Critical Care Flashcards
vasopressin release in septic shock
Vasopressin is secreted during the stress response, in response to increased serum osmolality, hypotension, and with hypovolemia. Plasma levels remain elevated for days after termination of the inciting event, with the magnitude and duration being dependent on the degree of stress, however these levels are rapidly depleted to levels unable to maintain hemodynamics with septic and severe hemorrhagic shock.
Exogenous corticosteroids stimulate the negative feedback loop and suppress both CRH and AVP production.
electrolyte abnormalities caused by hyperventilation
Respiratory alkalosis, such as from hyperventilation, can cause electrolyte abnormalities, such as hypocalcemia, hypokalemia, and hypophosphatemia. Hypocalcemia is caused by increased calcium binding to negatively charged plasma proteins as the proteins release hydrogen ions to restore physiologic pH.
CVP tracing summary
Normal CVP tracing summary:
a wave: atrial contraction, absent in atrial fibrillation
c wave: TV bulging into RA during RV isovolumetric contraction
x descent: TV descends into RV with ventricular ejection and atrial relaxation
v wave: venous return to and systolic filling of the RA
y descent: atrial emptying into RV through open TV
TrueLearn Insight : Below is a summary of the major CVP abnormalities:
Disorder CVP waveform changes
Atrial fibrillation Loss of a wave
AV dissociation Cannon a wave
Tricuspid regurgitation Tall c & v waves
Loss of x descent
Tricuspid stenosis Tall a & v waves
Minimal y descent
RV ischemia Tall a & v waves
Steep x & y descent
M or W configuration
Pericardial constriction Tall a & v waves
Steep x & y descent
M or W configuration
Cardiac tamponade Dominant x descent
Minimal y descent
causes of respiratory alkalosis
Respiratory alkalosis can be a result of central causes that increase respiratory drive, including stroke, aspirin overdose, anxiety, pain, and progesterone. Additionally, there are several pulmonary causes of respiratory alkalosis. These include pulmonary embolism, pneumonia, and asthma. Respiratory alkalosis also has significant metabolic effects, including hypocalcemia, hypokalemia, and hypophosphatemia.
calculation of SVR
SVR = 80 * (MAP - RAP) / CO. Typically, CVP is substituted for RAP. The conversion factor “80” is used to change units from “mm Hg/L/min” to “dynes x sec/cm^5.”
left IJV vs right IJV placement
Placement of a left-sided central line is associated with increased complications. There is an increased incidence of arterial puncture because the left internal jugular vein is often smaller and overlays the internal carotid artery more often than the right, which increase with head rotation more than 30 degrees. Additionally, the more tortuous course increases the incidence of malposition.
TrueLearn Insight : Although uncommon, carotid artery cannulation can lead to embolization. Carotid embolization on the left poses a greater risk as the left cerebral hemisphere is dominant in the majority of the population. This is also one of the reasons why right-sided carotid massage is preferred over left-sided massage. Another reason is that some investigations have found a greater cardioinhibitory effect on the right side.
PRES
Propofol infusion syndrome is a rare complication of high-dose (> 4-5 mg/kg/hr or > 65-80 mcg/kg/min), long-term (> 24 hours) propofol administration. It has been described more commonly in children
Propofol infusion syndrome is a rare complication of prolonged, high-dose propofol administration. Signs may include metabolic lactic acidosis, cardiac failure, renal failure, rhabdomyolysis, hyperkalemia, hypertriglyceridemia, hepatomegaly, and pancreatitis.
TrueLearn Insight : Phenol excretion during PRIS causes green-tinged urine.
Methemoglobinemia in G-6PD patients
Methylene blue is often the drug of choice when treating methemoglobinemia. Methylene blue is an antioxidant for the reduction of methemoglobin using nicotinamide adenine dinucleotide phosphate (NADPH) produced from the hexose phosphate pathway. In a patient with G6PD deficiency the hexose phosphate pathway is dysfunctional and free radicals develop, which causes red blood cell lysis. Therefore, methylene blue should be avoided in patients with G6PD deficiency. Additionally, methylene blue is a potent reversible monoamine oxidase inhibitor (MAOI) and may interact with serotonergic psychiatric medications leading to life-threatening serotonin syndrome.
Clostridium botulinum
Botulism is caused by the anaerobic bacillus, Clostridium botulinum. Flaccid neuroparalysis occurs due to the prevention of acetylcholine (ACh) release from vesicles at the NMJ. Acetylcholine is carried to the nerve terminal by vesicles which then fuse with the nerve terminal membrane via soluble N-ethylmaleimide-sensitive fusion associated protein receptor (SNARE) proteins. The collection of SNARE proteins facilitate exocytosis and then “repackaging” or reuptake of ACh. The various toxins of C. botulinum are zinc endopeptidases that cleave the SNARE proteins and stop the fusion and release of ACh into the nerve terminal, as well as prevent reuptake back into the terminal.
Common Chemo-Toxicities
Cisplatin, Carboplatin: acoustic nerve damage, nephrotoxicity
Vincristine: peripheral neuropathy
Bleomycin, Busulfan: pulmonary fibrosis
Doxorubicin: cardiotoxicity
Trastuzumab: cardiotoxicity
Cyclophosphamide: hemorrhagic cystitis
5-FU, 6-MP, methotrexate: myelosuppression
Accidental intrathecal injection of vincristine can cause ascending radiculomyeloencephalopathy, which is almost always fatal.
Vincristine is associated with peripheral neuropathy and patients on this medication are at increased risk for neuropathy during general anesthesia.
IO Placement sites
The four anatomical sites recommended for IO access are: the sternum, proximal tibia, distal tibia, and proximal humerus. Note, some general-purpose IO devices are not FDA-approved for sternal use.
IO vs central line in code situations
Major complications from IO access occur in less than 1% of insertions. During code situations, the AHA recommends IO access over central access due to a faster insertion time, higher first-attempt success rate, and lower infection incidence. Humeral IO have faster infusion rates compared to Tibial
Acute Respiratory acidosis
If a respiratory acidosis becomes chronic, pH nearly normalizes and HCO3- concentrations increase 4 to 5 mEq/L per 10 mm Hg sustained increase in PaCO2.
Which of the following is a recommendation for the management of a patient with sepsis or septic shock according to the Surviving Sepsis Campaign?
Sepsis and septic shock are medical emergencies and should be rapidly and aggressively managed as soon as a diagnosis is made. Broad-spectrum antibiotics should be initiated within the first hour. Sepsis-induced hypoperfusion should be treated with at least 30 mL/kg of intravenous crystalloid within the first three hours. For patients with septic shock, vasopressor therapy should be used in combination with volume resuscitation to target an initial MAP of 65 mm Hg.
Which of the following is likely to be the initial compensatory mechanism for acute respiratory acidosis that develops secondary to hypoventilation?
Homeostasis of body pH is complex and varies depending on the disturbance. Respiratory acidosis occurs when ventilation is inadequate. Initial compensation occurs though plasma protein buffers and is followed hours to days later by the renal response.
