ICU Flashcards
Thrombolytic reversal for bleeding compliczations
Epsilon aminocaproic acid
(ECA)
inhibitor of fibrinolysis.
competitively binds plasminogen,
preventing its interaction with fibrin
and activation to plasmin.
It is absorbed orally / intravenously.
ECA is contraindicated in disseminated intravascular coagulation because of the potential for uncontrolled clotting.
Cilostazol
is a phosphodiesterase enzyme inhibitor used as an antiplatelet agent.
Hyponatremia algorithmic approach
volume status,
serum
urine
urine osmolality.
first rule out pseudo hyponatremia caused by either hyperglycemia or mannitol infusion.
Correcting this patient’s sodium level by 1.6 mEq/L for every 100 mg/dL increase of the serum glucose above 100 mg/dL [(465–100)/100 × 1.6] results in a corrected level of 126 mEq/L.
nonketotic hyperglycemia typically have serum glucose levels approaching 1000 mg/dL.
Causes of hyponatremia in normovolemic patient:
(normal serum osmolality and question of pulmonary edema on chest radiograph) include:
syndrome of inappropriate antidiuretic hormone secretion (SIADH)
psychogenic polydipsia.
These 2 etiologies are differentiated by urine osmolality and urine sodium;
if the osmolality is less than 100 mOsm/kg:
psychogenic polydipsia is suspected,
patients with water intoxication have a urine sodium less than 10 mEq/L.
osmolality greater than 100 mOsm/kg:
suggests SIADH.
Urine sodium in SIADH is generally high (>20 mEq/L) due to an overall low urine volume;
This patient has SIADH as evidenced by vol sodium urine osmo urine na
normovolemic
hyponatremia (water in more than Na)
urine osmolality greater than 100 mOsm/kg
urine sodium greater than 20 mEq/L
adrenal insufficiency and cerebral salt wasting vol urine sodium urine osmo k
HYPOvol
urine sodium greater than 20 mEq/L
urine osmolality greater than 100 mOsm/kg,
HYPER K in adrenal insufficiency.
Diarrhea
vol
Na
Urine Na
Diarrhea
hypovolemic
hyponatremia,
urine sodium is typically less than 20 mEq/L
renal failure, heart failure, or cirrhosis
vol
Na
Patients with renal failure, heart failure, or cirrhosis may have a
hypervolemic
hyponatremia.
current guidelines recommend a delay of how long before withdrawing dual antiplatelet therapy for a nonurgent operation for bare metal vs drug-eluting stent
4–6 weeks after placement of a bare metal stent
6–12 months! after deployment of a drug-eluting stent
The incidence of perioperative death, myocardial infarction, and stent thrombosis may be as high as 30% within the first month, regardless of the type of implanted stent.
Although this risk decreases over time, some studies have suggested that the risk remains high for up to 2–3 years for drug-eluting stents.
The original indication for stent placement—stable angina versus acute coronary syndrome—appears, however, to be a more powerful predictor of perioperative cardiac complications than the type of stent deployed.
Contrast-induced acute kidney injury (CIAKI) is caused primarily by
renal vasoconstriction. Therefore, people with diminished renal vasodilatory capacity or factors contributing to this are at increased risk for CIAKI.
The most prominent risk factor appears to be preexisting renal impairment. The combination of diabetes and preexisting renal impairment appears to be particularly risky for developing CIAKI.
Factors increasing the risk impaired renal function, diabetes mellitus, reduced intravascular volume, cardiovascular response disease, use of diuretics, advanced age, FEMALE sex (more allergic to stuff), hypertension, hyperuricemia, concurrent use of nephrotoxic drugs, surgical interventions.
Evidence shows that even “prediabetic” patients (fasting hyperglycemia 100–125 mg/dL) have an increased risk of CIAKI when chronic kidney disease is present. High osmolality contrast agents are associated with a higher incidence of CIAKI than low-osmolality agents.
Both furosemide and mannitol INCREASE the risk of CIAKI!!
the most commonly encountered infection in the intensive care unit
Ventilator-associated pneumonia (VAP)
(NOT UTI!!)
risk of developing VAP increasing by approximately 1% per ventilator day.
The incidence of VAP in surgery patients, and in particular trauma patients, is significantly higher than in other intensive care unit populations, including patients admitted to the medical, neurosurgical, and pediatric intensive care units.
Unfortunately, the trauma patient is at significant risk secondary to altered mental status from traumatic brain injury, intoxication, and many other varied etiologies. Aspiration is commonly encountered in this patient population and is a major risk factor for the development of pneumonia.
Blood transfusion is an independent risk factor for VAP but is not part of the VAP bundle.
A restrictive transfusion trigger is suggested, as demonstrated in the Transfusion Requirements in Critical Care (TRICC) trial.
A restrictive transfusion strategy to maintain a Hb concentration of 7.0–9.0 g/dL was as effective as a strategy to maintain a Hb concentration of 10.0–12.0 g/dL.
The VAP bundle includes
a daily sedation holiday, stress gastritis prophylaxis, elevation of the head of bed, deep vein thrombosis prophylaxis, daily oral care.
Other measures that may help prevent VAP include enhanced use of noninvasive positive pressure ventilation and continuous aspiration of subglottic secretions.
ARDS with life-threatening refractory hypoxemia what are treatment
recruitment maneuvers, prone positioning, inhaled nitric oxide, high-frequency oscillatory ventilation, extracorporeal membrane oxygenation.
science definition of PEEP
the pressure in the lungs above atmospheric pressure
at the end of expiration.
PEEP is positive pressure applied at end-expiration to recruit collapsed alveoli and prevent derecruitment of open alveoli, thereby limiting atelectasis and ventilation-perfusion mismatch.
This recruitment results in increasing functional residual capacity.
PEEP also may improve lung compliance, especially in patients with acute respiratory distress syndrome (ARDS), by redistributing extravascular lung water from the alveoli to the interstitial space.
may reduce venous return and cardiac output by raising intrathoracic pressure.
used to decrease auto-PEEP in patients on mechanical ventilation.
Decreasing the tidal volume
or
dcr the respiratory rate, or increasing inspiratory flow,
Hypernatremia (defined a serum Na+ >148 mmol/L) generally indicates
a deficit of body water relative to sodium (i.e., decreased extracellular fluid volume).
Most hypernatremia is hospital acquired because of inadequate or inappropriate fluid therapy in patients with identifiable water losses, impaired thirst, or reduced access to free water (common in postoperative patients).
The manifestations of hypernatremia are primarily
neurologic.
Symptoms correlate with both the degree and rapidity of the change in serum Na+.
More severe symptoms (hyperreflexia, seizures, and coma) may be seen when the serum Na+ exceeds 160 mmol/L.
The treatment of hypernatremia is
to replace the free water deficit.
An estimate of the free water deficit can be calculated from the following formula:
Free water deficit = TBW × [(serum Na+/140) – 1]
Note. TBW = estimated total body water (normal TBW for men = 0.6 and women = 0.5 times the ideal body weight).
The current recommendations for patients with hypernatremia for longer than 24 hours is a correction of 0.5 mmol/L per hour or roughly a maximum correction of 10–12 mmol/L per day.
Hyponatremia
most common symptoms
Most patients with a serum Na+ greater than 125 mmol/L will be asymptomatic unless the change has been abrupt.
most common symptoms of hyponatremia are headache, nausea, vomiting, muscle cramps, lethargy, restlessness, disorientation, depressed reflexes.
Severe or rapidly evolving hyponatremia can lead to seizures, coma, permanent brain damage, respiratory arrest, brain-stem herniation, and death.
most common vol status associated with hyponatremia
Hyponatremia may be associated with high, normal, or low extracellular volume. Thus, the initial step in evaluating a patient with hyponatremia is to assess the patient’s volume status.
Hypervolemic hyponatremia results from
conditions that increase effective circulating volume
as a result of elevated plasma arginine vasopressin levels and reduced glomerular filtration rates (GFR).
It is often associated with congestive heart failure, cirrhosis, and renal failure. Patients will generally exhibit signs on physical exam of volume overload (e.g., peripheral and pulmonary edema, ascites, pleural effusions). The primary treatment is diuresis.
Hypovolemic hyponatremia usually involves
Na+ losses from either renal or nonrenal sources.
Diuretics (e.g., furosemide) are a common cause of renal losses.
Nonrenal losses include vomiting and insensible losses from fever, sweating, and diarrhea.
Clinical signs and symptoms include thirst, tachycardia, and possibly hypotension. The urine Na+ concentration is less than 10 mEq/L (unless renal loss is suspected).
Treatment is generally volume replacement with normal saline.
Euvolemic hyponatremia usually involves
generally lacks the clinical signs of hypovolemia or hypervolemia.
The urine Na+ is greater than 20 mEq/L.
frequently iatrogenic and often responds to fluid administration during the postoperative period.
The syndrome of inappropriate antidiuretic hormone secretion and adrenal insufficiency are also causes.
Fluid restriction is usually the first step in treatment.
Neurogenic shock
acute transection of the spinal cord. Clinical manifestations include warm skin, bradycardia, and hypotension secondary to a loss of sympathetic tone causing subsequent vasodilatation and increased venous capacitance.
Treatment includes administration of alpha-adrenergic vasoconstrictive agents, such as phenylephrine, to re-establish peripheral vascular tone and decrease venous capacitance.
Phenylephrine
alpha-1 selective agonist.
potent arterial vasoconstrictor when given intravenously.
associated with marked reflex bradycardia.
used during general anesthesia to reverse the vasodilatation of anesthetics.
