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- AAA
- Anticoagulation Reversal
- Aortic Dissection
- ARDS/Mechanical Vent
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- Brain Death
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- CSW/SIADH
- Cricothyrotomy
- Cuff Leak. What is it?
- Delirium/Antipsychotics
- DKA/Other Ketoacidosis
- EVD AND ICP MONITORS
- ETOH Withdrawal
- Extubation Readiness
- Febrile Neutropenia
- Fluids
- GI Bleeds
- Group A Streptococcus
- Hypertension PRNs
- Lido With Epi Recipe
- Lines & Tubes on CXR
- Lumbar Drains
- Lung Volume Recruitment
- Massive Transfusion
- O2 Delivery Devices
- Pacemaker Insertion
- Pain/Analgesia
- Pocket Pressor Recipes
- Pulmonary Embolism/PERT
- Respiratory Failure
- ROSC
- Sedation in ICU
- Seizures/Status
- Shock and Sepsis
- Subarachnoid Hemorrhage
- Swan Ganz Catheter Setup
- TBI/EVD/ICP monitoring
- TEVAR
- Toxicology/Overdose
- Tracheostomies AND THT
- Trauma Patients in ICU
- Tumor Lysis Syndrome
- Vasoactive Medications
- Ultrasound Guided Lines
Acute type b aortic dissection
- Type B Aortic Dissections can often be managed medically and should all be admitted to the Intensive Care Unit
- It is essential to achieve adequate control of their blood pressure and heart rate however they are also at high risk of complications of this essential management
- These patients most often have long-standing hypertension and their brain and kidneys, our 2 most blood pressure dependent organs, can suffer injury as a result of relative hypotension.
- Brain hypoperfusion manifests clinically as agitation and/or an altered level of consciousness and can result in strokes watershed global hypoperfusion.
- Kidney hypoperfusion will manifest as decreased urine output and a rising creatinine
- Additionally, when the coeliac and SMA are involved in the dissection, they may require higher pressures to maintain bowel perfusion
- Spinal cord perfusion is also at risk particularly if there is involvement of the artery of Adamkiewicz
- Balancing and monitoring their risk of hypertension and hypoperfusion can only be done in the ICU
- These patients should all be admitted to ICU (not PSCU) for at least the first 48 hours or more, and until they have been transitioned to oral agents and no longer requiring infusions
Risk Factors
- Chronic Hypertension
- Atheroscerlosis
- Aortic Aneurysms
- Connective Tissue Diseases (EDS, Marfans)
- Pregnancy
- Cocaine use
Presentation
- Sudden severe chest or upper back pain
- Suden severe abdominal pain
- Leg pain/weakness
Complications of the Aortic Dissection
Dynamic Obstruction
- The false lumen can exert pressure on the true lumen with the cardiac cycle causing dynamic obstruction and intermittent ischemia
Extension/Thrombus
Extension and//or thrombus into the ostia of the branched arteries can occur causing compression of the true lumen by the false lumen +/- thrombus formation
- Coeilic/SMA (bowel ischemia)
- Renal Arteries (AKI)
- Artery of Adamkiewicz (spinal (ischemia)
- Extension/Thrombus into renal arteries (AKI)
- Iliacs/femorals (ischemic limb)
Rupture
Rupture through Adventitia
Medical Management: Anti-impulse therapy
Slow the Heart Rate
Reduced (NOT low) blood Pressure
Reduced (NOT low) blood Pressure
- Slowing the heart rate reduces the number of times the Aorta sees a systolic pressure
Reduced (NOT low) blood Pressure
Reduced (NOT low) blood Pressure
Reduced (NOT low) blood Pressure
- Reducing the blood pressure lowers the impact of each pulsation
- NB: There is a balance between reducing the pressure enough and too much (see below under Iatrogenic Complications)
WHY CAN THE HYPERTENSION BE SO RESISTANT?
Endogenous Catecholamines and Hormones
- Aortic dissections are an inflammatory state that drives cortisol and hence endogenous epinephrine/norepinephrine levels up
- Pain alone will do that same and has to be treated
Longstanding Chronic Hypertension
Long standing hypertension causes
- remodeling of vasculature resulting in stiffening (via collagen deposition) and hypertrophy of the endothelium which further narrows the inner diameter and worsens hypertension
- The endothelium becomes damaged, reducing its ability to produce nitric oxide
- There is reduction in the total number of open capillaries and small arterioles in tissues, a phenomenon called "rarefaction," which significantly raises peripheral resistance.
RAAS Activation
The diminished diameter of the aorta is sensed by the juxtaglomerular apparatus in the kidney as diminished flow to the kidneys and activates the RAAS system
Anatomical Changes
The anatomical change in the diameter of the aorta unto itself increases the resistance of the vessel
Iatrogenic Complications of treatment (anti-impulse Therapy)
Hypotension (Hypoperfusion)
The brain and kidneys are the two most blood pressure dependent organs in our body
- They acclimate to hypertension and are very sensitive to the effects of relative hypotension
- Brain hypoperfusion will often manifest as either agitation or altered LOC. Occasionally you will see focal neurological deficits if they have asymmetrical Intracranial Atherosclerotic disease
Bowel Ischemia
CT demonstrating extension of the dissection into the SMA with narrowing of the ostia due to compression of the true lumen by the false lumen
This is a scenario where anti-impulse therapy can cause hypoperfusion to the gut (CT image also depicts pneumatosis coli)
The Posterior Spinal Arteries
- The Posterior Spinal Arteries supply the Dorsal Columns and the Posterior Horns
- Dorsal Columns and Posterior Horns convey sensations of fine touch, vibration, two-point discrimination, and proprioception from the skin and joints.
- PSAs arise from the vertebral arteries and have a rich rich and redundant blood supply from enumerable radicular arteries.
- The PSAs also form anastamoses with one another wihich futher promotes vascular supply to the Dorsal Columns and Posterior Horns
- This blood supply is not vulnerable which is why the sine qua non of spinal cord ischemia is a patient who has intact sensation but cannot move
The Anterior Spinal Arteries and The Artery of Adamkiewicz
- Anterior Spinal Artery arises from the vertebral arteries and is the longest artery in the body (from the foramen magnum to the conus medullaris.
- Supplies the anterior 2/3rds of the spinal cord including the Anterior Horns, Spinothalamic Tracts, and Corticospinal Tracts
- The Spinothalamic Tracts, and Corticospinal Tracts contain motor neurons
- The ASA has much less contribution from the radicular arteries and varies in diameter through its course (smallest diameter in the thoracic region)
- Luckily, the Artery of Adamkiewicz contributes to the ASA at T9-T12 in 75% of people (the rest have the artery located above or below)
- There is no way to know exactly where the artery is and so there is a chance that it will be included in the dissection and will be vulnerable to relative hypotension resulting in weakness or paralysis
IV Medication Options (as a bridge to Oral agents)
Labetalol
IV Hydralazine
IV Hydralazine
- Bolus Dose: 5-10 every 5 mins (no maximum dose)
- Infusion Dose: 1-5mg/min (but you can go higher if need be)
- Pros: 1:7 alpha to beta ratio and so it is effective in lowering blood pressure and heart rate.
- Cons: none
IV Hydralazine
IV Hydralazine
IV Hydralazine
- Bolus Dose: 10mg every 20 minutes PRN with a maximum dose of 40mg in 6 hours
- Pros: easy and familiar
- Cons: It takes 20 full minutes to see the full effects. and if you use too much it will be a 6 hour commitment (which is alright and fixable)
Nitroprusside
IV Hydralazine
Nitroprusside
- Infusion Dose 0.3-5ug/Kg/min
- Pros : extremely effective global vasodilation. Quick on and quick off (2 minute half life)
- Cons: it can cause cyanide toxicity with high doses and prolonged infusions particularly in the context of hepatic or renal compromise
Nitroglycerin
IV Hydralazine
Nitroprusside
- Bolus Dose: Often not required but you can give 5-10ugs at a time.
- Infusion Dose: 5-200ug/min but you can go higher
- Pros: quick onset ~2 mins/quick off ~3-5mins
- Cons: Patients can become tachyphylactic to its effects. Can cause a reflex tachycardia. Can cause headaches/nausea (potent vasodilator in the neurovasculature)