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The Texas Heart Institute Journal logoLink to The Texas Heart Institute Journal
. 2010;37(6):629–632.

Bedside Skills

A 50-Year Personal Retrospective

Ira Martin Grais 1
PMCID: PMC3014130  PMID: 21224929

Current dependence on the laboratory, noninvasive testing, and interventional techniques for diagnosis has diminished the time and effort devoted to the medical history and physical examination. Slowly, many practitioners are losing these bedside skills, and many others who were never taught them can't pass them on to the coming generations of students.1 Moreover, lower reimbursements for cognitive efforts expended during patient visits further diminish our attempts to maintain basic bedside or clinical techniques. Fifty years of clinical practice have taught me to respect these skills and not to give them up by relying solely on laboratory testing.

One of the most common clinical problems seen by an adult cardiologist is myocardial ischemia, often presenting as angina or dyspnea. Yet the practitioner knows that there is no single approach to the management of all patients with these symptoms. In one patient, the problem may be severe calcific aortic stenosis requiring valve replacement; in another, idiopathic hypertrophic subaortic stenosis requiring a myomectomy; and in a third, severe coronary atherosclerotic disease requiring bypass surgery or stenting. Each of these clinical entities requires a different approach, and this becomes more problematic when the patient has combined cardiac disorders or comorbidities.

Observing basic clinical principles will help lead to the correct diagnosis and treatment, as illustrated by the cases reported here. Four of these basic principles of clinical medicine are

  • Don't take the history from the patient; allow the patient to tell his or her story.

  • Observe. Selective attention is the heart of the physical examination.

  • When ordering a laboratory test, know what question you want answered and check on the results.

  • If an organ or an organ system fails, look for a precipitating cause.

As a senior medical student on an elective rotation in cardiology at what was then Presbyterian St. Luke's Hospital in Chicago, I learned the lesson of allowing patients to tell their own stories. The head of cardiology was Dr. John S. Graettinger, and in his department were a number of attending cardiologists and cardiology fellows. All of us participated in late-afternoon rounds.

I had examined a man with chest pain who was admitted for catheterization for aortic valve stenosis. I'd been told it was important to discover what level of effort brought on the chest discomfort. I thought I had learned this well and was presenting the case.

M. Grais: “This is a 60-year-old man who has been having effort-related mid-chest discomfort for several months. Despite this, he has not had to stop playing golf.” (As I continued to the next item in his history, Dr. Graettinger interrupted.)

Dr. Graettinger: “Just a minute, Marty. You say he was able to play golf without getting chest pain.”

M. Grais: “That's right.”

Dr. Graettinger: “Tell us something more about his golf game.”

M. Grais: “Well, he plays golf, but he doesn't have to stop because of chest pain.”

Dr. Graettinger: “I understand that, but give us more detail. For example, how many holes does he play?”

M. Grais: “I don't know.”

Attending 1: “Does he walk the golf course or ride a cart?”

Attending 2: “Does he have a caddie or does he pull a cart?”

Attending 3: “Does he ever have to stop to rest or can he play all the holes without resting?”

Attending 4: “Does he play on a flat golf course or is it hilly?”

Attending 5: “What time of day does he play golf? When it's hot or when it's cool? When it's sunny or in the shade?”

They all looked at me. No one smiled. I'm sure my face was red. I was speechless. A senior in medical school doesn't forget experiences like that. The inquisition embarrassed me but also provided critical insight into history-taking. This experience permanently altered how I interview patients about their chest pain.

I no longer simply ask people if they experience chest discomfort, followed by the usual questions about onset, duration, radiation, associated symptoms, methods of relief, and so forth. Instead, I'll ask more neutral questions about the patient's ordinary daily activity. Once I have the level of physical function clearly in mind, I ask, “Do you ever find you can't do these things you've described?” or “At this level of activity, do you ever find you can't do it for some reason?”

That's usually when the history of angina or dyspnea emerges. I'll hear something like, “Well, you know, Doc, funny you should ask. I used to be able to climb the stairs to the L (elevated train) without any trouble. But the last few months I have to slow down or stop halfway up, because I get this funny feeling or tightness here (and at this point the patient might make a clenched fist over the center of the sternum). It's not a pain or anything but I can't continue until it eases.” Watching the hand when someone describes pain can tell you more than the words. Rarely is angina described by pointing with the tip of a single finger. People who have trouble describing the character of pain orally will often tell you much with the way they position or move the hand.

A careful history and physical examination, with selective attention to the salient features of each, will usually provide the clues to the correct diagnosis or diagnoses. Also, the experienced practitioner knows that while testing can help make or confirm a diagnosis, the results do not necessarily help determine therapy for a given patient. The following cases illustrate how both routine and subtle findings can help determine diagnosis and therapy.

A Case of Angina with an Incomplete Examination

I was asked by an internist at another hospital to see his elderly patient with chest pain in our emergency department. Her ambulance had been diverted to our hospital because of difficulty in getting her blood pressure. Our staff had placed the patient in the Trendelenburg position and were putting in 2 intravenous lines, drawing blood, placing a Foley catheter, obtaining blood gases, getting a chest x-ray, hooking up an electrocardiograph, taking a history, and doing the usual nursing care and documentation. The head nurse reported that the patient's systolic blood pressure was 70 mmHg, yet the patient was alert and looking around, wondering what all the fuss was about. She was not pale or sweaty and actually looked comfortable. She certainly did not appear to be in shock. Since the blood pressure cuff was on her left arm, I moved it to her right arm, where the pressure was actually 160/60 mmHg. This was announced and 10 people attending the patient suddenly disappeared. She did have ischemic ECG changes and was admitted to our cardiac care unit. I called her internist to advise him of her status and the diagnosis of left subclavian artery stenosis.

Although this illustrates a rather obvious diagnosis, it is a classic mistake to take the blood pressure in only 1 arm, especially when you first see a patient. It is also wise not to rely on a blood pressure you have not taken yourself. Common things most commonly occur, and subclavian stenosis is not uncommon.

A Case of Angina with a Complicated Examination

An 80-year-old retiree who'd had replacement of his aortic valve for congenital bicuspid aortic stenosis, coronary artery bypass surgery for triple-vessel disease, and shunt placement in his left arm for renal dialysis was admitted to the cardiac care unit with recurrent chest pain and new T-wave inversions in the right and mid chest leads. His cardiac markers were negative for an acute myocardial infarction. After increased anti-anginal therapy and bed rest, the patient was experiencing less pain, and house staff felt he could be discharged.

However, the attending noted a left supraclavicular bruit and worried about the coronary anatomy. He requested a cardiac catheterization with additional attention to the left subclavian artery. Angiography showed a tight left subclavian stenosis proximal to the takeoff of the left internal mammary artery (LIMA) graft to the left anterior descending coronary artery, and this lesion also obstructed flow to the shunt in the left arm. The LIMA was patent; however, the left-arm shunt could have been stealing blood from the LIMA graft. After the placement of 2 stents corrected the subclavian artery obstruction, the patient's inverted T waves became upright and his angina disappeared.

In this patient, subclavian artery stenosis was suspected because of the left supraclavicular bruit. Blood pressure measurements were avoided in the left arm, to protect the hemodialysis shunt. These subtle findings emphasize the value of a careful physical examination as a mirror of applied pathophysiology.

Things Are Not Always as They Seem

A middle-aged hypertensive man with a previous right nephrectomy for cancer was referred for a cardiac catheterization because of deep precordial T-wave inversions thought to be ischemic. He had no history of angina or dyspnea and was being treated for his hypertension. During the complete physical examination, a systolic bruit extending into diastole was heard over the left kidney, suggesting that renal artery stenosis was the cause of the hypertension. Noninvasive imaging studies revealed an extrinsic mass compressing the left renal artery. At operation, the mass proved to be a solitary metastasis from his renal cancer. Postoperative blood pressures were normal, his T waves consistent with left ventricular strain improved, and the cardiac catheterization was deemed unnecessary.

A Case of Obvious Heart Failure

A man with known ischemic cardiomyopathy and an ejection fraction of 0.15 entered the hospital with gross heart failure. His B-type natriuretic peptide (BNP) level was 2,000 pg/mL. The attending asked the admitting resident, “Why is he in heart failure?” When the medical resident said that he didn't know, the attending asked, “Has anything changed in recent weeks?”

The resident responded, “Well, the only thing he told me was that 2 weeks ago he had a kidney stone and was too sick for surgery, so a urologist put him on sodium bicarbonate tablets to alkalinize the urine.” The attending asked how many tablets he was taking. The resident didn't know and asked the patient. He returned to the phone laughing and said, “He's been on 4 tablets, 4 times a day, for the last 2 weeks. There's 625 mg of sodium in each tablet, which is way more than allowed by his sodium-restricted diet.”

With additional furosemide and no sodium bicarbonate tablets, the patient lost considerable weight over the next 3 days and went home feeling well.

This case illustrates an obvious and salient principle in medicine: whenever an organ or an organ system fails, look for a precipitating cause. The BNP level as a biochemical marker of heart failure is quite useful but does not provide the reason for the heart failure or the best treatment. In this case, the history did.

A Case of Heart Failure due to Aortic Insufficiency

An elderly man came to the Veterans Administration Hospital with heart failure. On examination, he had 5 separate heart murmurs, including 1 of aortic insufficiency. Because he had murmurs that sounded like aortic stenosis and insufficiency, mitral stenosis and insufficiency, and tricuspid regurgitation, the most likely diagnosis was rheumatic heart disease.

However, the cardiologist suspected syphilitic aortitis and provided the following explanation: “First, the aortic insufficiency murmur radiates louder down the right sternal border than the left, suggesting that aortic root disease rather than aortic valve disease is causing the leak. Second, he has a loud apical S3 and no opening snap. This suggests that he does not have mitral stenosis, because with mitral stenosis diastolic flow is not fast enough to generate a left ventricular S3. Third, his aortic insufficiency is severe and could account for all the murmurs. Severe aortic insufficiency causes the aortic diastolic murmur. Subsequent ejection of the large volume of regurgitated blood creates an aortic systolic flow murmur. In time, the left ventricle becomes dilated and coaptation of the mitral leaflets is compromised, causing mitral insufficiency. The severe aortic insufficiency would cause an Austin Flint diastolic mitral flow rumble. Finally, with the onset of right-sided heart failure, the patient has developed a tricuspid regurgitation murmur. The presence of severe aortic insufficiency is indicated by all the runoff signs: wide pulse pressure with low diastolic pressure, pistol shots over the femoral arteries, Quincke pulse, Duroziez murmur, earlobe pulsation, wide excursion of the arterioles in the optic fundi, and a carotid pulsus bisferiens.”

One would hope that a Doppler echocardiogram would confirm such findings, yet relying on this test exclusively can lead us astray, as illustrated by the next patient, who also had aortic insufficiency.

Another Case of Heart Failure due to Aortic Insufficiency

A middle-aged man was referred to a cardiologist because of severe dyspnea on exertion. He had subtle signs of heart failure, a typical murmur of aortic insufficiency, and all the runoff signs described in the previous patient. A Doppler echocardiogram done at a prestigious medical center was read as mild aortic insufficiency, both initially and on repeat study. The cardiologist could not accept this interpretation, because the peripheral runoff signs suggested severe aortic insufficiency. He scheduled right and left cardiac catheterization. This confirmed torrential aortic regurgitation, requiring aortic valve replacement that resulted in resolution of the heart failure.

Subtle positive physical findings can override echocardiographic conclusions. Here the aortic valve was angled in such a manner that the aortic regurgitant jet was directed laterally instead of anteriorly, and this made quantitation difficult.

The Dog in the Nighttime Syndrome

Another clinical vignette teaches the importance of the absence of the expected.

An octogenarian with dementia and Parkinson's disease was admitted to the neurology service with pneumonia and a fever of 103 °F. He'd been given intravenous fluids and had developed severe dyspnea due to volume-overload pulmonary edema: hence the cardiology consultation.

Going through the chart and looking at the electrocardiogram, the cardiologist noted sinus rhythm at 60 beats/min. Why, he wondered, would an elderly man with pneumonia, a high fever, and pulmonary edema not have sinus tachycardia? Two common causes for such a paradoxical finding would be sick sinus syndrome and hypothyroidism. The patient's dementia, Parkinson's disease, and volume overload made evaluating the physical findings for hypothyroidism problematic. However, thyroid function tests confirmed the suspected severe hypothyroidism.

This case example is reminiscent of the famous vignette in the Sherlock Holmes story “Silver Blaze.” A favored racehorse named Silver Blaze had disappeared from its stables before the running of a big race, and the trainer was found dead from a knife wound. No one could find the horse or the killer, so Sherlock Holmes was consulted. At one point, Inspector Gregory and Holmes have the following exchange.

Gregory: “Is there any point to which you would wish to draw my attention?”

Holmes: “To the curious incident of the dog in the nighttime.”

Gregory: “The dog did nothing in the nighttime.”

Holmes: “That was the curious incident.”

Holmes noted that the horse lived in the stable with a dog and that the dog had not barked when the horse was taken. Clearly, the dog knew the person who took the horse. This clue leads to the solution of the crime. The story teaches much about observation. In the case of our febrile octogenarian with heart failure, his sinus node did not bark: the expected tachycardia was missing. The absence of something you expect to find can be as important as a positive finding.

Applying Pathophysiology While Taking the Blood Pressure Yourself

A 36-year-old rather muscular man presented at the Veterans Administration Hospital with effort dyspnea. He had no other symptoms. His supine blood pressure was 140/90 mmHg. His standing blood pressure remained 140/90 mmHg, but his pulse dropped from 80 to 40 beats/min. Had the patient suddenly developed heart block or was there a pulse deficit? I instantly moved my stethoscope from his arm to his cardiac apex and heard a heart rate of 80 beats/min while his pulse rate remained 40 beats/min. Further examination revealed a systolic ejection murmur typical of left ventricular outflow tract obstruction and a palpable left ventricular S4, but no signs of heart failure.

Various maneuvers confirmed that the murmur and S4 were consistent with idiopathic hypertrophic subaortic stenosis. The demonstrated orthostatic pulsus alternans strongly indicated a severe cardiomyopathy. Had I relied on someone else's recording of the blood pressure, I'd have missed the latter.

Summary

Medicine bears a long tradition of detailed medical history and physical examination. These standard techniques are now being shunned in favor of an emphasis on laboratory studies. Yet there should be no contest. The clinician needs both bedside skills and appropriately selected laboratory testing. High-touch and high-tech medicine are not incompatible. When the physician uses them together, he or she is less likely to be misled.

Footnotes

Address for reprints: Ira Martin Grais, MD, FACC, 6611 N. Central Park, Lincolnwood, IL 60712

E-mail: i-grais@sbcglobal.net

References

  • 1.Fred HL. Hyposkillia: deficiency of clinical skills. Tex Heart Inst J 2005;32(3):255–7. [PMC free article] [PubMed]

Articles from Texas Heart Institute Journal are provided here courtesy of Texas Heart Institute

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