ICU Flashcards

1
Q

Precedex
Max Dose:

A

1.5mcg/kg/hr

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2
Q

Hypercapnic respiratory failure is defined as….

A

Hypercapnic respiratory failure is defined as an increase in arterial carbon dioxide (CO2) (PaCO)> 45 mmHg with a pH < 7.35 due to respiratory pump failure and/or increased CO2 production.

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3
Q

Hypoxemic respiratory failure is defined as…

A

Hypoxemic respiratory failure is defined as SaO2 < 88% or a PaO2 < 60 mmHg with a normal or decreased partial pressure of carbon dioxide (PaCO2).

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4
Q

Normal PaO2 values =

A

Normal PaO2 values = 80-100 mmHg

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5
Q

Normal bicarb level =

A

Normal bicarb level = 22-28

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6
Q

AVAPS stands for…

A

Average Volume Assured Pressure Support (AVAPS)

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7
Q

Non-invasive positive pressure ventilation (NIPPV) includes

A

CPAP
BiPAP
AVAPS

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8
Q

NIPPV appropriate for HF w pulmonary edema?

A

CPAP

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9
Q

NIPPV appropriate for COPD exacerbation?

A

BiPAP

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10
Q

With BiPAP, the difference between IPAP and EPAP is called __________.

A

With BiPAP, the difference between IPAP and EPAP is called pressure support.

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11
Q

With AVAPS what do you set?

A

TV
I-Min
I-Max
EPAP

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12
Q

Normal CVP

A

8-12mmHg

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13
Q

Initial treatment for patients with suspected sepsis or septic shock includes initiation of fluid administration (_____mL/kg recommended) within the first hour and completion within three hours of initial presentation.

A

Initial treatment for patients with suspected sepsis or septic shock includes initiation of fluid administration (30 mL/kg recommended) within the first hour and completion within three hours of initial presentation.

Fluid boluses are preferred to treat hypotension before initiating vasopressors and should be continued until blood pressure and tissue perfusion is adequate or if patients are nonresponsive to fluid resuscitation. Multiple randomized trials and meta-analyses has provided no evidence of significant difference in mortality between albumin and crystalloid solutions in managing sepsis or septic shock.

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14
Q

Normal PA systolic < ____ mmHg

Normal PA diastolic < ____ mmHg

A

Normal PA systolic < 25 mmHg

Normal PA diastolic < 10 mmHg

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15
Q

Norepinephrine (Levophed)
MOA

A

Primarily agonistic at alpha1 and beta1 receptors, with little-to-no beta2 or alpha2 activity.

< 3 mcg/min - the beta1 effects may be more pronounced and increase cardiac output.

> 3 mcg/min - the alpha1 effects may predominate.

Three E’s in norepinephrine = 3mcg cut off

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16
Q

Normal Cardiac Index (CI)

A

2.5-4.0 L/min/M^2

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17
Q

Why Norepinephrine (Levophed) infusion should be through large-bore peripheral IV cath or CVC?

A

It is highly recommended to infuse norepinephrine through large-bore peripheral intravenous catheters or central venous catheters. Ideally, the peripheral infusion should be in the upper extremity, preferably through an antecubital vein, as this provides the least risk of ischemia secondary to extravasation. If possible, lower extremity veins should be avoided as occlusive vascular diseases are more likely to occur in the lower extremities. Extravasation into local tissue can cause significant ischemia and subsequent necrosis. Should extravasation be suspected, the infusion should stop immediately. An attempt should be made to remove (drawback) any of the injected medication. If continuing the infusion is necessary, it should be restarted at a different site, ideally in a different extremity. The local area should then be infiltrated with phentolamine.

Genenral rule > 10mcg/min you should place a CVC.

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18
Q

Normal PCWP < ___mmHg

A

< 12mmHg

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19
Q

Norepinephrine (Levophed)
Adverse Effects?

A

The most common adverse effects of norepinephrine relate directly to the activation of alpha1 receptors. In addition, excessive vasoconstriction can result in decreased end-organ perfusion, primarily caused by norepinephrine infusions without appropriately treating hypovolemia; this can be detrimental as most patients who require infusions of norepinephrine already have poor oxygen delivery or utilization.

Pulmonary vascular resistance may increase secondary to norepinephrine administration, which could have negative sequelae in patients with pulmonary hypertension. Decreased hepatic blood flow (secondary to alpha-mediated vasoconstriction) can lead to a transient increase in drugs that undergo hepatic metabolism.

Vasoconstriction secondary to alpha1 stimulation can result in reflex bradycardia via the baroreceptor reflex, which is generally not compensated for by the beta1 activity. The overall result is that cardiac output may decrease, or at most stay the same, despite beta1 agonism. At the same time, the increase in systemic vascular resistance increases the work of the heart by increasing afterload, thereby increasing myocardial oxygen demand. Because of these phenomena, the benefits of norepinephrine for cardiogenic shock are still unclear but merit consideration under certain conditions.

Ischemia/nencrosis w/ extravasation.

20
Q

Norepinephrine (Levophed)
Concentrations?

A

4 mg in 250 mL = 16 mcg/mL
8 mg in 250 mL = 32 mcg/mL
16mg in 250mL= 64mcg/mL
32 mg in 250 mL = 128mcg/mL

21
Q

Vasopressin
MOA

A

V1 - vasoconstriction
V2- increases aquaporins/water absorption collecting ducts

There are no inotropic or chronotropic effects. Only BP and SVR are increased with vasopressin

22
Q

Vasopressin
Dose?

A

0.01-0.04 U/min

23
Q

According to the 2021 Surviving Sepsis Campaign (SSC) International Guidelines for the Management of Sepsis and Septic Shock, infusion of vasopressin alongside norepinephrine early in the course of vasopressor therapy can reduce the amount of norepinephrine required to support blood pressures and may improve mortality in patients with sepsis.

Vasospressin should be added when levophed dose exceeds ________ mcg/min.

A

According to the 2021 Surviving Sepsis Campaign (SSC) International Guidelines for the Management of Sepsis and Septic Shock, infusion of vasopressin alongside norepinephrine early in the course of vasopressor therapy can reduce the amount of norepinephrine required to support blood pressures and may improve mortality in patients with sepsis.

Vasospressin should be added when levophed dose exceeds 20 mcg/min.

MORE:
Norepinephrine has been identified as the first agent of choice in patients with septic shock, but according to the 2021 Surviving Sepsis Campaign International Guidelines for the Management of Sepsis and Septic Shock, patients with inadequate mean arterial pressures who are receiving norepinephrine should have vasopressin added early to supplement vasoconstrictive effects instead of increasing dosages of norepinephrine. The guideline authors suggest that, when norepinephrine reaches titration levels of 0.25 to 0.5 mcg/kg/min, vasopressin can be added to slow the up-titration of norepinephrine. Results of several trials have provided evidence that vasopressin provides a catecholamine-sparing effect when it is added early on in the treatment of septic shock, and authors of systematic reviews performed by the SSC have reported reduced mortality in patients who receive norepinephrine and vasopressin compared to receiving norepinephrine alone.

Vasopressin is a hormone released by the posterior pituitary gland during times of hypotension or increased serum osmolality. It has vasoconstrictive effects on vascular smooth muscle via activating vasopressin hormone-specific proteins at the V1a receptor. Activation of the V2 receptor within the collecting duct of the renal tubule leads to reabsorption of water for intravascular reexpansion and the rebalancing of osmolarity. Data from some studies have provided evidence that, during septic shock, particularly after 24 to 48 hours of ongoing sepsis, a state of “relative vasopressin deficiency” can occur, contributing to deficient vascular tone, particularly within the splanchnic circulation. Thus, replacing vasopressin can counterbalance this deficiency and improve vascular tone in septic shock.

The SSC recommends using epinephrine as the third agent if blood pressure does not improve despite combined norepinephrine and vasopressin therapy. The addition of other pressors or inotropic agents should be considered after norepinephrine, vasopressin, and epinephrine are started.

24
Q

In what states does the body release Vasopressin/Arginine Vasopressin (AVP)/ Antidiuretic Hormone (ADH)?

A

Hyperosmolar states (strongest)
Hypovolemia

MORE:
ADH is the primary hormone responsible for tonicity homeostasis. Hyperosmolar states most strongly trigger its release. ADH is stored in neurons within the hypothalamus. These neurons express osmoreceptors that are exquisitely responsive to blood osmolarity and respond to changes as little as two mOsm/L. Therefore, slight elevations in osmolarity result in the secretion of ADH. ADH then acts primarily in the kidneys to increase water reabsorption, thus returning the osmolarity to baseline.

ADH secretion also occurs during states of hypovolemia or volume depletion. In these states, decreased baroreceptors sense arterial blood volume in the left atrium, carotid artery, and aortic arch. Information about low blood pressure sensed by these receptors is transmitted to the vagus nerve, which directly stimulates the release of ADH. ADH then promotes water reabsorption in the kidneys and, at high concentrations, will also cause vasoconstriction. These two mechanisms together serve to increase effective arterial blood volume and increase blood pressure to maintain tissue perfusion. It is also important to note that in states of hypovolemia, ADH will be secreted even in hypoosmotic states. Conversely, hypervolemia inhibits ADH secretion; therefore, in hyperosmotic hypervolemic states, ADH secretion will be reduced.

Osmolarity and volume status are the two greatest factors that affect ADH secretion. However, a variety of other factors promote ADH secretion as well. These include angiotensin II, pain, nausea, hypoglycemia, nicotine, opiates, and certain medications. ADH secretion is also negatively affected by ethanol, alpha-adrenergic agonists, and atrial natriuretic peptide. Ethanol’s inhibitory effect helps to explain the increased diuresis experienced during intoxicated states as well as increased free water loss; without appropriate ADH secretion, the kidneys excrete more water

25
Q

Three conditions treated with a synthetic form of Vasopressin called Desmopressin (DDAVP)?

A

Hemophilia A
Von Willebrand disease
Central Diabetes Insipidus

26
Q

Epinephrine (Adrenalin)
MOA?

A

a1, a2, b1, b2 agonist

Lose Dose (< 10mcg/min)– more b1/b2 effect

High Dose (>10mcg/min)- more a1/a2 effect

Epinephrine increases systemic vascular resistance, heart rate, cardiac output, and blood pressure.

10 letters in epinephrine = 10mcg cut off

27
Q

Epinephrine
Cardiac Arrest Dose?

A

1mg Q3-5min

28
Q

Phenylephrine (Neosynephrine)

A

alpha 1 agonist (pure)

Reflex bradycardia may occur due to selective vasoconstriction and elevation of blood pressure.

29
Q

Phenylephrine (Neosynephrine)
Dosing?

A

50-200mcg/min

30
Q

Dobutamine
MOA?

A

B1 > B2 > A1

In addition to the well-known beta-1 activity, dobutamine has been shown to have some beta-2 activity, which contributes to the reduction in the systemic vascular resistance, and alpha-1 activity, to an even lesser extent, whose vasoconstrictive effects are negated by the baroreceptor mediated response and beta-2 activity.

31
Q

Dobutamine
Dosing?

A

2.5 - 40mcg/kg/min

32
Q

Dopamine
MOA?

A

Dopamine is a precursor of norepinephrine and epinephrine, which acts in a dose-dependent fashion on dopaminergic receptors as well as alpha and beta receptors.

0.5-2mcg/kg/min- act on the visceral vasculature to produce vasodilation, including the kidneys, resulting in increased urinary flow.

5-10mcg/kg/min - beta > alpha (more inotropic)

> 10 mcg/kg/min - alpha > beta (more adrenergic0

33
Q

Milrinone
MOA?

A

Milrinone is a PDE-3 inhibitor that causes increased levels of cyclic AMP.

In cardiac myocytes, this results in cardiac stimulation and increased CO.

In smooth muscle of peripheral vessels, this results in vasodilation.

Thus, Milrinone is used to treat low CO as in decompensated HF.

34
Q

Ephedrine

A

Indirect and Direct Sympathomimetic

Ephedrine, a stereoisomer to better-known pseudoephedrine, is a sympathomimetic amine with unique effects due to its indirect mechanism than other sympathomimetic agents like pseudoephedrine and phenylephrine.

Ephedrine acts as both a direct and indirect sympathomimetic. It binds directly to both alpha and beta receptors; however, its primary mode of action is indirectly achieved by inhibiting neuronal norepinephrine reuptake and displacing more norepinephrine from storage vesicles. This action allows norepinephrine to remain in the synapse longer to bind postsynaptic alpha and beta receptors.

Ephedrine’s indirect mechanism results in a sustained or even increased heart rate due to norepinephrine’s ability to bind alpha and beta receptors, whereas more direct sympathomimetics like phenylephrine results in reflex bradycardia. While the indirect effect is most profound on arterial blood pressure, the direct vasoconstricting action functions more on the venous system. It is, therefore, effective in elevating central venous pressure when the patient is challenged with fluids.

Stimulation of alpha-1-adrenergic smooth muscle receptors within vasculature results in a rise in systemic vascular resistance and, consequently, systolic and diastolic blood pressure. Direct stimulation of beta-1 receptors by ephedrine and norepinephrine increases cardiac chronotropy and inotropy.

Finally, beta-2-adrenergic receptor stimulation in the lungs results in bronchodilation with ephedrine administration, though it is not as pronounced as its cardiovascular effects.

35
Q

Isoproterenol (Isoprenaline)
MOA?

A

Isoproterenol is a beta-1 and beta-2 adrenergic receptor agonist indicated primarily for bradydysrhythmias.

Indications: Heart block not requiring pacing, cardiac arrest from heart block when pacemaker therapy is unavailable; also used off-label for bradycardia, Torsades, Brugada syndrome, ventricular arrhythmias 2/2 AV blocks

36
Q

ACLS guidelines define high quality chest compressions as achieving ETCO2 pressures of at least ____-____ mmHg.

When ROSC occurs, the patients ETCO2 will increase to >____ mmHg.

A

ACLS guidelines define high quality chest compressions as achieving ETCO2 pressures of at least 10-20 mmHg.

When ROSC occurs, the patients ETCO2 will increase to > 40 mmHg.

37
Q

Cardiac Arrest:
First dose Amiodarone
Second dose Amiodarone

A

300mg Amiodarone
150mg Amiodarone

38
Q

Cardiac Arrest:
First dose Lidocaine
Second dose Lidocaine

A

1-1.5mg/kg
0.5-0.75mg/kg

39
Q

Shock energy for defibrillation in cardiac arrest (biphasic)

A

120-200J

40
Q

Reversible Causes of Cardiac Arrest

A

6H’s & 6T’s

Hypovolemia
Hypoxia
H+ (acidosis)
Hyper/hypokalemia
Hypoglycemia
Hypothermia

Thrombosis (MI)
Thrombosis (PE)
Tension PTX
Tamponade
Trauma
Toxins

41
Q

Rhythm?

A

V Fib

42
Q

Rhythm?

A

V Tach

43
Q

Types of Breaths

A

Mandatory

Assisted

Spontaneous

44
Q

Four common vent modes used in the ICU

A

Assist Control (AC)
Synchronized Intermittent Mandatory Ventilation (SIMV)
Pressure Control (PC)
Pressure Support Ventilation (PSV)

45
Q

Difference between AC and SIMV

A