Drop attacks

splash-water-1362224788t1gMedical terminology knows 5 reasons for people to fall unaided: common fall, syncope, collapse, seizure and drop attack.

A drop attack consist of the loss of lower extremity tone, leading to collapse, but decidedly without disturbance of consciousness (as opposed to syncopes) and without accompanying neurological or other signs or symptoms, in particular without dizziness or faintness, diplopia etc. Peculiarly, the attacks occur while walking, not standing or sitting. They seem to be quite prevalent, constituting a significant percentage of falls in the elderly.

The concept of drop attacks is very old and yet, there is not much published about it. As far as I got in my literature review, a 1986 series in Neurology has the most modern data (an astonishing 108 patients!). Apart from that you have to work through case reports and chapters in neurology textbooks, such as Neurological Differential Diagnosis – a cased-based approach.

The prototypical patient is a woman over forty who reports falling forward while hurriedly walking on the pavement, as if someone had pushed her, without warning, the legs giving way. She might even have injured herself. Once down, she could get up again after a few seconds, without feeling dizzy, nauseus or unsteady.

The differential diagnosis is huge, since so many diseases have been associated with drop attacks, and in some cases falsely so.

Hemodynamic ischemia

Take vertebrobasilar ischemia, for instance. Before the advent of MRI and CTA, many anomalies in the posterior circulation were interpreted as evidence of pathology, such as hypoplastic posterior communicating arteries, asymmetry of one vertebral artery or hypoplastic V4 segments. In practice, it seems to be nearly impossible to get isolated drop attacks (without vertigo!) from a hemodynamic basilar compromise. In a series of 83 proven basilar artery occlusions from basilar stenoses, prodromi included “drop attacks” in only 4 cases and these were accompanied by vertigo in 3 (Ferbert, Stroke 1990). Similarly rare, yet pathophysiologically more reasonable, is the case of a high grade carotid artery stenosis with contralateral hypoplastic A1-segment – when the compromised ICA supplies both anterior cerebral arteries.

It is interesting to note that the stroke rate of people with drop attacks was not increased as compared to age-matched controls in the 1986 series.

Systemic hypoperfusion (aka syncope without dizziness)

The classical mechanisms of syncope (orthostatic, neurocardiogenic etc., aortic stenosis) practically always lead to disturbance of consciousness or at least dizziness. There is just one exception: rhythmogenic drop attacks (Adam-Stokes attacks). In the above mentioned case series this constituted a sizable percentage (13%). Although I would think that a careful reevaluation reduce that number considerably, I concede that an event recorder is a reasonable investment for recurring drop attacks, not the least, because the gadgets have become so simple to implant.

A special case is carotid hypersensitivity syndrome, where a vagal mechanism due to head rotation or local pressure is usually hypothesized. To be honest, I haven’t seen many cases of this, despite the fact that I am working in a neurovascular lab much of my spare time, so it can’t be that frequent.

Epilepsy

Atonic (or astatic) seizures are well-known phenomena in pediatric neurology, arising in Lennox-Gastaut-syndrome, Doose syndrome and other epilepsies. It is rare as a manifestation of adult onset epilepsy, all the less in the elderly, yet the classical temporal lobe epilepsy can lead to temporal lobe syncopes or temporal lobe drop attacks in this age group as in any. 

In these modern times of weird autoimmune encephalitis variants, LGI1-antibody encephalitis has been reported to cause drop attacks even before it’s more typical facio-brachio-crural dystonic seizures.

Movement disorders

In (advanced) Parkinson’s you can be attacked by drops, usually with polypharmacy and fluctuating clinical course (on/off phenomena, freezing). Patients with Progressive Supranuclear Palsy tend to fall backward rather than forward, yet this can be described as a drop attack as well. Both diseases should present with clinical hints at the movement disorder.

Paroxysmal kinesiogenic dystonia has been proposed as an imitator of epilepsy and you could assume that this can lead to drop attacks as well, although I could not find a case report of this. At any rate of occurrence, a family history should help.

Negative myoclonus

This can be an expression of epilepsy (particularly, if focal as in benign partial epilepsy, see above) or a more generalized encephalopathy such as hepatic or toxic, leading to Asterixis (think of Pregabalin, Oxcarbazepine and toxic doses of any central acting drug). History, a hunt for the “flapping tremor” and lab works should rule this out.

Vestibular drop attacks

An acute and temporary disturbance in otolith function can lead to drop attacks. This has been eponymized by Tumarkin who coined the term otolith crisis in the thirties. The attacks are not the correlate of an acute Meniere’s endolymphatic hydrops, but due to unstable otolith function. In contrast to most other drop attacks there ought to be a sensation of vertigo, i.e., of movement of the outer world, yet only few patients can actually report this.

Theoretically, other vestibular disorders, in particular superior canal dehiscence syndrome, should be able to provoke vestibular drop attacks as well, yet there are no case reports.

(Cranio-)Cervical dysfunction

Quite a few diseases of the cervical myelon and the craniocervical junction can lead to temporary compression or dysfunction of either the pyramidal tract or the dorsal column afferent fibres, thus leading to either loss of tone or loss of feeling in the legs, hence the drop attack.

  • Posterior fossa tumors
  • Subacute combined degeneration (Vitamin B12)
  • Chiari Type I
  • Cervical spinal canal stenosis and other causes of cord compression

Other rare causes

  • Third ventricle tumors (colloid cyst, pineal cyst) – usually with postural headache
  • Isolated cataplexy as an abortive variant of narcolepsy
  • Coffin-Lowry-syndrome – stimulus-induced drop events
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How to do a presentation

Academically, Iclimbing_through_the_yellow_band_mt-_everest_-may_2007_a was raised in Mathematics, where a lecture is in fact a development of ideas on the black- or whiteboard. In the Mathematics research community things then went downhill with presentations in LaTeX trying to imitate Powerpoints horrible themes.

In Medicine, the situation has been disastrous even before Powerpoint – medical talks have always been boring with lots of facts and no investment into the choreography of the talk itself. Prezi took this even further, emphasizing the structure of the content rather than the talk.

For me it was the fascination with SMACC talks such as Vic Brazil’s famous Timing, Tribes and STEMIs and of course Cliff Reid’s impressive resuscitation talks, that led me first to the theory (Presentation zen, Nancy Duarte and the like) and then the practice (TED talks) of modern presentation creation.

This blog entry serves to collect the most helpful references for creating presentations. It also captures the basic steps I recommend for giving a small 20 min talk on a current topic in our departments’ continued education rounds.

5 steps for creating presentations

While three seems to play an important role in structuring you talk, I prefer rules of 5 for mnemonics, so here are my presentation creation 5.

  1. What
  2. So what?
  3. How
  4. Practice
  5. Present

What?

Choose a topic that interests you and your audience, priority on the latter. Don’t let the topic be dictated. Read up and become an expert. Helpful is Scott Weingarts tip to create a folder with a ppt-template, a note-file (eg mindmap), lots of subfolders (images, articles, videos, recordings) way ahead of the talk to let your subconscious work on the talk all those weeks, collecting articles, noting ideas.

So what?

Why should this topic be interesting for your audience? How do you want to change them? Write an elevator pitch for that.

How?

Choose one of three formats to structure your talk:

  •  Problem/solution: most frequent in medicine
  •  Narrative: most effective – use drama theory, suspense curves and the like
  •  Chronologic: most diffficult – take the audience through a historic tour

Now write the basic steps for Intro, Story, Closing on yellow postits and thus create the structure as a modifiable lattice.

Practice

I recommend 5 rehearsals for simple and 6 rehearsals for important talks

  1. Ad hoc: starting from your postits, talk the talk standing in front of an empty chair, then note necessary changes to your structure, write down good formulations as segues in differently coloured postits, fill in the missing data, examples etc.
  2. W/o slides: run through the talk again immediately and note at which point you need visual aids, the flipchart, videos etc to improve the talk. Use differently coloured postits as placeholders. Use the following weeks’ break to search for this stuff and take your time, letting it stew.
  3. To a person: give the talk with slides to a good friend or colleague, gathering as much feedback as you can – this is the first time you give the talk to an audience; make sure you achieve what you planned for, change the talk radically otherwise and start with 2 again. Work through each formulation, each slide. It helps to record the talk on video.
  4. Preparation: give the talk again in private at least a week ahead of the date. You might record this (audio only) Then give your subconscious time to improve the talk even further.
  5. Rehearsal: This is the final rehearsal 1-2 days before your talk. If you give the talk to a big audience, you should repeat this as a dress rehearsal to a small group, such as your peers, gathering feedback.

Present

Annouce and advocate your talk. Go to the venue and check everything out, if possible, 1 day before the talk. Get a clicker (not a pointer). Get to the talk on time. Be well-dressed and smart. Have someone announce your talk to make sure everyone is quiet. Stand before the audience and talk to them, not to the slides, looking them into the eyes, reacting. After the talk, get feedback and improve your talk.

5 steps for creating slides

  1. Not a teleprompter
  2. Not a handout
  3. Don’t distract
  4. Good design
  5. Good images

Not a teleprompter

Using your practice runs, you don’t need the slides as notes. Whenever the information on the slide is just for you to remember what to say, move it to the notes. Only citations may be read verbatim to the audience (it is always so cool, if you can cite by heart facing the audience).

Not a handout

If you feel the audience needs information to take home, prepare a handout. Your slides are not your handout. Every word on the slide needs to be checked whether it is inspirational or handout material. Long lists are handout material.

Don’t distract

Remove everything, every word, every object, every colour, every footer, every logo, everything that doesn’t serve your story. No template. Black background. No animations. No transitions.

Each slide should contain one thing, either a supporting image (fotos for emotions, graphs for illustration) or a slogan, maybe both.

If you absolutely need lists, keep them short, so that the eye can grasp the whole list in one glance (max. 5-6 entries)

Good design

Use all the theory of design (golden cut, font design, clear lines, few words) to improve your slides. Use a professional, if possible. Make it simple. Look at Apple’s advertisements and presentations to get the idea.

If you feel you have to excuse a busy slide, throw it out, redesign it. Most complex slides are better developed on the whiteboard.

Good images

Images are used to create emotions. Use good real fotos in high resolution, not artificial cartoons. You judt have to evoke the feeling. Make sure you have the right to use the images.

References

Obviously, I did not develop these concepts on my own. Here is an annotated list of useful links and references.

 

Life’s simple 3

When a stroke patient with symptomatic intracranial stenosis has been worked up, we SAMMPRIS him, by which we mean ASS, Clopidogrel and high dose statin. This is, of course, not the whole story – more important than drugs are the necessary lifestyle adjustments. We use this example to develop a system for stepwise improvement of risk factors and health behaviour.

In my view, the standard risk factors (pressure, sugar, fat and weight) can all be improved by concentrating on the simple three:

  1. Get active and work out
  2. Eat healthy
  3. Don’t smoke

This sounds reasonable, although the science behind 1 and 2 is not so simple. Just staying active (e.g. walking every day for at least 30 mins or running for 3 x 25 mins) might be healthy but need not really lower your blood pressure. Vastly more efficient are more intense workouts such as muscle strengthening (resistance) exercises or even high intensity interval training. The evidence for these measures is quite good. With regard to healthy eating, there seems to be no golden way to a good diet (in fact, most diets studied have been harmful), yet the mere fact that you are trying to be conscious about your food has a proven health promoting effect.

The current decade is probably the best to initiate health promoting behaviour, as smartphone/smartwatch/fitness bands abound and make it easier to watch your health without investing too much time. In particular these applications

  • can help to find out what improves weight or fitness
  • introduce a gamification factor to the otherwise boring issue
  • might lead to more insight about how your blood pressure, sugar or cholesterol react to specific measures
  • might allow to identify those patients where high dose statins are harmful by reducing fitness effects

References

Defining away sepsis

Why do we need new definitions for sepsis? We want the term to denote a syndrome with serious consequences, something that needs the full force of an ICU to recover.

No simple infections. So not a young girl with viral feverish URI (who happens to have leucocytes < 4). Neither a simple pneumonia. Maybe the myriad of negative sepsis studies stem from the fact that they included too many simple infections. What used to constitute severe sepsis, the endangered endorgans should become requisite in the definition of sepsis.

High sensitivity. What about the 90 yo dehydrated nursing home resident with positive nitrite stick and altered mental status? He might recover with some fluids and antibiotics, but then he also might not and deteriorate, so that he needs treatment response monitoring – he could be septic, but he also could just be cured in 2 hours.

I see the recent initiative to improve our definition of sepsis (dubbed Sepsis 3.0 by the FOAMED community) in this light. While the new definitions sound a bit esoteric, they are actually very practical, focussing on two situations:

  • Non-ICU: The normal ward, private practice or ER, where we need to recognize those patients with suspected infection that might deteriorate and need close monitoring, while ressources are not that good, that every patient can have an arterial blood or extensive lab works. Sepsis 3.0 recommends to use the qSOFA, also known as BAT score, where 2 out of 3 criteria suffice.
    • Blood pressure < 100
    • Altered mental status
    • Tachypnea 22 breaths/min
  • In ICU, we should screen with the daily labs we already have, using the SOFA score (routinely computed in electronic charts, also called CAR-LOG = coagulation-arterial pressure-renal-liver-oxygenation-GCS) and use a 2 point change as a threshold for sepsis, if infection is suspected. Septic shock is defined by need for noradrenaline to keep the MAP above 65 with remaining lactate geq 2 mmol/l, provided that enough fluids have been given.

Who is suspected? The beauty of the old and new definition of sepsis that “suspected infection” is not further specified. You might be warned by fever, CRP or leucocytosis, but also by a good story for an infection (postoperative patient, smelly urine). While some folks find this too vague, I think we always know when to suspect infection.

Think of sepsis when organs bail out. The article reminds us to think of sepsis (and thus suspect infection), whenever any organ failure occurs.

References

 

 

Climate change

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The earth might be warming up and so might our patients in the ICU. It is easy to fall into the Fever ➝ CRP ➝ antibiotics trap, but our goal is to be more responsible.

Contents

  • Raised temperature: fever vs. hyperthermia
  • Central fever
  • Stroke and fever
  • Temperature management strategies for stroke
  • Infectious causes of fever
  • Noninfectious causes of fever
  • References

Raised temperature

might be fever or hyperthermia.

Fever is more common and defined by a raised hypothalamic setpoint, due to

  • infectious or
  • other inflammatory reasons, or due to
  • central stimulation

of the hypothalamus (“central fever”, e.g. blood in brain, see below). Note that CRP does not really distinguish between the three causes of fever, while procalcitonin might at least hint at an infectious etiology. Also there is no proper consensus as to what constitutes fever.

Non-fever hyperthermia is failure of heat regulation with intact setpoint, e.g. in exsiccosis. Typically, antipyretics are ineffective in pure hyperthermia.

Fever control in the ICU has been studied, if not extensively, and never been shown to be helpful. Most recently, Acetaminophen was not effectively in improving anything (Young NEJM 2015). It may be harmful, especially in septic patients (see Schulman 2005 and Lee 2012).

Central fever

(see this 2016 review on the subject) is always suspected in neuro patients, but hard to prove.

Pathophysiology, it is due to damage to the hypothalamus or contact of this structure to blood 0r pus (this can be reproduced in animals). In brain injury, diffuse axonal damage and frontal lesions indicate shear stress on the hypothalamus and correlate with central fever.

Clinically, central fever might have less diaphoresis and tachycardia, but this is not very specific. The diagnosis relies on exclusion of other infectious and inflammatory causes. The literature (Predicting central fever in NICU, Hocker 2013) says

The combination of negative cultures; absence of infiltrate on chest radiographs; diagnosis of subarachnoid hemorrhage, intraventricular hemorrhage, or tumor; and onset of fever within 72 hours of admission predicted central fever with a probability of .90.

Therapywise, central fever is harder to treat, so that physical measures and endovascular cooling are often employed. I grew up with the lytic cocktail (blocking every neurotransmitter you know), but there is no proper literature on that.

You should bear in mind that there is another central neurologic complication with fever that complicates severe brain injury, namely paroxysmal sympathetic hyperactivity – this is a chapter on its own.

Stroke and fever

  • Very common: (40-61%) in the first 2d of stroke have elevated temperatures, depending on the definition
  • Very bad: Raised temperature correlates with bad outcome, both in animal experiments (40° x 3h leads to 3 times the stroke volume) and patients (e.g., Greer 2008).
  • Early is worse: Stroke is more vulnerable to fever in the first 24 hours – it accelerates the conversion of penumbra to stroke and all bad pathophysiologic cascades (apoptosis, inflammatory).
  • Can be controlled: Fever control is feasible in principle and regarded as one of the active components of stroke unit care.

Temperature management strategies for stroke

  • Hypothermia: Bi 2011, de Georgia 2004, Ictus-L 2006, Ovesen 2013 show no benefit
    EuroHyp-I (ongoing), Ictus 2/3 (terminated; no results yet) – endovascular methods, no evidence (but very effective)
  • Prophylactic
    • antipyretics: PAIS (den Hertog 2009), PISA (Dippel 2003) – only modest effect on temperature, no benefit (NRO, survival)
    • antibiotics: EPIAS, PANTHERIS – reduced infection rates, no benefit (NRO, survival)
  • Fever treatment: blankets/air cooling probably not better than drugs, endovascular highly effective – no benefit shown
    QASC trial shows that the combination of controlling fever, dysphagia and glucose is beneficial

Infectious causes of fever

  • Head: meningitis/encephalitis, brain abscess, ventriculitis, sinusitis, dental, HEENT (including epiglottitis)
  • Circulatory: CVC, endocarditis/myocarditis, peripheral cannula, aortitis, mediastinitis
  • Respiratory: pneumonia/bronchitis, empyema, VAP
  • GI: esophagitis, pancreatitis, diverticulitis, rectal/anal abscess, C. diff
  • Urogenital: prostatitis, pyelonephritis, cystitis, PID
  • Hematological: malaria, HIV
  • Integument: Osteomyelitis, cellulitis, fasciitis, myositis

Noninfectious causes of fever

  • Vascular: stroke, IVH, ICH, SAH, MI, ischemic bowel, DVT
  • Idiopathic inflammatory: Gout, postoperative, acalculous cholecystitis, pancreatitis, aspiration pneumonitis, GI bleed, ARDS
  • Traumatic: Hematoma, Ulcers
  • Toxic
    • Drug fever: high spiking fever, chills, maybe leucocytosis, eosinophilia; drugs are beta-lactams, PHE, iv contrast
    • Malignant neuroleptic syndrome, Serotonin syndrome (beware: linezolid, MCP, setrons), malignant hyperthermia
  • Autoimmune: vasculitis, hemolysis, transplant rejection, transfusion
  • Psychiatric: Withdrawal
  • Neoplastic: renal cell CA, tumor lysis, lymphoma, leucemia
  • Endocrine: Ovulation, Thyroiditis, Thyreotoxicosis, adrenal insufficiency

References

Get a grip!

roast_chicken
Not a HaNDL but a bavarian HeNDL

When a disease is discovered nowadays, it needs to be assigned a proper acronym – see CLIPPERS, MELAS, CADASIL. If we were living in the good ole eponymic days of, say, Steele-Richardson-Olszewski, the HaNDL syndrome would be named Swanson-Bartleson-Whisnant – the authors of a 1980s Neurology paper on the condition we covered in our rounds today. Or better: by Stigler’s law it should be named Berg-Williams-Syndrome after the 1995 Neurology article that coined the acronym HaNDL.

By all we know about the inflammatory pathophysiology of migraine, an increase in frequency and intensity of migraine auras should be able to produce a pleocytosis, but this is not the explanation for HaNDL, for it should enjoy all the epidemiologic characteristics of migraine then. And it doesn’t.

It is men of middle age (40-70, not young women) with only rarely (slightly more than chance predicts) any migraine in their history, who – sometimes after a preceding viral illness – suffer a series of episodes over days to weeks that resemble aura (except: less visual symptoms, more aphasia, more sensorimotor disturbances) in their development and migratory nature, but take way too long (a few hours rather than 10-60 minutes), accompanied or followed by headaches that resemble migraine with slightly less phobias (osmo-, kineto-, photo-, phonophobia). The usual workup (CT, MRI, labs) is negative, but there is a lymphocytotic pleocytosis of > 15/µl and often a raised CSF opening pressure.

Of course, as in any case of focal symptoms plus pleocytosis (aka encephalitis), we send off the standard microbiology tests (HIV, TPHA, borreliosis, PCR for HSV, VZV), start acyclovir and maybe ceftriaxone at once and wait until everything comes back negative. Then we are left with the hopes of a spontaneously resolving syndrome – by definition it should take weeks or months to clear.

In my experience, the usual migraine therapy (iv high dose NSAIDs = metamizol or ASS, plus antiemetics – MCP or dimenhydrinate) covers each episode but does not prevent the next. Steroids might, but don’t last long enough. I usually treat with spreading depression drugs (valproate, topiramate) and hope for the best.

The disease certainly is underrecognized, being replaced by “a minor encephalitis”. There should be some studies of  autoimmune mechanisms and antibodies, but I know of no proper results yet. So, if you are faced with your next HaNDL why not send of an experimental panel?

References

Borderlands

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First described in 1883, the concept of watershed strokes was further developed pathophysiologically in the 50s and 60s. (There is a proud  article in Stroke this week, discussing the  history of the concept.)

Terminology

Several terms are used in the literature: border-zone stroke, watershed stroke, misery perfusion, Letzte Wiese. Watershed is probably the best term, as it describes the idea that the land most distal to two supplying rivers suffers from even slight variations in flow in either. I personally apply the name Letzte Wiese only in specific cases – it captures an area  insufficiently supplied by just one vessel and thus can be applied only to internal border zone strokes.

Localization

For watershed strokes you need either quite severe hypoperfusion (as in hemorrhagic shock) or only minor hypoperfusion but at least one severely stenosed vessel.

  • The most frequent stenosis affects the proximal ICA, leading to the ACA/MCA and PCA/ACA border zones, as well as (sometimes) strokes in the MCA internal border zone.
  • High grade MCA stenosis can lead to watershed strokes in the internal border zone along and above the lateral ventricles (rosary pattern). In this case the region between the supplied region of the deep penetrating endarteries (mainly basal ganglia) and the small branches of the MCA main branches (which enter the brain from the cortex down) suffers, which amounts to the white matter in the centrum semiovale.
  • Finally the cerebellum knows watershed zones between the 3 feeding vessels, but this is not of practical relevance because treatment is similar to embolic strokes.

ICA stenosis

  • In chronic near occlusion of the ICA, the borderzone region can move if you give it enough time, with the PCA/MCA region moving forward and the ACA/MCA region backward.
  • To complicate matters further, the borderzones are variable depending on the localization of the stenosis and the integrity of the ECA collateral as well as the Circle of Willis (e.g., if A1 or the anterior communicating artery is hypoplastic or the PCA has the fetal variant).
  • In my experience you need at least 2 patent collaterals (out of ECA, ACA, PCA) to ensure hemodynamic stability even in near occlusion.
  • In the last years we learnt more about degenerative distal ICA stenosis just below the carotid T which is not well collateralized via the ECA pathway – this region unfortunately is not well imaged with CTA due to calcification-related artifacts, being  better amenable to duplex ultrasound and MRA.
  • Similar problems can arise with dissections extending to the intracranial sections of the ICA.
  • In very slowly progressive combined distal ICA and MCA stenosis (degenerative, vasculitis, Moya Moya disease) a web of tiny collaterals can form (Moya Moya picture), which has its own intricate pathophysiology.

Pathophysiology of hypoperfusion

Local hypoperfusion can be graded as follows:

  • Grade I: reduced CBF, enhanced CBV, functionally intact or only slightly compromised, near normal oxygen extraction, reduced vasodilatatory reserve
  • Grade II: severely reduced CBF, reduced CBV, reduced function, no or negative local vasodilatatory reserve (the latter is called the reverse Robin Hood phenomenon)

Practical management

  • When faced with an imaging pattern of watershed strokes, duplex ultrasound and angiography (CTA, MRA or even conventional angiography) are urgent to get as much information as possible about the flow patterns and the collateral situation.
  • Perfusion imaging: Severe proximal stenoses leads to difficulties in interpreting perfusion imaging, but this can be used to try to differentiate between grade I and II hemodynamic compromise.
  • To judge how imminent the danger is, functional ultrasound of the MCA (using CO2, apnea or – easier – acetazolamide 1g) is used.
  • If  in doubt, I recommend a trial of therapeutic hypertension (usually with 25-50-100µg Noradrenaline, only with intact coronaries!) to see whether the neurologic deficit fluctuates with blood pressure.
  • In this case, an emergency revascularization is necessary and without alternative. To bridge the time to surgery or stenting, you can use continuous therapeutic hypertension, aiming for an RR of > 180 or 200 mmHg.
  • Sensitivity to blood pressure drops: Quite often the reverse happens – someone accidentally treats an impressively high RR of 220 mmHg (which might actually be due to the brains own reaction to hypoperfusion) with an iv bolus of labetalol or urapidil and the patient deteriorates. If this happens, quickly counteract your medication (Noradrenaline again) and due your vascular studies.
  • Remember that patients with severe misery perfusion, the danger of hyperperfusion syndrome after revascularization is quite real and this is difficult to treat.

References