#* Clinical Practice Review

The cardiovascular system and its In adults, use both the ausculatory and palpatory methods. Usually the former is slightly higher than the lat- clinical considerations* ter. If the palpatory pressure is greater than the auscultatory pressure then accept this value as the systolic Donald J. Henderson BSc, DC** value. Should there be a difference over a wide range, e.g. 1494 Islington Ave., Islington, Ontario left 180/100/90 and right 120/95/90 then some arterial M9A 3L5 malformation should be suspected till proven otherwise (e.g. , brachial obstruction etc.) Pressure in both arms should be recorded at the beginn- Measurement of Blood Pressure ing and end of an initial examination. Vital Signs include temperature, , respiration, Pressure in the lower extremities can also be measured systemic arterial blood pressure as well as state of con- (using 18 cm cuff vs standard 12 cm cuff). Here the cuff is ciousness, skin colour and pupillary integrity. They may be applied over the lower 1/3 of the thigh and the examiner influenced by physical exertion, emotional tension, infec- auscultates over the popliteal fossa. Normally systolic tions, etc. Blood pressure is estimated by mercury or pressures are higher in the lower-limb (e.g. gravity, more aneroid manometers. The patient is usually seated or direct perfusion from aorta, larger muscle masses produc- supine with arm at heart level, relaxed and slightly flexed. ing increased resistance by arterial compression). This The arm should be supported. Apply the centre of the method should be done on children and young adults with sphygmomanometer cuff over the upper arm. The rubber hypertension to rule out coarctation of the aorta (con- tubing should run along the medial aspect of the arm with genital narrowing) which is characterized by elevated the distal portion of the cuff 2-3 cm. above the systolic pressure in arms and a lower pressure in legs (since antebrachial cubital fossa. While palpating radial pulse in- the brachial artery originates above and the popliteal flate cuff at least 40 mm. Hg. above the point where pulse artery below the stenosed segment of the aorta). is no longer detectable then slowly deflate cuff. The point If systolic pressure is high and diastolic values are low it where the first pulse is felt is a good indicater of the may suggest anemia, hyperthyroidism, aortic regurgita- palpatory systolic pressure (normally about 110-130 mm. tion, or . These readings (e.g. Hg.). For auscultatory pressures, re-inflate cuff above 170/80/75) are common in the elderly due to aortic 30-40 mm. Hg. above the point of radial pulse cessation. atherosclerosis and/or peripheral arteriosclerosis. This Place the bell or diaphragm upon the medial aspect of the high pulse pressure is produced by an increased cardiac antecubital fossa over the brachial artery. There should be output via increased stroke volume. no stethoscope contact with cuff or rubber tubing. The room should be quiet. Upon slow deflation the first sound Pulse Pressure heard will designate the value of systolic blood pressure. Below this the sounds will change in intensity and quality Pulse pressure is obtained by calculating the difference (Korotkov sounds). The point of sudden dullness and muf- between the systolic and diastolic pressure. Normal pulse fling should be noted and the point of cessation recorded. would be 30 or 40 mm Hg. (3:2:1 pressure ratio). Blood pressure by would then be recorded as Increased pulse pressure may suggest atherosclerosis of such 125/80/75 right arm, resting, sitting position. the large and aorta, hyperthyroidism, In auscultatory gap sounds may be detected at a high regurgitation, A-V fistula, vigorous exercise, fever, etc. level (e.g. 190 mm. Hg) only to have them disappear (say Decreased values may be seen in , mitral -170 mm. Hg) and reappear at a lower level (130). In this stenosis, heart failure, and massive . case if the cuff is not inflated high enough an erroneous normotensive (130) systolic pressure may be established when in fact the patient has systolic hypertension (190 mm. Venous Blood Pressure Hg). Venous blood pressure can be measured experimentally by manometer and pressure sensors within a . The nor- mal value is 40-80 mm H20 in large . Clinically it may *Originally presented to the Quebec Association in October, 1976, for be estimated by certain positions of the part under study. licence renewal credit. The veins on the dorsum of the hand in a dependent posi- tion are readily visible. With abduction of an outstretched **Faculty member, Canadian Memorial Chiropractic College, Toronto arm one should note the point at which the veins collapse. The Journal of the CCA / Volume 23 No. 2 / June 1979 61 Cardiovascular system

Normally they collapse at a level horizontal to the area of femoral, dorsalis pedis, posterior tibial, etc. The examiner the manubriosternal junction (atrial level). gently compresses the artery with the middle three fingers. A more reliable estimation would be to observe the The pulse flattens during diastole and is accentuated dur- jugular veins in relation to body position. Increased ing systole. venous distension may suggest right heart failure or car- The pulse should be taken for 1 minute duration noting diac tamponade (constrictive pericarditis). Observing the rate, rhythm, character and consistency of the arterial venous pulse waves may assist in a diagnosis of pulmonary wall. hypertension, complete A-V heart block, tricuspid valve disease, etc. Observation of external and internal (beneath SCM) jugular veins while elevating the torso at the hips to Rate 450 from the horizontal, one should see the most cephalad The rate will vary with age, sex, physical activity and extent of jugular pulse 1-2 cm above the manubrium. (The emotional status. neck should not be flexed and there should be no constric- tive Norms are:Children - 90-120/min. clothing). Tangential lighting assists in better Adults - 60-90/min. (female greater visualization. In marked elevation of venous pressure, the than male) cervical veins may be distended as high as the angle of the Athletes - approximately 50/min. mandible when patient is sitting. These tests employ gravi- ty and positioning to detect elevated venous pressure as Rate may be increased in: () seen in right heart failure. severe anemias Marked venous pressure elevation may co-exist with high fever dilatation of deep or superficial collateral veins. Venous massive hemorrhage pulsation may be evident which reflects coincident ac- cardiac arrhythmias tivities of the right side of the heart (i.e. atrial systole, hyperthyroidism tricuspid valvular closure, and ventricular systole - the congestive heart failure, etc. a,c,v waves). Venous pulsation should not be confused Rate may be decreased in: () with the carotid pulsation. In any event, if venous pressure increased intracranial pressure is increased, signs of peripheral congestion and engorge- obstructive jaundice ment of vessels should be checked suggesting right heart syncope failure. complete heart block, etc.

Normal and Abnormal Blood Pressures Rhythm The normal pressure range is variable and depends on Any alteration of rhythm is first noted by pulse, con- such factors as sex, climate, physical activity, emotional firmed by cardiac auscultation and established by EKG in tension. Obese extremities may cause erroneous high sys- complex arrhythmias. tolic readings since the pressure applied to the cuff must (a) Sinus Arrhythmia over come the resistance of tissue before compressing the This is of not clinical significance and is found in brachial artery. Upper limits of "normal" include: children, young adults and aged. Here the pulse rate will Under 40 - 140/90 increase with inspiration and decrease on expiration. Deep Under 50 - 150/90 respiration will accentuate the alterated rate. Under 60 - 160/90 (b) Premature Contractions (Extrasystoles) A patient should not be labelled "hypertensive" unless Here the patient will explain that their heart has "skip- multiple readings are taken over subsequent visits and ped a beat". Organic disease is not the rule. This is due to these readings are well above normal upper limits con- emotional tension, excess tobacco, alcohol, digitalis toxici- sistently. Low systolic pressures (90-100 mm. Hg) are not ty. The early stimulation of the ventricles occurs to the significant unless suggest pathology. detriment of end-diastolic blood volumes and the systolic Some causes of low blood pressure (hypotension) include pulse wave is barely detected. There may be scattered Addison's disease, acute mycardial infarction, hemor- pauses between periods of regular rhythm. rhage, , etc. Some causes of high blood pressure (c) Bigeminal Pulse (hypertension) include essential hypertension (idiopathic), This means that the beats are coupled or in pairs usually renal disease, phaeochromocytoma, coarctation of aorta, with the second beat weaker in character. This may suiggest neurogenic hypertension, etc. premature contractions as in an over-digitalized patient or a partial heart block where there is a defect in the A-V con- Pulse duction. (d) Trigeminal Pulse Pulse is checked by palpating an artery anywhere near One detects three pulse waves followed by a pause. This the surface where it can be compressed against a firm sur- also suggests premature contractions or partial heart face. Examples are radial, carotid, temporal, popliteal, block. 62 The Journal of the CCA / Volume 23 No. 2 / June 1979 Cardiovascular system

(e) Paroxysmal Atrial Tachycardia (PAT) shaped summit and a gradual down stroke quality is ap- Here the paroxysm of a regular rhythm but a rate of preciated. The heart may be ausculated while the carotid 150-220 beats/min. is noted at rest. Pressure over the pulse is palpated. carotid sinus ceases the tachycardia by the presso-receptor reflex. Pulse Types (f) Paroxysmal Ventricular Tachycardia (a) Pulsus Magnus This is a serious arrhythmia associated with signs and This is a strong bounding pulse with a rapid ascending symptoms of dizziness, weakness, dyspnea, precordial limb and equal rapid descending limb. The peak is sharp pain, pulse rate at 150-160 beats/min. with an irregular and brief. Normally associated with a wide pulse pressure, rhythm. There is no change with carotid sinus massage and an increased stroke volume, and decreased peripheral an EKG is required to confirm this problem. resistance. It is seen in anxiety, fever, exercise. Abnor- (g) Atrial Fibrillation malities associated with pulsus magnus include aortic Here a grossly irregular rhythm is noted (pulsus ir- regurgitation, hyperthyroidism, severe anemia, arterio- regularis perpetuus). The extreme irregularity of the pulse venous fistula and systolic hypertension. is matched by the extreme irregularity of the heart action. (b) Pulsus Parvus There is little regularity as to rhythm, rate or volume of the This is a small weak pulse with a delayed systolic peak. It pulse. When comparing the radial pulse to the of occurs in the presence of a narrowed pulse pressure (in- the heart a disparity of about 5-30 beats/min. is evident. creased in peripheral resistance, and decreased stroke This is called a pulse deficit. Since many of the ventricular volume). Causes of such a pulse include aortic stenosis, beats are so weak, although they may be heard at the apex, mitral stenosis, left ventricular failure secondary to an in- the pulse fails to come through at the wrist. This farct and constrictive pericarditis. phenomenon may be seen in other arrhythmias, e.g. (c) Pulsus Alternans premature contractions. Atrial fibrillation occurs often as This is a condition in which the pulse waves during a complication of mitral stenosis, arteriosclerotic heart regular rhythm are alternately strong and weak. This pulse disease, hyperthyroidism, and other conditions. type is due to an alternating contractile force of the left (h) Atrial Flutter ventricle. Pulsus alternans is virtually diagnostic of left This arrhythmia is characterized by a rapid regular pulse ventricular failure and is commonly associated with a ven- rate of about 140-160 beats/min. Here the atrial contrac- tricular (S3) diastolic . It may also be seen in tions occur at about 260-300/min., all the impulses of severe arterial hypertension and coronary artery disease. It which do not activate the ventricles. The neck veins reveal is detected more readily if the patient is standing or sitting. flutter waves occurring at a faster rate than that of the car- It can be assessed more accurately by sphygmomanometry diac apex which differentiates PAT since here the ratio is where only the strong beats are heard just below the 1:1. systolic value. As the cuff is slowly deflated the weaker (i) Heart Block beats are heard as well between the stronger beats giving an Heart Block occurs at the AV node where the pro- apparent doubled rate. Pulsus alternans should be dif- pagated impulse is in some way altered or impeded. There ferentiated from bigeminy produced by premature are three types: systoles. The former gives an equal regular rhythm bet- i) First degree partial block - pulse may be slowed and a ween strong and weak bests, the latter is variable both in decreased intensity of the first heart sound is noted at rhythm and volume with strong normal beats after pauses. the apex. (d) Pulsus Bisferiens ii) Second degree A-V block (Wenckebach) - bigemeny This is a "double-beating" pulse characterized by two may result. An alteration in A-V conduction may impulses occurring during systole. The initial upstroke of result in only every second, third or fourth atrial im- the pulse rises rapidly and is called the "percussion wave". pulse conducted to the ventricle (e.g. 2:1 Block - atrial A small dip intervenes and a second slow upstroke or rate 80, vent. rate 40 and 3:1 Block - atrial rate 120, "tidal" wave is detected. This occurs commonly in com- ventricular rate 40). bined aortic regurgitation and stenosis, aortic regurgita- iii) Third degree (cbmplete) block - no correlation between tion and in functional hypertrophic subaortic stenosis. atrial and ventricular rates. Pulse is very low, i.e. less (e) than 40/min. The heart rate is fixed and regular. This is characterized by a decrease in amplitude (or an Jugular Cannon 'a' waves are noted at jugular veins. imperceptibility of pulse) during inspiration. This is nor- Ventricular cells initiate their own impulse. mally present during forced inspiration but pathological during quiet respiration. During inspiration there is a decrease in venous return with resultant decrease in cardiac output. This increases venous pressure (Kussmaul's sign). The Quality and Character ofPulse Waves This can be determined by sphygmomanometry. There will This depends on the rate of any change noted and the be a normal drop of about 5-10 mm Hg of peak systolic magnitude of the pulse pressure. It is best evaluated at the pressure during inspiration. Should this drop exceed 10 carotid pulse where a brisk upstroke, a smooth dome mm Hg upon inspiration with a disapperance of radial The Journal of the CCA / Volume 23 No. 2 / June 1979 63 Cardiovascular system

pulse then the pulse is paradoxical and suggests pathology. This occurs in massive pericardial effusion, constrictive pericarditis, mediastinal tumors, severe pulmonary em- The art of auscultation involves silence, concentration physema, and heart failure. and knowledge. The examiner must concentrate on each sound at each valve area as he inches the bell or diaphragm (f) Anacrotic Pulse about the precordium. The intervals between each sound This is characterized by a small peak in the ascending should be noted as a sense of timing between beats is systolic wave and is generally of little clinical significance. developed. Two sounds are commonly heard. SI is syn- It is not palpable. The pulse wave pattern may be the result chronous with the apical impulse and corresponds to the of aortic stenosis. onset of ventricular systole. Acoustically the SI "lubb" is (g) Dicrotic Pulse represented by the mitral and tricupid valve closure. Nor- A second small peak in the ascending limb of the wave mally the coincident aortic and pulmonic valve opening is during early diastole is termed dicrotic pulse. It may be silent. S2 occurs at the termination of systole and cor- palpated in fevers as a small wave immediately following responds to the onset of ventricular diastole. Acoustically the pulse wave. It is most marked when the pulse pressure the S2 "dupp" is represented by closure of the aortic and is low. Too much palpatory pressure will obliterate it. It pulmonic valves and is coincident with A-V valvular open- may be present in mild to moderate aortic regurgitation. ing. The diastolic pause between S2 and the next SI is The pulse in general may be described in the following longer than the systolic interval between SI and S2. In terms: tachycardia it may be difficult to distinguish the sounds; i) Rate - pulsus frequens or rarus (rapid or slow) however, the sound coincident with carotid pulsation ii) Size - pulsus magnus or parvus Qarge or small) represents S1. iii) Type of wave - pulsus celer or tardus (quick or pro- Some topics have been discussed briefly and supplemen- longed) tal reading and practice must certainly follow. In any car- iv) Rhythm - pulsus regularis or irregularis (regular or ir- diovascular evaluation, full investigation would have to regular) supported by funduscopy, auscultation for and mur- v) Tension - pulsus durus or mollis (hard or soft) murs. Other special tests include EKG and elec- trophonocardiograph analysis, chest films, angiography and special lab tests. Of paramount importance, however, is a good case history and a complete physical examina- tion. Consistency ofthe Arterial Wall General The vessel wall may feel hard and irregular on light Bibliography palpation (pipe stem or goose neck artery). This may be 1. Bates B: A Guide to Physical Examination. JB Lippincott Co, palpated in marked arteriosclerosis. This may also be Toronto, 1974, pp 99-143 palpated by expressing blood from the distal segment of 2. Delph MH, Manning RT: Major's Physical Diagnosis. Eighth edi- the radial artery while occluding the proximal end by tion. WB Saunders Co, Toronto, 1975, pp 384-420 3. Hochstein E, Rubin AL: Physical Diagnosis. McGraw-Hill Book digital pressure, then palpate for arterial thickening. In Co, Toronto, 1964, pp 166-189, 248-280 youth the vessel is soft, pliable and barely palpable but 4. Parkins RA, Pegrum GD: The Basis of Clinical Diagnosis. Pitman with advancing years becomes thickened, rigid, and tor- Medical, Toronto, 1974, pp 85-125 tuous. The brachial and temporal arteries should be check- 5. Prior JA, Silberstein JS: Physical Diagnosis - The History and Ex- ed as well. Rarely a pulsatile nodule due amination of the Patient. Third edition. The CV Mosby Co, St. to a Louis, 1969, pp 211-267 microaneurysm may be palpated. This may be detected in 6. Rubenstein D. Wayne D: Lecture Notes on Clinical Medicine. JB polyarteritis nodosa or temporal (cranial) arteritis. Lippincott Co, Toronto, 1976, pp 45-66

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