End stage renal disease and lower white blood cell counts were associated with higher rates of heart rate normalization, while older age and higher intravenous fluid volume in the ED were associated with higher rates of respiratory rate normalization. In the unadjusted univariate analysis, mortality was significantly higher in patients persistently tachycardic throughout their ED stay 5.
Similarly, mortality was higher among persistently tachypneic versus those that normalized their respiratory rate 8. Of note, the absolute mortality rates were higher among patients with persistent tachypnea as opposed to tachycardia, and these data are illustrated in Fig. Our sensitivity analysis demonstrated similar results for predicting in-hospital mortality whether tachycardia was defined as 90 or beats per minute.
Similar results were also found when tachypnea was defined as 22, but not 18, breaths per minute data not shown. Relative mortality associated with the persistence of A tachycardia and B tachypnea.
Patients were categorized as to whether they temporarily normalized or were persistently elevated in the emergency department and whether they were persistently abnormal or normalized upon hospital admission.
Following model refinement, the final model for tachycardic patients included age, hypertension, end-stage renal disease, white blood count, hemoglobin, bicarbonate, hypotension, and either temporary normalization or normal heart rate upon admission. The final model for tachypneic patients included age, hypertension, white blood count, hemoglobin, bicarbonate, hypotension, and either temporary normalization or normal respiratory rate upon admission.
Hypotension remained a significant independent predictor and did not need to be forced into the final model. Other commonly available vital signs, such as temperature and pulse oximetry, were not significant predictors of outcome in the multivariate model, even when categorizing temperature as a binary normal versus abnormal rather than a continuous variable to account for the impact of hypothermia on data analysis.
In a post-hoc analysis, we added GCS to our final models to determine the impact of this readily available, bedside measure to influence the prediction of mortality. In our multivariate tachycardia model, GCS was indeed an independent predictor of mortality, though all other variables remained significant predictors. When added to the tachypnea model, GCS significantly predicted mortality, but normalization of tachypnea no longer reached statistical significance as an independent predictor of mortality.
Patient demographics and clinical characteristics of survivors versus non-survivors in patients presenting with either tachycardia or tachypnea. Unadjusted and adjusted odds ratios for in-hospital mortality among patients with and without persistent tachycardia and tachypnea. Finally, we attempted to determine whether persistent tachypnea and tachycardia were independently associated with increased risk of mortality, or whether they were different metrics that identified the same group of patients.
Eight hundred and fourteen patients demonstrated both initial tachycardia and tachypnea. Mortality was highest in patients who had persistence of both tachycardia and tachypnea throughout their ED stay at 8. Note that persistent tachypnea tends to carry a worse prognosis than persistent tachycardia. In this cross-sectional single center study of ED patients, we document the increased mortality associated with persistence of tachycardia and tachypnea.
Vital sign measurements are the cornerstone of clinical practice, and provide a simple fundamental method to assist in the evaluation of patients. Similarly, even transient normalization of these vital signs are associated with an improved prognosis compared to patients who never have a normal heart or respiratory rate measured in the ED.
The prognostic value persisted even when several different cutoffs for the definitions of tachycardia and tachypnea were investigated. These findings support the anecdotal practice of using normalization of vital signs for risk assessment of ED patients. Several findings of our study warrant further consideration. It would be reasonable to assume that patients failing to normalize these vital signs would be likely to have other indications of illness, such as hypotension, and that the relative utility of vital sign normalization might be negligible.
Our results were significant exclusive of measurements of hypotension, though the absolute risk of death was lower following exclusion of hypotensive patients. As illustrated by Table 4 , any episode of hypotension remains a stronger indicator of mortality odds ratios of 2. However, the risk associated with normalization of heart rate and respiratory rate remains significant even after controlling for the presence of hypotension and other clinical predictors of mortality. Combined, these data suggest that heart rate and respiratory rate normalization may be a particularly useful indicators in the cohort who require hospital admission but who do not exhibit hemodynamic instability through the manifestation of hypotenstion in the ED.
Similarly, altered mental status is a readily clinically available indicator with established utility to predict patient outcome in ED patients [ 10 , 11 ]. When included in our multivariate model, persistent tachycardia remained a significant independent predictor of mortality, supporting its clinical utility.
Persistent tachypnea was no longer statistically significant after addition of GCS our model, however. It could be that patients with significantly altered mental status were more likely to be intubated with resultant artificial respiratory rates. This confounder may have affected our study results, though that data was not recorded, making interpretation of persistent tachypnea less clear than tachycardia. It is important to note that the absolute mortality rates in the study are low, but are consistent with the mortality rate of an unselected cohort of patients admitted to a tertiary care facilities.
The present findings are not surprising given the fact that changes in heart and respiratory rate often precede hypotension, though perhaps these changes might serve as an early warning sign of clinical decompensation for clinicians. Pay-Per-View Access. Buy This Article. View Your Tokens. View Metrics.
Citing articles via Google Scholar. Email alerts Article Activity Alert. Newest Articles Alert. Latest Issue Alert. News Latest News Archive. Close Modal. This site uses cookies. By continuing to use our website, you are agreeing to our privacy policy. Assess the blood pressure and heart rate. Move the patient into a standing position.
After two minutes, reassess the blood pressure and heart rate with the patient in the standing position. A patient with a volume deficit will experience a decrease in preload, stroke volume and cardiac output.
Clinically, this will present as a decrease in systolic blood pressure and an increase in heart rate. If the systolic blood pressure decreases greater than 20 mmHg or the heart rate increases by greater than 20 to 30 beats per minute from the supine to standing vital signs, the patient is said to have orthostatic vital signs or postural hypotension.
The increase in heart rate has been found to be a more sensitive indicator of volume depletion. Be cautious when interpreting a decrease in systolic blood pressure when performing the orthostatic tilt test, especially on elderly patients. Thus, an increased heart rate of greater than 20 beats per minute becomes a better predictive indicator of volume depletion when performing this test.
If a sudden drop of greater than 10 mmHg in the systolic reading is found when assessing blood pressure, note the phase of respiration when the drop is occurring.
If a drop of greater than 10 mmHg of pressure is noted during the inspiratory phase of respiration, it may be an indication of pulsus paradoxus, which can be seen in cardiac tamponade, pericardial effusion, constrictive pericarditis, pulmonary embolism, cardiogenic shock, bronchial asthma or tension pneumothorax.
Another indication of pulsus paradoxus seen on physical examination is engorgement of the jugular veins on inspiration. This is known as Kussmaul's sign. When assessing a patient complaining of chest pain or midscapular pain, measure the blood pressure in both upper arms and compare the systolic readings.
If there is a difference of 10 to 20 mmHg in the systolic blood pressure between both extremities, it may be an indication of an aortic dissection. ACE inhibitors are drugs that cause blood vessels to dilate, thereby reducing the vascular resistance, which results in a decrease in blood pressure.
This lower vascular resistance reduces the myocardial workload and can improve the function of a weakened heart. In the patient who presents with a low blood pressure, consider the possibility of ACE inhibitor use. Pupils Assess the pupils for size, equality and reactivity.
Pupil signs may provide some evidence as to the integrity of the brainstem. Pupils may also provide a clue as to whether the coma patient has a structural lesion or if the condition is of a metabolic etiology. Pupils that are unequal, fixed and dilated in a comatose patient indicate a structural etiology or space-occupying lesion.
If the coma or altered mental status is due to a metabolic cause such as hypoxia, drug overdose or hypoglycemia, the pupils will remain equal and reactive to light; however, they may respond more sluggishly. When encountering a patient with an unknown etiology of coma, pupil signs may provide a clue as to the cause. Conclusion Abnormal findings in the vital signs may provide clear indications of certain conditions.
It is important to understand what is considered to be truly normal and abnormal. It is evident that some abnormal findings in one patient age group may be normal in another. Anytime an abnormal vital sign is identified, process it cognitively and consider it in relation to the whole patient assessment.
Esssentials of Paramedic Care, 2nd Ed. Advanced Medical Life Support, 3rd Ed. Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study.
BMJ , , Emergency Medicine Secrets, 2nd Ed. Joseph J. William S. Daniel D. He is the author of several EMS textbooks and a nationally recognized lecturer. Sign in. EMS World Expo. Current Issue. Issue Archives. Start Print Subscription. Renew Print Subscription. Start Digital Subscription.
Patient Care. Expo on Demand. CE Articles. Online Product Guide. Contact Us. Advisory Board. About Us. Copied to clipboard. Submit Feedback. Email Address. Here the authors present a unique etiology of a deep diabetic foot abscess and outline key components of the diagnosis and treatment.
Dr Margareth Pierre-Louis discusses the pros and cons of monitoring skin health with technology. Choices Significantly worse, frequent long waits. Moderately worse, occasional long waits. Minimally worse, infrequent long waits.
No real change or it's gotten better. Top Stories. Acute respiratory distress syndrome ARDS is caused by a severe inflammatory response in the body when there is a severe infection or after there has been trauma to the body. This inflammation causes fluid to leak into the lungs, which makes it extremely difficult to breathe and decreases the amount of oxygen going into the bloodstream.
The lack of oxygen can harm the brain, kidneys, and other internal organs. Most people who develop ARDS are already in the hospital because of another disease or injury. Shortness of Breath dyspnea — This is the feeling of being short of breath and having difficulty catching your breath. Rapid breathing tachypnea and heartbeat tachycardia — Healthy adults take 12 to 20 breaths per minute.
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