exercise 7.9 case study history and physical examination findings

LYRAD K. RILEY, MD, AND JEDDA RUPERT, MD

This is a corrected version of the article that appeared in print.

Am Fam Physician. 2015;92(11):1004-1011

Author disclosure: No relevant financial affiliations.

An elevated white blood cell count has many potential etiologies, including malignant and nonmalignant causes. It is important to use age- and pregnancy-specific normal ranges for the white blood cell count. A repeat complete blood count with peripheral smear may provide helpful information, such as types and maturity of white blood cells, uniformity of white blood cells, and toxic granulations. The leukocyte differential may show eosinophilia in parasitic or allergic conditions, or it may reveal lymphocytosis in childhood viral illnesses. Leukocytosis is a common sign of infection, particularly bacterial, and should prompt physicians to identify other signs and symptoms of infection. The peripheral white blood cell count can double within hours after certain stimuli because of the large bone marrow storage and intravascularly marginated pools of neutrophils. Stressors capable of causing an acute leukocytosis include surgery, exercise, trauma, and emotional stress. Other nonmalignant etiologies of leukocytosis include certain medications, asplenia, smoking, obesity, and chronic inflammatory conditions. Symptoms suggestive of a hematologic malignancy include fever, weight loss, bruising, or fatigue. If malignancy cannot be excluded or another more likely cause is not suspected, referral to a hematologist/oncologist is indicated.

Leukocytosis, often defined as an elevated white blood cell (WBC) count greater than 11,000 per mm 3 (11.0 × 10 9 per L) in nonpregnant adults, is a relatively common finding with a wide differential. It is important for clinicians to be able to distinguish malignant from non-malignant etiologies, and to differentiate between the most common nonmalignant causes of leukocytosis.

Leukocytosis in the range of approximately 50,000 to 100,000 per mm 3 (50.0 to 100.0 × 10 9 per L) is sometimes referred to as a leukemoid reaction. This level of elevation can occur in some severe infections, such as Clostridium difficile infection, sepsis, organ rejection, or in patients with solid tumors. 1 Leukocytosis greater than 100,000 per mm 3 is almost always caused by leukemias or myeloproliferative disorders. 2

Normal Variation

The normal range for WBC counts changes with age and pregnancy ( Table 1 ) . 3 Healthy newborn infants may have a WBC count from 13,000 to 38,000 per mm 3 (13.0 to 38.0 × 10 9 per L) at 12 hours of life (95% confidence interval). By two weeks of age, this decreases to approximately 5,000 to 20,000 per mm 3 (5.0 to 20.0 × 10 9 per L), and gradually declines throughout childhood to reach adult levels of 4,500 to 11,000 per mm 3 (4.5 to 11.0 × 10 9 per L; 95% confidence interval) by about 21 years of age. 3 There is also a shift from relative lymphocyte to neutrophil predominance from early childhood to the teenage years and adulthood. 4 During pregnancy, there is a gradual increase in the normal WBC count (third trimester 95% upper limit = 13,200 per mm 3 [13.2 × 10 9 per L] and 99% upper limit = 15,900 per mm 3 [15.9 × 10 9 per L]), and a slight shift toward an increased percentage of neutrophils. 5 In one study of afebrile postpartum patients, the mean WBC count was 12,620 per mm 3 (12.62 × 10 9 per L) for women after vaginal deliveries and 12,710 per mm 3 (12.71 × 10 9 per L) after cesarean deliveries. Of note, positive bacterial cultures were not associated with leukocytosis or neutrophilia, making leukocytosis an unreliable discriminator in deciding which postpartum patients require antibiotic therapy. 6 Patients of black African descent tend to have a lower WBC count (by 1,000 per mm 3 [1.0 × 10 9 per L]) and lower absolute neutrophil counts. 7

Normal Leukocyte Life Cycle and Responses

The life cycle of leukocytes includes development and differentiation, storage in the bone marrow, margination within the vascular spaces, and migration to tissues. Stem cells in the bone marrow produce cell lines of erythroblasts, which become red blood cells; megakaryoblasts, which become platelets; lymphoblasts; and myeloblasts. Lymphoblasts develop into various types of T and B cell lymphocytes. Myeloblasts further differentiate into monocytes and granulocytes, a designation that includes neutrophils, basophils, and eosinophils ( Figure 1 ) . Once WBCs have matured within the bone marrow, 80% to 90% remain in storage in the bone marrow. This large reserve allows for a rapid increase in the circulating WBC count within hours. A relatively small pool (2% to 3%) of leukocytes circulate freely in the peripheral blood 1 ; the rest stay deposited along the margins of blood vessel walls or in the spleen. Leukocytes spend most of their life span in storage. Once a leukocyte is released into circulation and peripheral tissues, its life span ranges from two to 16 days, depending on the type of cell.

Differentiation by Type of White Blood Cell

Changes in the normal distribution of types of WBCs can indicate specific causes of leukocytosis ( Table 2 ) . 8 Although the differential of the major types of WBCs is important for evaluating the cause of leukocytosis, it is sometimes helpful to think in terms of absolute, rather than relative, leukopenias and leukocytoses. To calculate the absolute cell count, the total leukocyte count is multiplied by the differential percentage. For example, with a normal WBC count of 10,000 per mm 3 (10.0 × 10 9 per L) and an elevated monocyte percentage of 12, the absolute monocyte count is 12% or 0.12 times the WBC count of 10,000 per mm 3 , yielding 1,200 per mm 3 (1.2 × 10 9 per L), which is abnormally elevated.

The most common type of leukocytosis is neutrophilia (an increase in the absolute number of mature neutrophils to greater than 7,000 per mm 3 [7.0 × 10 9 per L]), which can arise from infections, stressful conditions, chronic inflammation, medication use, and other causes ( Table 3 ) . 1 – 7 , 9 , 10 Lymphocytosis (when lymphocytes make up more than 40% of the WBC count or the absolute count is greater than 4,500 per mm 3 [4.5 × 10 9 per L]) can occur in patients with pertussis, syphilis, viral infections, hypersensitivity reactions, and certain subtypes of leukemia or lymphoma. Lymphocytosis is more likely to be benign in children than in adults. 4 Epstein-Barr virus infection, tuberculosis or fungal disease, autoimmune disease, splenectomy, protozoan or rickettsial infections, and malignancy can cause monocytosis (monocytes make up more than 8% of the WBC count or the absolute count is greater than 880 per mm 3 [0.88 × 10 9 per L]). 8

Eosinophilia (eosinophil absolute count greater than 500 per mm 3 [0.5 × 10 9 per L]), although uncommon, may suggest allergic conditions such as asthma, urticaria, atopic dermatitis or eosinophilic esophagitis, drug reactions, dermatologic conditions, malignancies, connective tissue disease, idiopathic hypereosinophilic syndrome, or parasitic infections, including helminths (tissue parasites more than gut-lumen parasites). 11 , 12 Isolated basophilia (number of basophils greater than 100 per mm 3 [0.1 × 10 9 per L]) is rare and unlikely to cause leukocytosis in isolation, but it can occur with allergic or inflammatory conditions and chronic myelogenous leukemia 13 ( Table 4 ) .

Nonmalignant Etiologies

A reactive leukocytosis, typically in the range of 11,000 to 30,000 per mm 3 (11.0 to 30.0 × 10 9 per L), can arise from a variety of etiologies. Any source of stress can cause a catecholamine-induced demargination of WBCs, as well as increased release from the bone marrow storage pool. Examples include surgery, exercise, trauma, burns, and emotional stress. 9 One study showed an average increase in WBCs of 2,770 per mm 3 (2.77 × 10 9 per L) peaking on postoperative day 2 after knee or hip arthroplasty. 10 Medications known to increase the WBC count include corticosteroids, lithium, colony-stimulating factors, beta agonists, and epinephrine. During the recovery phase after hemorrhage or hemolysis, a rebound leukocytosis can occur.

Leukocytosis is one of the hallmarks of infection. In the acute stage of many bacterial infections, there are primarily mature and immature neutrophils ( Figure 2 ) ; sometimes, as the infection progresses, there is a shift to lymphocyte predominance. The release of less-mature bands and metamyelocytes into the peripheral circulation results in the so-called “left shift” in the WBC differential. Of note, some bacterial infections paradoxically cause neutropenias, such as typhoid fever, rickettsial infections, brucellosis, and dengue. 1 , 14 Viral infections may cause leukocytosis early in their course, but a sustained leukocytosis is not typical, except for the lymphocytosis in some childhood viral infections.

An elevated WBC count is a suggestive, but not definitive, marker of the presence of significant infection. For example, the sensitivity and specificity of an elevated WBC count in diagnosing acute appendicitis are 62% and 75%, respectively. 15 , 16 For diagnosing serious bacterial infections without a source in febrile children, the discriminatory value of leukocytosis is less than that of other biomarkers, such as C-reactive protein or procalcitonin. 17 Although a WBC count greater than 12,000 per mm 3 (12.0 × 10 9 per L) is one of the criteria for the systemic inflammatory response syndrome (or sepsis when there is a known infection), leukocytosis alone is a poor predictor of bacteremia and not an indication for obtaining blood cultures. 18 , 19

Other acquired causes of leukocytosis include functional asplenia (predominantly lymphocytosis), smoking, and obesity. Patients with a chronic inflammatory condition, such as rheumatoid arthritis, inflammatory bowel disease, or a granulomatous disease, may also exhibit leukocytosis. Genetic causes include hereditary or chronic idiopathic neutrophilia and Down syndrome.

Malignant Etiologies

Leukocytosis may herald a malignant disorder, such as an acute or chronic leukemia ( Figure 3 ) , or a myeloproliferative disorder, such as polycythemia vera, myelofibrosis, or essential thrombocytosis. A previous article on leukemia in American Family Physician reviewed the features and differentiation of malignant hematopoietic disorders. 20 Many solid tumors may lead to a leukocytosis in the leukemoid range, either through bone marrow involvement or production of granulocyte colony-stimulating or granulocyte-macrophage colony-stimulating factors 1 , 3 , 21 ( Figure 4 ) . Chronic leukemias are most commonly diagnosed after incidental findings of leukocytosis on complete blood counts in asymptomatic patients. Patients with features suggestive of hematologic malignancies require prompt referral to a hematologist/oncologist ( Table 5 ) . 3 , 22

Approach to Evaluation

A systematic approach to patients with leukocytosis includes identifying historical clues that suggest potential causes ( Figure 5 ) . Fever and pain may accompany infections or malignancies; other constitutional symptoms, such as fatigue, night sweats, weight loss, easy bruising, or bleeding, might suggest malignancy. 22 Previous diagnoses or comorbid conditions that cause chronic inflammation should be noted, as well as recent stressful events, medication use, smoking status, and history of splenectomy or sickle cell anemia. A history of an elevated WBC count is important, because duration will help determine the likely cause. Leukocytosis lasting hours to days has a different differential diagnosis (e.g., infections, acute leukemias, stress reactions) than a case that persists for weeks to months (e.g., chronic inflammation, some malignancies).

The physical examination should note erythema, swelling, or lung findings suggestive of an infection; murmurs suggestive of infective endocarditis; lymphadenopathy suggestive of a lymphoproliferative disorder; or splenomegaly suggestive of chronic myelogenous leukemia or a myeloproliferative disorder; petechiae or ecchymoses; or painful, inflamed joints suggestive of connective tissue disease or infection.

Initial laboratory evaluation should include`a repeat complete blood count to confirm the elevated WBC level, with differential cell counts and a review of a peripheral blood smear. The peripheral smear should be examined for toxic granulations (suggestive of inflammation), platelet clumps (which may be misinterpreted as WBCs), the presence of immature cells, and uniformity of the WBCs. On evaluation of a leukocytosis with lymphocyte predominance, a monomorphic population is concerning for chronic lymphocytic leukemia, whereas a pleomorphic (varying sizes and shapes) lymphocytosis is suggestive of a reactive process. 4 , 23 With all forms of leukocytosis, concurrent abnormalities in other cell counts (erythrocytes or platelets) suggest a primary bone marrow process and should prompt hematology/oncology evaluation.

As indicated by the history and examination findings, physicians should consider performing cultures of blood, urine, and joint or body fluid aspirates; rheumatology studies; a test for heterophile antibodies (mononucleosis spot test); and serologic titers. Radiologic studies may include chest radiography (to identify infections, some malignancies, and some granulomatous diseases) and, as indicated by history, computed tomography or bone scan. If hematologic malignancy is suspected, additional confirmatory testing may include flow cytometry, cytogenetic testing, or molecular testing of the bone marrow or peripheral blood.

Data Sources : The primary literature search was completed using Essential Evidence Plus and included searches of the Cochrane, POEM, and NICE guideline databases using the search term leukocytosis. In addition, PubMed searches were performed using the terms leukocytosis and white blood cell. Search dates: October 31 and December 17, 2014, and September 2015.

The authors thank Melissa King, MD, Department of Hematology/Oncology, Eglin Air Force Base Hospital, for reviewing the manuscript, and Niquanna Perez, Eglin Air Force Base laboratory services, for procuring peripheral smear images.

The views expressed in this article are those of the authors and do not reflect the official policy or position of the U.S. government, the Department of Defense, or the U.S. Air Force.

Cerny J, Rosmarin AG. Why does my patient have leukocytosis?. Hematol Oncol Clin North Am. 2012;26(2):303-319.

Jain R, Bansal D, Marwaha RK. Hyperleukocytosis: emergency management. Indian J Pediatr. 2013;80(2):144-148.

Hoffman R, Benz EJ Jr, Silberstein LE, Heslop H, Weitz J, Anastasi J. Hematology: Basic Principles and Practice . 6th ed. Philadelphia, Pa.: Elsevier/Saunders; 2013:table 164–20.

Chabot-Richards DS, George TI. Leukocytosis. Int J Lab Hematol. 2014;36(3):279-288.

Lurie S, Rahamim E, Piper I, Golan A, Sadan O. Total and differential leukocyte counts percentiles in normal pregnancy. Eur J Obstet Gynecol Reprod Biol. 2008;136(1):16-19.

Dior UP, Kogan L, Elchalal U, et al. Leukocyte blood count during early puerperium and its relation to puerperal infection. J Matern Fetal Neonatal Med. 2014;27(1):18-23.

Lim EM, Cembrowski G, Cembrowski M, Clarke G. Race-specific WBC and neutrophil count reference intervals. Int J Lab Hematol. 2010;32(6 pt 2):590-597.

Berliner N. Leukocytosis and leukopenia. In: Goldman L, Schafer AI, eds. Goldman’s Cecil Medicine . 24th ed. Philadelphia, Pa.: Elsevier/Saunders; 2012.

Iskandar JW, Griffeth B, Sapra M, Singh K, Giugale JM. Panic-attack-induced transient leukocytosis in a healthy male: a case report. Gen Hosp Psychiatry. 2011;33(3):302.e11-302.e12.

Deirmengian GK, Zmistowski B, Jacovides C, O'Neil J, Parvizi J. Leukocytosis is common after total hip and knee arthroplasty. Clin Orthop Relat Res. 2011;469(11):3031-3036.

Ustianowski A, Zumla A. Eosinophilia in the returning traveler. Infect Dis Clin North Am. 2012;26(3):781-789.

Cormier SA, Taranova AG, Bedient C, et al. Pivotal Advance: eosinophil infiltration of solid tumors is an early and persistent inflammatory host response. J Leukoc Biol. 2006;79(6):1131-1139.

Munker R. Leukocytosis, leukopenia, and other reactive changes of myelopoiesis. In: Munker R, Hiller E, Glass J, Paquette R, eds. Modern Hematology: Biology and Clinical Management . 2nd ed. Totowa, N.J.; Humana Press; 2007.

Potts JA, Rothman AL. Clinical and laboratory features that distinguish dengue from other febrile illnesses in endemic populations. Trop Med Int Health. 2008;13(11):1328-1340.

Yu CW, Juan LI, Wu MH, Shen CJ, Wu JY, Lee CC. Systematic review and meta-analysis of the diagnostic accuracy of procalcitonin, C-reactive protein and white blood cell count for suspected acute appendicitis. Br J Surg. 2013;100(3):322-329.

Van den Bruel A, Thompson MJ, Haj-Hassan T, et al. Diagnostic value of laboratory tests in identifying serious infections in febrile children: systematic review. BMJ. 2011;342:d3082.

Yo CH, Hsieh PS, Lee SH, et al. Comparison of the test characteristics of procalcitonin to C-reactive protein and leukocytosis for the detection of serious bacterial infections in children presenting with fever without source: a systematic review and meta-analysis. Ann Emerg Med. 2012;60(5):591-600.

Dellinger RP, Levy MM, Rhodes A, et al.; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.

Coburn B, Morris AM, Tomlinson G, Detsky AS. Does this adult patient with suspected bacteremia require blood cultures? [published correction appears in JAMA . 2013;309(4):343]. JAMA. 2012;308(5):502-511.

Davis AS, Viera AJ, Mead MD. Leukemia: an overview for primary care. Am Fam Physician. 2014;89(9):731-738.

Granger JM, Kontoyiannis DP. Etiology and outcome of extreme leukocytosis in 758 nonhematologic cancer patients: a retrospective, single-institution study. Cancer. 2009;115(17):3919-3923.

Racil Z, Buresova L, Brejcha M, et al. Clinical and laboratory features of leukemias at the time of diagnosis: an analysis of 1,004 consecutive patients. Am J Hematol. 2011;86(9):800-803.

George TI. Malignant or benign leukocytosis. Hematology Am Soc Hematol Educ Program. 2012;2012:475-484.

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The written History and Physical (H&P) serves several purposes:

• It outlines a plan for addressing the issues which prompted the hospitalization. This information should be presented in a logical fashion that prominently features all of the data that’s immediately relevant to the patient's condition.
• It is a means of communicating information to all providers who are involved in the care of a particular patient.
• It allows students and house staff an opportunity to demonstrate their ability to accumulate historical and examination-based information, make use of their medical fund of knowledge, and derive a logical plan of attack.

The H&P is not:

• An instrument designed to torture Medical Students and Interns.
• Meant to cover unimportant/unrelated information.
• Should not require so much time to write that by the time it’s submitted, the information contained within is obsolete!

Knowing what to include and what to leave out will be largely dependent on experience and your understanding of illness and pathophysiology. If, for example, you were unaware that chest pain is commonly associated with coronary artery disease, you would be unlikely to mention other coronary risk-factors when writing the history. As you gain experience, your write-ups will become increasingly focused. You can accelerate the process by actively seeking feedback about all the H&Ps that you create as well as by reading those written by more experienced physicians. Several sample write-ups are presented at the end of this section to serve as reference standards.

The core aspects of the H&P are described in detail below.

"CC: Mr. Smith is a 70 year-old male admitted for the evaluation of increasing chest pain."

The HPI should provide enough information to clearly understand the symptoms and events that lead to the admission. This covers everything that contributed to the patient's arrival in the ED (or the floor, if admission was arranged without an ED visit). Events which occurred after arrival can be covered in a summary paragraph that follows the pre-hospital history.

A commonly used pneumonic to explore the core elements of the chief concerns is OLD CARTS, which includes: O nset, L ocation, D uration, C haracteristics, A ggravating/ A lleviating factors, R elated symptoms, T reatments, and S ignificance.

Some HPIs are rather straight forward. If, for example, you are describing the course of a truly otherwise healthy 40-year-old who presents with 3 days of cough, fever, and shortness of breath as might occur with pneumonia, you can focus on that time frame alone. Writing HPIs for patients with pre-existing illness(es) or a chronic, relapsing problems is a bit trickier. In such cases, it’s important to give enough relevant past history "up front," as having an awareness of this data will provide the contextual information that allows the reader to fully understand the acute issue. If, for example, a patient with a long history of coronary artery disease presents with chest pain and shortness of breath, an inclusive format would be as follows:

"HIP: Mr. S is a 70 yr old male presenting with chest pain who has the following coronary artery disease related history: -Status Post 3 vessel CABG in 2008. -Suffered recurrent chest pain in December 2015, which ultimately lead to catheterization and stent placement in a mid-LAD lesion. -He was re-cathed in January 2017 for recurrent chest pain at rest; at that time there was no significant change compared to catheterization of 12/15. The patient was therefore continued on medical therapy. -Known to have an Ejection Fraction of 40% with inferior and lateral akinesis by echo in January 2018 -No prior episodes of heart failure. -Last Exercise Tolerance Test was performed in January of 2018 and showed no ischemia at 8 METS of activity. Mr. S was in his usual state of health until last week (~ Saturday, November 18), when he began to experience recurrent episodes of chest pain, exactly like his past angina, after walking only one block. This represented a significant change in his anginal pattern, which is normally characterized as mild discomfort which occurs after walking vigorously for 8 or 9 blocks. In addition, 1 day prior to admission, the pain occurred while he was reading a book and resolved after taking a nitroglycerin tablet. It lasted perhaps 1 minute. He has also noted swelling in his legs over this same time period and has awakened several times in the middle of the night, gasping for breath. In order to breathe comfortably at night, Mr. S now requires the use of 3 pillows to prop himself up, whereas in the past he was always able to lie flat on his back and sleep without difficulty. Mr. S is known to have poorly controlled diabetes and hypertension. He currently smokes 2 packs of cigarettes/day. He denies fevers, chills, cough, wheezing, nausea vomiting, recent travel, or sick contacts."

That's a rather complicated history. However, it is obviously of great importance to include all of the past cardiac information "up front" so that the reader can accurately interpret the patient's new symptom complex. The temporal aspects of the history are presented in an easy to follow fashion, starting with the most relevant distant event and then progressing step-wise to the present.

From a purely mechanical standpoint, note that historical information can be presented as a list (in the case of Mr. S, this refers to his cardiac catheterizations and other related data). This format is easy to read and makes bytes of chronological information readily apparent to the reader. While this data is technically part of the patient's "Past Medical History," it would be inappropriate to not feature this prominently in the HPI. Without this knowledge, the reader would be significantly handicapped in their ability to understand the patient's current condition.

Knowing which past medical events are relevant to the chief concern takes experience. In order to gain insight into what to include in the HPI, continually ask yourself, "If I was reading this, what historical information would I like to know?" Note also that the patient's baseline health status is described in some detail so that the level of impairment caused by their current problem is readily apparent.

The remainder of the HPI is dedicated to the further description of the presenting concern. As the story teller, you are expected to put your own spin on the write-up. That is, the history is written with some bias. You will be directing the reader towards what you feel is/are the likely diagnoses by virtue of the way in which you tell the tale. If, for example, you believe that the patient's chest pain is of cardiac origin, you will highlight features that support this notion (e.g. chest pressure with activity, relieved with nitroglycerin, preponderance of coronary risk factors etc.). These comments are referred to as "pertinent positives." These details are factual and no important features have been omitted. The reader retains the ability to provide an alternative interpretation of the data if he/she wishes. A brief review of systems related to the current complaint is generally noted at the end of the HPI. This highlights "pertinent negatives" (i.e. symptoms which the patient does not have). If present, these symptoms might lead the reader to entertain alternative diagnoses. Their absence, then, lends support to the candidate diagnosis suggested in the HPI. More on the HPI can be found here: HPI .

Occasionally, patients will present with two (or more) major, truly unrelated problems. When dealing with this type of situation, first spend extra time and effort assuring yourself that the symptoms are truly unconnected and worthy of addressing in the HPI. If so, present them as separate HPIs, each with its own paragraph.

This includes any illness (past or present) that the patient is known to have, ideally supported by objective data. Items which were noted in the HPI (e.g. the cardiac catheterization history mentioned previously) do not have to be re-stated. You may simply write "See above" in reference to these details. All other historical information should be listed. Important childhood illnesses and hospitalizations are also noted.

Detailed descriptions are generally not required. If, for example, the patient has hypertension, it is acceptable to simply write "HTN" without providing an in-depth report of this problem (e.g. duration, all meds, etc.). Unless this has been a dominant problem, requiring extensive evaluation, as might occur in the setting of secondary hypertension.

Also, get in the habit of looking for the data that supports each diagnosis that the patient is purported to have. It is not uncommon for misinformation to be perpetuated when past write-ups or notes are used as the template for new H&Ps. When this occurs, a patient may be tagged with (and perhaps even treated for) an illness which they do not have! For example, many patients are noted to have Chronic Obstructive Pulmonary Disease (COPD). This is, in fact, a rather common diagnosis but one which can only be made on the basis of Pulmonary Function Tests (PFTs). While a Chest X-Ray and smoking history offer important supporting data, they are not diagnostic. Thus, "COPD" can repeatedly appear under a patient's PMH on the basis of undifferentiated shortness of breath coupled with a suggestive CXR and known smoking history, despite the fact that they have never had PFTs. So, maintain a healthy dose of skepticism when reviewing notes and get in the habit of verifying critical primary data.

Past Surgical History (PSH):

All past surgeries should be listed, along with the rough date when they occurred. Include any major traumas as well.

Medications (MEDS):

Includes all currently prescribed medications as well as over the counter and non-traditional therapies. Dosage, frequency and adherence should be noted.

Allergies/Reactions (All/RXNs):

Identify the specific reaction that occurred with each medication.

Social History (SH): This is a broad category which includes:

• Alcohol Intake: Specify the type, quantity, frequency and duration.
• Cigarette smoking: Determine the number of packs smoked per day and the number of years this has occurred. When multiplied this is referred to as "pack years." If they’ve quit, make note of when this happened.
• Other Drug Use: Specify type, frequency and duration.
• Marital/Relationship Status; Intimate Partner Violence (IPV) screen.
• Sexual History, including: types of activity, history of STIs.
• Work History: type, duration, exposures.
• Other: travel, pets, hobbies.
• Health care maintenance: age and sex appropriate cancer screens, vaccinations.
• Military history, in particular if working at a VA hospital.

Family History (FH): This should focus on illnesses within the patient's immediate family. In particular, identifying cancer, vascular disease or other potentially heritable diseases among first degree relatives

Obstetrical History (where appropriate):

Included the number of pregnancies, live births, duration of pregnancies, complications. As appropriate, spontaneous and/or therapeutic abortions. Birth control (if appropriate).

Review of Systems (ROS): As mentioned previously, many of the most important ROS questions (i.e. pertinent positives and negatives related to the chief concern) are generally noted at the end of the HPI. The responses to a more extensive review, covering all organ systems, are placed in the "ROS" area of the write-up. In actual practice, most physicians do not document an inclusive ROS. The ROS questions, however, are the same ones that are used to unravel the cause of a patient's chief concern. Thus, early in training, it is a good idea to practice asking all of these questions so that you will be better able to use them for obtaining historical information when interviewing future patients. A comprehensive list can be found here: ROS

Physical Exam: Generally begins with a one sentence description of the patient's appearance. Vital Signs: HEENT: Includes head, eyes, ears, nose, throat, oro-pharynx, thyroid. Lymph Nodes: Lungs: Cardiovascular: Abdomen: Rectal (as indicated): Genitalia/Pelvic: Extremities, Including Pulses:

Neurologic:

• Mental Status
• Cranial Nerves
• Sensory (light touch, pin prick, vibration and position)
• Reflexes, Babinski
• Coordination
• Observed Ambulation

Lab Results, Radiologic Studies, EKG Interpretation, Etc.:

Assessment and Plan:

It's worth noting that the above format is meant to provide structure and guidance. There is no gold standard, and there’s significant room for variation. When you're exposed to other styles, think about whether the proposed structure (or aspects thereof) is logical and comprehensive. Incorporate those elements that make sense into future write-ups as you work over time to develop your own style

SAMPLE WRITE UP #1

ADMISSION NOTE

CC: Mr. B is a 72 yo man with a history of heart failure and coronary artery disease, who presents with increasing shortness of breath, lower extremity edema and weight gain.

HPI: His history of heart failure is notable for the following:

• First MI was in 2014, when he presented w/a STEMI related to an LAD lesion. This was treated w/a stent. Echo at that time remarkable for an EF 40%.
• Despite optimal medical therapy, he had a subsequent MI in 2016. At that time, cardiac catheterization occlusions in LAD, OMB, and circumflex arteries. No lesions were amenable to stenting. An echo was remarkable for a dilated LV, EF of 20-25%, diffuse regional wall motion abnormalities, 2+MR and trace TR.
• Heart failure symptoms of DOE and lower extremity edema developed in 2017. These have been managed medically with lisinopril, correg, lasix and metolazone.

Over the past 6 months he has required increasing doses of lasix to control his edema. He was seen 2 weeks ago by his Cardiologist, Dr. Johns, at which time he was noted to have worsening leg and scrotal edema. His lasix dose was increased to 120 bid without relief of his swelling.

Over the past week he and his wife have noticed a further increase in his lower extremity edema which then became markedly worse in the past two days. The swelling was accompanied by a weight gain of 10lb in 2 days (175 to 185lb) as well as a decrease in his exercise tolerance. He now becomes dyspneic when rising to get out of bed and has to rest due to SOB when walking on flat ground. He has 2 pillow orthopnea, but denies PND.

Denies CP/pressure, palpitations or diaphoresis. Occasional nausea, but no vomiting. He eats normal quantities of food but does not salt or fluid intake. He also admits to frequently eating canned soup, frozen meals, and drinking 6-8 glasses liquid/day. He has increased urinary frequency, but decreased total amount of urine produced. He denies urinary urgency, dysuria or hematuria. He has not noted cough, sputum, fever or chills. He states he has been taking all prescribed medications on most days – missing a few (? 2-3) doses a week.

SAMPLE WRITE-UP #2

ADMISSION NOTE CC: Mr. S is a 65-year-old man who presents with 2 concerns: 1. Acute, painless decline in vision 2. Three day history of a cough.

HPI: 1. Visual changes: Yesterday morning, while eating lunch, the patient had the sudden onset of painless decrease in vision in both eyes, more prominent on the right. Onset was abrupt and he first noted this when he "couldn't see the clock" while at a restaurant. He also had difficulty determining the numbers on his cell phone. He denied pain or diplopia. Did not feel like a “curtain dropping” in front of his eyes. He had nausea and vomiting x2 yesterday, which has resolved. He did not seek care, hoping that the problem would resolve on its own. When he awoke this morning, the same issues persisted (no better or worse) and he contacted his niece, who took him to the hospital. At baseline, he uses prescription glasses without problem and has no chronic eye issues. Last vision testing was during visit to his optometrist 2 year ago. Notes that his ability to see things is improved when he moves his head to bring things into better view. Denies dizziness, weakness, headache, difficulty with speech, chest pain, palpitations, weakness or numbness. No history of atrial fibrillation, carotid disease, or heart disease that he knows of.

2. Cough: Patient has history of COPD with 60+ pack year smoking history and most recent PFT's (2016) consistent with moderate disease. Over the past few days he has noted increased dyspnea, wheezing, and sputum production. Sputum greenish colored. He uses 2 inhalers, Formoterol and Tiotropium every day and doesn’t miss any dosages. He was treated with antibiotics and prednisone a few years ago when he experienced shortness of breath. He has not had any other breathing issues and no hospitalizations or ED visits. Denies hemoptysis, fevers, orthopnea, PND, chest pain or edema.

ED course: given concern over acute visual loss and known vascular disease, a stroke code was called when patient arrived in ER. Neurology service evaluated patient and CT head obtained. Data was consistent with occipital stroke, which occurred > 24 hours ago. Additional details re management described below.

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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990.

Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition.

Chapter 7 an overview of the cardiovascular system.

Joel M. Felner .

The evaluation of the cardiovascular system includes a thorough medical history, a detailed examination of the heart and the peripheral arterial and venous circulations, and appropriate laboratory studies. In addition to the electrocardiogram and chest x-ray, the availability of sophisticated noninvasive techniques (e.g., echocardiography and nuclear cardiology) and the continued improvement of cardiac catheterization and angiography have significantly enhanced the clinical work-up of the patient with a cardiovascular problem. A careful assessment will enable the clinician to identify the etiologic, anatomic, and physiologic components of a specific cardiovascular disorder, as well as to determine overall cardiac function.

The medical history in a patient with a cardiac problem is usually centered on symptoms due to myocardial ischemia, dysrhythmias, and reduction in ventricular function. The majority of these individuals will consult a physician because of chest pain, dyspnea, palpitations, ankle edema, or syncope. Any or all of these symptoms may also have extra-cardiac causes. Because symptoms of heart disease may be absent at rest and appear only during stress, the medical history has unique diagnostic importance. The patient's daily activities should be assessed for their role in precipitating the symptoms and in identifying these symptoms as cardiac in origin. A purely symptom-based classification of heart disease has major limitations, however, since functional abnormalities are often more extensive than those represented by symptoms alone. In addition, the anatomic and physiologic disturbances may develop to advanced stages before symptoms appear. Examples of the manner in which the principal symptoms of heart disease may serve as a guide to diagnosis will be highlighted.

Chest pain or discomfort ( Chapter 9 ) has numerous cardiac causes (e.g., myocardial ischemia, pericarditis, pulmonary embolism, aortic dissection) as well as noncardiac etiologies (e.g., anxiety, cholecystitis, pneumonia). The pain of myocardial ischemia, characterized by a squeezing, strangling, or burning sensation, must be differentiated from pleuritic pain, which is sharp, stabbing, intensified by inspiration, and relieved by sitting up. Among the causes of myocardial ischemia are angina pectoris and myocardial infarction. Pleuritic pain usually accompanies pericarditis and pulmonary embolism.

Dyspnea (shortness of breath) ( Chapter 11 ) of cardiac origin must be distinguished from dyspnea due to pulmonary disease. Cardiac dyspnea, including paroxysmal nocturnal dyspnea (breathlessness at night) and orthopnea (dyspnea precipitated by assuming the recumbent position), is characteristically related to effort until the advanced stages of heart disease when it may become present at rest. Rapid progression of an episode of respiratory distress may result in a very severe form of dyspnea, acute pulmonary edema, i.e., "asthmatic" wheezes and a pink, frothy sputum.

Palpitations ( Chapter 10 ) describe an awareness of the heartbeat. Although the underlying disturbance usually requires electrocardiographic confirmation, occasionally the cadence of the palpitations may be ascertained at the bedside. Palpitations may often be of no consequence.

Syncope of cardiac origin ( Chapter 12 ) may be due either to an inability of the heart to maintain adequate cardiac output for a given level of activity or to a dysrhythmia that results in sudden loss of cardiac output. Left ventricular outflow tract obstruction (e.g., aortic stenosis or hypertrophic cardiomyopathy) commonly causes effort syncope, whereas syncopal episodes due to dysrhythmias can occur either at rest or during activity.

Edema ( Chapter 29 ), a detectable excess of fluid in the interstitial spaces, is most commonly located in the ankles and feet and is referred to as peripheral or ankle edema. When due to cardiac disease, it is usually a late sign of congestive heart failure, specifically, right heart failure.

Additional symptoms that may herald a cardiovascular problem include claudication (extertional cramping of the muscles) ( Chapter 13 ), most often of the lower extremities, fatigue, and hemoptysis ( Table 7.1 ).

Symptoms of Cardiovascular Diseases.

• Physical Examination

Instruments needed for the cardiovascular examination are listed in Table 7.2 . The examination involves inspection, palpation, and auscultation of the heart, arteries, and veins. The cardiac examination consists of evaluation of (1) the carotid arterial pulse and auscultation for carotid bruits; (2) the jugular venous pulse and auscultation for cervical venous hums; (3) the precordial impulses and palpation for heart sounds and murmurs; and (4) auscultation of the heart. The evaluation of the peripheral arteries, the aortic pulsation, elicitation of pulsus alternans, and a search for thrombophlebitis completes the cardiovascular examination ( Table 7.3 ).

Instruments Needed for Cardiovascular Examination.

Most Frequently Used Examination Sequence of the Cardiovascular System.

Special attention should be given to the patient's general appearance, since it can reflect the state of the circulation as well as noncardiac diseases that may involve the heart. The patient's color (pale, flushed, or cyanotic), facial features, body build, and obvious pulsations should be noted. The blood pressure and heart rate and rhythm are obtained with the vital signs, but must be integrated with the findings of the cardiovascular examination to arrive at the proper diagnosis.

Examination of the Heart

Carotid arteries.

Begin the cardiovascular examination by assessing the carotid arterial pulses ( Chapter 20 ). They are ordinarily examined while the patient is breathing normally and reclining with the trunk of the body elevated about 15 to 30 degrees ( Figure 7.1 ). In order to examine the carotid arteries, the sternocleidomastoid (SCM) muscle should be relaxed and the head rotated slightly toward the examiner. The examiner places the forefinger or thumb, depending on individual preference, slightly over the artery in the groove just lateral to the trachea. Care should be taken always to palpate in the lower half of the neck in order to avoid the area of the carotid bulb, lest a hypersensitive carotid sinus reflex be evoked with resultant bradycardia and hypotension. It is important that the carotid pulses be palpated using light pressure, one side at a time, since bilateral carotid compression may produce cerebral ischemia and syncope; extreme caution should be exercised in patients who have a history of syncope or transient neurologic symptoms.

Examination of the carotid arterial pulse. Place the patient in the supine position with the trunk elevated approximately 30 degrees, the head turned slightly toward the side being examined and the chin elevated. Palpate the carotid artery by gently pressing (more...)

Listen to the heart with the stethoscope in order to identify the first (S 1 ) and second (S 2 ) heart sounds while simultaneously palpating the carotid artery. The heart sounds are used as reference points for the cardiac examination in order to determine which events occur in systole (between S 1 and S 2 ) and which in diastole (between S 2 and S 1 ). While listening to the heart sounds, the examiner carefully and slowly applies more and more pressure to the carotid artery until the maximum pulse is felt; palpation should be continued for 5 to 8 seconds. The examiner should then slowly release the pressure on the artery while attempting to form a mental image of the pulse wave. It may be possible to detect an anacrotic notch (halt on the upstroke) or a bisferiens pulse (bifid or double peak) more easily with light pressure than with heavy pressure. In patients with evidence of carotid arterial disease, palpation of the vessels obviously should be gentle.

Divide the carotid pulse wave into three parts: (1) ascending limb or upstroke; (2) peak; and (3) descending limb. Initially concentrate on the amplitude (size) of the carotid pulse and note whether it is normal, decreased, or increased. If necessary, use your own carotid pulse as a control. Next, direct attention to analysis of the pulse contour and note if there is a single or double peak, a shudder or thrill, and the location of the peak within systole (i.e., early, mid, or late). Then concentrate on the upstroke and note whether it is normal, rapid, or slow. Finally, concentrate on the down-stroke of the pulse, which is difficult to palpate reliably. If there is a rapid fall-off, for instance, the majority of the clownstroke will be completed during systole.

The normal carotid arterial pulse wave is illustrated in Figure 7.2 together with the heart sounds. The upstroke of the carotid tracing is moderately rapid and smooth, and begins just after the initial component of the first heart sound. The summit of the carotid pulse is smooth and dome shaped, and occurs approximately in the middle of systole. The descending limb from the systolic peak is usually less steep than the ascending limb. In most normal individuals, the carotid incisura or dicrotic notch is not palpable; however, one can usually sense a change to a less steep down-slope.

These graphics represent the normal cardiac pulsations and heart sounds. The jugular venous pulsation normally has 3 positive waves—the a, c, and v waves and 2 negative troughs—x and y troughs. The "a" wave is approximately synchronous (more...)

There are a variety of abnormal arterial pulses including the hypokinetic pulse commonly seen with left ventricular failure; the hyper kinetic pulse commonly seen with mitral or aortic regurgitation; and the bisferiens pulse seen with aortic regurgitation or hypertrophic cardiomyopathy. During routine palpation of the carotid pulse, pay particular attention to the amplitude of the pulse following any premature beat, A diminished pulse amplitude following a premature beat is suggestive of hypertrophic cardiomyopathy.

Auscultation should be performed along the course of the carotid artery in order to detect any bruits. (See Figure 7.3 and Chapter 18 ). The location of maximum intensity of the bruit should be noted, as well as the pitch and duration of the sound. It is necessary for the patient to stop breathing during auscultation to eliminate the harsh sounds of tracheal breathing that could mask a low-pitched carotid bruit.

Auscultation of the carotid artery. Lightly apply the bell of the stethoscope over the course of the carotid artery, from the base of the neck to angle of the jaw, during full expiration.

Jugular Veins

The jugular venous pulse ( Chapter 19 ) is usually examined next. It includes observation of venous wave form, assessment of the response of the venous pressure to abdominal compression, estimation of the central venous pressure (CVP), and auscultation for cervical venous hums. Venous pulsations are examined by inspection of either the external or internal jugular veins, although the latter are generally more reliable because they more directly reflect right atrial hemodynamics.

The position of the patient is extremely important for the examination of the jugular veins ( Figure 7.4 ). Relax the neck muscles by placing a small pillow behind the neck. The head should not be rotated more than a few degrees, since rotation may tense the SCM muscle and obscure the transmission of venous pulsations. The trunk of the body should be elevated until maximal venous pulsations are noted. The degree of trunk elevation varies from subject to subject and must be established for each person. In most normal individuals, the maximum pulsation of the internal jugular vein is usually observed when the trunk is inclined to about 15 to 30 degrees. In patients with elevated venous pressure, it may be necessary to elevate the trunk more than 45 degrees to visualize the maximum venous pulsation. At times there is venous distention without visible waves and the pulsations are only seen with the patient upright at 90 degrees.

Anatomy of the blood vessels in the neck. Evaluation of the jugular venous pulse and the carotid artery are best accomplished with the patient supine, the neck muscles relaxed by placing a small pillow under the head and the trunk elevated until the maximal (more...)

Look for pulsations of the internal jugular vein by standing just behind the patient and looking down alongside the SCM muscle or by bending over in front of the patient and looking directly along the SCM muscles. Direct your study of the wave form to whichever internal jugular pulse is easier to see. For most patients, the right internal jugular vein is superior for accurate evaluation of the venous wave form. The internal jugular venous pulsations may be highlighted by shining a beam of light from a penlight tangentially across the skin overlying the left internal jugular vein. This technique may amplify the wave form by casting a shadow of its pulsations on the pillow or bed sheet behind the neck.

The normal jugular venous pulse consists of intermittent increases in the volume of blood in the veins caused by slowing or halting of blood flow in the right atrium. Because they are low-pressure impulses, venous pulsations are not palpable and therefore are interpreted by inspection rather than by palpation, in contrast to the carotid arterial pulse. Generally, internal and external jugular venous pulsations may be eliminated by applying gentle pressure below the point of observation. This procedure also may produce increased distention of the vein by blocking the flow of blood to the heart. The visible venous pulsations in the neck are slower and more undulating than the brisk, forceful arterial pulse waves. Respiration may produce marked changes in venous pulsations, whereas arterial pulses normally change relatively little. Under normal circumstances, inspiration decreases intrathoracic pressure and increases return of blood to the heart from the peripheral veins. The result is to reduce the mean level of venous pulsation and distention; the opposite occurs during expiration.

Abdominal pressure may also be used to distinguish venous from arterial neck pulsations. This test is best performed with the patient lying comfortably in bed at the optimal angle for observing the internal jugular venous pulsations. The patient is instructed to continue normal breathing in order to avoid performance of a Valsalva maneuver. Moderately firm pressure is then slowly applied for about 30 seconds with the palm of the hand pressing on the abdomen, usually on the right side (over the liver). Normally this maneuver produces no visible change in the arterial pulse, but a slight increase in the prominence of the jugular venous pulsations. In the presence of heart failure the jugular venous pulsations may be markedly increased. The response of jugular venous pulse to abdominal compression is known as the hepato-jugular reflux test. It is useful not only for distinguishing venous from arterial pulsations but also in unmasking occult abnormalities of circulatory function.

The normally visible jugular venous pulsations consist of two outward pulsations or positive waves ("a" and "v") and two descents or collapses or negative waves ("x" and "y") as shown in Figure 7.2 . The "c" wave, a positive wave that follows the "a" wave, may be recorded, but is seldom seen at the bedside. The carotid pulse may be used to time venous pulsations, but the heart sounds generally are preferable at the bedside. The "a" wave, the larger of the two visible positive waves, begins before S 1 and precedes the upstroke of the carotid pulse. The negative "x" and "y" waves occupy systole and diastole, respectively. The "v" wave occurs in late systole virtually synchronous with S 2 . Frequently, it is easier to visualize jugular descents because they are the largest and fastest movements.

The internal jugular veins are also used to estimate central venous pressure. The technique is similar to that for evaluation of the internal jugular venous wave form ( Figure 7.5 ). The patient is examined at the optimum degree of trunk elevation for inspection of the venous pulse. While the patient is breathing gently or preferably at the end of a normal expiration, the highest point of visible pulsation of the internal jugular vein is determined ( Figure 7.5 ). The CVP can then be estimated by measuring the vertical distance between the midright atrium and the top of the column of venous blood in relation to a fixed reference point, the sternal angle (of Louis). The vertical distance between the top of the column of venous blood and the level of the sternal angle is normally 2 cm. For convenience at the bedside, the sternal angle is chosen as a reference point because it has a relatively constant relationship, in all positions, to the midpoint of the right atrium (i.e., 5 cm above the mid-right atrium).

Estimation of the central venous pressure (CVP). Place the patient in the supine position with the head slightly elevated on a pillow to relax the sternocleidomastoid muscle. Elevate the trunk by adjusting the head of the bed so as to maximize the internal (more...)

The normal CVP is less than or equal to 7 cm H 2 O (i.e., 5 + 2 cm). The most common cause of an elevated CVP is failure of the right ventricle secondary to failure of the left ventricle. Earlobe and rarely eyeball pulsations are evidence of markedly elevated venous pressure.

Central venous pressure may also be estimated by examining the veins of the dorsum of the hand. To perform this determination, the patient should be in either a sitting or lying position at a 30-degree elevation or greater, and the hand should be kept below the level of the heart long enough for the veins of the dorsum of the hand to become distended. The arm is then slowly and passively raised while the physician observes the veins. Care should be taken that the arm is not flexed excessively at either the shoulder or the elbow and that the upper arm is not constricted by-clothing. Normally, the veins will be seen to collapse when the level of the dorsum of the hand reaches the sternal angle or the level of the suprasternal notch. The vertical distance above the sternal angle at which the veins collapse should be recorded as well as the position of the patient during the test.

Auscultation at the base of the neck, just above the clavicle and lateral to the clavicular attachment of the SCM muscle, with the patient sitting, enables one to determine if a cervical venous hum is present ( Chapter 18 ). The cervical venous hum is a continuous whining or roaring noise throughout systole and diastole produced by the flow of blood through the internal jugular veins. It occurs more frequently on the right than on the left, but may be present bilaterally. It is loudest with the patient sitting, during inspiration, and in diastole. It may be increased by turning the head away from the side being auscultated. It is obliterated by applying light pressure directly above the point of auscultation, the Valsalva maneuver, compression of the internal jugular vein, or lying down. An arterial bruit, in contrast, is loudest in systole, unaffected by light pressure, the Valsalva maneuver, and the patient's changing position. The venous hum is a frequent finding in normal individuals, but may also be a clue to high-output states (e.g., thyrotoxicosis).

Precordial Movements and Thrills

The precordial examination, performed next, consists of inspection and palpation of the anterior chest wall. Precordial movements ( Chapter 21 ) should be evaluated at the apex (left ventricle), lower left parasternal edge (right ventricle), upper left (pulmonary artery) and upper right (aorta) parasternal edges, and epigastric and sternoclavicular areas ( Figure 7.6 ). It is best to examine the precordium with the patient supine because if the patient is turned on the left side, the apical region of the heart is displaced against the lateral chest wall, distorting the chest movements. Inspect the chest wall by positioning yourself on the patient's right side and looking tangentially across the fourth, fifth, and sixth intercostal spaces. Ask the patient to take a deep breath and then to exhale slowly as you look for a discrete area of apical movement. The following are the factors to be considered about any precordial movement that can be seen or felt: (1) location; (2) amplitude; (3) duration; (4) time of the impulse in the cardiac cycle; and (5) contour.

Anteroposterior view of the chest indicating the major precordial areas to be examined. Try to detect by both inspection and palpation any abnormal pulsations that the underlying cardiac chambers and great vessels may produce. Auscultation is routinely (more...)

Locate the apex impulse by placing the palm and fingers of your right hand over the left precordium in the fourth, fifth, and sixth intercostal spaces near the midclavicular line ( Figure 7.7 ). If unable to palpate an impulse, move your hand laterally to the anterior axillary line. If still unable to locate the impulse, ask the patient to roll onto the left side and attempt to palpate the apex as just described ( Figure 7.8 ). Always state in which patient position the apex impulse was identified because the left lateral decubitus position distorts a normal apex and makes it appear or feel unduly sustained. If still unable to locate the apex impulse, inspect the right precordium in a manner similar to that used for the left precordium. On rare occasions the impulse may be visible in the right chest, providing the initial clue to the presence of dextrocardia.

Examination of the apex impulse in the supine position. Place the patient in the supine position elevating the trunk approximately 30–45 degrees. Position yourself on the patient's right side and place the flat part of your right hand over the (more...)

Examination of the apex impulse with the patient in the left lateral decubitus position. If the apex impulse cannot be located with the patient supine, ask the patient to roll to his left side and attempt to palpate the apex with the fingers of your right (more...)

Record the location of the apex impulse by noting its distance from either the midsternal or midclavicular line and the intercostal space in which it is felt. Also record the approximate diameter (cm) of the apex. The amplitude and duration of the apical pulsation may be more important than its location and size; therefore, state whether the impulse is of normal, increased, or diminished force and whether it occupies half or more than half of systole. If necessary, palpate your own apex impulse for comparison. In addition, if a single pulsation is palpated, determine whether its force is uniform throughout systole or whether there is a late systolic accentuation or bulge.

In a normal individual the apex impulse is a tapping, early systolic outward thrust that occurs in the fifth intercostal space in the midclavicular line. It is localized to a small area not more than 1 to 2 cm (dime-sized) in diameter. The outward thrust is brief, lasting about one-half of systole, and is of minimal amplitude. Normally, diastolic pulsations are not palpable. Left ventricular hypertrophy, for instance, results in exaggeration of the normal left ventricular thrust both in amplitude and duration. It is nondisplaced, sustained (occupying more than one-half of systole), and 2 to3 cm (quarter-sized). Left ventricular dilation, in contrast, results in downward and lateral displacement of the apex below the fifth interspace.

The lower left parasternal region of the chest is best evaluated by looking at the chest from the side and by placing the heel of the hand over or just to the left of the sternum ( Figure 7.9 ). If a left parasternal impulse or lift is appreciated, determine if the impulse is sustained throughout systole, vigorous or slight, and begins with or after the onset of the apex impulse. Determine its onset by placing your right hand over the apex impulse and your left palm over the left parasternal impulse. The right ventricle is really an anterior structure, and when enlarged, it may lift the anterior portion of the chest including the sternum. In normal individuals the parasternal region usually retracts (moves inward) during ejection and is not palpable.

Palpation of the left parasternal impulse. Place the patient in the supine position with the trunk elevated 30–45 degrees. Place the heel of your right hand, with the hand slightly cocked up, together with downward pressure (arrow) of your left (more...)

Right ventricular hypertrophy and/or dilation results in a sustained systolic lift of the lower parasternal region of the chest. This lift is present in patients with high right ventricular pressure (pulmonary arterial hypertension or pulmonic stenosis) or volume overload (tricuspid regurgitation or atrial septal defect), but is infrequently seen in chronic lung disease if right-sided heart failure is not present. The pulsations of the main pulmonary artery are also often visible and palpable, especially in patients with parasternal pulsations.

Patients with acute myocardial infarction or with angina pectoris may have an outward paradoxical precordial movement that often can be seen or palpated at the apex, the anterior precordium, or in an "ectopic" area. The impulse is usually sustained throughout systole, frequently with a second systolic bulge, and is often difficult to distinguish from that of left ventricular hypertrophy by palpation alone if the bulge occurs in the region of the apex. In order to time systolic and diastolic cardiac movements accurately, it is essential to inspect and palpate the precordium while actually listening to the heart sounds.

The early diastolic and late diastolic (presystolic) precordial movements are the visible and palpable counterparts of the third (S 3 ) and fourth (S 4 ) heart sounds, respectively. They may be felt at the cardiac apex with the patient in the left lateral decubitus position. Careful inspection of the precordium with the naked eye or observing the motions of a wooden stick taped over the cardiac apex best demonstrates any precordial impulses that correlate with audible S 3 and S 4 sounds. The right-sided S 4 , seen and felt at the lower left sternal edge, occurs slightly earlier in diastole than the left-sided S 4 . It often correlates with a very prominent jugular "a" wave and a sustained outward movement (lift) in the lower left parasternal area.

Heart murmurs that can be palpated are referred to as thrills ( Chapters 26 and 27 ). The diastolic rumble of mitral stenosis and the systolic murmur of mitral regurgitation may be palpated at the cardiac apex. The harsh systolic murmur of aortic stenosis may cut across the palm of the hand toward the right side of the neck, while the thrill of pulmonic stenosis cuts across the palm of the hand to the left side of the neck. The thrill due to ventricular septal defect is usually located in the third and fourth intercostal spaces near the left sternal border. Heart sounds may also be palpable. For instance, the loud S 1 of mitral stenosis may be palpated at the apex.

Heart Sounds and Murmurs

Auscultation ( Chapters 22 – 28 ) of the heart is performed after examining the jugular venous pulse, carotid pulse, and precordial movements because acoustic events can best be interpreted after the other components of the cardiac examination have been evaluated. Auscultation of the heart should, therefore, not be performed as an isolated event because heart sounds, murmurs and pulse tracings must all be integrated in order to understand normal and altered cardiac physiology and anatomy. Attempt to study two and occasionally three aspects of the cardiac examination simultaneously. Then pictorially display the heart sounds and correlate them, by use of a diagram, with any murmurs heard, the jugular venous wave form, the carotid pulse, and the apex impulse to best understand the patient's cardiac problem ( Figure 7.2 ).

Proper use of a quality stethoscope is essential for an accurate auscultatory examination. The important parts of the stethoscope are the ear pieces, the tubing, and the chest pieces. The ear pieces must fit the ear canal snugly without going to an uncomfortable depth. The tubing should be as short as possible, but long enough to be comfortable and convenient for the user; 10 to 12 inches is an ideal length. The chest pieces, the bell, and the diaphragm should be combined into one housing. A diaphragm pressed firmly on the chest filters out low-frequency vibrations and amplifies high-frequency vibrations. It is routinely used to hear the first and second heart sounds, systolic murmurs, and the diastolic murmur of aortic regurgitation. The bell should be applied to the chest with very light pressure, barely creating an air seal, so low-frequency sounds and murmurs are appreciated. It is used to hear the third and fourth heart sounds and the diastolic murmur (rumble) of mitral stenosis. A trumpet-shaped bell is much better than a shallow one.

Auscultation usually begins at the aortic area (upper right sternal edge). The stethoscope is then moved sequentially to the pulmonary (upper left sternal edge), tricuspid (lower left sternal edge), and mitral (apex) areas. It is helpful to palpate the carotid pulse or apex impulse simultaneously to time the acoustic events as systolic or diastolic. A finger on the carotid artery will sense the systolic thrust that is virtually coincident with S 1 . Use of a more distant artery for this purpose leads to error because of the time it takes the pulse wave to reach the periphery.

The heart sounds are usually the first auscultatory events identified. They are brief, discrete, auditory vibrations of varying intensity (loudness) and frequency (pitch). The first heart sound ( Chapter 22 ) identifies the onset of systole. It is normally split into mitral (M 1 ) and tricuspid (T 1 ) components that are temporally related to closure of the respective atrioventricular (A-V) valves. The second heart sound ( Chapter 23 ) identifies the end of systole and the onset of diastole. It is normally split into aortic (A 2 ) and pulmonic (P 2 ) components that are temporally related to closure of the respective semilunar valves. The second sound is louder than S 1 in the aortic listening area; S 1 is louder at the apex.

In the aortic area, listen for the first and second heart sounds, the aortic ejection sound, and the murmurs of aortic stenosis and aortic regurgitation with the stethoscope diaphragm. Then move the diaphragm to the second and third left intercostal spaces in order to appreciate the aortic and pulmonic components of S 2 , the pulmonary ejection sound, and the murmurs of pulmonic stenosis and pulmonary and aortic regurgitation. Continue to the fourth and fifth intercostal spaces along the left sternal border and listen for the murmurs of tricuspid regurgitation and tricuspid stenosis and the murmur produced by ventricular septal defect. Right ventricular S 3 and S 4 sounds (gallops) can best be heard in this area with the stethoscope bell. The diaphragm should be moved to the third and fourth intercostal spaces to the right of the sternum to judge whether a murmur of aortic regurgitation is louder along the left or right sternal border.

The diaphragm should then be positioned at the cardiac apex where S 1 and S 2 should again be studied. An aortic ejection sound, a mid to late systolic click, the opening snap of mitral stenosis, the systolic murmur of mitral regurgitation, and occasionally the high-pitched murmur of aortic regurgitation are also heard in this area with the diaphragm.

The bell of the stethoscope should then be positioned over the apical impulse with the patient turned to the left lateral position to listen for low-frequency diastolic sounds and murmurs.

Have the patient exercise (5 to 10 sit-ups), or cough if myocardial infarction is suspected, to "bring out" the murmur of mitral stenosis and the S 3 and S 4 gallop sounds. The third and fourth heart sounds ( Chapters 24 and 25 ) are low pitched and may be audible as well as palpable. They are best heard at the cardiac apex when generated from the left ventricle and at the lower left sternal edge when generated from the right ventricle.

The technique known as inching may help determine whether extra cardiac sounds are systolic or diastolic. The examiner moves the stethoscope inch by inch from the aortic area to the apex while focusing attention on S 2 . Determine whether the extra sound precedes (systolic) or follows (diastolic) S 2 . The acoustic events can best be appreciated by a careful review of the hemodynamic curves of the cardiac cycle.

Several additional areas should be ausculted ( Figure 7.10 ), including (1) the inferior edge of the sternum and epigastrium, especially in patients with chronic obstructive lung disease, in whom heart sounds and murmurs are difficult to hear in the more conventional listening areas; (2) the first and second intercostal spaces below the left midclavicular area for the continuous (systolic and diastolic) murmur of patent ductus arteriosus; (3) the interscapular area of the back for the systolic murmur of coarctation of the aorta; (4) over the lung areas; (5) over the head, eyes, liver, sacrum, abdomen, as well as over tumors or bony overgrowths; and (6) over all scars to identify the continuous murmur of a peripheral A-V Fistula.

Figure 7.10

Anteroposterior view of the chest showing some additional areas shaded for auscultation. The first and second left intercostal spaces at the mid clavicular line (MCL). The fifth intercostal space to the right of the sternum. The epigastric area just below (more...)

Murmurs ( Chapters 26 and 27 ) are prolonged series of auditory vibrations that should be characterized according to (1) timing in the cardiac cycle (systolic, diastolic, continuous); (2) intensity (loudness); (3) frequency (pitch); (4) configuration (shape); (5) duration (long or short); (6) radiation (to other auscultatory areas); and (7) variation, if any, with respiration or other maneuvers (position change, Valsalva, etc.).

The classic way to time murmurs and heart sounds is with a finger on the carotid arterial pulse. The heart sound virtually coinciding with the carotid upstroke (pulse) is S l and the heart sound just after the carotid pulse is S 2 . The intensity of a murmur is graded I to VI with I faint, III loud, IV palpable, and VI loud enough to be heard with the stethoscope just off the chest. The frequency of a murmur varies from low (rumbling) to mid (harsh) to high (blowing). The configuration is described as crescendo (increases progressively in intensity), decrescendo (decreases progressively in intensity), crescendo-decrescendo (diamond-shaped), or plateau (even). Of all the parameters by which a murmur is analyzed, its time of occurrence in the cardiac cycle and the precordial area of maximal intensity are easiest to learn and thus are most reliable.

The influence of respiration on the second sound is extremely important. The examiner will wish to note respiratory variation both during quiet breathing and at times during exaggerated breathing. The interval between the two audible components of S 2 normally increases on inspiration and virtually disappears on expiration. The Valsalva maneuver may be used to exaggerate the effects of respiration. Variation in the cardiac cycle, as with atrial fibrillation or heart block, may also exert profound influences on S 2 and on S 1 . When S 2 is split, determine the relative loudness of each component (A 2 and P 2 ).

Examination of the Peripheral Arteries

The evaluation of the peripheral arterial pulses ( Chapter 30 ) is an integral part of the cardiovascular examination. Palpation of the peripheral arteries may yield the following information: (1) frequency and regularity of the pulsations; (2) condition and patency of the peripheral arteries; and (3) characteristics of the arterial pulse wave. All of the following pulses should be examined thoroughly by palpation: temporals, brachials, radials, aortic, femorals, popliteals, posterior tibials, and the dorsalis pedii ( Figure 7.11 ). When applicable, pulses should be examined bilaterally and graded as to quality of the impulse on a scale of 0 to 3 with 2 being normal, 0 absent, 1 decreased, and 3 increased. In addition, hair distribution should be checked on the toes and feet.

Figure 7.11

Location of the arteries that are routinely examined. The temporalis artery is located in front of the ear where it is very superficial and readily palpated. Pulses in the upper extremities can be identified at the brachial artery, just medial to the (more...)

To examine the brachial artery, palpate along the course of the artery just medial to the biceps tendon and lateral to the medial epicondyle of the humerus. To examine the radial artery, palpate along the radial–volar aspect of the subject's forearm at the wrist.

The abdominal aorta is an upper abdominal, retroperitoneal structure that is best palpated by applying firm pressure with the flattened fingers of both hands to indent the epigastrium toward the vertebral column. The normal aortic pulse should be less than 6 cm in diameter. Auscultation should be performed over the aorta and along both iliac arteries into the lower abdominal quadrants to detect bruits.

The femoral artery is best palpated with the fingertips of the examining hand pressed firmly into the groin. Auscultation should be performed in this area as well.

The popliteal artery passes vertically through the deep portion of the popliteal space. It may be difficult or impossible to palpate in obese or very muscular individuals. The pulse is detected by pressing deeply into the popliteal space with the supporting fingertips.

The posterior tibial artery lies just posterior to the medial malleolus and is felt most readily by curling the fingers of the examining hand around the ankle.

The dorsalis pedis artery usually lies near the center of the long axis of the foot. Place the fingertips transversely across the dorsum of the forefoot near the ankle. This pulse often requires some searching and is congenitally absent in approximately 10% of normal individuals.

Information should be obtained by simultaneously palpating the radial and femoral arteries and noting the relative time of onset of the pulse at the two locations. Normally, the pulse wave arrives in these locations virtually simultaneously. In a patient with coarctation of the aorta, both onset and peak of the weak femoral pulses are delayed. Compared to the carotid pulse, the pulse wave in these more peripheral vessels arrives later and is characterized by a steeper initial wave that reaches a higher systolic peak, whereas the diastolic and the mean arterial pressures are lower.

Palpating peripheral arteries is the most important single maneuver in establishing whether or not chronic occlusive arterial disease is present. One may obtain an impression of thickness and hardness of the walls of the brachial, radial, and dorsalis pedis arteries by "rolling" the compressed vessel against the underlying tissue. Auscultation of the peripheral arteries is also very important. A systolic bruit over the abdominal aorta, iliac, or femoral arteries when the patient has been supine for more than 10 minutes usually signifies intimal disease, but not necessarily significant occlusion.

Pulsus alternans refers to a characteristic pulse pattern in which the beats occur at regular intervals, but with an alternation of the height of the pulse. This valuable sign should be searched for by palpating the femoral artery; less often, the radial artery may disclose that alternate pulses vary in amplitude. Have the patient hold his or her breath while you feel the pulse to make certain that the alternation of pulse volume is independent of respiration. The pulse rhythm should be regular, since alternation of the strength of cardiac beats commonly results from bigeminal rhythm. Rarely, pulsus alternans may feel irregular because of a slight delay in sensing the weaker beat.

When pulsus alternans is prominent, it may be confirmed and quantified by use of a sphygmomanometer. As the pressure is lowered in the sphygmomanometer, the examiner should routinely observe whether every Korotkoff sound is heard with equal intensity. As the cuff pressure is lowered further, the frequency of the sounds may suddenly double as the weaker beats also become audible. In most instances, the weak pulses are only slightly weaker than the strong beats. On rare occasions, a weak beat may be so small that no palpable pulse is detected at the periphery, so-called total alternans. Pulsus alternans is produced by an alternation in left ventricular contractile force associated with an alternation of left ventricular fiber length; it is a very valuable sign of left ventricular dysfunction. In most instances, it is found in association with a third heart sound.

Examination for Thrombophlebitis

The presence or absence of thrombophlebitis ( Chapter 30 ) is an integral part of the cardiovascular database. Thrombophlebitis refers to venous inflammation with secondary thrombosis of the involved vein. It is most commonly noted in the deep veins of the leg and superficial veins of the arm. Superficial thrombophlebitis can be seen and felt, making the diagnosis easy in most cases. Most deep vein thromboses are clinically silent and cannot be detected by routine examination. When thrombophlebitis is confined to small venous channels beneath the subcutaneous tissue or in the pelvis, the lesions are neither visible nor palpable. Mild pain in the calf may be the only symptom, and tenderness may be the only sign.

The examiner should also compare the skin temperature in the two calves, since active phlebitis may create local warmth. Calf circumference should also be determined in all suspected cases. Pain is a prominent feature of muscular, synovial, or vascular leg diseases, and various tests have been used to identify the specific etiology. Homans's test (dorsiflexion sign) is used to detect irritability of the posterior leg muscles through which inflamed or thrombosed veins course. The Lowenberg cuff test is another helpful clinical maneuver for detection of calf vein thrombosis.

A summary of only the most common conditions associated with an abnormality on the cardiovascular examination is shown in Table 7.4 .

Common Conditions Associated with an Abnormality on the Cardiovascular Examination.

An orderly process of history taking and physical examination together with selective application of modern laboratory technology should enable the clinician to arrive at an accurate diagnosis, estimate the degree of severity, formulate a logical plan of treatment, and better understand the pathophysiologic abnormalities in the patient with a cardiovascular problem.

• Cite this Page Felner JM. An Overview of the Cardiovascular System. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 7.
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