RESUMEN
The use of pulse wave analysis may guide the provider in making choices about blood pressure treatment in prehypertensive or hypertensive patients. However, there is little clinical guidance on how to interpret and use pulse wave analysis data in the management of these patients. A panel of clinical researchers and clinicians who study and clinically use pulse wave analysis was assembled to discuss strategies for using pulse wave analysis in the clinical encounter. This manuscript presents an approach to the clinical application of pulse waveform analysis, how to interpret central pressure waveforms, and how to use existing knowledge about the pharmacodynamic effect of antihypertensive drug classes in combination with brachial and central pressure profiles in clinical practice. The discussion was supplemented by case-based examples provided by panel members, which the authors hope will provoke discussion on how to understand and incorporate pulse wave analysis into clinical practice.
Asunto(s)
Presión Sanguínea/fisiología , Hipertensión/diagnóstico , Análisis de la Onda del Pulso/métodos , Adulto , Anciano , Antihipertensivos/uso terapéutico , Determinación de la Presión Sanguínea , Arteria Braquial/fisiología , Femenino , Humanos , Hipertensión/tratamiento farmacológico , Hipertensión/fisiopatología , Masculino , Persona de Mediana Edad , Flujo Pulsátil/fisiología , Análisis de la Onda del Pulso/estadística & datos numéricos , Análisis de la Onda del Pulso/tendenciasRESUMEN
BACKGROUND/OBJECTIVE: We examined the changes in ventilation during sleep at high altitude using the LifeShirt monitoring system on 2 climbers who were attempting to summit Mount Aconcagua (6956 m). METHODS: Prior to the summit attempt, we measured cardiovascular and pulmonary function at 401 m (Rochester, MN) and gathered respiratory and cardiovascular data during sleep using the LifeShirt monitoring system with exposure to normobaric normoxia and normobaric hypoxia (simulated 4300 m). We then monitored the ventilatory response during sleep at 3 altitudes (4100 m, 4900 m, and 5900 m). RESULTS: During normoxic sleep, subjects had normal oxygen saturation (O(2sat)), heart rate (HR), respiratory rate (RR), tidal volume (V(T)) and minute ventilation (V(E)), and exhibited no periodic breathing (O(2sat) = 100 +/- 2%, HR = 67 +/- 1 beats/min, RR = 16 +/- 3 breaths/min, V(T) = 516 +/- 49 mL, and V(E) = 9 +/- 1 L/min, mean +/- SD). Sleep during simulated 4300 m caused a reduction in O(2sat), an increase in HR, RR, V(T), and V(E), and induced periodic breathing in both climbers (O(2sat) = 79 +/- 4%, HR = 72 +/- 14 beats/min, RR = 20 +/- 3 breaths/min, V(T) = 701 +/- 180 mL, and V(E) = 14 +/- 3 L/min). All 3 levels of altitude had profound effects on O(2sat), HR, and the ventilatory strategy during sleep (O(2sat) = 79 +/- 2, 70 +/- 8, 60 +/- 2%; HR = 70 +/- 12, 76 +/- 6, 80 +/- 3 beats/min; RR = 17 +/- 6, 18 +/- 4, 20 +/- 6 breaths/min; V(T) = 763 +/- 300, 771 +/- 152, 1145 +/- 123 mL; and V(E) = 13 +/- 1, 14 +/- 0, 22 +/- 4 L/min; for 4100 m, 4900 m, and 5900 m, respectively). There were strong negative correlations between O(2sat) and V(E) and ventilatory drive (V(T)/T(i), where T(i) is the inspiratory time) throughout the study. CONCLUSIONS: Interestingly, the changes in ventilatory response during simulated altitude and at comparable altitude on Aconcagua during the summit attempt were similar, suggesting reductions in FiO(2), rather than in pressure, alter this response.