We know that we need to reduce the blood pressure for a lot of good reasons. It reduces the chances of ischemic heart disease, slows down atherosclerosis, delays decline in renal function and reduces the incidence of stroke. Is there any other reason for keeping the BP within an arbitrary normal? The risk of dementia in hypertension is increased if there is associated atrial fibrillation. Here is an excerpt from Univadis.
Dementia risk in mid-life patients with atrial fibrillation (AF) can be reduced by controlling high blood pressure to <130 mmHg, according to research presented at the European Heart Rhythm Association (EHRA) 2019 Congress.
Researchers examined associations between systolic blood pressure (SBP) and incidence of dementia among 196,388 patients with AF aged 50 years and older, focusing on the effects of age. The risk of dementia according to SBP levels was assessed in age groups of 50-59 years, 60-69 years, 70-79 years and 80 years or older.
After a median follow-up of 4.3 years, the researchers found SBP ≥130 mmHg at 50-59 years and ≥140 mmHg at 60-69 years significantly increased dementia risk, with SBP 120-129 mmHg as reference. Sub-analysis among those with a follow-up BP measurement 1.8 years after baseline BP measurement revealed that lowering SBP to <130 mmHg for initially uncontrolled (≥140 mmHg) patients could alter their dementia risk to as low as that of initially well-controlled patients in aged 50 to 60 years. The study found, however, that lowering BP in patients above 70 years may not have as big of an impact on dementia risk.
I would like to emphasise control of blood pressure with or without atrial fibrillation, from the age 50 years. If we are controlling BP for the first time at the age of 70 years much of the damage has been already done. Those patients who have been treated for hypertension from their 50s need to be given the benefit of regular medication and monitoring. Do treat the 70 years plus but do not expect spectacular results.
Is there any risk from the use of high dose nifedipine and can we use amlodipine instead?
Use of high-dose nifedipine could increase the risk of out-of-hospital cardiac arrest (OHCA), according to the results from the European Sudden Cardiac Arrest Network (ESCAPE-NET) presented at the European Heart Rhythm Association 2019 (EHRA) conference at the weekend.
Using data from the Dutch Amsterdam Resuscitation Studies Registry (ARREST) 2005-2011 and the Danish Cardiac Arrest Registry (DANCAR) 2001-2014, researchers examined whether the widely used dihydropyridines nifedipine and amlodipine are associated with increased OHCA risk.
The study found that the current use of high-dose (≥60 mg/day), but not low-dose (<60 mg/day), nifedipine was significantly associated with an increased risk of OHCA compared with nonuse of dihydropyridines, with an odds ratio of 1.5 in ARREST and 1.5 in DANCAR. High-dose nifedipine was also associated with an increased OHCA risk when compared with any dose of amlodipine, with odds ratios of 2.3 and 1.6 in the ARREST and DANCAR registries, respectively.
There was no risk associated with amlodipine. So be careful with the use of nifedipine.
How should we provide analgesia to critically ill patients? How should we sedate them? Should we use benzodiazepines in the ICU?
Distress, due to pain, fear/anxiety, dyspnea, or delirium is common among critically ill patients, especially those who are intubated or are having difficulty communicating with their caregivers. Distress may manifest clinically as agitation that is often associated with ventilator asynchrony and vital sign abnormalities. Regardless, distress needs to be treated to comfort the patient, ameliorate agitation that may interfere with supportive care, and attenuate increases in sympathetic tone, which may have untoward physiological effects.
Morphine sulfate, fentanyl, and hydromorphone are the intravenous opioids that are most commonly used to manage distress due to pain in critically ill patients. Oral opioids such as oxycodone, methadone, and morphine are also given to patients where oral or enteral administration is preferred. Remifentanil is also an option; advantages include its rapid onset of action and prompt clearance that are independent of hepatic and renal function, although there is debate as to whether its use is associated with a higher risk of tolerance.
Propofol infusion can be used to sedate critically ill patients. It is an anesthetic agent which is very rapidly acting with onset of action within minutes but is rapidly metabolised by the liver so has to be given by continuous IV infusion. It is very useful for patients who need to be woken up for repeated neurological examinations.
Benzodiazepines such as midazolam and lorazepam are best suited for sedation in the intensive care unit (ICU) because they can be administered by either intermittent or continuous infusion and have a relatively short duration of effect. Intravenous diazepam is used less often to sedate patients in the ICU. It can be administered by intermittent infusion, but not continuous infusion. Propylene glycol is the carrier (solvent) that is used to administer lorazepam or diazepam intravenously. Infusion of either drug may be complicated by propylene glycol toxicity. This leads to severe metabolic acidosis.
Dexmedetomidine is a highly selective, centrally acting alpha-2-agonist with anxiolytic, sedative, and some analgesic effects. It has no deleterious effects on respiratory drive. Dexmedetomidine may reduce the duration of mechanical ventilation and intensive care unit (ICU) stay when compared with traditional sedatives in the ICU
According to a recent study published in the American Journal of Respiratory and Critical Care Medicine, patients who received a low nighttime dose of dexmedetomidine were more likely to remain delirium-free during their ICU stay compared with patients who received a placebo (80% vs 54%, respectively). This finding is consistent with previous studies suggesting that dexmedetomidine may reduce the risk for delirium in ICU patients more effectively than benzodiazepines.
Skrobik Y, et al. Am J Respir Crit Care Med. 2018 May 1;197(9):1147-1156. doi: 10.1164/rccm.201710-1995OC. Reade MC, et al. New Engl J Med. 2014;370:444-454.