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Home , Blood pressure, Fourth heart sound, Heart sounds, Hypovolemia, Korotkoff sounds, Pulse pressure

14 , Tones, and Diagnoses

GEORGE BOJANOVf MD

CONTENTS

BLOOD PRESSURE HEART TONES SUMMARY SOURCES

1. In 1916, French physician Rene Laennec invented the first Fundamental to providing comprehensive care to patients is , which was constructed from stacked paper rolled the ability to obtain an accurate and carefully into a solid cylinder. Prior to his invention, physicians around perform and interpret a . The optimal the world would place one of their ears directly on the patient's selection of further tests, treatments, and use of subspecialists chest to hear heart or sounds. After Dr. Laennec's initial depends on well-developed skills for taking patient history and success, several new models were produced, primarily of wood. a physical diagnosis. An important part of a normal physical His stethoscope was called a"monaural stethoscope." The "bin- examination is obtaining a blood pressure reading and auscul- aural stethoscope" was invented in 1829 by a physician named tation of the heart tones, which both represent critical corner- Camman in Dublin and later gained wide acceptance; in the stones in evaluating a patient's hemodynamic status and 1960s, the Camman stethoscope was considered the standard diagnosing and understanding physiological and anatomical for superior . pathology. It is essential that care professionals and bioengi- Naive ideas about circulation and blood pressure date as far neers understand how these important diagnostic parameters back as ancient Greece. It took until the 18th century for the are obtained, their sensitivities, and how best to interpret them. first official report to describe an attempt to measure blood pressure, when published a monograph on 1.1. Physiology of Blood Pressure "haemastatics" in 1733. He conducted a series of experiments Blood pressure is the force applied on the arterial walls as the involving cannulation of in horses and invasive direct heart pumps blood through the . The rhyth- blood ; unfortunately, his method was mic contractions of the left result in cyclic changes in not applicable for humans at that time. There were many sub- the blood pressure. During ventricular , the heart pumps sequent contributions to the art of measuring and understand- blood into the circulatory system, and the pressure within the ing blood pressure during the next two centuries. One of the arteries reaches its highest level; this is called systolic blood greatest of these was described in a publication in Gazetta pressure. During , the pressure within the arterial sys- medica di Torino called "A New " by Dr. tem falls and is called diastolic blood pressure. Riva-Rocci in 1896; it is recognized as the single most impor- The mean of the systolic and diastolic blood during tant advancement in practical noninvasive methods for blood the represents the time-weighted average arterial pressure estimation in humans. pressure; this is called mean arterial blood pressure. Alternat- ing systolic and diastolic pressures create outward and inward movements of the arterial walls, perceived as arterial pulsation From: Handbook of Cardiac Anatomy, Physiology, and Devices Edited by: P. A. Iaizzo © Humana Press Inc., Totowa, NJ or arterial . is the difference between sys- tolic and diastolic blood pressures. 181 182 PART II1: PHYSIOLOGY AND ASSESSMENT / BOJANOV

Blood pressure is measured in units called millimeters of able bladder is applied to the and inflated until the arterial (mmHg). A "normal" systolic blood pressure is less pulse felt distal to the cuff placement disappears. Then, the than 140 mmHg; a"normal" diastolic blood pressure is less than pressure in the cuff is released at a speed of approx 3 mmHg per 90 mmHg. Blood pressure higher than normal is called hyper- heartbeat until the arterial pulse is felt again. The pressure at tension, and one lower than normal is called . which the arterial pulsations start is the systolic blood pressure. Hence, normal is between 60 and 90 Diastolic blood pressure and mean arterial pressure cannot be mmHg. Mean arterial pressure is normally considered a good readily estimated using this method. Furthermore, the mea- indicator of tissue and can be measured directly using sured systolic blood pressure using the method is automated blood pressure cuffs or calculated using the follow- often an underestimation of the true arterial systolic blood pres- ing formulas: sure because of the insensitivity of the sense of touch and the MAP = DBP + PP/3 or MAP = [SBP + (2 x DBP)]/3 delay between blood flow below the cuff and the appearance of where PP = SBP - DBP; MAP is mean arterial pressure, DBP arterial pulsations distal to the cuff. is diastolic blood pressure, PP is pulse pressure, and SBP is 1.2.1.2. Doppler Method systolic blood pressure. The Doppler method is a modification of the palpation Blood flow throughout the circulatory system is directed by method and uses a sensor (Doppler probe) to determine blood pressure gradients. By the time blood reaches the right , flow distal to the blood pressure cuff. The Doppler effect is the which represents the end point of the venous system, pressure shift of the frequency of a sound wave when a transmitted sound has decreased to approx 0 mmHg. The two major determinants wave is reflected from a moving object. When a sound wave of blood pressure are: (1) , which is the volume shifts (e.g., as caused by blood movement in an ), it is of blood pumped by the heart per minute; and (2) systemic detected by a monitor as a specific swishing sound. The pres- , which is the impediment offered by the sure of the cuff, at which blood flow is detected by the Doppler vascular bed to flow. Systemic vascular resistance is controlled probe, is the arterial systolic blood pressure. by many factors, including vasomotor tone in , termi- This method is more accurate (less subjective) in estimating nal arterioles, or precapillary sphincters. Blood pressure can be systolic blood pressure compared to the palpation method. It calculated using the formula has also been quite a useful method in detecting systolic blood BP = CO x SVR pressure in patients who are in , have low-flow states, are where BP is blood pressure, CO is cardiac output, and SVR is obese, or are pediatric patients. Disadvantages of the Doppler systemic vascular resistance. method include: (1) inability to detect diastolic blood pressure; Blood pressure decreases by 3-5 mmHg in arteries that are (2) necessity for sound-conducting gel between the skin and the 3 mm in diameter. It is approx 85 mmHg in arterioles, which probe (because air is a poor conductor of ultrasound); (3) like- accounts for approx 50% of the resistance of the entire systemic lihood of a poor signal if the probe is not applied directly over circulation. Blood pressure is further reduced to around 30 an artery; and (4) potential for motion and electrocautery unit mmHg at the point of entry into and then becomes artifacts. approx 10 mmHg at the venous end of the capillaries. 1.2.1.3. Auscultation (Riva-Rocci Method) The speed of the advancing pressure wave during each car- The auscultation method uses a blood pressure cuff placed diac cycle far exceeds the actual blood flow velocity. In the around an extremity (usually an upper extremity) and a stetho- , the pressure wave speed may be 15 times faster than the scope placed above a major artery just distal to the blood pres- flow of blood. In an end artery, the pressure wave velocity may sure cuff (e.g., the if using the cuff on the upper be as much as 100 times the speed of the forward blood flow. extremity). Inflation of the blood pressure cuff above the sys- As the pressure wave moves peripherally through the arterial tolic blood pressure flattens the artery and stops blood flow system, wave reflection distorts the pressure waveform, caus- distal to the cuff. As the pressure in the cuff is released, the ing an exaggeration of systolic and pulse pressures. This artery becomes only partially compressed, which creates con- enhancement of the pulse pressure in the periphery causes the ditions for turbulent blood flow within the artery and produces systolic blood pressure in the to be 20-30% higher the so-called , named after the individual who than the aortic systolic blood pressure and the diastolic blood first described them. Korotkoff sounds are caused by the vibra- pressure to be approx 10-15% lower than the aortic diastolic tions created when blood flow in partially flattened arteries blood pressure. Nevertheless, the mean blood pressure in the transforms from laminar into turbulent, and they persist as long radial artery will closely correspond to the aortic mean blood as there is an increased turbulent flow within a vessel. Systolic pressure. blood pressures are determined as the pressures of the inflated 1.2. Methods of Measuring Blood Pressure cuffs at which Korotkoff sounds are first detected. Diastolic Arterial blood pressure can be measured both noninvasively blood pressures are determined as the cuff pressure at which and invasively; these methods are described next. Korotkoff sounds become muffled or disappear. Sometimes, in patients with chronic , there is an 1.2.1. Noninvasive Methods "" that represents disappearance of the normal 1.2.1.1. Palpation Korotkoff sounds in a wide pressure range between the systolic Palpation is a relatively simple and easy way to assess sys- and the diastolic blood pressures. This condition will lead to tolic blood pressure. A blood pressure cuff containing an inflat- inaccurately low blood pressure assessments. Korotkoff sounds CHAPTER 14 / BLOOD PRESSURE, HEART TONES, AND DIAGNOSES 183 can also be difficult to detect in patients who are in low-flow rapidly adjust the cuff pressure, which can be displayed as a states or in those with marked peripheral . The beat-to-beat tracing. Thus, in healthy patients, the blood pres- use of microphones and electronic amplification of such signals sure measured on the finger will correspond to the aortic blood can greatly increase the sensitivity of this method. Yet, consid- pressure; this will not be true for patients with low peripheral erations for systematic errors include motion artifact and elec- perfusion, like those with peripheral artery disease, hypother- trocautery interference. mia or low-flow states. 1.2.1.4. Oscillometry 1.2.1.7. Arterial Tonometry Oscillometry is defined as the blood pressure measurement Tonometry devices can determine beat-to-beat arterial blood method that uses automated blood pressure cuffs. Arterial pul- pressures by adjusting the pressure required to partially flatten sations cause oscillations in the cuff pressure. These oscilla- a superficial artery located between a tonometer and a bony tions are at their maximum when the cuff pressure equals the surface (e.g., radial artery). These devices commonly consist of mean arterial pressure and decrease significantly when the cuff an electronic unit and a pressure-sensing head. The pressure- pressures are above the systolic blood pressure or below the sensing head includes an air chamber with adjustable air pres- diastolic blood pressure. Advantages of this approach are the sure and an array of independent pressure sensors that, when ease and reliability of use. Some of the potential technical prob- placed directly over the artery, assess intraluminal arterial pres- lems include motion artifacts, electrocautery unit interference, sures. The resultant pressure record resembles an invasive arte- and inability to measure accurate blood pressure when patients rial blood pressure waveform. Limitations to these methods elicit arrhythmias. include motion artifacts and the need for frequent calibrations. 1.2.1.5. Blood Pressure Cuff Pressure 1.2.2. Invasive Methods of Blood Pressure Measurement When using blood pressure cuffs for such measurements, it 1.2.2.1. Indications is important to select them in accordance with the patient's Indications for the use of direct blood pressure size. Blood pressure cuffs for adult and pediatric patients come (arterial cannulation) include hemodynamic instability, intra- in variable sizes. An appropriate size means that the cuff's operative monitoring in selected patients, and use of vasoactive bladder length is at least 80% and the cuff width is at least 40% drugs like , epinephrine, , and the like. of the arm circumference. If the cuff is too small, it will take 1.2.2.2. Cannulation Sites more pressure to occlude arterial blood flow completely, and the resultant measured pressures will be falsely elevated. If The arteries most often selected for cannulation are the the cuff is too large, however, the pressure inside the cuff radial, ulnar, brachial, femoral, dorsalis pedis, or axillary. Can- needed for complete occlusion of the arterial blood flow will nulation of an artery should be avoided if there is: (1) docu- be less, and the measured pressures will be falsely low. mented lack of collateral circulation, (2) a skin infection on Blood pressure is most commonly taken while the patient is the site of cannulation, and/or (3) a preexisting vascular defi- seated with the arm resting on a table and slightly bent, which ciency (e.g., Raynaud's disease). The radial artery is the most positions the arm at the same level as the patient's heart. This often selected artery for invasive blood pressure monitoring same principle should be applied if the patient is in a supine because of its easily accessed superficial location and good collateral flow to the region it supplies. position; the blood pressure cuff should be level with the heart. If the location of the blood pressure cuff during blood pressure 1.2.2.3. Techniques measurements is above or below the patient's heart level, reg- The two frequently utilized techniques for arterial cannula- istered blood pressure will be either lower or higher than the tion are: (1) a over a needle or (2) Seldinger's tech- patient's actual blood pressure. This difference can be repre- nique. When using the first technique, the operator enters the sented as the height of a column of water interposed between the with a needle that has a catheter placed over it. blood pressure cuff and the heart levels. To convert centimeters After free blood flow is documented through the needle, the of water (cmH20) to millimeters of mercury, the measured catheter is advanced over the needle into the artery, and the height of the water column should be multiplied by a conversion needle is withdrawn. The catheter is then connected to the pres- factor of 0.74 (1 cmH20 = 0.74 mmHg). sure-transducing system. When using Seldinger's technique, All of the aforementioned methods for assessing blood pres- the operator first enters the artery with a needle. After free sure do so indirectly by registering blood flow below the blood blood flow is confirmed through the free end of the needle, the pressure cuff. Other noninvasive methods include plethysmog- operator places a wire through the needle into the blood vessel raphy and arterial tonometry. and withdraws the needle. Then, a plastic catheter is advanced 1.2.1.6. Plethysmography into the artery over the steel wire, the wire is removed, and the catheter is connected to a transducer system. Both methods The plethysmographic method for blood pressure measure- require sterile techniques and skilled operators. ment uses the fact that arterial pulsations cause a transient increase in the of an extremity and thus in the 1.2.2.4. Considerations volume of the whole extremity. A finger plethysmograph Arterial cannulation provides beat-to-beat numerical infor- determines the minimum pressures needed by a finger cuff to mation and tracing waveforms of arterial blood pressures and is maintain constant finger blood volume. A light-emitting diode considered a gold standard in blood pressure monitoring. Inva- and a photoelectric cell detect changes in the finger volume and sive arterial pressure monitoring systems or kits commonly 184 PART II1: PHYSIOLOGY AND ASSESSMENT / BOJANOV include a catheter (20-gauge catheter for adults), tubing, a trans- When connected to the patient, such monitoring systems ducer, and an electronic monitor for signal amplification, filter- provide digital readings of systolic, diastolic, and mean blood ing, and analysis. Such pressure transducers are usually based pressures and, commonly, pressure waveforms. Watching the on the strain gauge principle: Stretching a wire of silicone crys- trend of the waveform and its shape can provide other important tal changes its electrical resistance. The catheter, the connective information as well. More specifically, the top of the waveform tubing, and the transducer are filled with . A pressure bag represents the systolic pressure, and the bottom is the diastolic provides a continuous saline flush of the system at a rate of blood pressure. The dicrotic notch is caused by the closure of 3-5 mL]h. The system should also allow for intermittent flush the and the backsplash of blood against the closed boluses as needed. valve. The rate of the upstroke of the arterial blood pressure The quality of the information gathered depends on the wave depends on the ; the rate of the dynamic characteristics of the whole system. The complex downstroke is affected by the systemic vascular resistance. waveform obtained from the arterial pulse can be expressed as Exaggerated variation in the size of the waves with respiration a summation of simple sine and cosine waves using a method suggests . Integrating the areas under the wave- called "Fourier analysis." Most invasive blood pressure moni- forms can be used for calculations of the values of the mean toring systems have natural frequencies of approx 16-24 Hz, arterial pressures. See also Chapter 16 for more details on pres- which must exceed the frequency of the arterial pulse waveform sure waveforms. to reproduce it correctly. This natural frequency is described as 1.2.2.5. Complications the frequency at which the system oscillates when disturbed. Potential complications associated with arterial cannulation Another property of the catheter-tubing-transducer system is include , hematoma, infection, , ischemia the "dumping coefficient." The dumping coefficient character- distal to the cannulation site, vasospasm, embolization with air izes how quickly oscillations in the system will decay. bubbles or thrombi, nerve damage, , , Both the natural frequency and the dumping coefficient are and inadvertent intraarterial drug injection. primarily determined by the length, size, and compliance of the catheter and tubing and by presence of air bubbles or cloths 1.3. Diagnoses trapped in the fluid column. This chapter does not go into 1.3.1. details of how to determine and change the system character- Inspiration can decrease arterial pressure by more than istics. Briefly, "underdumping" the system will exaggerate 10 mmHg; the inspiratory venous pressure stays relatively artifacts like a "catheter whip" and can result in a significant unchanged. Normally, the arterial and venous blood pressures overestimation of the systolic blood pressure. "Overdumping" fluctuate throughout the respiratory cycle, decreasing with will blunt the response of the system and lead to an underes- inspiration and rising with expiration. This fluctuation in the timation of the systolic blood pressure. In addition, systems blood pressure under normal conditions is less than 10 mmHg. with low natural frequencies will show amplifications of the Inspiration increases venous return, therefore increasing the pressure curves, causing overestimation of the systolic blood right heart output transiently, according to the Frank-Starling pressures. Diastolic blood pressures will also be affected by law. As the blood is sequestered in the altering the above factors, but to a lesser degree. Note that during inspiration, the left heart output is reduced transiently, system response characteristics can be optimized by using accounting for the normal lower systolic pressure during short and low-compliance tubing and by avoiding air trapping this phase. The right ventricle contracts more vigorously and when the system is flushed. mechanically bulges the toward the When an invasive blood pressure system is connected to a left ventricle, reducing its size and accounting for the lower patient, it should be zero referenced and calibrated. Zero refer- systolic blood pressure. encing is performed by placing the transducer at the level of the Certain conditions drastically reduce the transmural or dis- midaxillary line, which corresponds to the level of the patient's tending (filling) pressure of the heart and interfere with the heart. The system is opened to air and closed to the patient, and diastolic filling of the two ventricles. In such cases, there is an then the transducing system is adjusted to a 0 mmHg baseline. exaggeration of the inspiratory fall in the systolic blood pres- For this, it is not necessary for the transducer to be at the level sure, which results from reduced left ventricular volume of the midaxillary line as long as the stopcock, which is opened and the transmission of negative intrathoracic pressure to the aorta. Common causes for such reductions include pericardial to air during the zero reference, is at that level. The system is effusion, adhesive , , pulmonary then opened to the patient and ready for use. emphysema, severe , paramediastinal effusion, endocar- System calibrations are separate procedures and involve dial fibrosis, myocardial amyloidosis, scleroderma, mitral connecting the invasive blood pressure systems to mercury with right , tricuspid stenosis, hypov- manometers, closing the systems to the patient, and pressuriz- olemia, and/or pulmonary . Associated clinical signs ing the systems to specified pressures. Then, the gains of the include a palpable decrease in pulse with inspiration and monitor amplifiers are adjusted until displayed pressures equal decrease in the inspiratory systolic blood pressure more than 10 the pressures in the mercury manometers. Recommendations mmHg compared to the expiratory pressure. are to perform zero referencing at least every clinical shift and calibration at least once daily. It should be noted that some of 1.3.2. Pulsus Alternans the more contemporary transducer designs rarely require exter- An alternating weak and strong peripheral pulse is usually nal calibration. caused by alternating weak and strong heart contractions. It CHAPTER 14 / BLOOD PRESSURE, HEARTTONES, AND DIAGNOSES 185 may be found in patients with severe heart failure, various de- 1.3.8. Dicrotic Pulse grees of , or arrhythmias. Pulsus alternans is charac- Not to be confused with a bisferiens pulse, in which both terized by a regular rhythm and must be distinguished from peaks occur in systole, the dicrotic pulse is characterized by a , which is usually irregular. second peak that is in diastole immediately after the second 1.3.3. Bigeminal Pulse heart sound. The normally small wave that follows aortic valve closure (dicrotic notch) is exaggerated and measures more than A bigeminal pulse is caused by occurrences of premature 50% of the pulse pressure on direct pressure recordings. It usu- contractions (usually ventricular) after every other beat, which ally occurs in conditions such as cardiac tamponade, severe results in alternation in the strength of the pulse. Bigeminal heart failure, and , in which a low stroke pulse can often be confused with pulsus alternans. However, in volume is ejected into a soft elastic aorta. Rarely, a dicrotic contrast to the latter, in which the rhythm is regular, in pulsus pulse is noted in healthy adolescents or young adults. bigeminus the weak beat always follows a shorter pulse inter- val. 2. HEART TONES 1.3.4. Pulse Deficit 2.1. Physiology and Normal Pulse deficit is the inability to detect arterial pulsations Heart tones are caused primarily by vibrations created by when the heart beats, as can be observed in patients with atrial pressure differentials during closure of the heart valves. Nor- fibrillation, in states of shock, or with premature ventricular mal opening of the heart valves is a relatively slow process and complexes and the like. The easiest way to detect pulse deficit makes no audible sounds. The heart tones are relatively brief is to place a finger over the radial artery while monitoring the and characterized by varying intensity (loudness), frequency QRS complexes on an electrocardiogram monitor. A QRS (pitch), and quality (timbre). To understand heart tones better, complex without a detected corresponding pulse represents a it is necessary to review briefly the physiology of cardiac pulse deficit. In the presence of atrioventricular dissociation, events. The electric impulse for cardiac contraction starts from when atrial activity is irregularly transmitted to the ventricles, the sinus node, located in the right atrium, thus causing the right the strength of the peripheral arterial pulse depends on the atrium to contract first. Contraction of the ventricles--the left timing of the atrial and ventricular contractions. In a patient is slightly more rapid--results in closure before with rapid heartbeats, the presence of such variations suggests closure of the . Ejection, on the other hand, starts ventricular ; with an equally rapid rate, an absence in the right ventricle because the right ventricular ejection nor- of variation of pulse strength suggests a supraventricular mally occurs at a much lower pressure than the left ventricular mechanism. ejection. Ejection ends first in the left ventricle, causing the aortic valve to close slightly before the pulmonic valve. 1.3.5. Wide Pulse Pressure The first heart sound (S 1) arises from closure of the mitral Wide pulse pressure, or as it is often called "water hammer valve (M 1), followed by closure of the tricuspid valve (T 1). The pulse," is observed in cases of severe aortic regurgitation and initial component of the first heart sound (M1) is most promi- consists of an abrupt upstroke ( wave) followed by nent at the cardiac apex. The second component (T 1), if present, rapid collapse later in systole with no dicrotic notch. normally presents at the left lower sternal border; it is less com- 1.3.6. Pulsus Parvus et Tardus monly heard at the apex and is seldom heard at the base. When The phenomenon of pulsus parvus et tardus is observed in the first heart sound is dramatically split, like in Ebstein's cases of and is caused by reductions in stroke anomaly of the tricuspid valve (associated with delayed right volumes and prolonged ejection phases, which produce reduc- ventricular activation), its first component is normally louder. tions and delays in the volume increments inside . As mentioned, the intensity of the sound will increase with "Tardus" refers to delayed or prolonged early systolic accelera- increases of the pressure gradients across a particular valve. tions; "parvus" refers to diminished amplitudes and rounding of With increases in the pressure gradients, the blood velocities the systolic peaks. and the resultant forces for valve closure will increase, causing loud and easily detectable sounds. Another factor that affects 1.3.7. Bisferiens Pulse the intensity of the sound produced by an atrioventricular valve A bisferiens pulse is characterized by two systolic peaks-- is the valvular position at the onset of systole. When ventricu- the percussion and tidal waves--separated by a distinct lar contraction occurs against a wide-open valve, the leaflets midsystolic dip; the peaks are often equal, or one may be larger. will achieve higher velocity and thus a louder heart sound It occurs in conditions in which a large is ejected compared to a valve with partially closed leaflets at the begin- rapidly from the left ventricle and is observed most commonly ning of systole. in patients with pure aortic regurgitation or with a combina- The second heart sound ($2) is caused by closure of the tion of aortic regurgitation and stenosis. A bisferiens pulse aortic and the pulmonic valves, normally with a first component also occurs in patients with hypertrophic obstructive cardi- caused by the aortic valve closure (A2), followed by the pul- omyopathy. In these patients, the initial prominent percussion monic valve closure (P2). wave is associated with rapid ejection of blood into the aorta The physiological third heart sound ($3) (Fig. 1) occurs during early systole, followed by a rapid decline as obstruc- shortly after A2, and is a low-pitched vibration caused by the tion becomes prominent in midsystole and by a tidal wave. rapid ventricular filling during diastole. $3 can commonly be Very rarely does it occur in individuals with a normal heart. heard in children, adolescents, and young adults. When detect- 186 PART IIh PHYSIOLOGY AND ASSESSMENT/BOJANOV

Systole Diastole S1 P2 J Pulmo~rc Area $3 i Fig. 1. Normal heart physiology introducing the third heart sound (see text for details). S 1, first heart sound; $3, third heart sound; A2, aortic valve closure; P2, pulmonic valve closure.

Systole Diastole $1 A2 P2 S4 /! _h Tri, spidArea Mitral Area Fig. 2. Normal heart physiology introducing the (see text for details). S 1, first heart sound; $4, fourth heart sound; A2, Fig. 3. Auscultatory areas, including the aortic, pulmonic, mitral, and aortic valve closure; P2, pulmonic valve closure. tricuspid auscultation areas.

able after the age of 30 years, $3 is considered "ventricular between $2 and S 1 than between S 1 and $2 because systole is gallop" and is a sign of possible pathology; in most such cases, shorter than diastole. S 1 is also of longer duration and lower there is diastolic dysfunction associated with ventricular fail- pitch, and $2 is of shorter duration and higher pitch. S 1 is best ure. Yet the third heart sounds sometimes persist beyond age 40 heard at the heart apex, and $2 is best auscultated over the years, especially in women. aortic and pulmonic areas. The physiological fourth heart sound ($4) (Fig. 2) is a soft, Although the normal heart sounds represent normally occur- low-pitched noise heard in late diastole, just before S1. $4 is ring phenomena in a normal heart, cardiac pathology can change generated by rapid ventricular filling during atrial systole, the intensity or the time occurrence of the sounds and even which causes vibrations of the left ventricular wall and the create new ones, often called murmurs (e.g., because of valvu- mitral apparatus. Normally, $4 is heard in infants, small chil- lar or congenital anomalies). dren, and adults over 50 years of age. A loud $4, especially 2.3. Abnormal Heart Sounds associated with shock, is a pathological sign and is referred to as an $4 gallop. Conditions that can accentuate S1 include mitral stenosis (most often), left-to-right shunts, hyperkinetic circulatory states, 2.2. Auscultatory Areas accelerated atrioventricular conduction, and tricuspid stenosis. The heart sounds generated by the various valves are best Diminished S 1 can be caused by mitral and tricuspid stenosis, heard over so-called auscultatory areas, which bear the valve moderate or severe aortic regurgitation, slow atrioventricular names, but do not specifically correspond to the anatomical conduction, or hypocontractility states. A diminished S 1 can locations of the valves. also be caused by thick chest walls, such as in individuals with The aortic auscultation area is located in the second inter- excessively developed body musculature or in patients with costal space at the right sternal border (Fig. 3). The pulmonic emphysema. auscultation area is located in the second intercostal space at A variability in the S1 sound can be observed in states caus- the left sternal border. The mitral auscultation area is found ing variation in the velocity of the atrioventricular valve clo- at the heart's apex, which is in the fifth intercostal space, left sures, such as , atrioventricular block, from the sternum. This area is also called a left ventricular or ventricular pacemakers, , and so on. An accen- apical area. The tricuspid auscultation area is located at the tuatedS2 is present in: (1) diastolic or , (2) left lower sternal border. For patients with a left thoracic heart aortic coarctation, (3) aortic dilation, (4) of the position (normal situs), auscultation should begin at the aorta, and (5) ; it is characterized by a cardiac apex and continue with the left lower sternal border loud pulmonary component of the second heart sound. A dimin- (inflow), proceeding interspace after interspace up the left ished $2 is detected most often with aortic valvular stenosis, sternal border to the left base and then to the right base (out- pulmonic stenosis, and pulmonary emphysema. flow). This type of examination permits the clinician to think Splitting of $2 can be normal during inspiration. When con- physiologically, following the inflow-outflow direction of the sidered abnormal, it is associated with: (1) delayed activation blood flow. of the right ventricle; (2) prolonged right ventricular ejection To distinguish between the first and the second heart sounds time relative to left ventricular ejection time (like in pulmonic easily, it should be pointed out that there is a longer pause stenosis, mitral regurgitation, ventricular septal defect); or CHAPTER 14/BLOOD PRESSURE, HEART TONES, AND DIAGNOSES 187

(3) increased impedance of the pulmonary vasculature (as in 2.4. Dynamic Auscultation massive or pulmonary hypertension). The term dynamic auscultation refers to the technique of Persistent splitting of the $2 refers to cases in which the aortic adjusting circulatory dynamics by means of respiration or and pulmonic components of the second heart sound remain various other physiological or pharmacological maneuvers to audible during both inspiration and exhalation. Persistent determine their effects on the dynamics of heart sounds and splitting may be because of a delay in the pulmonary compo- murmurs. Variables that can affect sound and murmurs include: nent, as occurs with complete right bundle branch block, or (1) changes in venous return representing the cardiac ; can be caused by early timing of the aortic component associ- (2) changes in systemic vascular resistances; (3) changes in ated with mitral insufficiencies. Directional changes in the contractility; (4) changes in or rhythm; or (5) any interval of the split (greater with inspiration, lesser with exha- maneuver that affects the pressure gradients within the heart. lation) in the presence of both components define the split as Diagnostic maneuvers often used for altering heart sounds persistent, but not fixed. include inspiration, expiration, a recumbent position, a left Fixed splitting of $2 is commonly found in patients with semilateral position, , standing, sitting up, or leaning atrial septal defects, severe pulmonic stenoses, or right ven- forward. tricular failures. This term applies when the interval between Inspiration causes decreased intrathoracic pressure, increased the aortic and pulmonary components is not only wide and venous return, increased right ventricular preload, and decreased persistent, but also remains unchanged during the respiratory pulmonary vascular resistance. A voluntary inspiration can be cycle. used to increase the intensity of $3 and $4 gallops, tricuspid and Paradoxical splitting refers to a reversed sequence of semi- pulmonic stenosis or regurgitation murmurs, or mitral and tri- lunar valve closure, with the pulmonary component (P2) pre- cuspid clicks. Inspiration also causes splitting of $2, which is ceding the aortic component (A2). Paradoxical splitting of $2 caused by prolonged right ventricular ejection. Expiration is caused by a delay in the A2 varying with the inspiratory cycle causes just the opposite--decreased venous return to the heart and can be caused by: ( 1) a complete left bundle branch block; (preload) and decreased right-sided flow. Sounds and murmurs (2) premature right ventricle contractions; (3) ventricular originating on the left side of the heart tend to be accentuated tachycardia; (4) severe aortic stenosis; (5) left ventricular during expiration. outflow obstruction; (6) hypertrophic cardiomyopathy; (7) Change in the patient's position can affect the intensity of coronary artery disease; (8) myocarditis; or (9) congestive car- the heart sounds as well, mostly by increasing the ventricular diomyopathy. preload and ventricular sizes and by bringing the heart closer Normally, blood flow in the heart is primarily laminar and to the chest wall. The recumbent position accentuates mur- does not produce murmurs. Murmurs can be detected when- murs of mitral and tricuspid stenosis. The left semilateral ever there is a pathology causing turbulent flow, such as with position accentuates left-sided $3 and $4, mitral opening snap, abnormal shunts, obstructions to flow, or induced reverse flow. and mitral regurgitation murmurs. Standing affects general Turbulent flow creates vibrations that can be heard as mur- by pooling blood in the lower extremities and murs. Murmurs are described on the basis of appearance in decreasing heart filling pressures and ventricular sizes. Thus, relation to the cardiac cycle and on the basis of changes in standing is used to accentuate mitral and tricuspid clicks. Sit- intensity (loudness), frequency (pitch), configuration (shape), ting up accentuates the tricuspid valve opening snap, and sit- quality, duration, or direction of radiation. For example, inten- ting up and leaning forward are the best maneuvers for sity or loudness is graded from 1 to 6. Based on time of exist- enhancing murmurs of aortic and pulmonic regurgitation or ence relative to the cardiac cycle, murmurs are classified as aortic stenosis murmurs. Exercise commonly causes increases systolic, diastolic, or continuous. Depending on their life cycle in heart rates, shortens diastole, elevates left atrial pressure, during systole or diastole, they are further subclassified into and shortens the time for closure of the heart valves. Hence, early, mid-, and late systolic or diastolic murmurs: physiological changes during exercise increase amplitudes of • Early systolic murmur begins with S1 and ends before the S 1, $2, $3, $4, mitral opening snaps, existing mitral regurgi- midsystole. tations or stenoses, or murmurs. • Midsystolic murmur starts after S 1 and ends before $2. Two other pathological sounds that might be heard when • Late systolic murmur begins in the middle of systole and auscultating the heart are clicks and opening snaps. Clicks are ends at $2. caused by rapid movement of valvular structures. Systolic • Holosystolic murmur starts with S 1 and continues for the duration of the whole systole. clicks are referred to as ejection or nonejection clicks, depend- • Early diastolic murmur begins with $2. ing on their timing relative to the systole. Ejection clicks, which • Middiastolic murmur begins after $2. occur early in systole, indicate semilunar valve anomalies and, • Late diastolic murmur begins just before S 1. in rare conditions, great vessel lesions. Nonejection clicks are • Continuous murmur continues during both systole and heard in mid-to-late systole and represent mitral (more often) diastole. or tricuspid valve prolapse. A tricuspid valve opening snap is Based on changes in intensity, murmurs are described as: (1) usually heard when there is tricuspid valve stenosis and in crescendo, increasing in intensity; (2) decrescendo, decreasing conditions associated with increased blood flow across the tri- in intensity; (3) crescendo-decrescendo, when the intensity of cuspid valve (e.g., presence of large ). The the murmur first increases and then decreases; and (4) plateau, mitral vah,e opening snap when present is considered caused for which the intensity of the murmur remains constant. by elevated left atrial pressure forces causing rapid valve open- 188 PART IIh PHYSIOLOGY AND ASSESSMENT/BOJANOV

Systole Diastole blood is ejected through the aortic root. The musical second $1 P2 component of the aortic stenosis murmur originates from peri- Aortic odic high-frequency vibrations of the fibrocalcific aortic cusps Stenosis $4 and can be quite loud and heard even from a distance. When |__ present it can be accentuated by expiration, sitting up, and lean- ing forward. The high-frequency apical midsystolic murmur of Fig. 4. Representation of aortic stenosis murmur caused by a stenotic aortic stenosis should be distinguished from the high-frequency aortic valve. This is normally a holosystolic crescendo--decrescendo apical murmur of mitral regurgitation, a distinction that may be murmur best heard at the aortic auscultatory area. S 1, first heart sound; difficult or impossible, especially if the aortic component of the $4, fourth heart sound; P2, pulmonic valve closure. second heart sound is soft or absent. The murmur caused by stenosis is a char- acteristic midsystolic murmur originating in the right side of Systole Diastole the heart and best auscultated over the pulmonic auscultation Sl area. This murmur begins after the first heart sound or with a Aortic pulmonary ejection sound, rises to a peak in crescendo, and Insufficiency then decreases in a slower decrescendo slightly before a i delayed or soft pulmonary component of the second heart Fig. 5. Representation of , an early decrescendo sound. The length and the profile of the murmur are dependent diastolic murmur originating in the left side of the heart and best heard on the degree of pulmonic obstruction. over the aortic and pulmonic auscultation areas. S 1, first heart sound; The murmur caused by aortic insufficiency (Fig. 5) is an A2, aortic valve closure; P2, pulmonic valve closure. early decrescendo diastolic murmur originating in the left side of the heart and best heard over the aortic and pulmonic auscul- tation areas. This murmur begins with the aortic component of Systole Diastole the second heart sound. The intensity and the configuration of such a murmur tend to reflect the volumes and rates of regur- S1 P2 gitant flows. Radiation of this murmur to the right sternal bor- Mitral der commonly signifies aortic root dilation, as in Marfan Stenosis syndrome. In chronic aortic regurgitation, the aortic diastolic B pressure always significantly exceeds the left ventricular dias- Fig. 6. The mitral stenosis murmur, a decrescendo-crescendo tolic pressure, so the decrescendo is subtle, and the murmur is holodiastolic murmur, is caused by a stenotic mitral valve. Best heard well heard throughout diastole. The diastolic murmur of acute at the mitral auscultation area, this murmur is accentuated by exercise severe aortic regurgitation differs from the chronic aortic re- and by assuming a recumbent position. S 1, first heart sound; A2, aortic gurgitation murmur primarily in that the diastolic murmur is valve closure; P2, pulmonic valve closure; OS, opening snap. relatively short because the aortic diastolic pressure rapidly equilibrates with the rapidly rising diastolic pressure in the nondilated left ventricle. The aortic insufficiency murmur is accentuated by expiration, sitting up, or leaning forward. ing to the point of maximum excursion. The mitral valve open- A pulmonary regurgitation murmur is an early diastolic ing snap is detected most often in cases of mitral stenosis and murmur originating from the right side of the heart. Often, the less often in ventricular septal defects, second or third atrio- second heart sound is split, and the murmur proceeds from its ventricular blocks, patent ductus arteriosus, hyperthyroidism, latter part. It is loud primarily because the elevated pressure exerted on the incompetent pulmonary valve begins at the and the like. The mitral valve opening snap is similar in quality moment that right ventricular pressure drops below the pulmo- to a normal heart sound and is often confused with a splitting nary arterial diastolic pressure. The high diastolic pressure of $2. The of mitral valve opening snap generates high-velocity regurgitant flow and results in a high- vs other heart sound has been described in detail elsewhere and frequency blowing murmur that may last throughout diastole. is not a topic of this chapter. Because of the persistent and significant difference between the 2.5, Specific Murmurs pulmonary arterial and right ventricular diastolic pressures, the The aortic stenosis murmur (Fig. 4) is caused by a stenotic amplitude of the murmur is usually relatively uniform through- aortic valve and is commonly a holosystolic crescendo-decre- out most of the diastole. scendo murmur best heard at the aortic auscultatory area. The A mitral stenosis murmur (Fig. 6) is caused by a stenotic high-velocity jet within the aortic root results in radiation of the mitral valve and is considered a decrescendo-crescendo murmur upward, to the right second intercostal space, and fur- holodiastolic murmur. It is heard best at the mitral auscultation ther into the neck. Although the murmur in the second right area and is accentuated by exercise and by assuming a recum- intercostal space is harsh, noisy, and impure, the murmur heard bent position. A mitral stenosis murmur that lasts up to the first when auscultated over the left apical area is pure and often heart sound, even after long cardiac cycles, indicates that the considered musical. The harsh basal murmur is believed to be stenosis is severe enough to generate a persistent gradient even caused by the vibrations created when the high-velocity jet of at the end of long diastoles. CHAPTER 14 / BLOOD PRESSURE,HEART TONES, AND DIAGNOSES 189

The murmur caused by tricuspid stenosis is middiastolic in Systole Diastole origin and differs from the mitral stenosis middiastolic mur- mur in two important respects: (1) the loudness of the tricuspid Mitral S~2 murmur increases with inspiration, and (2) the tricuspid mur- Regurgitation mur is auscultated over a relatively localized area along the left lower sternal border. Detectable inspiratory increases in loud- Fig. 7. Caused by an insufficiency of the mitral valve, the mitral regur- ness occur because of augmentations of the right ventricular gitation murmur is a systolic murmur best heard at the mitral auscul- volumes, decreases in right ventricular diastolic pressures, and tation area. S 1, first heart sound; A2, aortic valve closure; P2, pulmonic increases of the gradients and flows across the stenotic tricus- valve closure. pid valve. This murmur is best detected over the left lower sternal border because it originates within the inflow portion of the right ventricle and is then transmitted to the overlying chest Systole Diastole $1 P2 wall. A2 A mitral regurgitation murmur (Fig. 7) is caused by an insuf- Tricuspid ill I1[ Regurgitation ficiency of the mitral valve and is a systolic murmur best heard ~ at the mitral auscultation area. It is accentuated by exercise and left semilateral positioning. Acute severe mitral regurgitation is Fig. 8. The tricuspid regurgitation murmur is often associated with often accompanied by an early systolic murmur or holosystolic infective . It is a systolic murmur best heard at the tricus- murmur that has a decrescendo pattern, diminishing or ending pid area and is accentuated by inspiration. S 1, first heart sound; A2, before the second heart sound. The physiological mechanism aortic valve closure; P2, pulmonic valve closure. responsible for this early systolic decrescendo murmur is pri- marily acute severe regurgitation into a relatively normal-size left atrium with limited distensibility. The regurgitant flow is Systole Diastole maximal in early systole and minimal in late systole, and the murmur typically follows this pattern. $1 P2 Another described early systolic murmur is the tricuspid Atrial ~ regurgitation murmur (Fig. 8), often associated with infective Septal endocarditis. The mechanisms responsible for the timing and Defect configuration of this murmur are analogous to those described Fig. 9. Murmurs associated with atrial septal defects are normally for mitral regurgitation. It is a systolic murmur best heard at the systolic murmurs caused by increased blood flows through the pul- tricuspid area and is best accentuated by inspiration. monic valves; such murmurs are best heard over the pulmonic auscul- The murmurs associated with atrial septal defects (Fig. 9) tation area. S 1, first heart sound; A2, aortic valve closure; P2, pulmonic are commonly systolic murmurs caused by increased blood valve closure. flows through the pulmonic valves and are best heard over the pulmonic auscultation area. Most often, the atrial septal defect involves the fossa ovalis, is midseptal in location, and is of the ostium secundum type. This type of defect is a true deficiency Systole Diastole of the atrial septum and should not be confused with a patent $1 P2 foramen ovale. The magnitude of the left-to-right shunt through Patent ~._ A2 I an atrial septal defect depends on the size of the defect and the relative compliance of the ventricles as well as the relative , Ur 'oU:us resistances in both the pulmonary and the systemic circula- Fig. 10. Commonly associated with patent ductus arteriosus, this tions. The increased pulmonic valve flows cause a delay (split- murmur is caused by a turbulent continuous flow through the ductus ting) in the pulmonic components of the second heart sound. connecting the aorta with the main . S 1, first heart The murmur commonly associated with patent ductus arte- sound; A2, aortic valve closure; P2, pulmonic valve closure. riosus (Fig. 10) is caused by a turbulent continuous flow through the ductus connecting the aorta with the main pulmonary artery. Itis a continuous "machinery" murmur, heard in both systole and diastole, because aortic pressures are higher than the pres- Systole Diastole sures in the pulmonary artery throughout the cardiac cycle. S1 P2 Other associated clinical findings in such patients include Ventricular~ bounding peripheral , an infraclavicular and interscapu- Septal lar systolic murmur, precordial hyperactivity, hepatomegaly, Defect and either multiple episodes of apnea and or respi- ratory dependency. Fig. 11. Murmurs associated with ventricular septal defects are sys- tolic murmurs primarily caused by blood flow from the left to the right The murmurs associated with ventricular septal defects ventricle (or the right to the left ventricle in Eisenmenger' s syndrome). (Fig. 11) are systolic murmurs, with intensity depending on S1, first heart sound; A2, aortic valve closure; P2, pulmonic valve the size of the defect; they are primarily caused by blood flow closure. 190 PART II1: PHYSIOLOGY AND ASSESSMENT / BOJANOV from the left to the right ventricle or the right to the left ven- SOURCES tricle in Eisenmenger's syndrome. Eisenmenger's syndrome Barash, R.G., Cullen, B.F., and Stoelting, R.K. (eds.) (2001) Clinical is the reversing of left-to-right shunt in patients with atrial , 4th Ed. Lippincott, Williams, and Wilkins, Philadelphia, PA. septal defects, ventricular septal defects, or patent ductus Braunwald, E. (ed.) (1997) Heart Disease: A Textbook of Cardiovascu- arteriosus. Such murmurs are best heard at the mitral auscul- lar , 5th Ed. Saunders, Philadelphia, PA. tation area or at the heart apex. Faulconer, A. and Keys, T.E. (eds.) (1993) Foundations of Anesthesi- ology, Vols. 1 and 2. The Wood Library-Museum of Anesthesiol- 3. SUMMARY ogy, Park Ridge, IL. In conclusion, I would like to reiterate the clinical impor- Kaplan, J.A., Reich, D.L., and Konstadt, S.N. (eds.) (1999) Cardiac Anesthesia, 4th Ed. Saunders, Philadelphia, PA. tance of deeply understanding and using the basic physiologi- McVicker, J.T. (2001) Blood pressure measurement--does anyone do cal principles in interpreting "simple things" like blood it right? An assessment of the reliability of equipment in use and the pressure and heart tones should not be underestimated. It measurement techniques of clinicians. J Fam Plann Reprod Health should also be noted that the descriptions of the general scien- Care. 27, 163-164. tific and clinical principles used in this chapter have been Miller, R.D. and Cucchiara, R.F. (eds.) (1994) Anesthesia, 4th Ed., simplified for clarity and can vary significantly in a clinical Vols. 2 and 2. Churchill Livingstone, New York, NY. population. Even the most sophisticated electronic monitors Mohrman, D.E. and Heller, L.J. (eds.) (1997) Cardiovascular Physiol- cannot necessarily reduce the need for acquiring sound clini- ogy, 4th Ed. McGraw-Hill, New York, NY. cal skills such as inspection, palpation, percussion, ausculta- O'Brien, E., Pickering, T., Asmar, R., et al. (2002) Working Group on Blood Pressure Monitoring of the European Society of Hyperten- tion, and so on. Even though "fancy" methods for monitoring sion, international protocol for validation of blood pressure measur- can facilitate clinical decision making, to date there is almost ing devices in adults. Blood Press Monit. 7, 3-17. no evidence that they reduce morbidity and mortality; yet, Stoelting, R.K. (1999) Pharmacology and Physiology in Anesthetic they can add significantly to the overall cost of care. Practice, 3rd Ed. Lippincott-Raven, Philadelphia, PA.