in the midclavicular line at the 5th intercostal space on the left side. It may be necessary to roll the patient onto his left side (the left lateral position) to detect it. Occasionally, the impulse is undetectable especially in patients who are obese, have a muscular chest wall or those with a barrel cbest (Bickley and

y C ^ 2 ^ ^ ^ ^ ^ ^ ^ _ _ _ ^ Clavicle

^r^-

^--^

Figure 2: How lo measure jugular yeiioiis pressure QV'l'} 1. Position ihe patient at 4S. 2. Ask them to flex their head alightly and look straight ahead. The aim is to relax the stertiomastoid muscle. 3. Observe the internal jugular vein's transmitted pulsations just above the elavicle. 4. Note the top of the pulsation. 5. Estimate the vertical height from the sternal angle to the top of the pulsation (it should be less than 4ctn). Venous pulsations need to be distinguished from arterial pulsations. The JVP has an undulating wai'eform with two pulsations per cardiac cycle, becomes pronounced if the abdomen is compressed over the area of the liver (liepalojugular reflex) and is rarely palpable (Epstein et al, 2003).

506

Utitisli Joiiriul ol" Niirsmy. 2nuti,Viil 13. No

CARDIAC ASSESSMENT
Szilaygi, 2003). The apical beat may be displaced if the heart becomes enlarged and the quality of the beat may indicate increased cardiac output, mitral stenosis or hypertrophy (Epstein et al,2003). Auscultation The purpose of auscultation is to establish whether heart sounds are normal and if there are any additional sounds.The stethoscope must be placed directly on the skin and, ideally, the environment should be quiet. When a stethoscope is used listen to the heart, the resonance of a single heartbeat corresponds to two heart sounds, otberwise known as 'lub dub', which originate from the closure of heart valves. The atria till with blood and tben contract, pushing the blood into the ventricles. This is the beginning of systole and, to prevent backtlow as the ventricles contract, the valves between the atria and ventricles close securely. Thus, the first heart sound (lub or SI) occurs as a result of the closure of the tricuspid and bicuspid valves. As systole continues, blood leaves the ventricles through open aortic and pulmonary valves and when these valves shut the second heart sound (dub or S2) is produced. This denotes the end of systole and there is a short gap before the next set of heart sounds. This short period between S2 and the next SI is diastole which signifies the time when the ventricles are filling with blood. As valve closure on the right side occurs slightly later than the Iett side as a result of pressure changes during inspiration, the nurse may distinguish two components for each sound which may be a normal finding termed pbysiological splitting. The nurse may also distinguish a whooshing noise, known as a heart murmur, which denotes abnormal turbulent tlow which may occur if a valve is damaged. When a valve does not close properly, the valve is 'incompetent'. The sound produced is due to blood being refluxed or regurgitated backwards when the chamber contracts. Conversely, if the valve does not open adequately, it is known as sclerosis or stenosis. If the murmur is heard between the two heart sounds (that is, during systole), they are termed systolic murmurs. If, however, they are heard during diastole they are designated as diastolic murmurs. The skill of distinguishing these abnormalities from the normal heart sounds occurs through practice and exposure to patients with conditions. However, correct use of a stethoscope with two heads (a diaphragm and a bell) amplifies appropriate sounds. The chest should be auscultated with the diaphragm of the stethoscope throughout the precordium to detect the high pitched sounds ot SI, S2, pericardial friction rubs and murmurs from aortic and mitral regurgitation (Bickley and Szilaygi, 2003). The bell is used to detect low pitched sounds of a mitral stenosis murmur and further heart sounds termed S3 and S4. The sites tor auscultation are outlined in Figure 3 and murmurs deriving from certain valves are louder in particular areas which are named accordingly. It is worth noting that these areas are not directly above the valves concerned. Tbere are various additional techniques used to accentuate murmurs (Timmis and Mills, 2002; Bickley and Szilaygi, 2003; Epstein et al, 2003).
Figure 3: Cardiac auscultation. The diaphragm of the stethoscope is used throughout the precordium to detect the high pitched sounds and the bell is used to detect low pitched sounds at the apex then mot'ed medially along the lower sternal border. ICS = intercostal space.

\ 2nd ICS Aortic area /

2nd ICS Pulmonic area

'

Left sternal border - - 3 r d , 4th and 5th ICS Tricuspid area

ICS-lntercostal space

Apex Usually in the 5th ICS midclavicular line Mitral area

Further examinations Ideally, all major arteries should be assessed to check whether pulses are present and for bruits and aneurysms. There may be evidence of varicose veins, ulcers or oedema and acute arterial obstruction will classically present as a cold, pulseless, painful limb. Patients with heart failure may have evidence of crackles on lung auscultation and an enlarged spleen or liver. Extra information may be gleaned by assessing tbe retina for changes related to hypertension and DM. Finally, all intormation must be accurately recorded. Not only is this a professional requirement (NMC, 2004) but it provides a record of patient problems, the action taken, a baseline against which improvements or deterioration can be made, and facilitates continuity of care. Conclusions This article has enabled nurses to understand the most common cardiac symptoms experienced and be equipped to enquire into them. In addition, it has addressed vital signs and physical examination. Discussion of some aspects in this article have been introductory, for example, heart sound.s. Furthermore, a comprehensive assessment would also include diagnostic investigations, a fiinctional assessment and an assessment of all body systems. It is envisaged that nurses undertaking advanced roles would seek to further develop their clinical skills through continuing education and experience. uH

Untishjouriul of Nufiiiig, 2l)()6,Vol 15. No 9

507

Beers MH. Herkow K, eds (21)05) Approach to the Cauiuc Patient, in Merck .Manual of Diagnosis and Tlieriipy, Merck & Co., Inc. Available www.nicrck. coni/mrkshared/nimamial/sectionl6/chapteriy7/l97b.jsp (accessed 14 December 2{)U5) Bickley LS, Szilaygi PC! (2(KI3) Bates' Qnide to Phyncal Exaiiiiimlion and History Taking. 8th edn. Lippiiicott Williams and Wilkms, Philadelphia Brashers VL (21)04) Alterations of cardiovascular tlinction. In: Heuther SE, McCance KL eds. Ihidenlnnding piilhophysiohi^ 3rd edti. Mosby, Missouri: 6.19-708 Department of Health (2()0U) .\'aiiotial Scn'ice l-nnncu'orl^ for (A'ro'uny Heart Disease. HMSO, London Doherty B (21)02) Cardiorespir.itory physical assessmriit for the acutely ill: I. Br
EpstL-iii O , Pcrkin ClIX C o o k s o n |, d e B o n o D P (21)03) Clinical Hxaininatioii 3rd e d n . Mosby, LoTidon

Springhonse (2(M)2) Asses.inient made incredibly easy! 2nd edn. Springhousc, Pliiladclphia Timmis A, Milk P (2002) The cardiovascular system. In: Swash M ad. Hutchison's Clinical Methods. 3rd edn.WB Saunders, London: 79-124 United Kingdom C.entral C'onncil for Nnrsiiig ami Midwifery and Health Visiting (1992) 'Die Scope of Ihofessional l^actici: UKtX", Lomitni White M (2002) The cardiovascular system. In: C~ross S. Rimmcr M eds. .\'urie Practitioner: Manual Cyf Clinical Skills. Bailliere Tindall, London: 11636 Wood GC;,Timmis A (20lH) Rapid assessment of chest pain:The rationale is dear, but evidence is needed. Br Med J 323(7313): 5KC-7

Estes MEZ (2002) Healtli Afsessnient and Physical Examinalion. 2nd edn. Dclniar Learmnt;, New York Fallon E, Rnqnes J (l'W7) Acute Chest Pain. AACN Clwical Issues 8(3): 383-97 Foxton J (2()(H) tkimnary heart disease: Risk factor management, i^un Stand 19(13):47-54 Gieadle J (2003) Hi.^tory and F^xamitiation .it .i (Ikitiee. Blackwell Science. Oxford Halton C; Ulackwood K (2(M)3) Leaiire No!e^ On Clinical SkilL 4th udn. Blackwell Science. Oxford Jowi'tt Nl,Thompson D R (2003) Conipn-hcnsiiv coronary eare. 3rd edn. Bailliere Tind.ill, London McArthiir-Rouse F (2001) Critical care outreach services aiid early warnini' scorini; systems: a review of the litcratun.-.J/]rfi' Nurs 36(5): 696-704 Nursing and Midwifery C^ouncil (2004) Tlic NMC Code of Professional Condiid. HMSO. London
N H S M a n a g e m e n t Executive {\^)'>]) Junior Doctors the Nnv Deiii. D e p a r t m e n t

KEY POINTS
I Patient assessment consists of patient history, vital signs, physical examination and diagnostic investigations. I The patient may present with one of several cardiac symptoms and the anaiysis of chest pain is most significant. I Physical examination takes a whole patient approach and is based upon the principles of inspection, palpation, percussion and auscultation. I Undertaking advanced nursing roles is underpinned by the need for continuing education and experience to develop competence.

of Health, London Resusciation Council UK (2000) Advanced Ufi-Support Guidelines. Resuscitation Council UK, London Roper N, Logan W, Tierney A (1980) llie Ulenientf of Niming. t:hnR-hill Liviiii^tone. Oxford Riishforth H,Warner J.Burgc D.Cksper EA (1998) Nursing physical a.ssessment skills: implications for UK practice. RrJ Nurs 7(1()): 965-70 Ryan H, Cadman C, Haiin L (21K)4) Setting standards for assessment of ward patients at risk of detcnorarion. Brf Nurs 13(20): 1186-90

Don't miss an issue.


The best way to ensure you receive every issue of B J N | is to piace an order with your iocai newsagent. Once set up, your copy of B J N wili \ie heid for you to coliect, saving you the time and the frustration of having to search the newsstand. Some newsagents may even offer a home deiivery service making it even easier to obtain your copy. So don't miss an issue, simply complete the form below and take to your local newsagent today.

# #

British journal of Nursing

BIN

Obesity: -^.
leal
IS
of Nurs/n

itual
gious ids imoting ;ep In :ler people lood pressure measurement
TLEDINE COLUMN ' LEGAL *SI>ECrS OF DEATH - MISOMDUCT CTCASE I

NEWSAGENT ORDER FORM:


... Pk-asc rcser\r/deliver* a cop\ nl D J I N nn ,i rcijiil.n- b.isis. ciijimu'ininL^ uitli the iic.\t issue for: Title/Mr/Mrs/Ms:
Address:

First name:

Surname:

Postcode:

Daytime Telephone N o :

British lourmi of NureJng Britlh l l f N ^

BJN

508

i!. 2(10(1. Vol Li. N o ')