Chest pain-onset? Location? Radiation? Quality? Rating on scale of 1 to 10 (10 being the worst)? Duration? How often? See Table 17-1 for a description of various types of cardiovascular pain.
What brings it on? What relieves it? Does activity make it worse? Does it have a pattern or radiate? (See Figs. 17-4 and 17-5.) Are there any other associated symptoms, such as nausea, vomiting, sweating? Irregular heartbeat, palpitations? Does your heart pound or beat too fast? Does your heart skip or jump? Difficulty breathing or shortness of breath? Dizziness? Light-headedness? Swelling in feet, ankles or legs? Heart burn-Onset? How often? Relief? History of heart defect? Murmur? Rheumatic fever? Heart surgery? Cardiac balloon interventions? Last electrocardiogram and results? Cholesterol levels? Medications for heart disease? Usual blood pressure? Family history of hypertension, myocardial infarction, coronary heart disease, elevated cholesterol levels, or diabetes mellitus? Smoking? Packs per day? Over how many years? Attempts and/or desire to quit? Twenty-four-hour dietary recall? Alcohol consumption each day? Form of exercise? How often? Any change in activities of daily living over the last 5 years? Over the last 10 years? Ability to care for self? Any activities limited because of chest pain, shortness of breath, or fatigue? Effects of heart disease on sexual activities? Number of pillows used to sleep on at night? Daily stressors? Forms of relaxation? Fears regarding heart disease?
It should be assumed that chest pain is due to cardiac ischemia until determined otherwise through a thorough assessment. This may be life threatening because of lack of oxygen, causing damage to cells in the heart muscle. This is a medical emergency.
Risk for coronary heart disease related to hypertension, increased low-density lipoprotein (LDL) cholesterol and decreased high-density lipoprotein cholesterol, diabetes mellitus, minimal exercise, cigarette smoking, diet high in saturated fat and trans fatty acids, postmenopausal without estrogen replacement (in females), family history, and upper body obesity.
See Figure 17-2 for a diagram of the heart chambers, valves, and circulation. Additional data gathered during assessment of the blood pressure, skin, nails, head, thorax and lungs, and peripheral pulses all play a part in the complete cardiovascular assessment. Provide the client with as much modesty as possible. Explain that the client will need to move to different positions to facilitate auscultation of heart sounds. Tell the client you will be listening to the heart in several areas and that this does not necessarily mean that anything is wrong. Note: If a client has large breasts, ask them to pull the breast upward and to the side when you are auscultating for heart sounds.
| ASSESSMENT PROCEDURE | NORMAL FINDINGS | ABNORMAL FINDINGS |
|---|---|---|
| Inspection | ||
| Observe the jugular venous pulse. Inspect the jugular venous pulse by standing on the right side of the client. The client should be in a supine position with the torso elevated 30-45 degrees. Make sure the head and torso are on the same plane. Ask the client to turn the head slightly to the left. Shine a tangential light source onto the neck to increase visualization of pulsations as well as shadows. Next, inspect the suprasternal notch or the area around the clavicles for pulsations of the internal jugular veins. Note: Be careful not to confuse pulsations of the carotid arteries with pulsations of the internal jugular veins. | The jugular venous pulse is not normally visible with the client sitting upright. This position fully distends the vein, and pulsations may or may not be discernible. | Fully distended jugular veins with the client's torso elevated more than 45 degrees indicate increased central venous pressure that may be the result of right ventricular failure, pulmonary hypertension, pulmonary emboli, or cardiac tamponade. Distention of jugular vein on one side may be caused by a kink or aneurysm. |
| Evaluate jugular venous pressure (Fig. 17-6). Evaluate jugular venous pressure by watching for distention of the jugular vein. It is normal for the jugular veins to be visible when the client is supine. To evaluate jugular vein distention, position the client in a supine position with the head of the bed elevated 30, 45, 60, and 90 degrees. At each increase of the elevation, have the client's head turned slightly away from the side being evaluated. Using tangential lighting, observe for distention, protrusion, or bulging. Note: In acute care settings, a more accurate way to measure jugular pressure is by use of invasive cardiac monitors (pulmonary artery catheters) to precisely measure pressures (Kelly & Rabbani, 2013). | The jugular vein should not be distended, bulging, or protruding at 45 degrees or greater. | Distention, bulging, or protrusion at 45, 60, or 90 degrees may indicate right-sided heart failure. Document at which positions (45, 60, and/or 90 degrees) you observe distention. Clients with obstructive pulmonary disease may have elevated venous pressure only during expiration. An inspiratory increase in venous pressure, called Kussmaul sign, may occur in clients with severe constrictive pericarditis. |
| Auscultation | ||
| Auscultate the carotid arteries. Auscultate the carotid arteries if the client is middle-aged or older or if you suspect cardiovascular disease. Place the bell of the stethoscope over the carotid artery and ask the client to hold their breath for a moment so breath sounds do not conceal any vascular sounds (Fig. 17-7). Note: Always auscultate the carotid arteries before palpating because palpation may increase or slow the heart rate, changing the strength of the carotid impulse heard. | No blowing, swishing, or other sounds are heard. | A bruit, a blowing or swishing sound caused by turbulent blood flow through a narrowed vessel, is indicative of occlusive arterial disease. However, if the artery is more than two-thirds occluded, a bruit may not be heard. Pulse inequality may indicate arterial constriction or occlusion in one carotid. Weak pulses may indicate hypovolemia, shock, or decreased cardiac output. A bounding, firm pulse may indicate hypervolemia or increased cardiac output. Variations in strength from beat to beat or with respiration are abnormal and may indicate a variety of problems. A delayed upstroke may indicate aortic stenosis. |
| Pulses are equally strong: a 2+ or normal with no variation in strength from beat to beat. Contour is normally smooth and rapid on the upstroke and slower and less abrupt on the downstroke. The strength of the pulse is evaluated on a scale from 0 to 4 as follows: Pulse Amplitude Scale 0 = absent 1+ = weak 2+ = normal 3+ = increased 4+ = bounding | ||
| Palpation | ||
| Palpate the carotid arteries. Palpate each carotid artery alternately by placing the pads of the index and middle fingers medial to the sternocleidomastoid muscle on the neck (Fig. 17-8). Note amplitude and contour of the pulse, elasticity of the artery, and any thrills. | Arteries are elastic and no thrills are noted. Pulses are equally strong: a 2+ or normal with no variation in strength from beat to beat. Contour is normally smooth and rapid on the upstroke and slower and less abrupt on the downstroke. | Loss of elasticity may indicate arteriosclerosis. Thrills may indicate a narrowing of the artery. Pulse inequality may indicate arterial constriction or occlusion in one carotid. Weak pulses may indicate hypovolemia, shock, or decreased cardiac output. |
| Palpation | ||
| Note: Palpate the carotid arteries individually because bilateral palpation could result in reduced cerebral blood flow. Be cautious with older clients because atherosclerosis may have caused obstruction and compression may easily block circulation. | The strength of the pulse is evaluated on a scale from 0 to 4 as follows: Pulse Amplitude Scale 0 = absent 1+ = weak 2+ = normal 3+ = increased 4+ = bounding | A bounding, firm pulse may indicate hypervolemia or increased cardiac output. Variations in strength from beat to beat or with respiration are abnormal and may indicate a variety of problems. A delayed upstroke may indicate aortic stenosis. |
| Inspection | ||
| Inspect chest to identify landmarks that aid in assessment of the heart (Fig. 17-9). Check for visibility of point of maximum impulse (PMI) and any abnormal pulsations. | ||
| Inspect for any pulsations on anterior chest over heart. With the client in supine position with the head of the bed elevated between 30 and 45 degrees, stand on the client's right side and look for the apical impulse and any abnormal pulsations. Note: The apical impulse was originally called the PMI. However, this term is no longer used because a maximal impulse may occur in other areas of the precordium as a result of abnormal conditions. | The apical impulse may or may not be visible. If apparent, it would be in the mitral area (left midclavicular line, fourth or fifth intercostal space). The apical impulse is a result of the left ventricle moving outward during systole. | |
| Palpation | ||
| The client should be lying down. Palpate using the fingertips and palmar surfaces of fingers in an organized fashion, beginning in the aortic area and moving down the chest toward the tricuspid area (Fig. 17-10). | ||
| Palpate the apical impulse. Remain on the client's right side and ask the client to remain supine. Use one or two finger pads to palpate the apical impulse in the mitral area (fourth or fifth intercostal space at the midclavicular line). You may ask the client to roll to the left side to better feel the impulse using your finger pads (Fig. 17-11). | The apical impulse is palpated in the mitral area and may be the size of a nickel (1-2 cm). Amplitude is usually small-like a gentle tap. The duration is brief, lasting through the first two-thirds of systole and often less. In obese clients or clients with large breasts, the apical impulse may not be palpable. | The apical impulse may be impossible to palpate in clients with pulmonary emphysema. If the apical impulse is larger than 1-2 cm, displaced, more forceful, or of longer duration, suspect cardiac enlargement. |
| Note: If this apical pulsation cannot be palpated, have the client assume a left lateral position. This displaces the heart toward the left chest wall and relocates the apical impulse farther to the left. | ||
| Palpate for abnormal pulsations. Use your palmar surfaces to palpate the apex, left sternal border, and base. | No pulsations or vibrations are palpated in the areas of the apex, left sternal border, or base. | A thrill or a pulsation is usually associated with a grade IV or higher murmur. |
| Percussion | ||
| Percussion may be done to define cardiac borders by identifying areas of dullness, but it is generally unreliable. Size of heart can be more accurately determined by chest x-ray. | ||
| Auscultation | ||
| Auscultate in an orderly, systematic fashion beginning with the aortic area. Move across and then down the chest. Focus on one sound at a time. Auscultate each area with the stethoscope diaphragm applied firmly to the chest. Repeat the sequence using the stethoscope bell applied lightly to the chest. Auscultate with the client in the supine position. Then listen specifically over the apex with the bell while client is in the left lateral position. Assist client to a sitting position and auscultate the pericardium with the diaphragm. Then have the client lean forward and exhale while you listen over the aortic area with the diaphragm. | ||
| Auscultate heart rate and rhythm. Place the diaphragm of the stethoscope at the apex and listen closely to the rate and rhythm of the apical impulse. | Rate should be 60-100 beats/min, with regular rhythm. A regularly irregular rhythm, such as sinus arrhythmia when the heart rate increases with inspiration and decreases with expiration, may be normal in young adults. Resting pulse rate (RPR) varies by age, fitness level, gender, ethnicity/racial background, and other factors (El-Wazir, 2019). | Bradycardia (<60 beats/min) or tachycardia (>100 beats/min) may result in decreased cardiac output. Refer clients with irregular rhythms (e.g., premature atrial contraction or premature ventricular contractions, atrial fibrillation, atrial flutter with varying blocks) for further evaluation. These types of irregular patterns may predispose the client to decreased cardiac output, heart failure, or emboli. |
| If you detect an irregular rhythm, auscultate for a pulse rate deficit. This is done by palpating the radial pulse while you auscultate the apical pulse. Count for a full minute. | The radial and apical pulse rates should be identical. | A pulse deficit (difference between the apical and peripheral/radial pulses) may indicate atrial fibrillation, atrial flutter, premature ventricular contractions, and varying degrees of heart block. |
| Auscultate to identify S1and S2 (Fig. 17-12). Auscultate the first heart sound (S1 or "lub") and the second heart sound (S2 or "dub"). Remember these two sounds make up the cardiac cycle of systole and diastole. S1 starts systole, and S2 starts diastole. The space, or systolic pause, between S1 and S2 is of short duration (thus S1 and S2 occur very close together); the space, or diastolic pause, between S2 and the start of another S1 is of longer duration. Note: If you are experiencing difficulty differentiating S1 from S2, palpate the carotid pulse: the harsh sound that you hear from the carotid pulse is S1 | S1 corresponds with each carotid pulsation and is loudest at the apex of the heart. S2 immediately follows after S1 and is loudest at the base of the heart. | |
| Listen to S1. Use the diaphragm of the stethoscope to best hear S1 (Fig. 17-13). | A distinct sound is heard in each area but is loudest at the apex. May become softer with inspiration. A split S1 may be heard normally in young adults at the left lateral sternal border. | Accentuated, diminished, varying, or split S1 are all abnormal findings. |
| Listen to S2. Use the diaphragm of the stethoscope (see Figs. 17-12 and 17-13). Ask the client to breathe regularly. Note: Do not ask the client to hold their breath. Breath holding will cause any normal or abnormal split to subside. | Distinct sound is heard in each area but is loudest at the base. A split S2 (into two distinct sounds of its components-A2 and P2) is normal and termed physiologic splitting. It is usually heard late in inspiration at the second or third left interspaces. | Any split S2 heard in expiration is abnormal. |
| Auscultate for extra heart sounds. Use the diaphragm first, then the bell to auscultate over the entire heart area. Note the characteristics (e.g., location, timing) of any extra sound heard. Auscultate during the systolic pause (space heard between S1 and S2). Auscultate during the diastolic pause (space heard between end of S2 and the next S1). Note: While auscultating, keep in mind that development of a pathologic S3 may be the earliest sign of heart failure. | Normally no sounds are heard. A physiologic S3 (Fig. 17-14) heart sound is a benign finding commonly heard at the beginning of the diastolic pause in children, adolescents, and young adults. It is rare after age 40. The physiologic S3 usually subsides upon standing or sitting up. A physiologic S4 heart sound (Fig. 17-15) may be heard near the end of diastole in well-conditioned athletes and in adults older than age 40 or 50 with no evidence of heart disease, especially after exercise. | Ejection sounds or clicks (e.g., a midsystolic click associated with mitral valve prolapse). A friction rub may also be heard during the systolic pause. A pathologic S3 (ventricular gallop) may be heard with ischemic heart disease, hyperkinetic states (e.g., anemia), or restrictive myocardial disease. A pathologic S4 (atrial gallop) toward the left side of the precordium may be heard with coronary artery disease, hypertensive heart disease, cardiomyopathy, and aortic stenosis. A pathologic S4 toward the right side of the precordium may be heard with pulmonary hypertension and pulmonic stenosis. S3 and S4 pathologic sounds together create a quadruple rhythm, which is called a summation gallop. Opening snaps occur early in diastole and indicate mitral valve stenosis. A friction rub may also be heard during the diastolic pause. |
| Auscultate for murmurs. A murmur is a swishing sound caused by turbulent blood flow through the heart valves or great vessels. Auscultate for murmurs across the entire heart area. Use the diaphragm and the bell of the stethoscope in all areas of auscultation because murmurs have a variety of pitches. Also auscultate with the client in different positions as described in the next section because some murmurs occur or subside according to the client's position. | Normally no murmurs are heard. However, innocent and physiologic midsystolic murmurs may be present in a healthy heart. See Table 17-2 for classification of murmurs. | Pathologic midsystolic, pansystolic, and diastolic murmurs. See Table 17-2 for classification of murmurs. |
| Auscultate with the client assuming other positions. Ask the client to assume a left lateral position. Use the bell of the stethoscope and listen at the apex of the heart. | S1 and S2 heart sounds are normally present. | An S3 or S4 heart sound or a murmur of mitral stenosis that was not detected with the client in the supine position may be revealed when the client assumes the left lateral position. |
| Ask the client to sit up, lean forward, and exhale. Use the diaphragm of the stethoscope and listen over the apex and along the left sternal border. | S1 and S2 heart sounds are normally present. | Murmur of aortic regurgitation may be detected when the client assumes this position. |
| ASSESSMENT PROCEDURE | NORMAL FINDINGS AND VARIATIONS |
|---|---|
| Inspect chest wall in semi-Fowler position from an angle for PMI. | PMI is easily visible because heart is larger in proportion to chest size (Fig. 17-16). Heart lies more horizontally up to age 5-6 years. Thus, the PMI may be lateral to the MCL. |
| Palpate peripheral pulse points in relation to apical pulse and to each other: femoral, radial, brachial, and carotid. Palpate femoral and brachial pulses at the same time. | Symmetrical and equal rate, strength, and rhythm. |
| ASSESSMENT PROCEDURE | NORMAL FINDINGS AND VARIATIONS |
|---|---|
| Percuss heart size. Note: This is rarely done owing to inaccuracy of the method. | Percussion area is slightly larger because of horizontal position and overlying thymus gland. |
| Auscultate S1 and S2 at: | |
| Pulmonic area (Erb point). | S1 is louder than S2, or S2 is louder than S1. Splitting of S2 is heard best at Erb point (25% to 33% of all children). This is a frequent site of innocent murmurs (grade 3 or lower), which are common throughout childhood. They are of short duration with no transmission to other areas; are low pitched, musical, or of groaning quality that is variable in intensity in relation to position, respiration, activity, fever, and anemia with no other associated signs of heart disease. Other murmurs may indicate pathology. |
| Tricuspid area | S1 louder, preceding S2 |
| Mitral area | S1 loudest |
| Auscultate for sinus arrhythmia | Varies with respiration; very common and disappears with age. Heart rate may increase with inhaling and decrease with exhaling. If a child holds their breath, rhythm will become regular. |
| Auscultate for pulse rate | See Table 17-3 for normal pediatric pulse rates. |
In addition to the focus questions for adults, inquire about the following: Mother's use of therapeutic drugs or drug abuse during pregnancy? Poor weight gain? Signs of delayed development (e.g., slowed social development, language development, or motor skills)? Difficulty in feeding (breast, bottle, acceptance of new foods)? Inability to tolerate physical activity or play with peers? Squatting behavior? Excessive irritability or crying? Circumoral cyanosis or central cyanosis?
See Table 17-3 for average heart rates of infants and children.
Be cautious with palpating carotid arteries in older clients because atherosclerosis may have caused obstruction and compression may easily block circulation.
Decreased elasticity of heart and arteries; reduced pumping ability of heart
Apical impulse may be difficult to palpate because of increased anteroposterior chest diameter.
Location of heart sounds and PMI may be varied owing to kyphosis or scoliosis.
African Americans have the world's highest rates of hypertension, with 40% of non-Hispanic African American men and women having hypertension (AHA, 2016). Their hypertension develops earlier in life and is more severe than other ethnic groups. As for cholesterol, Hispanic males have the highest LDL cholesterol worldwide, followed by White women, and Asians have the lowest levels (AHA, 2019a).
Hispanics and Blacks have increasing stiffness of carotid arteries with age in comparison to Whites. As they age, Hispanics have an increased carotid diameter, which is not seen in Whites and Blacks (Markert et al., 2011). The widening of the carotid diameter in Hispanics may account for their significantly reduced rate of mortality from ischemic stroke than the rate for non-Hispanic Whites.
In the United States, heart disease causes more deaths than other conditions among all ethnic groups. However, all cardiovascular diseases are higher in the southern states; therefore, that region is sometimes referred to as the "Stroke Belt" (Moawad, 2020).
Surprisingly, in what has been called the "Hispanic paradox," those of Hispanic ethnicity have a higher prevalence of diabetes and obesity-and higher death rates related to diabetes, chronic liver disease/cirrhosis, and environmental conditions conducive to disease-compared with Whites but have a lower overall cardiovascular disease and mortality rate by 2 years than Whites (CDC, 2015).
| Decreased cardiac output | Congenital heart disease |
| Congestive heart failure | Endocarditis |
| Myocardial ischemia | Angina |
| Cardiogenic shock | Dysrhythmia |