3) So let's start with a case: 65yo ♂️, presents to the #ED with #headache, lethargy & confusion. PMH: #HTN, #hyperlipidemia, #DM2, COPD. Initial VS: HR 85, BP 205/120, T 37.2 RR 12, SpO2 92% on RA. Family reports that he has been more lethargic over the past 2 days.
4) On exam, he opens eyes to voice, is A&Ox3, & moves all extremities w/o focal deficits. He reports 9/10 #headache & blurry vision.
5) CTH reveals no acute intracranial hemorrhage. Family states that he is Rx'd lisinopril for HTN, but is not good about taking it as prescribed. Is this hypertensive emergency?
a) Yes, SBP > 200
b) No, SBP not > 220
c) Yes, HTN+organ damage
d) Need to know his baseline to say
6) YES! Yes, this is a #HTN#emergency. Contrary to popular misconceptions, there is no numerical BP that "defines" HTN emergency. A HTN emergency is substantially elevated BP accompanied by hypertension-mediated organ damage (HMOD), so the correct answer is C.
7) Another "practical" definition of hypertensive emergency, which separates it from hypertensive "urgency," is that parenteral #antihyperternsives are required to bring it under control and address that end-organ damage.
8) End-organs include kidney🫘, brain🧠, retina👁️, heart🫀, & large arteries. As the name implies, HTN emergencies are time-sensitive & need rapid intervention in order to preserve end-organ function.
9) There are multiple possible presentations of HTN emergencies, but the most common are malignant hypertension, hypertensive #encephalopathy, and hypertensive thrombotic microangiopathy. See 🔓emcrit.org/ibcc/htn/
10) Other possible presentations are associated with #cerebral#hemorrhage, acute #stroke, acute coronary syndrome #ACS, cardiogenic pulmonary edema, aortic aneurysm/dissection, & severe preeclampsia and eclampsia.
11) Malignant hypertension comes on rapidly and is associated with extremely elevated #BP (>200/120). It is commonly associated with bilateral retinopathy, with #papilledema being frequently present.
12) Patients w/hypertensive #encephalopathy may present with a number of neurological symptoms including lethargy, #seizures, cortical blindness, even #coma. It is important to R/O other causes of these symptoms, such as acute ischemic #stroke or intracerebral hemorrhage #ICH.
13) In hypertensive thrombotic microangiopathy, patients develop #hemolysis and #thrombocytopenia related to the #HTN. As with hypertensive encephalopathy, it’s important to rule out other potential causes of these findings.
14) In all cases, the goal is to ⬇️the blood pressure. How much & how fast depend on the symptoms and the cause. In #aortic#dissection, rapid control is important to prevent further dissection while in acute ischemic stroke, higher pressures may be well-tolerated.
15) IV beta blockers like labetalol are a great option for reducing BP in the acute setting. What other drug do you most commonly give in hypertensive emergencies?
16) Check out the results of the poll to see what your fellow #nurses & other #ICU clinicians are seeing in use. And check out this busy but comprehensive flow chart for GETTING TO the therapeutic decision from 🔓emcrit.org/ibcc/htn/
17) All of the choices in tweet 15 would be appropriate, but most commonly in hypertensive emergencies, a continuous infusion is preferred over IVP dosing. It’s important for nurses to understand how to titrate the gtt they’re using including how frequently to adjust the rate.
18) Altho #nitroprusside is sometimes used in cases of extreme hypertension, its downsides make it less than ideal except in specific circumstances (acute cardiogenic pulmonary edema & aortic disease) & it can ➡️reflex tachycardia, so should be given w/a beta-blocker.
19) The mainstay drugs for BP control in hypertensive emergencies are labetalol IVP & nicardipine gtts. Esmolol is rapidly titratable beta-blocker that can be given as a continuous infusion. Clevidipine may be the best choice, but it’s not universally available (yet).
22) So back to those options: Labetalol IVP is rec'd as 1st line in guidelines, but often is insufficient to really control ⬆️⬆️hypertension. Esmolol is a beta-blocker option administered as a gtt. But it generally doesn’t work much better & gives your pt quite a bit of volume.
23) #Nicardipine is a calcium channel blocker that is the real workhorse for acute BP lowering in most hospitals.
24) To titrate, start at 5mg/hr & ⬆️ by increments of 2.5 to a max of 15. Nicardipine has a longish half-life, so it’s not rapidly titratable. Wait 15-30 mins before increasing. Once the BP reaches target, ⬇️the dose slightly to avoid overshooting and inducing hypotension.
25) Besides the sluggish titration response, nicardipine tends to be somewhat dilute and therefore gives your patient a little more volume than may be desirable.
26) #Clevidipine is also a CCB, but w/ a much shorter half-life, making it truly titratable and good for rapid, tight control of #BP. It’s better at BP control than nitroprusside & better at maintaining tight control of BP than nicardipine (🔓pubmed.ncbi.nlm.nih.gov/18806012/).
27) Start at 1-2mg/hr & double every 2 mins. As you get close to the target BP, slow titration to every 5-10 mins & increase slowly. The risk of overshooting & causing hypotension is lower than with nicardipine because of the short half-life. The normal dose range is 1-32 mg/hr.
28) Caution: Usually, the only lipid-emulsion infusing in our patients is propofol. Having a 2nd white infusion can be confusing, so ensure that both lines are clearly labeled to avoid errors. Consider using opposite arms if propofol & clevidipine are infusing simultaneously.
29) Clevidipine may not be available in all hospitals due to cost or other formulary factors. If not available, nicardipine is probably the second best option for controlling BP in hypertensive emergencies.
So back to our case.
30) Our patient was given bolus doses of IV labetalol, but that did not adequately reduce BP. A clevidipine gtt was started and we were able to achieve goal BP. Our patient is in the ICU 24h later.
31) Clevidipine has been infusing at a stable dose for the past 12h with good control of the BP. You get an order to start scheduled oral labetalol. Should you turn off the clevidipine drip before giving the labetalol? Answer before you scroll ⤵️!
32) The correct answer is no. The half-life of clevidipine is extremely short, ~1 minute, & most patients will see a return to their previous BP within 5-15 min of discontinuation unless the cause of HTN is reversed (in cases of secondary HTN) or another agent has taken effect.
33) In this case, the oral labetalol will need to achieve its steady state before discontinuing the clevidipine so that we don’t see an⬆️in the BP. Expect to continue the clevidipine gtt, titrating the dose ⬇️to keep the BP in goal range, until the labetalol takes full effect.
34) Because of the short half-life, there is little worry about hypotension, as clevidipine can be down-titrated rapidly or even stopped if BP begins to fall.
35) You are able to wean the clevidipine off once the labetalol has taken effect and the patient’s blood pressure is now well controlled on oral agents. His confusion and blurry vision have resolved and he is ready to be downgraded from the ICU.
1) Welcome to our #accredited#tweetorial on optimal mgt of #hyperkalemia in the patient with #CKD. Earn 0.5h #CME/CE credit by following this thread. I am Sourabh Sharma MD DNB FASN 🇮🇳 @iamnephrologist & u have found the ONLY source for CE credit delivered entirely on Twitter!
3) This program is intended for #healthcare providers and is supported by educational grants from Actelion, Bayer, Chiesi, & AstraZeneca. Faculty disclosures are listed at cardiometabolic-ce.com/disclosures/. Prior programs, still available for credit, are at cardiometabolic-ce.com
9) Many risk factors modulate the propensity of LDL-C to traverse the endothelium and enter the arterial intima. See 🔓academic.oup.com/eurheartj/arti….
10) It now appears that the passage of #LDL into the #intima is not a merely passive process whereby the concentration in blood & the permeability of the endothelium determine LDL accumulation.
11) It’s #Transcytosis (an active process), through a vesicular pathway involving #caveolae, scavenger receptors (#SRB1) and activin like receptor kinase 1 (#ALK1). Hence for a given blood level of LDL-C the amount of atherosclerosis is variable.
1) Welcome to an #accredited#tweetorial on the role of ⬆️ #LDL-C levels in the pathogenesis & pathophysiology of #ASCVD. I am Kausik Ray MD FRCP @profkausikray, Professor of Public Health & Cardiologist @imperialcollege London AND President of European Atherosclerosis Society
3) #Atherosclerosis starts in childhood, progresses in fits and spurts and presents in middle to late life in the form of major adverse cardiovascular events #MACE.
3) @PaulDThompsonMD took on education re mechanisms & use of ezetimibe & bempedoic acid. He proposes a case: 45 ♂️ w/history of inferior wall #MI treated with primary angioplasty.