Cardiac System

Preferred Practice Patterns

The most relevant practice patterns for the diagnoses discussed in this chapter, based on the American Physical Therapy Association’s Guide to Physical Therapist Practice, second edition, are as follows:

• Primary Prevention/Risk Reduction for Cardiovascular/Pulmonary Disorders: 6A

• Impaired Aerobic Capacity/Endurance Associated with Deconditioning: 6B

• Impaired Aerobic Capacity/Endurance Associated with Cardiovascular Pump Dysfunction or Failure: 6D

Please refer to Appendix A for a complete list of the preferred practice patterns, as individual patient conditions are highly variable and other practice patterns may be applicable.

Physical therapists in acute care facilities commonly encounter patients with cardiac system dysfunction as either a primary morbidity or comorbidity. Recent estimates conclude that although the death rate associated with cardiovascular disease has declined in recent years, the overall burden of the disease remains high.¹ Based on current estimates, 82,500,000 (more than one in three) Americans have one or more types of cardiovascular disease (CVD).¹ In 2009 CVD ranked first among all disease categories and accounted for 6,165,000 hospital discharges.¹ In the acute care setting, the role of the physical therapist with this diverse group of patients remains founded in examination, evaluation, intervention, and discharge planning for the purpose of improving functional capacity and minimizing disability. The physical therapist must be prepared to safely accommodate for the effects of dynamic (pathologic, physiologic, medical, and surgical intervention) changes into his or her evaluation and plan of care.

The normal cardiovascular system provides the necessary pumping force to circulate blood through the coronary, pulmonary, cerebral, and systemic circulation. To perform work, such as during functional tasks, energy demands of the body increase, therefore increasing the oxygen demands of the heart. A variety of pathologic states can create impairments in the cardiac system’s ability to meet these demands successfully, ultimately leading to functional limitations. To fully address these functional limitations, the physical therapist must understand normal and abnormal cardiac function, clinical tests, and medical and surgical management of the cardiovascular system.

Body Structure and Function

The heart and the roots of the great vessels (Figure 3-1) occupy the pericardium, which is located in the mediastinum. The sternum, the costal cartilages, and the medial ends of the third to fifth ribs on the left side of the thorax create the anterior border of the mediastinum. It is bordered inferiorly by the diaphragm, posteriorly by the vertebral column and ribs, and laterally by the pleural cavity (which contains the lungs). Specific cardiac structures and vessels and their respective functions are outlined in Tables 3-1 and 3-2.

TABLE 3-1

Primary Structures of the Heart

Structure	Description	Function
Pericardium	Double-walled sac of elastic connective tissue, a fibrous outer layer, and a serous inner layer	Protects against infection and trauma
Epicardium	Outermost layer of cardiac wall, covers surface of heart and great vessels	Protects against infection and trauma
Myocardium	Central layer of thick muscular tissue	Provides major pumping force of the ventricles
Endocardium	Thin layer of endothelium and connective tissue	Lines the inner surface of the heart, valves, chordae tendineae, and papillary muscles
Right atrium	Heart chamber	Receives blood from the venous system and is a primer pump for the right ventricle
Tricuspid valve	Atrioventricular valve between right atrium and ventricle	Prevents back flow of blood from the right ventricle to the atrium during ventricular systole
Right ventricle	Heart chamber	Pumps blood to the pulmonary circulation
Pulmonic valve	Semilunar valve between right ventricle and pulmonary artery	Prevents back flow of blood from the pulmonary artery to the right ventricle during diastole
Left atrium	Heart chamber	Acts as a reservoir for blood and a primer pump for the left ventricle
Mitral valve	Atrioventricular valve between left atrium and ventricle	Prevents back flow of blood from the left ventricle to the atrium during ventricular systole
Left ventricle	Heart chamber	Pumps blood to the systemic circulation
Aortic valve	Semilunar valve between left ventricle and aorta	Prevents back flow of blood from the aorta to the left ventricle during ventricular diastole
Chordae tendineae	Tendinous attachment of atrioventricular valve cusps to papillary muscles	Prevents valves from everting into the atria during ventricular systole
Papillary muscle	Muscle that connects chordae tendineae to floor of ventricle wall	Constricts and pulls on chordae tendineae to prevent eversion of valve cusps during ventricular systole

TABLE 3-2

Great Vessels of the Heart and Their Function

Structure	Description	Function
Aorta	Primary artery from the left ventricle that ascends and then descends after exiting the heart	Ascending aorta delivers blood to neck, head, and arms Descending aorta delivers blood to visceral and lower body tissues
Superior vena cava	Primary vein that drains into the right atrium	Drains venous blood from head, neck, and upper body
Inferior vena cava	Primary vein that drains into the right atrium	Drains venous blood from viscera and lower body
Pulmonary artery	Primary artery from the right ventricle	Carries blood to lungs

FIGURE 3-1 Anatomy of the right coronary artery and left coronary artery, including left main, left anterior descending, and left circumflex coronary arteries. (From Becker RC: Chest pain: the most common complaints series, Boston, 2000, Butterworth-Heinemann.)

Note: The mediastinum and the heart can be displaced from their normal positions with changes in the lungs secondary to various disorders. For example, a tension pneumothorax shifts the mediastinum away from the side of dysfunction (see Chapter 4 for a further description of pneumothorax).

The cardiovascular system must adjust the amount of nutrient- and oxygen-rich blood pumped out of the heart (cardiac output [CO]) to meet the spectrum of daily energy (metabolic) demands of the body.

The heart’s ability to pump blood depends on the following characteristics ²:

• Automaticity: The ability to initiate its own electrical impulse

• Excitability: The ability to respond to electrical stimulus

• Conductivity: The ability to transmit electrical impulse from cell to cell within the heart

• Contractility: The ability to stretch as a single unit and then passively recoil while actively contracting

• Rhythmicity: The ability to repeat the cycle in synchrony with regularity

Cardiac Cycle

Blood flow throughout the cardiac cycle depends on circulatory and cardiac pressure gradients. The right side of the heart is a low-pressure system with little vascular resistance in the pulmonary arteries, whereas the left side of the heart is a high-pressure system with high vascular resistance from the systemic circulation. The cardiac cycle is the period from the beginning of one contraction, starting with sinoatrial (SA) node depolarization, to the beginning of the next contraction. Systole is the period of contraction, whereas diastole is the period of relaxation. Systole and diastole can also be categorized into atrial and ventricular components:

• Atrial diastole is the period of atrial filling. The flow of blood is directed by the higher pressure in the venous circulatory system.

• Atrial systole is the period of atrial emptying and contraction. Initial emptying of approximately 70% of blood occurs as a result of the initial pressure gradient between the atria and the ventricles. Atrial contraction then follows, squeezing out the remaining 30%.³ This is commonly referred to as the atrial kick.

• Ventricular diastole is the period of ventricular filling. It initially occurs with ease; then, as the ventricle is filled, atrial contraction is necessary to squeeze the remaining blood volume into the ventricle. The amount of stretch placed on the ventricular walls during diastole, referred to as left ventricular end diastolic pressure (LVEDP), influences the force of contraction during systole. (Refer to the Factors Affecting Cardiac Output section for a description of preload.)

• Ventricular systole is the period of ventricular contraction. The initial contraction is isovolumic (meaning it does not eject blood), which generates the pressure necessary to serve as the catalyst for rapid ejection of ventricular blood. The left ventricular ejection fraction (EF) represents the percent of end diastolic volume ejected during systole and is normally approximately 60%.²

Cardiac Output

CO is the quantity of blood pumped by the heart in 1 minute. Regional demands for tissue perfusion (based on local metabolic needs) compete for systemic circulation, and total CO adjusts to meet these demands. Adjustment to CO occurs with changes in heart rate (HR—chronotropic) or stroke volume (SV—inotropic).³ Normal resting CO is approximately 4 to 8 liters per minute (L/min), with a resting HR of 70 beats per minute (bpm); resting SV is approximately 71 ml/beat.² The maximum value of CO represents the functional capacity of the circulatory system to meet the demands of physical activity.

CO also can be described relative to body mass as the cardiac index (CI), the amount of blood pumped per minute per square meter of body mass. Normal CI is between 2.5 and 4.2 L/min/m². This wide normal range makes it possible for cardiac output to decline by almost 40% and still remain within the normal limits. Although several factors interrupt a direct correlation between CI and functional aerobic capacity, a CI below 2.5 L/min/m² represents a marked disturbance in cardiovascular performance and is always clinically relevant.⁴

Factors Affecting Cardiac Output

Preload.

Preload is the amount of tension on the ventricular wall before it contracts. It is related to venous return and affects SV by increasing left ventricular end diastolic volume in addition to pressure and therefore contraction.² This relationship is explained by the Frank-Starling mechanism and is demonstrated in Figure 3-2.

FIGURE 3-2 Factors affecting left ventricular function. (Modified from Braunwal E, Ross J, Sonnenblick E et al: Mechanisms of contraction of the normal and failing heart, ed 2, Boston, 1976, Little, Brown.)

Frank-Starling Mechanism.

The Frank-Starling mechanism defines the normal relationship between the length and tension of the myocardium.⁵ The greater the stretch on the myocardium before systole (preload), the stronger the ventricular contraction. The length-tension relationship in skeletal muscle is based on the response of individual muscle fibers; however, relationships between cardiac muscle length and tension consist of the whole heart. Therefore length is considered in terms of volume; tension is considered in terms of pressure. A greater volume of blood returning to the heart during diastole equates to greater pressures generated initially by the heart’s contractile elements. Ultimately facilitated by elastic recoil, a greater volume of blood is ejected during systole. The effectiveness of this mechanism can be reduced in pathologic situations.³

Afterload.

Afterload is the force against which a muscle must contract to initiate shortening.⁵ Within the ventricular wall, this is equal to the tension developed across its wall during systole. The most prominent force contributing to afterload in the heart is blood pressure (BP), specifically vascular compliance and resistance. BP affects aortic valve opening and is the most obvious load encountered by the ejecting ventricle. An example of afterload is the amount of pressure in the aorta at the time of ventricular systole.²

Cardiac Conduction System

A schematic of the cardiac conduction system and a normal electrocardiogram (ECG) are presented in Figure 3-3. Normal conduction begins in the SA node and travels throughout the atrial myocardium (atrial depolarization) via intranodal pathways to the atrioventricular (AV) node, where it is delayed momentarily. It then travels to the bundle of His, to the bundle branches, to the Purkinje fibers, and finally to the myocardium, resulting in ventricular contraction.⁶ Disturbances in conduction can decrease CO (refer to the Health Conditions section for a discussion of rhythm and conduction disturbances).⁷

FIGURE 3-3 Schematic representation of the sequence of excitation in the heart. (From Walsh M, Crumbie A, Reveley S: Nurse practitioners: clinical skills and professional issues, Boston, 1999, Butterworth-Heinemann.)

Neural Input.

The SA node has its own inherent rate. However, neural input can influence HR, heart rate variability (HRV), and contractility through the autonomic nervous system.2,8

Parasympathetic system (vagal) neural input generally decelerates cardiac function, thus decreasing HR and contractility. Parasympathetic input travels through the vagus nerves. The right vagus nerve stimulates primarily the SA node and affects rate, whereas the left vagus nerve stimulates primarily the AV node and affects AV conduction.2,8

Sympathetic system neural input is through the thoracolumbar sympathetic system and increases HR and augment ventricular contractility, thus accelerating cardiac function.²

Endocrine Input.

In response to physical activity or stress, a release in catecholamines increases HR, contractility, and peripheral vascular resistance for a net effect of increased cardiac function (Table 3-3).²

TABLE 3-3

Cardiac Effects of Hormones

Data from Guyton AC, Hall JE: Textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.

Local Input.

Tissue pH, concentration of carbon dioxide (CO₂), concentration of oxygen (O₂), and metabolic products (e.g., lactic acid) can affect vascular tone.² During exercise, increased levels of CO₂, decreased levels of O₂, decreased pH, and increased levels of lactic acid at the tissue level dilate local blood vessels and therefore increase CO distribution to that area.

Cardiac Reflexes

Cardiac reflexes influence HR and contractility and can be divided into three general categories: baroreflex (pressure), Bainbridge reflex (stretch), and chemoreflex (chemical reflex).

Baroreflexes are activated through a group of mechanoreceptors located in the heart, great vessels, and intrathoracic and cervical blood vessels. These mechanoreceptors are most plentiful in the walls of the internal carotid arteries.² Mechanoreceptors are sensory receptors that are sensitive to mechanical changes such as pressure and stretch. Activation of the mechanoreceptors by high pressures results in an inhibition of the vasomotor center of the medulla that increases vagal stimulation. This chain of events is known as the baroreflex and results in vasodilation, decreased HR, and decreased contractility.

Mechanoreceptors located in the right atrial myocardium respond to stretch. An increased volume in the right atrium results in an increase in pressure on the atrial wall. This reflex, known as the Bainbridge reflex, stimulates the vasomotor center of the medulla, which in turn increases sympathetic input and increases HR and contractility.² Respiratory sinus arrhythmia, an increased HR during inspiration and decreased HR during expiration, may be facilitated by changes in venous return and SV caused by changes in thoracic pressure induced by the respiratory cycle. At the beginning of inspiration when thoracic pressure is decreased, venous return is greater; therefore a greater stretch is exerted on the atrial wall.⁹

Chemoreceptors located on the carotid and aortic bodies have a primary effect on increasing rate and depth of ventilation in response to CO₂ levels, but they also have a cardiac effect. Changes in CO₂ during the respiratory cycle also may result in sinus arrhythmia.²

Coronary Perfusion

For a review of the major coronary arteries, refer to Figure 3-1. Blood is pumped to the large superficial coronary arteries during ventricular systole. At this time, myocardial contraction limits the flow of blood to the myocardium; therefore myocardial tissue is perfused during diastole.

Systemic Circulation

For a review of the distribution of systemic circulation, refer to Figure 3-4. Systemic circulation is affected by total peripheral resistance (TPR), which is the resistance to blood flow by the force created by the aorta and arterial system. Two factors that contribute to resistance are (1) vasomotor tone, in which vessels dilate and constrict, and (2) blood viscosity, in which greater pressure is required to propel thicker blood. TPR, also called systemic vascular resistance, and CO influence BP.² This relationship is illustrated in the following equation:

FIGURE 3-4 Schematic of systemic circulation. (From Thibodeau GA: Structure and function of the body, ed 13, St Louis, 2007, Mosby.)

Cardiac Evaluation

Cardiac evaluation consists of patient history, physical examination (which consists of observation, palpation, BP measurement, and heart sound auscultation), laboratory tests, and diagnostic procedures.

Patient History

In addition to the general chart review presented in Chapter 2 the following pertinent information about patients with cardiac dysfunction should be obtained before physical examination^3,10–12:

• Presence of chest pain (see Chapter 17 for an expanded description of characteristics and etiology of chest pain)

• Location and radiation

• Character and quality (crushing, burning, numbing, hot)

• Frequency

• Angina equivalents (what the patient feels as angina [e.g., jaw pain, shortness of breath, dizziness, lightheadedness, diaphoresis, burping, nausea, or any combination of these])

• Aggravating and alleviating factors

• Precipitating factors

• Medical treatment sought and its outcome

• Presence of palpitations

• Presence of cardiac risk factors (Box 3-1)

Box 3-1

Cardiac Risk Factors

Primary and Secondary Prevention

LDL, Low-density lipoprotein; HDL, high-density lipoprotein.

Data from Grundy SM, Pasternak R, Greenland P et al: Assessment of cardiovascular risk by use of multiple-risk-factor assessment equations: a statement for healthcare professionals from the American Heart Association and the American College of Cardiology, Circulation 100:1481-1492, 1999; Belkic KL, Landsbergis PA et al: Is job strain a major source of cardiovascular disease risk? Scand J Work Environ Health 30(2):85-128, 2004.

• Family history of cardiac disease

• History of dizziness or syncope

• Previous myocardial infarction (MI), cardiac studies, or procedures

Clinical Tip

When discussing angina with a patient, use the patient’s terminology. If the patient describes the angina as “crushing” pain, ask the patient if he or she experiences the crushing feeling during treatment as opposed to asking the patient if he or she has chest pain. The common medical record abbreviation for chest pain is CP.

Physical Examination

Observation

Key components of the observation portion of the physical examination include the following 3,7:

• Facial color, skin color and tone, or the presence of diaphoresis

• Obvious signs of edema in the extremities

• Respiratory rate

• Signs of trauma (e.g., paddle burns or ecchymosis from cardiopulmonary resuscitation)

• Presence of jugular venous distention (JVD), which results from the backup of fluid into the venous system from right-sided congestive heart failure (CHF) (Figure 3-5)

FIGURE 3-5 Measurement of jugular venous distention (JVD). The JVD reading is the maximum height, in centimeters, above the sternal angle at which venous pulsations are visible. (Modified from Thompson JM, McFarland GK, Hirsch JE et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.)

• Make sure the patient is in a semirecumbent position (45 degrees).

• Have the patient turn his or her head away from the side being evaluated.

• Observe pulsations in the internal jugular neck region. Pulsations are normally seen 3 to 5 cm above the sternum. Pulsations higher than this or absent pulsations indicate jugular venous distention.

Palpation

Palpation is the second component of the physical examination and is used to evaluate and identify the following:

• Pulses for circulation quality, HR, and rhythm (Table 3-4, Figure 3-6)

TABLE 3-4

Pulse Amplitude Classification and Pulse Abnormalities

^*Corrigan’s pulse is a bounding pulse visible in the carotid artery that occurs with aortic regurgitation.

Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S, editors: Cardiac nursing, ed 4, Philadelphia, 2000, Lippincott.

FIGURE 3-6 Arterial pulses. (From Pierson FM: Principles and techniques of patient care, ed 4, St Louis, 2008, Saunders.)

• Extremities for pitting edema bilaterally (Table 3-5)

TABLE 3-5

Pitting Edema Scale

Scale	Degree	Description
1+ Trace	Slight	Barely perceptible depression
2+ Mild	0-0.6 cm	Easily identified depression (EID) (skin rebounds in <15 sec)
3+ Moderate	0.6-1.3 cm	EID (rebound 15-30 sec)
4+ Severe	1.3-2.5 cm	EID (rebound >30 sec)

Data from Woods SL, Sivarajian Froelicher ES, Underhill-Motzer S, editors: Cardiac nursing, ed 4, Philadelphia, 2000, Lippincott; Hillegass EA, Sadowsky HS, editors: Essentials of cardiopulmonary physical therapy, ed 2, Philadelphia, 2001, Saunders.

When palpating HR, counting the pulse rate for 15 seconds and multiplying by 4 is sufficient with normal rates and rhythms. If rates are faster than 100 bpm or slower than 60 bpm, palpate the pulse for 60 seconds. If the rhythm is irregularly irregular (e.g., during atrial fibrillation) or regularly irregular (e.g., premature ventricular contractions [PVCs]), perform auscultation of heart sounds to identify the apical HR for a full minute. In these cases, palpation of pulse cannot substitute for ECG analysis to monitor the patient’s rhythm, but it may alert the therapist to the onset of these abnormalities.

Clinical Tip

Use caution in palpating pulses because manual pressure on the carotid sinus may cause reflexive drops in HR, BP, or both.

Blood Pressure

BP measurement with a sphygmomanometer (cuff) and auscultation is an indirect, noninvasive measurement of the force exerted against the arterial walls during ventricular systole (systolic blood pressure [SBP]) and during ventricular diastole (diastolic blood pressure). BP is affected by peripheral vascular resistance (blood volume and elasticity of arterial walls) and CO. Table 3-6 lists normal BP ranges. Occasionally, BP measurements can be performed only on certain limbs secondary to the presence of conditions such as a percutaneous inserted central catheter, arteriovenous fistula for hemodialysis, blood clots, scarring from brachial artery cutdowns, or lymphedema (e.g., status post mastectomy). BP of the upper extremity should be measured in the following manner:

TABLE 3-6

Normal Blood Pressure Ranges

Age Ranges	Systolic	Diastolic
Age 8 years	85-114 mm Hg	52-85 mm Hg
Age 12 years	95-135 mm Hg	58-88 mm Hg
Adult	<120 mm Hg	<80 mm Hg
Prehypertension	120-139 mm Hg	80-89 mm Hg
Hypertension
Stage 1	140-159 mm Hg	90-99 mm Hg
Stage 2	≥160 mm Hg	≥100 mm Hg
Normal exercise	Increases 5-12 mm Hg per MET increase in workload	±10 mm Hg

MET, Metabolic equivalent.

Data from Chobanian AV, Bakris GL et al: Seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure, Hypertension 42(6):1206-1252, 2003; American College of Sports Medicine, Armstrong LE, et al: ACSM’s guidelines for exercise testing and prescription, Philadelphia, 2005, Lippincott Williams & Wilkins.

1. Check for posted signs, if any, at the bedside that indicate which arm should be used in taking BP. BP variations of 5 to 10 mm Hg between the right and left upper extremity are considered normal. Patients with arterial compression or obstruction may have differences of more than 10 to 15 mm Hg.¹²

2. Use a properly fitting cuff. The inflatable bladder should have a width of approximately 40% and length of approximately 80% of the upper arm circumference.¹³

3. Position the cuff 2.5 cm above the antecubital crease.

4. Rest the arm at the level of the heart.

5. To determine how high to inflate the cuff, palpate the radial pulse, inflate until no longer palpable, and note the cuff inflation value. Deflate the cuff.

6. Place the bell of the stethoscope gently over the brachial artery.

7. Reinflate the cuff to 30 to 40 mm Hg greater than the value in step 5. Then slowly deflate the cuff. Cuff deflation should occur at approximately 2 to 3 mm Hg per second.¹³

8. Listen for the onset of tapping sounds, which represents blood flow returning to the brachial artery. This is the systolic pressure.

9. As the pressure approaches diastolic pressure, the sounds will become muffled and in 5 to 10 mm Hg will be completely absent. These sounds are referred to as Korotkoff sounds (Table 3-7).^12,13

TABLE 3-7

Korotkoff Sounds

Phase	Sound	Indicates
1	First sound heard, faint tapping sound with increasing intensity	Systolic pressure (blood starts to flow through compressed artery)
2	Start swishing sound	Blood flow continues to be heard; sounds are beginning to change because of the changing compression on the artery
3	Sounds increase in intensity with a distinct tapping	Blood flow is increasing as artery compression is decreasing
4	Sounds become muffled	Diastolic pressure in children <13 years of age and in adults who are exercising, pregnant, or hyperthyroid (see phase 5)
5	Disappearance	Diastolic pressure in adults—occurs 5-10 mm Hg below phase 4 in normal adults. In states of increased rate of blood flow, it may be >10 mm Hg below phase 4. In these cases, the phase 4 sound should be used as diastolic pressure in adults.

Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S, editors: Cardiac nursing, ed 4, Philadelphia, 2000, Lippincott, 2000; Bickley LS, Szilagyi PG: Bates’ guide to physical examination and history taking, Philadelphia, 2003, Lippincott Williams & Wilkins.

Clinical Tip

In situations when it is difficult to auscultate or discern a distinct diastolic pressure, the patient’s blood pressure may be noted as systolic BP/P (i.e., “BP is 90 over palp”) or systolic BP over 2 diastolic pressures (e.g., 140/85/62) denoting the onset of muffling sounds and the disappearance of sounds.¹³

Physical Therapy Considerations

• Recording preexertion, paraexertion, and postexertion BP is important for identification of BP responses to activity. During recovery from exercise, blood vessels dilate to allow for greater blood flow to muscles. In cardiac-compromised or very deconditioned individuals, total CO may be unable to support this increased flow to the muscles and may lead to decreased output to vital areas, such as the brain.

• If you are unable to obtain BP on the arm, the thigh is an appropriate alternative, with auscultation at the popliteal artery.

• Falsely high readings occur if the cuff is too small or applied loosely, or if the brachial artery is lower than the heart level.

• Evaluation of BP and HR in different postures can be used to monitor orthostatic hypotension with repeat measurements on the same arm 1 to 5 minutes after position changes. The symbols that represent patient position are shown in Figure 3-7.

FIGURE 3-7 Orthostatic blood pressure symbols.

• The same extremity should be used when serial BP recordings will be compared for an evaluation of hemodynamic response.

• A BP record is kept on the patient’s vital sign flow sheet. This is a good place to check for BP trends throughout the day and, depending on your hospital’s policy, to document BP changes during the therapy session.

• An auscultatory gap is the disappearance of sounds between phase 1 and phase 2 and is common in patients with high BP, venous distention, and severe aortic stenosis. Its presence can create falsely low systolic pressures if the cuff is not inflated enough (prevented by palpating for the disappearance of the pulse before measurement), or falsely high diastolic pressures if the therapist stops measurement during the gap (prevented by listening for the phase 3 to phase 5 transitions).¹³

Auscultation

Evaluation of heart sounds can yield information about the patient’s condition and tolerance to medical treatment and physical therapy through the evaluation of valvular function, rate, rhythm, valvular compliance, and ventricular compliance.³ To listen to heart sounds, a stethoscope with a bell and a diaphragm is necessary. For a review of normal and abnormal heart sounds, refer to Table 3-8. The examination should follow a systematic pattern using the bell (for low-pitched sounds) and diaphragm (for high-pitched sounds) and should cover all auscultatory areas, as illustrated in Figure 3-8. Abnormal sounds should be noted with a description of the conditions in which they were heard (e.g., after exercise or during exercise).

TABLE 3-8

Normal and Abnormal Heart Sounds

Sound	Location	Description
S1 (normal)	All areas	First heart sound; signifies closure of atrioventricular valves and corresponds to onset of ventricular systole
S2 (normal)	All areas	Second heart sound; signifies closure of semilunar valves and corresponds with onset of ventricular diastole
S3 (abnormal)	Best appreciated at apex	Immediately following S2; occurs early in diastole and represents filling of the ventricle. In young, healthy individuals, it is considered normal and called a physiologic third sound. In the presence of heart disease, it results from decreased ventricular compliance (a classic sign of congestive heart failure)
S4 (abnormal)	Best appreciated at apex	Immediately preceding S1; occurs late in ventricular diastole; associated with increased resistance to ventricular filling; common in patients with hypertensive heart disease, coronary heart disease, pulmonary disease, or myocardial infarction, or following coronary artery bypass grafts
Murmur (abnormal)	Over respective valves	Indicates regurgitation of blood through valves; can also be classified as systolic or diastolic murmurs. Common pathologies resulting in murmurs include mitral regurgitation and aortic stenosis
Pericardial friction rub (abnormal)	Third or fourth intercostal space, anterior axillary line	Sign of pericardial inflammation (pericarditis), associated with each beat of the heart; sounds like a creak or leather being rubbed together

Data from Bickley LS, Szilagyi PG: Bates’ guide to physical examination and history taking, Philadelphia, 2003, Lippincott Williams & Wilkins.

FIGURE 3-8 Areas for heart sound auscultation. (Courtesy Barbara Cocanour, PhD, University of Massachusetts, Lowell, Department of Physical Therapy.)

TABLE 3-9

Electrocardiograph Interpretation

Data from Meyers RS, editor: Saunders manual of physical therapy practice, Philadelphia, 1995, Saunders; Aehlert B, editor: ACLS quick review study guide, St Louis, 1994, Mosby; Davis D, editor: How to quickly and accurately master ECG interpretation, ed 2, Philadelphia, 1992, Lippincott Williams & Wilkins.

Holter Monitoring.

Holter monitoring is 24- or 48-hour ECG analysis conducted to detect cardiac arrhythmias and corresponding symptoms during a patient’s daily activity.¹² Holter monitoring is different than telemetric monitoring because the ECG signal is recorded and later analyzed.

Indications for Holter monitoring include the evaluation of syncope, dizziness, shortness of breath with no other obvious cause, palpitations, antiarrhythmia therapy, pacemaker functioning, activity-induced silent ischemia, and risk of cardiac complications with the use of HRV.

Heart Rate Variability.

HRV has been discussed in the literature to possibly reflect cardiac autonomic nervous system regulation. A common overall measure of HRV is the standard deviation of all RR intervals on an ECG during a 24-hour period (SDNN).⁸ Evidence regarding the potential clinical utility of HRV for cardiology is growing; however, it continues to be used primarily in research.¹⁴ In healthy populations, low HRV is a risk factor for all causes of cardiac mortality^15–17 and for new onset of hypertension.¹⁸ Low HRV is also a risk for mortality in patients who have had an MI^19–21 or have coronary artery disease²² or CHF.²³ Evidence suggests that altered HRV during exercise may provide valuable information for risk assessment.²⁴ This is likely related to the increasingly accepted relationship between delayed heart rate recovery (HRR) after exercise and cardiac risk. Delayed HRR (<46 bpm) 3 minutes after an exercise test is a predictor of long-term (~15 years) mortality.²⁵ HRR is discussed further in the section on Physical Therapy Intervention.

Telemetric Electrocardiogram Monitoring.

Telemetric ECG monitoring provides real-time ECG visualization via radiofrequency transmission of the ECG signal to a monitor. Benefits of telemetry include monitoring with no hardwire connection between the patient and the visual display unit and real-time graphic display of the ECG signal using the standard ECG monitor attachment.

Clinical Tip

Some hospitals use an activity log with Holter monitoring. If so, document physical therapy intervention on the log. If no log is available, record the time of day and physical therapy intervention in the medical record.

Complete Blood Cell Count

Relevant values from the complete blood cell count are hematocrit, hemoglobin, and white blood cell counts. Hematocrit refers to the number of red blood cells per 100 ml of blood and therefore fluctuates with changes in the total red blood cell count (hemoglobin) and with blood volume (i.e., reduced plasma volume results in relatively more red blood cells in 100 ml of blood). Elevated levels of hematocrit (which may be related to dehydration) indicate increased viscosity of blood that can potentially impede blood flow to tissues.¹² Hemoglobin is essential for the adequate oxygen-carrying capacity of the blood. A decrease in hemoglobin and hematocrit levels (10% below normal is called anemia) may decrease activity tolerance or make patients more susceptible to ischemia secondary to decreased oxygen-carrying capacity.^11,26 Slight decreases in hematocrit resulting from adaptations to exercise (with no change in hemoglobin) are related to increases in blood volume. The concomitant exercise-related decreases in blood viscosity may be beneficial to post-MI patients.²⁷

Elevated white blood cell counts can indicate that the body is fighting infection, or they can occur with inflammation caused by cell death, such as in MI. Erythrocyte sedimentation rate (ESR), another hematologic test, is a nonspecific index of inflammation and commonly is elevated for 2 to 3 weeks after MI.²⁶ Refer to Chapter 7 for more information about these values.

Coagulation Profiles

Coagulation profiles provide information about the clotting time of blood. Patients who undergo treatment with thrombolytic therapy after the initial stages of MI or who are receiving anticoagulant therapy because of various cardiac arrhythmias require coagulation profiles to monitor anticoagulation in an attempt to prevent complications such as bleeding. The physician determines the patient’s therapeutic range of anticoagulation using the prothrombin time (PT), partial thromboplastin time, and international normalized ratio.²⁶ Refer to Chapter 7 for details regarding these values and their significance to treatment.

Patients with low PT and partial thromboplastin time are at higher risk of thrombosis, especially if they have arrhythmias (e.g., atrial fibrillation) or valvular conditions (e.g., mitral regurgitation) that produce stasis of the blood. Patients with a PT greater than 2.5 times the reference range should not undergo physical therapy because of the potential for spontaneous bleeding. Likewise, an international normalized ratio of more than 3 warrants asking the physician if treatment should be withheld.²⁶

Blood Lipids

Elevated total cholesterol levels in the blood are a significant risk factor for atherosclerosis and therefore ischemic heart disease.²⁸ Measuring blood cholesterol level is necessary to determine the risk for development of atherosclerosis and to assist in patient education, dietary modification, and medical management. Normal values can be adjusted for age; however, levels of total cholesterol more than 240 mg/dl are generally considered high, and levels of less than 200 mg/dl are considered normal.

A blood lipid analysis categorizes cholesterol into high-density lipoproteins (HDLs) and low-density lipoproteins (LDLs) and provides an analysis of triglycerides. HDLs are formed by the liver and are considered beneficial because they are readily transportable and do not adhere to the intimal walls of the vascular system. People with higher amounts of HDLs are at lower risk for coronary artery disease.26,28 HDL levels of less than 33 mg/dl carry an elevated risk of heart disease. A more important risk for heart disease is an elevated ratio of total cholesterol to HDL. Normal ratios of total cholesterol to HDL range from 3 to 5.¹²

LDLs are formed by a diet excessive in fat and are related to a higher incidence of coronary artery disease. LDLs are not as readily transportable as HDLs because LDLs adhere to intimal walls in the vascular system.²⁶ Normal LDL levels are below 100 mg/dl.¹²

Triglycerides are fat cells that are free floating in the blood. When not in use, they are stored in adipose tissue. A person’s triglyceride levels increase after he or she eats foods high in fat and decrease with exercise. High levels of triglycerides are associated with a risk of coronary heart disease.²⁶

Clinical Tip