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.
Fenoldopam
peripheral arterial dilator via activation of dopamine receptors.
It is used in clinical situations of
hypertensive emergencies
postoperative hypertension.
short (10-minute) half-life.
One of its side effects is an increase in intraocular pressure and is contraindicated in patients with glaucoma.
Inamrinone
Inamrinone
(amrinone and milrinone)
cyclic AMP phosphodiesterase inhibitor
results in elevated levels of cyclic AMP in cardiac and smooth muscles.
increased myocardial contractility
and
dilatation of both arterial and venous
overall effect is an increase in cardiac output.
most effective in patients with congestive heart failure.
Vasopressin
antidiuretic hormone
[synthetic analog, desmopressin (DDAVP)]
are posterior pituitary hormones
have antidiuretic and vasoconstrictive effects.
Vasopressin clinically has both antidiuretic and vasoconstrictive properties.
used in the treatment of diabetes insipidus and is used as a potent vasopressor in vasodilatory shock.
Because of its potent vasoconstrictive properties, it is also used as an adjuvant drug in bleeding esophageal varices and lower gastrointestinal bleeding.
DDAVP, its longer-acting synthetic analog, has almost no clinical vasoconstrictive properties but is a potent antidiuretic.
preferred drug for treatment of pituitary diabetes insipidus.
It is also used as an adjuvant in the treatment of hemophilia A
and
Von Willebrand disease,
because it increases the factor VIII activity in these patients.
Desmopressin also can increase Von Willebrand factor from endothelial cells and can be adequate treatment in type I Von Willebrand disease.
Nitroglycerin
release of nitric oxide,
smooth muscle relaxation.
systemic vasodilatory effect more prominent on the veins.
Nitroglycerin lowers cardiac oxygen demand by decreasing preload.
generally 2 classifications of shock:
hypodynamic
and
hyperdynamic.
Patients with hypodynamic shock have
a low cardiac index
and
high systemic vascular resistance.
hypovolemic,
cardiogenic,
obstructive
Causes of obstructive shock
tension pneumothorax,
acute pulmonary embolism,
pericardial tamponade.
Causes of hyperdynamic shock are
sepsis,
adrenal insufficiency,
neurogenic shock,
anaphylaxis.
(Previously, hyperdynamic shock was classified as distributive shock)
The underlying hemodynamic effect is the maldistribution of blood flow.
Cervical cord injury from a cervical spine fracture may cause distributive shock due to interruption of the sympathetic chain and unopposed vagal tone. These patients present with low blood pressures and bradycardia.
Ventilator bundle vs dcr in VAP
The most important factor in reducing VAP is the reduction in time on the ventilator;
weaning protocols driven by respiratory therapy and nursing are key in reducing time on the ventilator.
Minimizing sedation is also effective in reducing time on the ventilator and is a recommended part of the “ventilator bundle” … spontaneous awakening and breathing trial reduced mortality in ventilated patients, there is no direct association between the daily interruption of sedation and VAP. (BUT there is DCR days on the vent !)
OTHER part of the bundle but NOT related to VAP:
histamine 2 receptor blockers - to dcr gastritis
prophylaxis against deep venous thrombosis, also unrelated to VAP
maintaining the head of the bed at more than 30° to reduce the risk of aspiration;
assessing daily for liberation from the ventilator.
The use of chlorhexidine as an oral decontaminant reduces VAP.
NOT - Tooth brushing alone is not associated with a decrease in VAP.
NOT - Early tracheostomy is advocated by many intensivists due to greater ease of ventilator weaning and increased patient comfort and family satisfaction. Unfortunately, it has no effect on the incidence of VAP (EVEN with dcr days on the VENT?)
The 1-year mortality associated with CIAKI is up to
30%.
only intervention clearly proven to prevent CIAKI,
Hydration!
NOT bicarb / mucomyst
In fact, there is evidence that sodium bicarbonate administration might be associated with an increased risk of CIAKI.
Intravenous hydration appears to be more efficacious compared with ad lib oral hydration.
A randomized trial showed that 0.9% saline is superior
fluid administration within 12 hours before and for 12 hours after contrast administration is superior to bolus administration at the time of contrast administration.
Calculate number needed to treat
NNT is the inverse of the ARR or 1/ARR. In the example in the question, the mortality in the treatment group was 10% compared with 30% in the control group. The NNT is 1/20%, or 1/0.2 = 5. Therefore, in the example, 5 patients need to be treated with Protocol A to prevent 1 death.
physio effects of hypothermia
During induction of hypothermia,
peripheral vasoconstriction causes shunting of blood away from the extremities and to the central system, resulting in a
rise in central venous pressure (CVP)
and
diuresis
but a relative hypovolemia.
This mechanism is reversed during rewarming:
leading to vasodilation, a decrease in CVP, and unmasking of the hypovolemia caused by previous hypothermia-induced diuresis. The initial diuresis causes fluid and electrolyte shifts and results in hypokalemia, hypophosphatemia, and hypomagnesemia during cooling. During rewarming, hyperkalemia can occur. Opportunistic infections are more common because of the reduction of inflammatory and immune responses, especially when cooling is prolonged more than 24 hours. Hypothermia induces small decreases in platelet function and coagulation; however, these effects are not usually clinically significant.
results in earlier liberation from mechanical ventilation
daily spontaneous breathing trials (SBT),
[in which patients breathe through a T-tube or using a small amount of continuous positive airway pressure, results in earlier liberation from mechanical ventilation.]
AND
sedation holiday
This approach was compared with sedation targeted to patient comfort along with SBTs. The group with paired sedation discontinuation and SBT had more ventilator-free days, fewer days in intensive care, and fewer days in the hospital. Although these results are early, both sedation vacation and SBT are recommended standard practice and should be paired when possible.
Delirium is defined as
acute disturbance of consciousness that fluctuates over a short period of time and is accompanied by inattention, disorganized thinking, and perceptual disturbances.
Presence of delirium is best ascertained by administration of the
Confusion Assessment Method for the ICU (CAM-ICU). This assessment can be administered by a nurse and requires only 1–2 minutes. It is 98% accurate in detecting delirium.
The CAM-ICU assessment requires that the patient be able to respond to verbal commands.
Treatment first involves a search for underlying causes. Once life-threatening causes are ruled out, patients should be reoriented and provided with necessary visual and hearing aids if used previously. Invasive devices and restraints should be removed if possible. Medications associated with delirium should be discontinued when possible
impairment in patients who are mechanically ventilated.
treatment of delerium
A traditional antipsychotic medication such as haloperidol may be useful.
commonly used drug in the ICU associated with delerium
H2 blockers
metoclopramide
sterioids
Delirium effect on prognosis
Delirium is not benign. Patients with delirium have twice the mortality at 6 months, and duration of delirium is independently associated with long-term cognitive impairment in patients who are mechanically ventilated
Hyponatremia should be thought of as
an excess of water
rather than a sodium deficit.
Hyponatremia It is usually associated with what fluid patterns
decreased plasma osmolality,
Large quantities of both plasma lipids or proteins can cause pseudo hyponatremia.
When plasma osmolality is low in a hyponatremic patient (normal is 285–295 mOsm/kg), the patient’s volume status must be assessed through history, physical examination, and measurement of urinary sodium.
Hypotonic hypovolemic hyponatremia occurs when there is a deficit of both total body sodium and water, with the sodium deficit exceeding the water deficit. Water loss can be renal or extrarenal. Vomiting or diarrhea often cause extrarenal hypovolemic hyponatremia. Diuretics are the most common cause of renal hypovolemic hyponatremia. Renal causes include cerebral salt wasting, which is a salt-losing deficiency seen in patients with intracranial injury. The underlying etiology is unclear, but the result is that the kidneys are not able to reabsorb sodium, leading to a volume-contracted state with a relative hyponatremia. In this situation, the renal inability to reabsorb sodium is reflected in the urine sodium, which is more than 20–25 mEq/L. Treatment is replacement of fluid volume and sodium without restriction of fluids. Often hypertonic saline is required.
Cerebral salt wasting must be differentiated from the syndrome of inappropriate antidiuretic hormone secretion (SIADH). SIADH is a euvolemic condition in which vasopressin secretion continues despite a low plasma tonicity/osmolality. It is commonly seen in patients with central nervous system disturbances as well. Plasma osmolality is less than 270 mOsm/kg, urine sodium is more than 20 mEq/L. The patient’s volume status is an essential differentiator between SIADH and cerebral salt wasting, because both can be seen in neurologically injured patients. The treatment of SIADH is fluid restriction and slow sodium replacement, again often with hypertonic saline.
Diabetes insipidus is a condition in which there is impaired (by contrast with inappropriate/elevated) secretion of vasopressin. It leads to a profound diuresis and rapidly developing hypernatremia. Excess free water replacement leads to a hypervolemic relative hyponatremia with high urine output. Nephrotic syndrome is also a hypervolemic condition in which hypoalbuminemia and lowered plasma oncotic pressure lead to an effective volume contraction and low flow state that stimulates vasopressin release and causes renal sodium and water retention and causes peripheral edema.
Lorazepam
is recommended by the Society of Critical Care Medicine as the preferred agent for the sedation of critically ill patients.
lorazepam contains propylene glycol, and systemic accumulation is associated with continuous lorazepam infusion.
toxicity includes hyperosmolar metabolic acidosis, lactic acidosis, acute tubular necrosis, intravascular hemolysis, central nervous system depression, seizures, cardiac arrhythmias, and hypotension.
quetiapine
Compared with haloperidol treatment or with placebo, is associated with a reduced need for other medications and faster resolution of delirium.
Use of quetiapine for hospital-acquired delirium is currently considered off label.
Dexmedetomidine
is a highly selective alpha-2-receptor agonist that acts at the locus coeruleus and spinal cord to produce both sedative and antishivering effects.
Dexmedetomidine does not significantly affect the respiratory rate and may be associated with reduced requirements for concurrent analgesic and sedative use compared with the benzodiazepines.
.
Treatment with what drug is an independent risk factor for delirium in several studies
midazolam
Haloperidol is recommended in many practice guidelines as first-line therapy for what in the icu and what potential side effect
hyperactive delirium in the intensive care unit. It is given intravenously in the intensive care unit
has a rapid onset (5–20 minutes)
a long half-life (18–54 hours).
Some treatment recommendations for hyperactive delirium advise giving haloperidol intravenously every 15–20 minutes and doubling the dose until agitation is controlled.
High doses of haloperidol (>400 mg/day) are associated with QTc prolongation and ventricular arrhythmias, including torsade de pointes.
Lorazepam and midazolam cause what kind of amneia
induce anterograde amnesia but do not cause retrograde amnesia.
Society of Critical Care Medicine recommends that midazolam be used only for short-term therapy (<48 hours).
By contrast, lorazepam is longer acting and is metabolized in the liver to inactive metabolites that are excreted in the urine. Is recommended for longer-term use as a sedative.
Because lorazepam is suspended in propylene glycol, toxicity from propylene glycol and metabolites (lactate and pyruvate) can be seen with lorazepam infusion. Toxicity includes hyperosmolarity and metabolic acidosis. Serum concentrations of propylene glycol are not readily available; physicians are advised to monitor the osmol gap daily in patients receiving more than 50 mg per day of lorazepam.
Propofol
sedative and hypnotic properties, as well as amnestic properties.
provides 1.1 kcal/mL from fat.
Propofol causes systemic vasodilation and hypotension, particularly in hypovolemic patients.
Propofol infusion syndrome (PRIS) is a syndrome of metabolic acidosis, bradyarrhythmia, and progressive myocardial failure that was first reported in pediatric patients on high-dose infusions of propofol.
The syndrome can include rhabdomyolysis, heart failure, renal failure, severe metabolic acidosis, bradyarrhythmias, cardiac arrest, and hypotension that can occur with infusion rates greater than 83 µg/kg/min, infusion for more than 48 hours, and concomitant use of catecholamine vasopressors or glucocorticoids.
Dexmedetomidine
Dexmedetomidine is an alpha-2 agonist that causes anxiolysis and sedation without respiratory depression. It has a rapid onset of action, approximately 15 minutes, and a short half-life of 2–2.5 hours. Dexmedetomidine is metabolized in the liver and through the cytochrome P450 system and has no active metabolites. It is becoming more widely used as an intensive care unit sedative–hypnotic agent, because it produces an effect that is termed “cooperative sedation,” meaning that arousability is maintained, despite deep sedation levels. It is thought to be advantageous in patients in whom a proper sedation level is difficult to achieve because of agitation on awakening. Dexmedetomidine causes bradycardia and hypotension, because it decreases plasma catecholamines.
Labetalol
is a selective alpha-1-adrenergic
nonselective beta-antagonist.
The onset of action is 2–5 minutes,
its half-life is 5–6 hours.
Due to the beta-blocking effects, cardiac output is maintained or mildly reduced.
Labetalol maintains cardiac output, unlike pure beta-antagonists, as well as cerebral, coronary, and renal perfusion.
It is often used in pregnancy-induced hypertension because there is little placental transfer.
Esmolol
ultra-short-acting cardioselective beta-adrenergic antagonist.
Its onset of action is less than 1 minute and the half-life is less than 10 minutes. It decreases blood pressure by decreasing heart rate and myocardial contractility. Its use is relatively contraindicated in patients with bradycardia because it further reduces heart rate.
Caution should also be used in patients with decompensated heart failure as it may decrease myocardial function.
Sodium nitroprusside
has a very rapid onset of action, and its half-life is 3–4 minutes.
It is both an arterial and venous dilator.
reduces both afterload and preload.
Although it is extremely potent and predictable, several properties limit its utility.
Nitroprusside decreases cerebral blood flow and increases intracranial pressure!!
which makes its use difficult in patients with stroke or hypertensive encephalopathy.
It can cause a steal syndrome in patients with coronary artery disease and increases mortality when used after acute myocardial infarction!!
Finally, patients can develop cyanide toxicity with its use.
Nitroglycerin
has its onset in 2–5 minutes with a
duration of action of 10–20 minutes.
Nitroglycerin is primarily a venodilator and decreases blood pressure by reducing preload and cardiac output.
This often leads to reflex tachycardia.
It may cause arterial vasodilation at higher dose, but this effect is highly variable. This limits its usefulness, and
nitroglycerin is not considered first-line therapy.
Low-dose nitroglycerin is generally used with other agents as combination therapy in patients with acute coronary syndrome or pulmonary edema.
Nicardipine is a second-generation calcium channel blocker. Its onset of action is 5–15 minutes, and the half-life is approximately 1 hour. It has high vascular selectivity and strong dilatory activity in the cerebral and coronary circulations. These properties may make nicardipine especially useful for the treatment of hypertension in patients with stroke, coronary artery disease, or systolic heart failure.
Nicardipine
is a second-generation calcium channel blocker. Its onset of action is 5–15 minutes,
and the half-life is approximately 1 hour.
It has high vascular selectivity and strong dilatory activity in the cerebral and coronary circulations.
These properties may make nicardipine especially useful for the treatment of hypertension in patients with stroke, coronary artery disease, or systolic heart failure.
Dopamine
has complex, dose-dependent alpha- and beta-receptor affinity and effects.
At low doses (0.5–2 µg/kg/min), dopamine stimulates D1 receptors, resulting in selective vasodilatation of the renal, splanchnic, cerebral, and coronary vasculature.
At slightly higher doses (2–5 µg/kg/min), dopamine stimulates norepinephrine release and has mixed receptor activity.
Infusions of 5–10 µg/kg/minute stimulate beta-1 receptors, which increases heart rate and contractility.
At doses greater than 10 µg/kg/min, alpha effects predominate, causing vasoconstriction in most vascular beds.
There is considerable variability in the response to dopamine, especially in critically ill patients. Tachyarrhythmias are the most common untoward effect.
Dobutamine
is a synthetic catecholamine that has affinity for both beta-1 and -2 adrenergic receptors.
The beta-1 activity primarily increases isotropicity and heart rate.
The beta-2 effect causes mild vasodilator effects.
It is commonly used to support cardiac decompensation in shock states.
Norepinephrine
has potent alpha-adrenergic activity.
It has modest affinity for beta-adrenergic receptors at low doses; thus, it has minimal effect on heart rate and cardiac output.
At clinically relevant doses (0.01–3 µg/kg/minute) the alpha-adrenergic activity predominates and increases blood pressure by vasoconstriction.
Norepinephrine is generally considered a first-line agent, along with dopamine, in patients who need hemodynamic support for septic shock.
Epinephrine
has both alpha- and beta-agonist properties that vary depending on dose.
At low doses, beta-receptor activity predominates so the net result is an increase in cardiac output, decreased systemic vascular resistance, and variable effect on blood pressure.
beta-1 stimulation causes an increase in heart rate (chronotropy) and stroke volume (inotropy).
This increases cardiac output and myocardial oxygen consumption.
beta-2 stimulation also causes vasodilation in skeletal muscle arterioles, offsetting some of the alpha-induced vasoconstriction.
At higher doses, alpha-receptor stimulation results in generalized vasoconstriction and increased blood pressure.
Epinephrine’s main limitations are its potential provocation of dysrhythmias (mostly sinus tachycardia), potential for myocardial ischemia, and visceral vasoconstriction.
Doses used clinically range from 0.01 to 0.10 µg/kg/minute.
Phenylephrine
has pure, potent alpha-adrenergic activity.
It has no affinity for beta-adrenergic receptors and minimal direct effect on heart rate or cardiac contractility.
Increased blood pressure may cause reflex bradycardia, but otherwise arrhythmia potential is minimal.
Its most common use is in neurogenic shock and as second-line treatment in septic shock.
Norepinephrine
released by the adrenal medulla.
alpha- and beta-1 adrenergic receptor agonist.
increases cardiac contractility by its effect on the beta-1 adrenergic receptor
causes even greater vasoconstriction by its effect on the alpha-receptor.
Norepinephrine is 1 of the first-line pressors recommended in the Surviving Sepsis guidelines.
Epinephrine
naturally occurring catecholamine produced by the adrenal medulla (converted from NorEpi)
its production and release are regulated by the sympathetic innervation of the adrenal gland.
beta-1,
beta-2,
alpha-adrenergic receptor agonist.
potent chronotrope and inotrope.
entricular fibrillation,
pulseless electrical activity,
asystole.
Phenylephrine
is a selective alpha-1 adrenergic receptor agonist
potent vasoconstrictor
used in hyperdynamic shock from cervical cord injury.
Patients with hyperdynamic shock have a high cardiac index and low systemic vascular resistance. Causes of hyperdynamic shock are sepsis, adrenal insufficiency, neurogenic shock, and anaphylaxis.
Vasopressin
produced in the posterior pituitary gland.
potent vasoconstrictor
It acts on the v1 smooth muscle receptor.
decreased levels seen in patients with septic shock and is recommended in the Surviving Sepsis guidelines if patients remain hypotensive despite norepinephrine infusion. careful, max out norepi first)
Vasopressin is an alternate to epinephrine for the treatment of adult refractory ventricular fibrillation.
Dobutamine
Dopatrex made for heart failure
synthetic adrenergic agonist derived from dopamine.
beta-1 and beta-2 adrenergic receptor agonist.
both inotropic and chronotropic effects and is used in patients with low cardiac indexes who are not hypovolemic.
It lowers systemic vascular resistance.
