#electronic notes

Aortic abdominal aneurysm is defined by a dilation of the abdominal aorta greater than 1.5x normal.

Normal diameter is 2cm. Thus, >3cm is considered aneurysmal. 90% are infrarenal (1.5-2cm below), and the risk of rupture is greater in women when sizes are equivalent.

Most are discovered incidentally/are asymptomatic.

When they do present:

Excruciating back/abdomen/groin pain.

Hypovolemic shock (tachycardia + hypotension)

Flank ecchymosis [bruise]. aka Grey-Turner sign.

USPSTF recommends one time screening if:

male 65-75 hx smoking

male 65-75 familial hx first degree family requiring AAA repair/died of AAA

[no established guidelines for women]

Risk factors same as those in atherosclerosis.

No established guidelines on surveillance. Can use ultrasound (most common) or CT. First screen six months after discovery. If it's not expanding, use the following:

<4cm in size = screen every 2 years

4-4.5cm = annual

>4.5cm = every six months

Surgical indications:

Symptomatic

>5.5cm

Growing >0.5cm/6mo or >1cm/year

Saccular aneurysms (potential for infection)

Surgical options:

EVAR/Endovascular aneurysm repair:

lower perioperative morbidity/mortality

but does not eliminate risk of future rupture

best for patients with high operative risk

Limitations of EVAR: need an adequate length of femoral artery (10mm), appropriate aortic neck length (10-15mm), and aortic neck angle (<60 degrees)

Complications from EVAR:

stent migration/kinking

undersized stent = poor seal

oversized stent = incomplete expansion, may not fix in place

parts of the stent separate

infection (has a mortality rate of 25%)

endoleak (five types)

Open repair:

higher perioperative morbidity/mortality

but definitive repair

better in younger patients w/ low operative risk

PVD = occlusion of larger arteries NOT including coronary, cerebral, or aortic arch.

Risk factors:

Smoking

Family hx

Diabetes

Hypertension (HTN)

Dyslipidemia

Obesity

Essentially the same RFs that cause other cardiovascular diseases.

Root cause: atherosclerosis (hardening of the vascular walls) or inflammation. The former is most common. In either case you can get stenosis, thrombus, or embolus formation leading to acute or chronic ischemia downstream.

PVD problems necessitating surgery:

Carotid artery occlusive disease (CAOD)

Abdominal aortic aneurysm (AAA)

Peripheral artery occlusive disease (PAOD)

CAOD typically presents with:

Stroke-like/neurologic symptoms (variable)

Transient ischemic attack (TIA) < 24h

Reversible ischemic neurologic deficit 24-72h

Cerebrovascular accident (CVA/stroke) - permanent.

Amaurosis fugax - transient loss of vision.

CAOD alters the flow of blood through the carotids... listen for bruits.

Dx: carotid doppler is non-invasive with high sensitivity/specificity for recognizing any stenosis. but it is poor for quantifying the degree. thus, if you find stenosis, do angiography (CTA/MRA).

Medical management: statins, anti-platelet therapy, modification of risk factors/lifestyle, control of HTN/diabetes.

Surgical management: Only if symptomatic or stenosis exceeds 60-70%. In an evolving stroke, perform surgery emergently. If the stroke has already completed, wait 4-6 weeks to avoid reperfusion injury.

Two options in surgery:

Balloon/stent [smashes plaque against the walls to reopen] if patient is high risk in surgery/not completely occluded

But endarterectomy [removal of plaque] is preferred.

ABCs are paramount. (as they are with trauma. airway, breathing, circulation.)

There are four types of vascular access options: Peripheral IV, central line, PICC line, and intraosseous. The first two are covered in relative detail below.

Peripheral IVs are exactly what they sound like: access through a vein in the extremities. Needles should be no smaller than 20 gauge (using gauge, higher number = smaller needle), particularly with blood where using too small of a needle can cause physical lysis of the RBCs. Also recall that in trauma, you want two peripheral access points to introduce fluid (18 gauge). This is preferable to a central line. You cannot feed a patient TPN through peripheral IVs. Vasopressor introduction through peripheral IVs should be done with caution--extravasation of a pressor into the tissue can cause compartment syndrome. If you have to, use phenylephrine preferentially.

A *central line/central venous catheter can be placed in three major veins: femoral, subclavian, and jugular. Femoral placements have the highest odds of infection [in my notes I wrote "2 close 2 ur nasty bits"]. Jugular access has the lowest infection rates. However, subclavian and jugular access can result in accidental pneumothorax because they're much closer to the thoracic cavity. And in any of these access points, you can accidentally insert into the artery. Advantages of central line placement: TPN feeding, multiple drug infusion, IV drips, vasopressor delivery. If you need peripheral access but can't get it, this is an acceptable alternative.

Fluids: Lactated ringers are preferred in trauma if you use crystalloids. The rule for maintaining fluid levels is 100/50/20: 100ml/kg/day for the first 10kg, 50ml/kg/day for the next 10kg, and 20ml/kg/day for the remaining kilos after 20kg. [For a 100kg patient, the formula would then be 100ml(10kg) + 50ml(10kg) + 20ml(80kg) = 3100ml/day.] The hourly version of this rule is 4/2/1.

The initial goal of fluid resuscitation is to restore tissue perfusion and normal oxidative metabolism. Use 6-10L of crystalloids or 2-4L of colloids, with predetermined boluses titrated to clinical endpoints. If the patient doesn't respond to fluids, you need to start using vasopressors.

Signs that the patient is responding = mean arterial pressure > 60mmHg or higher, clinical improvement (mental status, urine output, etc.) Be sure to treat the underlying cause.

According to the SAFE study, 4% albumin and normal saline had similar 28-day outcomes. But normal saline trended in favor of trauma patients, and albumin trended in favor of septic patients.

While it may sound difficult to track in a critical care situation, keeping accurate fluid input/output records is a must, and not just for legal purposes. It's how you'll know if you've given too little [hypovolemic] or too much [cardiac overload, pulmonary edema, abdominal hypertension] fluid.

Possible pressors: epinephrine, norepi, phenylephrine, dopamine, dobutamine [d'ohbutamine is still stuck in my head], vasopressin. Will cross these drugs in depth on Sunday when I review pharm.

When to do a blood transfusion?

Patient's Hgb is < 7.

Underlying cardiac disease may require it around Hgb 9-10. Keep an eye on vitals and oxygen delivery capacity.

Transfusions for cancer patients is hotly debated [and hopefully then, not testable.]

Risks from transfusions:

allergic reaction/anaphylaxis

transfusion-associated cardiac overload

transfusion-related acute lung injury

Transfusion protocol:

1:1:1 packed red blood cells, fresh frozen plasma, and platelets.

this is standard because infusions of blood or crystalloid by themselves dilute clotting factors/platelets, which can cause disseminated intravascular coagulopathy [in short, a mass of clotting events all over the body followed by massive bleeding as clotting factors are used up/clot lysis is massively stimulated in response]. This relates to the triangle of death.

Triangle of death:

coagulopathy, metabolic acidosis, and hypothermia are all related in bringing a patient closer to death.

hypothermia halts the coag cascade -> coagulopathy leads to poor perfusion -> poor perfusion causes cells to convert to anaerobic metabolism -> this increases lactic acid/metabolic acidosis -> this decreases myocardial performance/poor cardiac function -> hypothermia. [it's why emergency rooms have the heat jacked up like a sauna.]

worth noting that patients often show up to the ED already in a state of coagulopathy and slightly cold/poorly perfusing.

Once in the hospital setting, constantly be looking for infection. The hospital is a dirty place, despite the best advances in protocol.

The five W's of infection:

Wind (atelectasis): ventilators do a poor job at keeping all alveoli open. The reopening of these alveoli -> cytokine response -> predisposition to pneumonia. Incentive spirometry.

Water (UTIs): Indwelling foley catheters pose a risk of infection every time they are inserted, and if left, are a pathway for infection. You want foley caths out ASAP. If someone spikes a fever, get a urine sample.

Wound: Infections present 5-7 days post-op. Erythema, warmth, tenderness, pus, and fever are all strong signs. If found, give empiric antibiotics while you wait for the culture results to come back.

Walking: Get your patients ambulatory ASAP. Deep vein thrombosis can break off and throw a pulmonary embolism, which accounts for 10% of all hospital deaths. You ALWAYS prophylax for DVTs with heparin or enoxaparin (low molecular weight heparin). Compression stalkings are also helpful in reducing blood pooling/stasis in the lower extremities.

[it just says "wonder drug." what?]

ARDS/ALI (acute respiratory distress syndrome/acute lung injury) occurs due to a body-wide inflammatory state (from something like sepsis/trauma). Endothelial injury -> increased capillary permeability -> proteinaceous fluid crosses into alveoli. Damage to alveolar lining also raises pulmonary edema. ARDS has a 50% mortality rate.

Abdominal compartment syndrome: increased intra-abdominal pressure resisting the diaphragm, compressing the bladder, obstructing renal and other organ vasculature leading to a myriad of symptoms. Consider laparotomy with temporary enclosure, to relieve pressure and allow time to find the cause. Can be measured with bladder pressure:

Normal is 0-5 cm H20

Grade I = 10-15

Grade II = 15-25

Grade III = 25-35

Grade IV = 35+

* Instructions for accessing each of the three central line points:

Femoral: recall the NAVEL mnemonic that orders the nerve, artery, and vein (and lymphatics) from lateral to medial. If you can't find the pulse or the situation is traumatic, the go-to rule is that the vein is two finger widths lateral to the pubic tubercle.

Subclavian: Needle goes under the bend of the clavicle, directed to the suprasternal/manubrial notch.

Someone with a traumatic CNS injury (brain, cervical, or high thoracic spinal cord) may go into neurogenic shock due to a disconnect in the autonomic nervous system. Lack of vagal tone -> bradycardia. Lack of sympathetic tone -> systemic vasodilation -> hypotension. You need to give this patient vasopressors to augment the loss of the ANS.

Endocrine disorders (adrenal insufficiency or a thyroid disorder) can cause combined cardiogenic and distributive shock. You would treat this with corticosteroids (solucortef).

Sepsis can cause septic shock via myocardial depression from inflammatory mediators such as endotoxin, IL-1, IL-6, nitric oxide, and TNF-alpha. Most sepsis patients are over 65 years old.

SvO2 - mixed venous oxygen saturation. The percentage of blood bound to Hgb that returns to the right side of the heart. It’s a measure of how much oxygen is being extracted from blood by the body. Normally 60-80%, it can dip lower when perfusion into the tissues is insufficient [more oxygen is extracted].