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Throat, Respiratory & Cardiovascular Disorders

Throat, Respiratory & Cardiovascular Disorders

A thorough examination of all systems is required to detect peripheral and systemic effects of cardiac disorders as well as evidence of noncardiac disorders that may have an impact on the heart. The following items are examined:

Vital sign monitoring
Auscultation and pulse palpation
Observation of veins
Palpation and examination of the chest
Percussion, palpation, and auscultation of the heart
Examination of the lungs, including percussion, palpation, and auscultation
Examination of the extremities and abdomen
Cardiac auscultation is covered in a separate section. Despite the increasing use of cardiac imaging, bedside auscultation is still useful because it is always available and can be repeated as many times as needed for free.
Other patient data is also collected during the examination.

Signs of Life
Vital indicators include

High blood pressure
Heart rhythm and rate
The rate of respiration
In addition to vital signs, patient weight and peripheral oxygen saturation are frequently obtained (SpO2).

Blood pressure (BP) is taken in both arms and, in the case of suspected congenital cardiac or peripheral vascular disorders, in both legs. The bladder of an appropriately sized cuff encircles 80% of the circumference of the limb, and the width of the bladder is 40% of the circumference. Systolic pressure is the first sound heard as the mercury column falls; diastolic pressure is the disappearance of the sound (5th-phase Korotkoff sound). A pressure differential of up to 15 mm Hg between the right and left arms is normal; a greater differential indicates a vascular abnormality (e.g., dissecting thoracic aorta) or a peripheral vascular disorder. Typically, leg pressure is 20 mm Hg higher than arm pressure. The patient should take an accurate blood pressure reading.

For more than 5 minutes, sit in a chair (not on the examination table), feet on the floor, back supported.
Maintain the limb at heart level with no clothing covering the cuff placement area.
For at least 30 minutes before the measurement, refrain from exercising, consuming caffeine, or smoking.
Blood Pressure Monitoring
Blood Pressure Monitoring

If arrhythmia is suspected, heart rate and rhythm are assessed by palpating the carotid or radial pulse or by cardiac auscultation; some heartbeats during arrhythmias are audible but do not generate a palpable pulse.

A high respiratory rate may indicate cardiac decompensation or a primary lung disorder. In patients with heart failure or anxiety, the rate rises, then falls or becomes intermittent in the moribund. Pleuritic pain may be indicated by shallow, rapid breathing.

Acute rheumatic fever or a cardiac infection can cause a rise in temperature (eg, endocarditis). Low grade fever is very common after a myocardial infarction. Other causes are investigated only if the fever lasts more than 72 hours.

Weight is taken on a standing scale with the patient at each clinic visit, ideally while wearing a similar amount of clothing. Weight gain in patients with heart failure may indicate hypervolemia, whereas weight loss may indicate cardiac cachexia (unintentional, non-edematous weight loss of more than 5% in the previous 12 months—1). To determine whether weight changes are related to changes in volume status and/or amount of muscle or fat, a history and additional findings from the physical examination (jugular veins, lung, and extremity examinations) are required.
Throat, Respiratory & Cardiovascular Disorders
SpO2 (peripheral arterial oxygen saturation) is measured. Pulse oximetry (SpO2) determines the oxygen saturation of hemoglobin in arterial blood and provides a quick, noninvasive estimate of tissue oxygenation. A probe attached to a finger or earlobe is used to obtain pulse oximetry. The general consensus is that SpO2 values of 95% are normal, whereas values of 95% indicate hypoxemia. The target SpO2 in patients with chronic obstructive pulmonary disease is 88 to 92%, which is a notable exception to this cutoff value. When hypoxemia is present, potential cardiac causes include pulmonary edema in heart failure patients and right-to-left intracardiac shunts (a patent foramen ovale in patients with pulmonary hypertension, congenital heart disease including tetralogy of Fallot).

Ankle-brachial index (ABI) (ABI)
The ankle-brachial index (ABI) is the ratio of ankle to arm systolic blood pressure (BP). The ankle blood pressure is measured in both the dorsalis pedis and the posterior tibial artery while the patient is recumbent, and the arm blood pressure is measured in both arms at the brachial artery. The index is calculated for each lower extremity by dividing the higher of the two brachial artery systolic pressures by the higher of the two dorsalis pedis pressures. This ratio is usually greater than one. If the pedal pulses are not easily palpable, a Doppler probe can be used to measure blood pressure at the ankle.

A low ankle-brachial index ( 0.90) indicates peripheral arterial disease, which can be mild (index 0.71 to 0.90), moderate (0.41 to 0.70), or severe ( 0.40). A high index (> 1.30) may indicate noncompressible leg vessels, as seen in blood vessel calcification conditions such as diabetes, end-stage renal disease, and Mönckeberg arteriosclerosis. A high index may indicate that additional vascular studies are required (toe-brachial index or arterial duplex studies).

Changes in orthostatic pressure
The patient’s blood pressure and heart rate are measured while supine, seated, and standing; a 1-minute interval is required between each change in position. A difference in blood pressure of 10 mm Hg and a change in heart rate of 20 beats per minute is considered normal; the difference in blood pressure is slightly higher in older patients due to vascular elasticity loss.

The paradox of the pulse
During inspiration, systolic arterial blood pressure can drop by up to 10 mm Hg, causing pulse rate to increase to compensate. Pulsus paradoxus is defined as an exaggeration of this normal response with a greater decrease in systolic blood pressure or a weakening of the pulse during inspiration. Pulsus paradoxus is a condition that occurs in

Tamponade of the heart (commonly)
Constrictive pericarditis, severe asthma, and chronic obstructive pulmonary disease are all examples of this condition.
Hypovolemic shock, severe pulmonary embolism, and restrictive cardiomyopathy (rarely)
Because negative intrathoracic pressure increases venous return and thus right ventricular (RV) filling during inspiration, the interventricular septum bulges slightly into the left ventricular (LV) outflow tract, decreasing cardiac output and thus BP. This mechanism (and the resulting drop in systolic blood pressure) is exacerbated in disorders that cause high negative intrathoracic pressure (eg, asthma) or that restrict RV filling (eg, cardiac tamponade, cardiomyopathy) or outflow (eg, congestive heart failure) (eg, pulmonary embolism).

Pulsus paradoxus is measured by inflating a blood pressure cuff to just above systolic BP and slowly deflating it (eg, 2 mm Hg/heartbeat). When Korotkoff sounds are first heard (at first, only during expiration) and when Korotkoff sounds are heard continuously, the pressure is measured. The “amount” of pulsus paradoxus is the difference between the pressures.

General information
1. Cardiac cachexia, Lena A, Ebner N, Anker MS. L24-L27 in Eur Heart J Suppl 21 (Suppl L), 2019.
Pulses in the periphery
For symmetry and volume, major peripheral pulses in the arms and legs are palpated (intensity). The arterial wall’s elasticity is observed. The absence of pulses may indicate an arterial disorder (for example, atherosclerosis) or a systemic embolism. Obese or muscular people may have difficulty feeling their peripheral pulses. In disorders with a rapid runoff of arterial blood, the pulse has a rapid upstroke and then collapses (eg, arteriovenous communication, aortic regurgitation). In hyperthyroidism and hypermetabolic states, the pulse is rapid and bounding; in hypothyroidism, it is slow and sluggish. Auscultation over peripheral vessels may detect a bruit due to stenosis if pulses are asymmetric.

Carotid artery pulses
Both carotid pulses being observed, palpated, and auscultated may indicate a specific disorder (see table Carotid Pulse Amplitude and Associated Disorders). Arteriosclerosis and aging cause vessel rigidity, which tends to eliminate the characteristic findings. Even in very young children with severe aortic stenosis, the carotid pulse may be normal.

Murmurs and bruits can be distinguished by auscultation over the carotid arteries. Murmurs originate in the heart or great vessels and are typically louder over the upper precordium and lessen as they progress toward the neck. Bruits are higher-pitched, can only be heard over the arteries, and appear more superficial. A venous hum must be distinguished from an arterial bruit. A venous hum, unlike an arterial bruit, is usually continuous, is best heard with the patient sitting or standing, and is eliminated by compression of the ipsilateral internal jugular vein.

Carotid Pulse Amplitude and Related Disorders
Veins on the periphery
Varicosities, arteriovenous malformations (AVMs), and shunts, as well as overlying inflammation and tenderness due to thrombophlebitis, are all looked for in the peripheral veins. An AVM or shunt causes a continuous murmur (which can be heard on auscultation) as well as a palpable thrill (because resistance is always lower in the vein than in the artery during systole and diastole).

Veins on the neck
The veins in the neck are examined to determine the venous wave height and waveform. Height is proportional to right atrial pressure, and waveform reflects cardiac cycle events; both can be seen best in the internal jugular vein.

The jugular veins are typically examined while the patient is reclining at 45 degrees. Normally, the top of the venous column is just above the clavicles (upper limit of normal: 4 cm above the sternal notch in a vertical plane). Heart failure, volume overload, cardiac tamponade, constrictive pericarditis, tricuspid stenosis, superior vena cava obstruction, or reduced right ventricle compliance all cause an increase in the venous column. When such conditions are severe, the venous column can extend to jaw level, and its top can only be detected when the patient sits or stands upright. In hypovolemia, the venous column is depleted.

Venous Jugular Distention
Venous Jugular Distention

Despite continued abdominal pressure, the venous column can be briefly elevated by firm hand pressure on the abdomen (hepatojugular or abdominojugular reflux); the column falls back in a few seconds (maximum 3 respiratory cycles or 15 seconds) (because a compliant RV increases its stroke volume via the Frank-Starling mechanism). However, during abdominal pressure, the column remains elevated (> 3 cm) in disorders that cause a dilated and poorly compliant RV or in obstruction of RV filling by tricuspid stenosis or right atrial tumor.

During inspiration, the venous column normally falls slightly as lower intrathoracic pressure draws blood from the periphery into the vena cava. A rise in the venous column during inspiration (Kussmaul sign) is seen most commonly in chronic constrictive pericarditis, right ventricular myocardial infarction, and chronic obstructive pulmonary disease (COPD), but it can also be seen in heart failure and tricuspid stenosis.

Waves in the jugular vein (see figure) Normal jugular vein waves) can usually be distinguished clinically, but they are more visible on the screen during central venous pressure monitoring.

Jugular vein waves are normal.
The a wave is caused by right atrial contraction (systole), and the x descent is caused by atrial relaxation. The transmitted carotid pulse causes the c wave, an interruption of the x descent; it is rarely detected clinically. Right atrial filling during ventricular systole causes the v wave (tricuspid valve is closed). The y descent is caused by rapid right ventricle filling during ventricular diastole prior to atrial contraction.

Jugular vein waves are normal.
In pulmonary hypertension and tricuspid valve stenosis, the a waves are increased. In atrioventricular dissociation, giant a waves (Cannon waves) occur when the atrium contracts while the tricuspid valve is closed. When there is poor RV compliance, the a waves disappear and are accentuated (eg, in pulmonary hypertension or pulmonic stenosis). In tricuspid regurgitation, the v waves are very prominent. In cardiac tamponade, the x descent is steep. When RV compliance is poor, the y descent is very abrupt because when the tricuspid valve opens, an elevated column of venous blood rushes into the RV, only to be abruptly stopped by the rigid RV wall (in restrictive myopathy) or the pericardium (in constrictive pericarditis).

Palpation and examination of the chest
The contour of the chest and any visible cardiac impulses are examined. The precordium is palpated for pulsations and thrills (which determine the apical impulse and thus cardiac situs).

Chest deformities can occur as a result of a variety of disorders.

Shield chest and pectus carinatum (a prominent birdlike sternum) may be associated with Marfan syndrome or Noonan syndrome (which may be accompanied by aortic root or mitral valve disease) (which may be accompanied by pulmonic stenosis, atrial septal defects, or hypertrophic cardiomyopathy). A localized upper chest bulge may indicate a syphilis-related aortic aneurysm.

Pectus excavatum (depressed sternum) with a narrow anteroposterior chest diameter and an abnormally straight thoracic spine may be associated with hereditary cardiac defects (eg, Turner syndrome, Noonan syndrome) and, in rare cases, Marfan syndrome.

The patient is lying at a 30 to 45 degree angle. The clinician approaches the patient from the right side and palpates the precordium in a systematic manner.

In healthy people, the apical impulse should be palpable between the 4th and 5th intercostal spaces, just medial to the midclavicular line, and cover an area 2 to 3 cm in diameter.

A palpable lifting sensation under the sternum and anterior chest wall to the left of the sternum indicates severe right ventricular hypertrophy. In rare cases, the precordium bulges asymmetrically to the left of the sternum due to congenital disorders that cause severe RV hypertrophy.

A sustained thrust at the apex (which can be distinguished from the less focal, more diffuse precordial heave of RV hypertrophy) indicates LV hypertrophy.

Patients with a dyskinetic ventricular aneurysm may experience abnormal focal systolic impulses in the precordium. In patients with severe mitral regurgitation, an abnormal diffuse systolic impulse lifts the precordium. Because the left atrium expands, anterior cardiac displacement occurs. When the LV is dilated and hypertrophied, an apical impulse is found that is diffuse and inferolaterally displaced (eg, in mitral regurgitation).

Thrills are a buzzing sensation that occurs when there is a particularly loud murmur. Their location hints at the cause (see table Location of Thrills and Associated Disorder).

Thrill Location and Related Disorder
Exaggerated pulmonic valve closure in pulmonary hypertension can cause a sharp impulse at the 2nd intercostal space to the left of the sternum. A similar early systolic impulse at the cardiac apex could indicate closure of a stenotic mitral valve; opening of the stenotic valve can sometimes be felt at the start of diastole. On auscultation, these findings are consistent with an augmented first heart sound and an opening snap of mitral stenosis.

Examination of the Lungs
The lungs are examined for pleural effusion and pulmonary edema, both of which can occur with cardiac disease such as heart failure. Percussion, palpation, and auscultation are all part of the lung examination.

The primary physical maneuver used to detect the presence and level of pleural effusion is percussion. Finding areas of dullness during percussion indicates the presence of underlying fluid or, less frequently, consolidation.

Tactile fremitus (vibration of the chest wall felt while a patient speaks) is reduced in pleural effusion and pneumothorax and increased in pulmonary consolidation (eg, lobar pneumonias).

Lung auscultation is an important part of the examination of patients with suspected cardiac disease.

The nature and volume of breath sounds can help distinguish cardiac from pulmonary disorders. Crackles, rhonchi, wheezes, and stridor are examples of adventitious sounds. Crackles and wheezes are abnormal lung sounds that can occur in heart failure as well as non-cardiac diseases.

Crackles are sporadic, accidental breath sounds. Fine crackles are brief high-pitched sounds, whereas coarse crackles are prolonged low-pitched sounds. Crackles are similar to the sound of crinkling plastic wrap and can be produced by rubbing strands of hair together between two fingers near one’s ear. They are most commonly associated with atelectasis, alveolar filling processes (for example, pulmonary edema in heart failure), and interstitial lung disease (for example, pulmonary fibrosis); they indicate the opening of collapsed airways or alveoli.
Wheezes are whistling, musical breath sounds that occur more frequently during expiration than during inspiration. Wheezing, which is usually associated with dyspnea, can be a physical finding or a symptom. Wheezes are most commonly associated with asthma, but they can also occur in cardiac conditions such as heart failure.
Crackles icon
AUDIO \sWheezing icon
Examination of the Abdomen and Extremities
The abdomen and extremities are checked for signs of fluid overload, which can occur with both heart failure and noncardiac disorders (eg, renal, hepatic, lymphatic).

Ascites is a symptom of significant fluid overload in the abdomen. Visible abdominal distention caused by marked ascites is tense and nontender to palpation, with shifting dullness on abdominal percussion and a fluid wave. The liver may be distended and slightly tender, and there may be hepatojugular reflux.

Fluid overload manifests itself in the extremities (primarily the legs) as edema, which is swelling of soft tissues caused by increased interstitial fluid. On inspection, edema may be visible, but minor amounts of edema in very obese or muscular people may be difficult to detect visually. Thus, the examiner’s fingers are used to palpate the extremities for the presence and degree of pitting (visible and palpable depressions caused by pressure from the examiner’s fingers, which displaces the interstitial fluid). The extent of the edema, symmetry (comparing both extremities), warmth, erythema, and tenderness are all evaluated. Edema over the sacrum, genitals, or both may be present with significant fluid overload.

Tenderness, erythema, or both, especially if unilateral, point to an inflammatory cause (eg, cellulitis or thrombophlebitis). Nonpitting edema indicates lymphatic or vascular obstruction rather than fluid overload.

Ultrasonography at the Point of Care (POCUS)
(Also see Echocardiography.)

Point-of-care ultrasonography (POCUS) is an adjunct to the physical examination that employs small, inexpensive, battery-operated ultrasound devices that are operated at the bedside by the clinician. Doppler techniques in both two dimensions and color can be used. A brief, focused ultrasound examination has been shown to improve detection of various cardiac anomalies, confirm findings from physical examination, and sometimes make a diagnosis in the absence of physical findings. Identification is a common application (1, 2)

Systolic dysfunction of the left ventricle (with global or regional wall motion abnormality)
Anomaly of the left ventricular regional wall motion (with reduced or normal systolic function)
Left heart filling pressures are elevated (enlarged left atrium)
Structure and operation of a valve
Edema of the lungs (vertical B-lines in the lung fields)
Pleural edema
Congestion of the veins throughout the body (dilated inferior vena cava)
Cardiovascular tamponade and pericardial effusion
To ensure high image quality and accurate interpretation, adequate training in performing brief ultrasound examinations is required (2). POCUS should be used to supplement rather than replace physical examinations.

Ultrasound at the Point of Care
1. Kimura BJ: Better at the bedside: point-of-care cardiac ultrasound techniques in physical examination. doi: 10.1136/heartjnl-2016-309915.
2. Spencer KT, Kimura BJ, Korcarz CE, et al: American Society of Echocardiography Recommendations for Focused Cardiac Ultrasound. J Am Soc Echocardiogr, 2013;26:567-581. doi:10.1016/j.echo.2013.04.001 quiz link
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Jugular vein waves are normal.
Jugular vein waves are normal.

Home>Nursing homework help
For this, you will take on the role of a clinician who is building a health history for the following patient:

Chief Complaint
(CC) A 65-year-old male with chronic obstructive pulmonary disease (COPD) presents to the clinic with a cough he has had for the past 2 weeks.

Subjectivedenies chest pain, denies night sweats, admits to having a fever but does not know the temp.

VS(BP) 115/75, (P) 89, (RR) 16, (T) 100.4°F (38°C), O2 sat 98% on room air.

Generalpatient appears tired; skin color pale, patient is diaphoretic and sweaty, height 5′3″; weight 175 lbs

HEENTEYES: no injection, no increase in lacrimation or purulent drainage;
EARS: normal
TM: Normal
NOSE: Bilateral erythema and edema of turbinates with significant yellow drainage on the right. Obstructed air passages

Respiratorylung crackles in LLL, no wheezes or rhonchi noted; does not clear with coughing; dullness to percussion over the LLL; shallow respirations and is 30, accessory muscles use not present

Neck/Throatno neck swelling or tenderness with palpation; neck is supple; no JVD; thyroid is not enlarged;
trachea midline

HeartRegular rate and rhythm, no murmur, S3, or S4

Answer the following :

What other subjective data would you obtain?
What other objective findings would you look for?
What diagnostic examination do you want to order?
Name 3 differential diagnoses based on this patient presenting symptoms?
Give rationales for your each differential diagnosis.

Submission Instructions:

Requirements: at least 500 words ( 2 complete pages of content) formatted and cited in current APA style 7 ed with support from at least 3 academic sources which need to be journal articles or books from 2019 up to now. NO WEBSITES allowed for reference entry. Include doi, page numbers, etc. Plagiarism must be less than 5%.

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