My patient is asking about the benefits of smoking cessation. How soon should she realize the health benefits of quitting her habit?

She should realize the health benefits of smoking cessation (SC) almost immediately! As the effect of nicotine wears off, just 15-20 minutes after her last cigarette, her heart rate and blood pressure should begin to fall.1,2Other health benefits, some within a year others longer, soon follow. 3,4 Between 2-12 weeks after SC, your patient may notice an improvement in her breathing and pulmonary function tests.

Between 1-9 months, the cilia in the lungs should begin to regenerate and regain normal function, allowing her to adequately clear mucus and bacteria with a decrease in cough and shortness of breath.

At 1 year, the risk of cardiovascular disease (eg, myocardial infarction, stroke) falls by one-half.

At 5 years, the risk of mouth, throat, esophagus, and bladder cancer also drops by one-half.

It takes 10 years for the risk of lung cancer to drop by one-half, and 15 years for it to approach that of non-smokers asymptotically. 4Fun fact: Did you know that in hypertensive patients who smoke, the blood pressure lowering effect of beta-blockers may be partly abolished by tobacco smoking,  whereas alpha-blockers may maintain their antihypertensive effects? 5References

  1. Omvik P. How smoking affects blood pressure. Blood Press. 1996;5:71–77.
  2. Mahmud A, Feely J. Effect of smoking on arterial stiffness and pulse pressure amplification. Hypertension. 2003;41(1):183-187.
  3. US Surgeon General’s Report, 1990, pp. 193, 194, 196, 285, 323
  4. US Surgeon General’s Report, 2010 and World Health Organization. Tobacco Control: Reversal of Risk After Quitting Smoking. IARC Handbooks of Cancer Prevention, Vol. 11. 2007, p. 341.
  5. Trap-Jensen. Effects of smoking on the heart and peripheral circulation. Am Heart J 1988;115:263-7.

Contributed by Felicia Hsu, Medical Student, Harvard Medical School

My patient is asking about the benefits of smoking cessation. How soon should she realize the health benefits of quitting her habit?

How does hyperventilation cause coronary vasospasm?

Hyperventilation may be an important cause of coronary vasospasm and chest pain. 1 The mechanism likely revolves around the competition between the effects of hydrogen and calcium ions on the smooth muscle of coronary arteries. 2

Respiratory alkalosis induced by hyperventilation causes a reduction of hydrogen ions which, under physiologic conditions, compete with calcium ion, an important trigger for arterial smooth muscle contraction. Lower hydrogen ion concentrations tips the balance in favor of calcium’s effects on transmembrane channels and myofibrillar ATP-ase of the smooth muscle and causes vasoconstriction.2

In fact, hyperventilation has been used to reproduce coronary spasm during angiography in patients with non-obstructive coronary artery disease and angina symptoms.The efficacy of hyperventilation in inducing an alkalotic state during this test is verified by obtaining an arterial blood gas after 6-minutes of hyperventilation.  A basic Tris-buffer to enhance alkalotic provocation was also used in earlier studies. 2

In addition to producing spasm and angina, hyperventilation-induced alkalosis has been associated with frank transmural myocardial infarction and ischemia-related arrhythmias such as ventricular tachycardia. 2,4,5

So in the appropriate context, hyperventilation may not be so benign!


  1. Freeman LJ, Nixon PGF. Chest pain and the hyperventilation syndrome-some aetiologic considerations. Postgrad Med J 1985;61:957-61.
  2. Yasue HM, Nagao S, Omote A, et al. Coronary arterial spasm and Prinzmetal’s variant form of angina induced by hyperventilation and Tris-buffer infusion. Circulation 1978;58:56-62.
  3. Zaya M, Mehta PK, Merz NB, etal. Provocative testing for coronary reactivity and spasm. J Am Coll Cardiol 2014; 63:103-9.
  4. Magarian GJ, Jones S, Calverley T. Hyperventilation testing for coronary vasospasm: induction of spontaneous ventricular tachycardia in association with transmural ischemia without obstructive coronary disease. 1990; 120:1447-49.
  5. Chelmowski MK, Keelan MH. Hyperventilation and myocardial infarction. Chest 1988;93:1095-96.



Contributed by Ramya Chitra Mosarla, Medical Student, Harvard Medical School

How does hyperventilation cause coronary vasospasm?

Is checking for orthostatic hypotension less than 1 minute after standing clinically useful?

Not only can it be useful in identifying those with history of dizziness upon standing but it may also predict a higher risk of falls, fracture, syncope and mortality long term. 1

Clinicians (myself included) have often assumed that drops in blood pressure (BP) and brief feeling of light-headedness soon after active standing are too common and “physiologic” to be of clinical utility,1,2 and have often discouraged checking for orthostatic hyotension (OH) sooner than 1 minute.

However, a 2017 report involving over 11,000 middle-aged participants (Atherosclerosis Risk in Communities Study) may make us rethink our position. This prospective study  found a significant association between participant-reported history of dizziness on standing and OH (defined as a drop in BP systolic ≥20 mmHg or diastolic ≥10 mmHg) but only at 1st measurement (mean of 28.0 seconds after standing), not at subsequent ones over a 2 minute period.

The more intriguing finding was the association between OH documented < 1 minute after standing and increased risk of falls, fracture, syncope, and mortality over a median follow-up period of 23 years. Although there were limitations to the study (eg, excluding many patients likely to have more severe OH), it appears that “premature” checking for OH less than a minute after standing  may not be useless!

Most, including the CDC, agree that rechecking the BP at 3 minutes is still indicated to identify those with sustained or delayed OH. 2,3

Also go to a related P4P post:


  1. Juraschek SP, Daya N, Rawlings AM, et al. Comparison of early versus late orthostatic hypotension assessment times in middle-age adults. JAMA Intern Med 2017;1177:1316-1323.
  2. Singer W, Low PA. Early orthostatic hypotension and orthostatic intolerance-more than an observation or annoyance. JAMA Intern Med 2017;1177:1234-25.
  3.  CDC. Accessed February 7, 2017.
Is checking for orthostatic hypotension less than 1 minute after standing clinically useful?

Can my patient contract influenza more than once in a season?

It’s not common but reinfection with influenza can definitely occur, either due to the same viral strain, or due to a different one altogether.

One study reported influenza reinfection due to H1N1 in otherwise healthy patients within 12-20 days of the original infection after an apparent period of full recovery. 1 There was no evidence of resistance to oseltamivir among isolates and all patients recovered after the second infection.

Reinfection with the same viral strain within 2-3 weeks of the initial bout of influenza shouldn’t be too surprising since it takes 4-7 weeks for antibody response to the infection to peak. 2 Reexposure to the same circulating strain of influenza virus (the season can last 6 weeks or longer) can then result in reinfection when the body hasn’t had enough time to make significant amount of protective antibodies following the first infection.

Another explanation is that more than 1 strains of influenza virus often circulate during any given season.   This places patients at risk of infection due to strains of influenza virus that do not confer significant cross-immunity between each other,  resulting in getting “the flu twice in 1 season.” 3


  1. Perz CM, Ferres M, Labarca JA. Pandemic (H1N1) 2009 reinfection, Chile. Emerg Infect Dis 2010;16:156-57.
  2. Treanor JJ. Influenza viruses, including avian influenza and swine influenza. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious diseases. 7th ed. New York: Elsevier; 2010. p 2265-2293.
  3. Rettner R. Can you get the flu twice in 1 season? Scientific American, LiveScience, February 4, 2018. . Accessed February 5, 2018.


Can my patient contract influenza more than once in a season?

What is the difference between “Moderate” and “High complexity” medical decision making under the Centers for Medicare and Medicaid Services (CMS) rule?

The level of medical decision making (“Straightforward/Low complexity”, “Moderate complexity”, “High complexity”) or MDM should reflect the intensity of the cognitive labor performed by the clinician.

The MDM level is determined by 3 important factors:

  • The nature and number of clinical problems
  • The amount and complexity of data reviewed by the clinician
  • The risk of morbidity and mortality to the patient

As for the nature of clinical problems, in contrast to stable problems (1 point), the following receive higher points:

  • Established problems that are worsening (2 points)
  • New problems for which no further workup is planned (3 points)
  • New problems for which additional workup is planned (4 points)

As for the amount and complexity of data reviewed by the clinician, the following receive higher points (2 points each)

  •  Review and summarization of old records and/or obtaining history from someone other than patient and/or discussion of case with another health care provider
  • Independent visualization of image, tracing or specimen itself (not simply review of report)

More routine activities such as simply reviewing or ordering lab, radiology, or other tests, discussing tests results with performing physician, or obtaining old records and/or history from someone other than patient receive only 1 point each.

The 3rd element of MDM scoring system is based on the risk of complications and/or morbidity or mortality determined by the severity of the presenting problem(s), complexity of the diagnostic procedure(s) ordered, and management options selected.

Patients may be considered “High risk” of complications and/or morbidity or mortality when any of following is documented: 

A. Presenting problem(s)

  • ≥1 chronic illnesses with severe exacerbation, progression, or side effects of treatment
  • Acute or chronic illnesses or injuries that may pose a threat to life or bodily function, eg, multiple trauma, acute MI, pulmonary embolus, severe respiratory distress, progressive severe rheumatoid arthritis, psychiatric illness with potential threat to self or others, peritonitis, acute renal failure
  • An abrupt change in neurologic status, eg, seizure, TIA, weakness or sensory loss

B. Diagnostic procedure(s) ordered

  •  Cardiovascular imaging studies with contrast with identified risk factors
  • Cardiac electrophysiologic tests
  • Diagnostic endoscopies with identified risk factors
  • Discographies

C. Management options selected

  •  Elective major surgery (open, percutaneous or endoscopic with identified risk factors)
  • Emergency major surgery (open, percutaneous or endoscopic)
  • Parenteral controlled substances
  • Drug therapy requiring intensive monitoring for toxicity
  • Decision not to resuscitate or to de-escalate care because of poor prognosis

Less severe conditions such as pyelonephritis, pneumonitis, colitis, or head injury with brief loss of consciousness, and less complicated procedures such as diagnostic endoscopies and elective major surgery with no identified risk factor are considered “Moderate risk”.

 To qualify for “High complexity” care, at least 2 of the following must be present:

  • High (≥4 points) score in number of diagnoses or treatment option
  • High ((≥4 points) score in the amount and complexity of data gathered
  • High risk of complications and/or morbidity or mortality

Otherwise, your patient encounter qualifies for “Moderate” or lower complexity  care.

For further details on how to determine the MDM level on your individual patient go to:

Contributed by Jodie Medeiros, CPC, COC, ICDCT-CM, Billing Specialist, Mass General Hospital, Boston, MA


What is the difference between “Moderate” and “High complexity” medical decision making under the Centers for Medicare and Medicaid Services (CMS) rule?

My patient is admitted with diabetic ketoacidosis (DKA) and is testing positive for cocaine. Can cocaine cause DKA?

Cocaine use has been generally linked to DKA but whether it’s through its antagonizing effect on insulin action or more indirectly through its association with non-compliance with insulin, or both, is not totally clear.

A retrospective study found cocaine users to account for 14% of all DKA admissions.1 Cocaine users were also less likely than controls to have an intercurrent illness identified as a precipitant for DKA, and more likely to have missed taking insulin prior to admission. Another study also reported active cocaine use to be associated with DKA, but found its effect to be independent of non-compliance. 2

Yet another retrospective study limited to patients admitted with hyperglycemia, found no significant association between active cocaine use and development of hyperglycemic crisis.

There are reasons to believe that cocaine may contribute to DKA. Cocaine has been proposed as a possible precipitant of DKA due to its ability to potentially enhance counterregulatory mechanisms designed to antagonize the effect of insulin by increasing catecholamine and cortisol levels. 1,3

So next time you have a patient with DKA, consider cocaine as a possible precipitant, particularly when the cause of DKA is unclear.



  1. Warner EA, Greene GS, Buchsbaum MS et al. Diabetic ketoacidosis associated with cocaine use. Arch Intern Med 1998; 158:1799-802.
  2. Nyenwe E, Loganathan R, Blum S, et al. Active use of cocaine: An independent risk factor for recurrent diabetic ketoacidosis in a city hospital. Endocr Pract 2007;13:22-29.
  3. Modzelewski KL, Rybin DV, Weinberg JM, et al. Active cocaine use does not increase the likelihood of hyperglycemic crisis. J Clin Transl Endocrinol 2017;9:1-7


Contributed in part by Quin L Sievers, Medical Student, Harvard Medical School

My patient is admitted with diabetic ketoacidosis (DKA) and is testing positive for cocaine. Can cocaine cause DKA?