CRNA Interview Questions

Contrary to all other arteries in body, coronaries are perfused during

diastole

Timing of IABP is always performed using __ as a guide for balloon timing.

arterial waveform

Atropine keep

In order to understand the pharmacology of atropine we first need to understand the role of the PSN and the heart. binds with acetycholine receptors blocking parasympathetic response thereby blocking a decreased heart rate

The vagus (parasympathetic) nerves that innervate the heart release acetylcholine(ACh) as their primary neurotransmitter. ACh binds to muscarinic receptors (M2) that are found principally on cells comprising the sinoatrial(SA) and atrioventricular(AV) nodes. Muscarinic receptors are coupled to the Gi-protein; therefore, vagal activation decreases cAMP leading to decreased Ca in the cells also leading to decreased chronotropy and inotropy. Gi-protein activation also leads to the activation of KACh channels that increase potassium efflux and hyperpolarizes the cells.

Atropine is a muscarinic receptor antagonist. Therefore, it binds to the muscarinic receptor preventing ACh from binding and activating that receptor, blocking vagal nerve activity on the heart. This results in increased heart rate and decreased conduction time.

Used in SB and 1st degree, 2nd degree type 1 AV Blocks
CHB, 2ndDegree type II, and heart txp (due to cutting of vagus nerve) patients will not be affected by this drug

Dose 1mg IVP Q3-5min; Max dose 3mg
Onset of action: 30 seconds

Blocks acetylcholine receptors, accelerates heart rate in bradycardia, dries mucous membranes in organophosphate poisoning, and may worsen bradycardia associated with certain heart blocks.

How do Beta-agonists and insulin drive K back into the cells?

Insulin increases the phosphorylation of the insulin receptor substrate protein (IRS-1), which leads to the activation of atypical protein kinase C and the insertion of extra Na+/K+ ATPase pumps into the membrane. With food intake, insulin secretion also occurs, and potassium is safely sequestered inside cells.

β-agonists increase the activity of Na+/K+ ATPase pumps in skeletal muscle. Specifically, this is a β2 effect. The reason for this is thought to be the need to increase the availability of these transmembrane pumps to keep up with the demand of exercising muscle (a quantitatively much larger volume of ions will be in traffic across the muscle cell membrane if it keeps depolarising and repolarising all the time).

Pulse Pressure

SBP- DBP= PP
reflects the volume of blood ejected from the LV on a single beat or the "stroke volume"

Rapid Sequence Intubation (RSI)

The use of medications to sedate and paralyze a patient to achieve endotracheal intubation rapidly;

SOAP- ME
Suction
Oxygen: bag valve mask connected to 15L O2
Airways: Oral and nasal airway rescue ventilation at bedside; intubation ready to go.
Positioning and pre-oxygenation: high flow O2 on with patient in position to tube
Monitoring and medication: patient hooked up to monitor properly; all medication verified and drawn up
End tidal CO2: to verify proper intubation

MODS (multiple organ dysfunction syndrome)

progressive dysfunction of 2 or more organ systems from uncontrolled inflammation response from a severe illness. Sepsis and septic shock are the most common causes. MODS is the most common cause of mortality in the ICU. Mortality is 100% if there is failure of 5 or more organs (basically all of them)

cardiomyopathy

Dilated:
usually caused by ICM, valve disease, ETOH, renal failure, or infection.
Impaired systolic function leading to increases in intracardiac volume, ventricular dilation, and systolic HF.

SSX: JVD, pulmonary congestion, peripheral edema.., displaced apical pulse

Hypertrophic:
can come in two forms (1) Hypertrophic Obstructive CM (HOCM) and (2) hypersensitive or valvular hypertrophic CM (VHCM)

HOCM: most common inherited. Thickening of the septal wall may cause outflow obstruction to the LV outflow tract. This poses a significant risk for ventricular dysrhythmias.

VHCM: due to increased resistance to ventricular ejection. Usually in those w HTN or AS. Hypertrophy of the myocytes is due to compensation for the increased myocardial workload. we will see Diastolic dysfunction first, then Systolic dysfunction later on.

Restrictive:
restrictive filling and an increased diastolic pressure of either or both ventricles w normal systolic function and wall thickness.
Usually occurs w diseases such as scleroderma, amyloidosis, sarcoidosis, lymphoma, etc. The myocardium becomes rigid and noncompliant causing a decrease in ventricular filling and raising filling pressure.

Albumin

protein in blood; maintains the proper amount of water in the blood

Bodies priority of blood flow

Cerebral - 15% of blood flow
Cornaries - 5%
Renal - 25%
GI - 25%
Skeletal Muscle - 25%
Skin - 5%

Normal ECG Values

PR interval - 0.12-0.2; time from initial depolarization of the atria to initial depolarization of ventricles
QRS - <0.12; depolarization of ventricles
QT - <460; first ventricular depolarization to last ventricular repolarization
T wave - ventricle repolarization
P wave - atrial depolarization
QRS - ventricle depolarization

Cardiac Tropisms; Define each

Chronotropy - Heart Rate (SA Node)
Ionotrophy - Contractility via Ca loading
Dromotropy - Conduction through the AV node
Bathmotropy - Excitability via alteration of RMP
Lusitropy - Relaxation

Difference between hypoxia and hypoxemia

Hypoxia is a reduction in oxygen supply.The body's tissues are not adequately oxygenated. Examples- hyper-metabolic states, anemia, carbon monoxide poisoning. Hypoxemia is a reduction in the partial pressure of O2 in arterial blood (SaO2). examples- pneumonia, ards, PE

Vitamin K dependent clotting factors

II, VII,IX,X

Intrinsic vs extrinsic clotting

intrinsic pathway is activated by internal trauma.Collagen activates factor XII which starts the cascade. The clotting factors VIII, IX, XI, and XII are involved in intrinsic. The extrinsic pathway is activated by external trauma. Trauma causes the release of tissue factor which activates factor VII.Factor VII is the only extrinsic factor.
All lead to common pathway (X prothrombin which is activated to thrombin).

Warfarin

mechanism-works by inhibiting vitamin k dependent factors.
vitamin K is an essential cofactor for the activation of factors II, VII, IX, and X. These factors are synthesized as precursors, and require post-translational carboxylation by gamma glutamyl carboxylase. Reduced vitamin K is required as a cofactor for this reaction. In its absence, the secreted factors are inactive, and the extrinisic pathway is affected.
monitor Pt/inr which is extrinsic pathway because it affects VII the quickest and VII has shortest half-life of all vit K factors so it will show affect soonest

High oral bioavailablility (~ 100%)Maximum blood concentration about 90 minutes after administration

Terminal half-life of warfarin after a single dose is approximately 1 week;Effective half-life ranges from 20 to 60 hours

Lung Compliance

Can be thought of as volume changes as a result of pressure change. Usually in regard to the lungs and chest wall.

Lungs and chest wall are inversely correlated with their elastic properties. Example:
Consider two rubber bands. One thin, the other thick. The thin rubber band has a smaller amount of elastic "tissue" than the thick. It stretches easily and is very compliment. In contrast, the thicker rubber band has a larger amount of elastic "tissue" and is difficult to stretch and much less compliant, but when stretched, has the ability to snap back with greater elastic recoil.

Basically compliance is measuring the extent to which the lungs the lungs will expand (change in volume) for each unit increase in the trans-pulmonary pressure (gradient between alveolar and pleural pressure.

Lung compliance = Change in vol/Change in trans pulmonary pressure (alveolar - pleural pressure)

Why does this matter? Compliance determines 65% of the work of breathing. If the lung has low compliance, it requires more work from muscles to inflate the lungs. It is useful to understand to decide ventilation management.

What causes recoil? Elasticity (elastin (stretchable protien) and collagen) + surface tension (tension between molecules at the air-fluid interface)

Examples of increased compliance: emphysema (no recoil or elasticity)

Examples of decreased compliance: pulmonary fibrosis (very restrictive, all the recoil, cannot be elastic and expand)

Lungs with low compliance are stiff lungs and will require much greater pressure to reach a given volume compared to lungs that have high compliance. There are several factors that affect lung compliance including alterations in the ribs (ie. fractures), ossification of the costal cartilage, obesity, muscular or neural changes to intercostal muscles (ie. paralysis or strain/pain), po

isoproterenol

Isoproterenol is a beta-1 and beta-2 adrenergic receptor agonist indicated primarily for bradydysrhythmias.Bpth beta-1 and beta-2 adrenergic receptors exert their effects through a G-alpha stimulatory second messenger system.G-alpha protein dissociates from the intracellular domain and activates adenylate cyclase. Activated adenylate cyclase subsequently converts intracellular ATP to cAMP. The principal second messenger in this pathway, cAMP, activates protein kinase A (PKA). Activated PKA phosphorylates L-type calcium channels in cardiac myocytes, resulting in increased intracellular calcium. PKA also causes an increase in calcium release from ryanodine receptors on the sarcoplasmic reticulum.

onset- imediate

Dopamine

Vasopressin (pressor)

_____________________________________

V3 receptor subtype

V3 receptors are mainly found on cells within the central nervous system, especially in the adenohypophysis; their stimulation modulates corticotropin secretion.

Nitroprusside (Nipride) keep

Sodium nitroprusside is a water-soluble salt comprised of ferrous iron complexed with nitric oxide (NO) and five cyanide ions. Acting as a prodrug, SNP reacts with sulfhydryl groups on erythrocytes (as well as albumin and other proteins) to produce nitric oxide (NO). t does this by binding to oxyhaemoglobin to release cyanide, methaemoglobin and nitric oxide.Upon binding to vascular smooth muscle, NO triggers intracellular cGMP-mediated activation of protein kinase G and subsequent inactivation of myosin light chains, resulting in relaxation of vascular smooth muscle. The result of this signaling cascade is peripheral vasodilation of both arteries and veins (with slightly more selectivity for veins).

onset- less 2 minutes
half life- 2 minutes

can cause coronary steal
careful fo cyanide/thiocynate toxicity- Nitroprusside combines with hemoglobin and is subsequently metabolized to 5 cyanide ions and cyanmethemoglobin. Cyanide then converts to thiocyanate via rhodanese-mediated donation of a sulfur group (from thiosulfate or cysteine); this final step can quickly become overwhelmed with large quantities of the drug.

**Mainly arterial dilator; Converted to NO;
NO activates smooth muscle guanylyl cylcase (GC) to turn GTP to cGMP. Increased cGMP inhibits Ca entry into the cell therefore decreasing intracellular Ca concentration and causing smooth muscle relaxation; Additionally NO leads to activation of K channels causing hyperpolarization and further relaxation.

Nicardipine

precedex keep

Dexmedetomidine is an alpha agonist having sedative, anxiolytic, hypnotic, analgesic, and sympatholytic properties. It produces these effects by inhibiting central sympathetic outflow by blocking the alpha 2 receptors in the brainstem, thereby inhibiting the release of norepinephrine.α 2 receptors inhibit adenylyl cyclase activity and cause decrease of cyclic adenosine monophosphate (cAMP). PKA is not able to be activated by cAMP, so proteins such as phosphorylase kinase cannot be phosphorylated by PKA. neuronal hyperpolarization is a key element in the mechanism of action of dexmedetomidine and is achieved by efflux of potassium and suppression of calcium entry. Loss of intracellular potassium and inhibition of calcium entry suppress neuronal firing and can inhibit signal transduction.


Rapid administration can result in temporary vasoconstriction/hypertension. Alpha 2 receptors are stimulated which actually cause vasoconstriction.Dexmedetomidine and all the other imidazoline derivatives have peripheral α2-receptor effects on the vascular smooth muscle, which tend to produce vasoconstriction

Alpha-2-adrenoceptor stimulation resulting in inhibition of neurotransmitter release is mediated through a decrease in calcium-ion conductance. The decrease in calcium-ion conductance involves direct regulation of calcium entry by voltage-gated calcium ion channels

The most common adverse effects of dexmedetomidine are hypotension, bradycardia, and hypertension. Hypotension and bradycardia are the results of the stimulation of presynaptic alpha receptors, which leads to a decreased release of norepinephrine; this is in addition to the decrease in the central sympathetic outflow.

Maintains hypercapnic arousal response (in contrast to opioids which blunt this response).

onset- 5 mins
1/2 life- 90 mins

Etomidate (Amidate). keep

Etomidate has a favorable hemodynamic profile on induction, with minimal blood pressure depression, making it ideal for shock trauma, hypovolemic patients, or patients with significant cardiovascular disease.
Etomidate interacts with gamma-Aminobutyric acid type A (GABA) receptors by binding directly to specific sites and increasing the affinity of the inhibitory neurotransmitter GABA (positive modulation of GABA-mediated activity).[6] GABA is the principal inhibitory neurotransmitter within the central nervous system (CNS) and works with the adrenergic neurotransmitter system to counterbalance the action of excitatory neurotransmitters.

Etomidate binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.

Inhibits steroidogenesis (cholesterol converting to steroid hormones) which makes it no good to use long term as a drip

Initial 0.3mg/kg (range 0.2-0.6mg/kg) over 30-60 seconds for induction of anesthesia
Onset: 30-60 seconds
Dose: 0.2-0.6 mg/kg

Digoxin keep

its a cardiac glycoside
By inhibiting Na+/K+ ATPase, digoxin increases intracellular sodium, which increases sodium-calcium exchange by the Na+/Ca2+ exchanger during Phase 1 of the cardiac action potential.The resulting increase in intracellular calcium promotes inotropy. Sodium is generally pumped out of the cell by the activity of Na+/K+ ATPase, which means inhibiting it will increase the sodium availability, subsequent calcium entry, and therefore inotropy.It also acts as a vagotonic agent, which slows conduction through the AV node, and decreases the duration of the action potential mainly by reducing the duration of Phase 2. The slope of Phase 4 is increased, promoting automaticity, but then automaticity is overall suppressed by the vagotonic effects

side effects-Bradycadia, AV block, shortened QT interval, tachyarrhythmias (including VF and Vt which can be bidirectional), nausea, anorexia, depressed level of consciousness, and arterial vasoconstriction, main toxicity effects are n/v and cns visual changes

dig effects are potentiated by hypokalemia because it normally binds to the same spot as potassium

therapeutic level is .5-1.5

Arterial Line; How does it work? Explain damping,leveling, zeroing, flushing; Draw and label waveforms and explain what is happening in waveform.

Arterial cannula is inserted into the artery and connected to fluid-filled non-compliant tubing. The tubing is connected to a pressure bag which prevents any back flow of blood from the artery. Transducer or wheatstone bridge (wheatstone bridge - an electrical circuit used to measure an unknown electrical resistance) intercepts pressure signals from the artery and turns them into electrical waves that become interpreted into a waveform.

Damping is anything that absorbs a shock. This can be soft tubing, air bubbles, long or narrow tubing. These can decrease the amplitude of the oscillations. We used a flush test for damping purposes. Ideally we only see two bounces or oscillations. Over-dampened lines will lose their DN and will not have more than one oscillation. This is due to a clot at the catheter tip, air bubble in the tubing. Under damped will over estimate the systolic and there will be many oscillations post flush.

Zeroing is the use of atmospheric pressure (760 mmHg) as a reference standard which all other pressures are measured. Basically differs what is pressure in the atmosphere and what is pressure in the body.

Leveling is a point at which the zero is set or reference point. This is typically done at the phlebostatic axis which is at the mid axillary line and the 4th intercostal space. This point corresponds with the position of the right atrium and the aortic root. This relates to the idea that these points are also reference points for the bodies atrial and arterial baroreceptors where pressure is measured.
(For every 10 cm below the phlebostatic axis, there is an increase of 7.4mmHg of pressure)


The systolic upstroke (anacrotic limb) marks the systolic phase and can be correlated with the opening of the aortic valve and left ventricular contraction. The dicrotic notch correlates with the closure

Breathing; Explain the physiology. What is the pressure of the atmosphere?

A couple of things to note is the concept of diffusion and Boyles Law.

Amospheric pressure is 760 mmHg

Boyles law states that pressure and volume are inversely related ; as pressure decreases, volume increases and vis versa
Diffusion states that things always moves from HIGHER concentration to LOWER concentration in order to find equilibrium. The same applies regarding pressure.

Inspiration: As the diaphragm moves downward and intercostal muscles move outward, intrapleaural volume increases due to lung expansion and intrapleural pressure decreases. This causes the air from the atmosphere (which has a higher pressure) to move from higher pressure to lower pressure (the lungs).From there the air will continue to enter the lungs until the pressure in the lungs equal the pressure in the atmosphere. (760 mmHg)

Expiration: is, however is a passive process. The ventral respiratory group in the medulla is triggered by stretch receptors which tells the diaphragm and intercostal muscles to relax by decreasing their action potentials. The diaphragm then goes back up and volume in the lungs then decreases and pressure increases causing air to become exhaled.

cAMP; What is Cyclic AMP? What receptors can it affect? How does it work on these receptors? Give example.

Secondary Messenger

Receptors linked with decreased cAMP: M2 (cardiac inhibition) and M4 (CNS inhibition)
Receptors linked with increased cAMP: Beta-1 (cardiac contraction) & 2 (smooth muscle relaxation)

Example: epinephrine binds to beta receptor site on molecule > G protein becomes activated as GDP leaves and GTP comes in> GTP activates adenylyl cylclase and converts ATP into cAMP> cAMP activates PKA and leads in increased Ca into the cell

Central Venous Pressure; Normal value, label wave form and what each wave means.

Leveled at the phlebostatic axis to correlate with the right atrium. Usually the line is located in the SVC which have very similar pressures to the RA. Usually used to measure right ventricular preload and assess fluid responsiveness. (Normal value is 2-8mmHg)

a wave: atrial contraction (absent with a-fib); p wave

c wave: c is for cusp. The cusp of the tricuspid valve protruding backwards during RV contraction. QRS wave

x descent: atrial relaxation and downward movement of RV

v wave: blood filling the atrium; right after t wave; large V wave suggests TR due to the back flow of blood from RV contraction

y descent: decrease in pressure due to the early opening of the tricuspid valve in early ventricular diastole right before atrial contraction

Dead space VS Intrapulmonary Shunting

Both of these are known as V/Q mismatch or ventilation/perfusion mismatch.

Shunting is simply blood flow without ventilation. This can be seen in pneumothorax, atelectasis, pneumonia/ pulmonary edema (due to increased secretions blocking gas exchange. Capnography: Arterial CO2 will rise since it is not able to get exchanged due to lack of exam with oxygen; EtCO2 will decreases because no CO2 from the blood will be exchanged to be exhaled.

Dead space is ventilation without and blood flow to an alveoli. An example of this would be shock (decreased perfusion), PE/air emboli (blocked flow of blood), hypoxic pulmonary vasoconstriction (decreased lumen leading to increased resistance and decreased blood flow.

Dobutamine (Dobutrex)

Weaning Parameters

EtCO2; What is it? Describe the waveform.

Excellent for assessing ventilation status; Normal is about 33-37 mmHg
The exhaled amount of CO2 from the patient is absorbed by a infrared light emission source and then reach a detection point showing how much CO2 is present.
A - Describes the air the sensor first sees. This will be physiological dead space from portions of the lungs that do not undergo gas exchange (larynx, main stem bronchi, trachea)
B - alveolar air finally reaches the sensor
C - D; D alveolar plateau when the last of the CO2 is at the sensor; mostly alveolar gas
E - inhalation

Neuromuscular Junction Physiology

Within the neuromuscular junction, a stimulus causes an action potential and depolarization down the alpha motor neuron motor neuron (Na channels open causing Na to flow into the motor neuron -> voltage gated Ca channels open -> Ca causes acetylcholine to be released from their vesicles and into the synaptic cleft -> acetylcholine binds to acetylcholine gated receptor-channels (nicotinic receptors) on the motor end plate of the plasma membrane of muscle fibers -> motor end plate depolarize causing muscle contraction from influx of Na kickstarting action potential

Norepinephrine keep

Strong Alpha-1 receptor agonist; on the arterial side of the a1 receptors, we can see an increase in SVR, BP, and afterload; On the venous side of a1 of receptors we can see increased preload leading to increase SV and increased CO

Moderate Beta-1 receptor agonist; regarding nodal cells we will see increased conductivity or chronotropy; we also see increase activity of contractile cells leading to increased inotropy

First line for septic shock. Usually used for hypotension unresponsive to fluid replacement; cardiogenic shock

0.5-30 mcg/min
immediate onset; duration 1-2 min

Class: alpha beta adrenergic agonist (a1, a2, b1)

MOA: Direct stimulation of the adrenergic receptor. Predominant a, with modest b. Increases SVR and MAP with little change on HR/ CO. Can cause reflex bradycardia.


Considerations: caution w/ peripheral admin

-beta 1 (inotropy)
-alpha 1 and 2
-strong vasoconstrictor
-septic shock d/t peripheral vasodilation
-helps heart pumps too inc. CO

Used to increase mean arterial pressure after adequate fluid resuscitation, primarily acts on alpha-1 adrenergic receptors causing vasoconstriction, and commonly used as a vasopressor in septic shock and distributive shock.

Catecholamine Vasoconstrictor
Receptors: A 1&2 (vasoconstriction) and B1 (inotropy) A1>B1

AE: tachyarrythmias, angina, HTN, and local necrosis w/ extravasation. headaches, tremors, restlessness


Dose: 0-50 mcg/min

Parasympathetic; What nerves and what are the target organs? What controls the nerves?

CN 3, 7, 9, and 10 and the sacrum
Ocular motor, facial, glossopharyngeal, and vagus respectively. (This is the cariosacral outflow)

Remember: pre ganglion releases Ach and Post Ganglion releases Ach as well.

Hypothalamus can control the PNS

CN III (Occularmotor) acts on ciliary ganglion:
- Pupil; constrict

CN VII (Facial Nerve)
- Increases secretions by acting on salivary glands

CN IX (Glossopharyngeal)
- Secretions too

CN X (Vagus, controls 90% of PSN)
- Pulmonary Plexus: Bronchoconstriction, increased secretions
- Cardiac Plexus; mostly acts on nodal cells (SA and AV node) and decreases action potentials resulting in negative chronotropy

Propofol (Diprivan). keep

Acts on GABA A subunit causing prolonged opening of Cl- channels, leading to hyperpolarization of the postsynaptic cell -> cell having a more difficult time producing an action potential of a neuron because the RMP is now further away from the threshold potential > leads to inhibition of post synaptic neuron

Dose up to 50 mcg/kg/min
No antagonist

Fast on and fast off; onset is <1 min and duration is 3-8 min

Eliminated hepatic and renal

Monitor lipids, blood pressure

Decreased preload, mainly due to sympathetic inhibition.

Decreased afterload: systemic vascular resistance decreases with propofol.SVR dropped by about 30%. In short, arterial vasodilation is the effect of the sympathetic nervous system being turned off, and not a direct effect of propofol.

contractility is maintained. minimal effects on cardiac output

Succinylcholine keep

Used for induction; Depolarizing Neuromuscular Blocker
Onset is 30 sec, lasts 5-10 min
Eliminated through Plasma Cholinesterase, so it is NON REVERSIBLE

works by overwhelming the neuromuscular junction with acetylcholine causing a prolonged refractory period

Side effects: severe muscle contraction causing muscle fatigue, hyperkalemia due to activation of Na/K pump causing an outflow of K from the cells (watch out for arrhythmias)

Fasiculations from the strong muscle contraction during the increased acetylcholine release

Fasiculations can be decreased by giving a defasiculating dose of a non-depolarizing muscle blocker to take the space of acetylcholine on the nicotinic receptor on the motor end plate

Vent Circuit; Explain and draw out the typical ventilator circuit

This is a dual limb circuit. The ventilator is connected to a tubing the pushes humidified air into the patient. There are four potential positions for a bacterial viral filter. Exhaled air by the patient passes through the bacterial viral filter and is then released into the atmosphere

Voltage Gated Ion Channel?

Channel that opens and closes in response to changes in membrane potential.

Epinephrine (Adrenaline) keep

Strong beta agonist in lower doses; increased chronotropy via nodal cells and inotropy via contractile cells
In higher doses, an alpha-1 agonist; increased SVR and venous return
Additionally a Beta-2 agonist, acts on bronchioles resulting in bronchodilation; acts on mast cells decreasing histamine release (histamine causes bronchoconstriction);
**epinephrine acts on beta-2 receptors in liver causing rise in lactate via stimulation of glycogenolysis

Indications: Cardiogenic shock, septic shock, symptomatic bradycardia, anaphylaxis

A special note regarding epinephrine. Its binding to Gs-protein-coupled β2-adrenoceptors versus Gq-protein-coupled α1-adrenoceptors is concentration dependent because β2-adrenoceptors have a higher affinity for epinephrine than α1-adrenoceptors. Therefore, at low epinephrine concentrations vasodilation occurs, whereas at high concentrations vasoconstrictor responses become dominant. It generates more pyruvate then the cells are able to uptake via citric acid cycle and thus excess pyruvate turns into lactate. Excess lactate then can be reconverted into pyruvate and participate in aerobic metabolism under oxygenated conditions.

Dose: 0.02 - 0.2 mcg/kg/min
Onset: 1-2 min
Duration: 2-10 min

Class: alpha/beta adrenergic agonist.

MOA: Direct stimulation of adrenergic receptors. Increase BP. Positive Inotrope, chronotrope and peripheral vasoconstriction.


Dose: 0.01-0.05 mcg/kg/min b>a. 0.06-1 mcg/kg/min a>b

Onset/Duration: <5 minutes

Metabolism: liver, kidney, peripheral tissues. Monoamine oxidase

Considerations: dose dependent, increases myocardial o2 consumption. Stimulates increase in lactate from skeletal muscles via glycolysis and pyruvate generation

A catecholamine released by the adrenal medulla,


a1 b1 b2 agonist.

lowest doses b2 bronchodilation

typical doses positive inotrope primarily b1

higher doses a1

Catecholamine inopressor
Receptors: A1 & 2/B1 & 2
Result: increase BP, HR, CO, PRV and bronchodilation
AE: tachyarrthmias, angina, necrosis w/ extravasation, hyperglycemia (B2 breaks down glycogen), increases lactate even though perfusion is improved
Dose: 0-0.3 mcg/kg/min
Low dose acts more on B1 (inotropy)
High dose acts more on A1 (vasoconstriction)]

Stimulates alpha 1, beta 1 and beta 2 adrenergic receptors resulting in relaxation of smooth muscle of the bronchial tree, cardiac stimulation (increase myocardial oxygen consumption), and dilation of skeletal muscle vasculature

small doses can cause vasodilation via beta 2 receptors.

large doses may produce constriction of skeletal and vascular smooth muscle (alpha effects predominate)

-alpha 1 and 2
-Beta 1 and beta 2
-mcg/kg/min
-anaphylaxis (relax bronchial smooth muscle) .05 to .1 mg IV q5 min
-use in heart failure when the patient is severely hypotensive (.5 - 20 mcg/kg/min)
-use in cardiac tamponade

Phenylephrine Keep

Phenylephrine is primarily an alpha-1 adrenergic receptor agonist with minimal to no beta-adrenergic activity; therefore, it is ideal for elevating mean arterial pressure. It does so by causing venous and arterial vasoconstriction and increasing cardiac preload without having any significant direct effect on cardiac myocytes.

The α1-adrenoceptors are the predominant α-receptor located on vascular smooth muscle. These receptors are linked to Gq-proteins that activate smooth muscle contraction through the IP3 signal transduction pathway and Rho-kinase pathway.

Because of phenylephrine's sole alpha-receptor stimulation, it can cause baroreceptor-mediated reflex bradycardia; due to the increase in BP the baroreceptors in the carotid sinus sense this and relay this to the cardiovascular centres in the medulla. in order to remain in homeostasis the vagus nerve stimulates the release of ACh to bind to M2 (Gi pathway) receptors in the cardiac nodal cels resulting in decreased HR.

1/2life- 2.5-3hrs
pressor duration- 10-15 mins
onset immediate

Milrinone keep

Inodilator; the most potent of all inodilators
PDE3 inhibitor preventing cAMP breakdown;

INOTROPY PORTION:
cAMP plays in important role in cardiac muscle contraction. Activation of the SNS causes the release of endogenous catecholamines which bind to Beta-1 Receptors that are couple with Gs-proteins. The Gs proteins activate adenylyl cyclase to form cAMP form ATP. cAMP increases contractility, heart rate, and conduction velocity. cAMP is broken down by phosphodiestase (PDE) into AMP making it useless.

VASODILATION PORTION:
One major thing to note is that cAMP causes relaxation in smooth muscle, because it inhibits myosin light chain kinase (enzyme responsible for phosphorylation of smooth muscle myosin and causing contraction) Beta-2 agonists stimulate the Gs protein complex and form cAMP. Normal cAMP is degraded by PDE, but due to PDE3 inhibition, cAMP can increase and causes smooth muscle relaxation in the vessels.

Indications: Heart failure, afterload reduction, increase in contractility. Cardiogenic shock.

Renally cleared, can accumulate and cause major vasodilation.

Hydralazine Keep

Hydralazine is a direct arteriole vasodilator. theorized to be associated with intracellular calcium homeostasis. Specifically, it acts to inhibit inositol trisphosphate (IP3)-induced release of calcium from the smooth muscle cells sarcoplasmic reticulum and inhibits myosin phosphorylation within the arterial smooth muscle.This reduces peripheral vascular resistance and leads to a compensatory baroreceptor-mediated release of epinephrine and norepinephrine, which, as a result, increases venous return and cardiac output. Given hydralazine's stimulation of the sympathetic nervous system, it consequently leads to tachyphylaxis and tachycardia. It is sometimes given with a beta-blocker or diuretic for better patient tolerance

another proposed mechasnism-hydralazine causes smooth muscle hyperpolarization through the opening of K+-channels.

For oral dosing, the blood-pressure-lowering effects occur within 20 to 30 minutes with a total duration of 2 to 4 hours.

contraindicated- Coronary artery disease: this is due to hydralazine's stimulation of the sympathetic nervous system. This leads to increased cardiac output and oxygen demand which can provoke myocardial ischemia.

Isosorbide keep

Isosorbide undergoes bioactivation (prodrug) in the endoplasmic reticulum through the cytochrome P450 enzymes to release NO which activates the enzyme soluble guanylyl cyclase in the vascular smooth muscles, thereby increasing the levels of intracellular cGMP and the associated protein kinases such as cGMP- dependent protein kinases(cGK-I). The cGMP activates the myosin light chain phosphatase (MLCP), causing dephosphorylation of the myosin light chain. cGMP-cGK-I inhibits the (IP3)-dependent calcium release, decreasing the intracellular calcium.
The decreased intracellular calcium inhibits the myosin light chain kinase(MLCK). The MLCK, along with the unphosphorylated myosin light chain, causes the myosin head to detach from the actin component of the smooth muscle, resulting in smooth muscle relaxation and causing vasodilation. Isosorbide dilates the venous capacitance vessels, arterioles, and coronary arteries. But Its maximal effect is seen in venous capacitance vessels.

oral dinitrate-4-6 hrs
oral mononitrate- 6-10hrs

contraindications-PDE inhibitors such as tadalafil and sildenafil work by inhibiting the phosphodiesterase (PDE) enzyme, which is involved in breaking down the cGMP. Concomitant use of isosorbide with PDE inhibitors will cause increased cGMP, resulting in life-threatening hypotension

Propofol infusion syndrome

it is characterized by profound metabolic acidosis and bradycardia which may ultimately lead to cardiac arrest.

proposed to be caused by either "a direct mitochondrial respiratory chain inhibition or impaired mitochondrial fatty acid metabolism

Since propofol is formulated in a lipid emulsion, the solvent, as well as the drug itself, contribute to hyperlipidemia and hypertriglyceridemia. The accumulation of free fatty acids promotes cardiac arrhythmias.

Diltizem

Nitroglycerin

As with other nitrates used to treat anginal chest pain, nitroglycerin converts to nitric oxide (NO) in the body. NO then activates the enzyme guanylyl cyclase, which converts guanosine triphosphate (GTP) to guanosine 3',5'-monophosphate (cGMP) in vascular smooth muscle and other tissues. cGMP then activates many protein kinase-dependent phosphorylations, which enhances the reuptake of calcium into the sarcoplasmic reticulum, increases extracellular calcium, and opens the calcium-gated potassium channel.This ultimately results in the dephosphorylation of myosin light chains within smooth muscle fibers. This activity causes the relaxation of smooth muscle within blood vessels, resulting in the desired vasodilatory effect.

The risk of syncope significantly increases with the concurrent use of a phosphodiesterase-5 (PDE-5) inhibitor.

Impella facts

impella 2.5, CP,5.5,RP

can be used for high risk pci, cardiogenic shock

purge system works by creating a barrier of purge fluid flowing in the opposite direction as the blood flow. purge pressure must be higher than systolic
purge pressure is automated to be at least 300 mmhg.

lowers lvedp which lowers wall stress which lowers myocardial contractility which helps decrease myocardial oxygen utilization. Lower wall stress combined with coronary perfusion of impella improves coronary blood flow

direct flow devices unload ventricle so raises diastole and raises map

Clevidipine keep

Clevidipine is a dihydropyriodine. It is a lipid emulsion.clevidipine inhibits L-type calcium channels in a voltage-dependent manner and exhibits a high degree of vascular selectivity in vitro. The BP-lowering effects of the drug are rapid and dose dependent, and are achieved by decreasing systemic vascular resistance .

Offset of effect within 5-15 minutes. Clevidipine had greater effects on arterial vasodilation and lesser effects on venodilation compared with sodium nitroprusside.

elimination- Dosing of CLEVIPREX is independent of hepatic and renal function due to metabolism by plasma and tissue esterases.The initial phase is rapid (half-life of approximately 1 minute) and accounts for the majority of clevidipine exposure after an intravenous bolus dose and for 85-90% of its elimination; the terminal elimination half-life is approximately 15 minutes.In most patients, full recovery of BP is achieved 5-15 minutes after the infusion is stopped.

transvenous pacemaker

indications- Unstable Bradycardia (2nd Degree II or 3rd Degree Heart Block)
Sick Sinus with Pauses
Overdrive Pacing for unstable tachydysrhythmias, especially Torsades de Pointes (polymorphic VT due to long QT)
Sometimes: Prophylactic for new LBBB or RBBB with left axis deviation due to acute MI

Inserted typically through RIJ. It is threaded into RV. preferences of sites- RIJ >> L Subclav >> LIJ >> R Subclav >> Femoral

will only be VVI mode because it cannot see or pace the atria. The tip is ideally located in apex of RV.

if loss of capture try increasing MA or left lateral decubiits. If pt unstable start transcutaneous pacing, epi push/drip, atropine, dopamine if you have to.

Highlight TTM / side effects of cooling

Mechanism- Hypothermia decreases the metabolic rate by 5% to 7% per 1 C decrease in core body temperature.This is one of the main mechanisms underlying its protective effects since oxygen deprivation and the accumulation of lactate and other waste products of anaerobic metabolism are central to the progression of ischemic cerebral cell death. The accumulation of aspartate, glutamate, and other excitatory neurotransmitters also plays a significant role in neuronal death following cerebral ischemia. The severity of excitotoxicity and neuronal damage is proportional to the quantity of these neurotransmitters.Hypothermia decreases production and suppresses the various inflammatory processes that occur following global ischemia and reperfusion.

The inflammatory response that follows reperfusion has both beneficial and detrimental effects, with some mediators being transiently neuroprotective. However, this exaggerated response may last up to 5 days, and persistently high levels of cytokines are destructive over this protracted time course. Hypothermia suppresses the inflammatory cascade and, in turn, prevents the exacerbation of cerebral injury by inflammation.

Adenosine keep

Purinergic adenosine receptors found throughout the body. There are four types of adenosine receptors: A1, A2a, A2B, and A3, affecting the immune, nervous, circulatory, respiratory, and urinary systems. Most notably, receptors found in the cardiac atrioventricular (AV) nodal tissue and within the peripheral vasculature are what exhibit clinical manifestations when administering adenosine.

It acts on receptors in the cardiac AV node, significantly slowing conduction time. This effect occurs via the A1 receptor, adenosine inhibits adenyl cyclase, reducing cAMP and thus causing potassium to flood out of the cell and inhibiting calcium entry it reducing its positive ion content and thus hyperpolarizing. hyperpolarization of the resting membrane potential while slowing of calcium influx causes suppression of calcium-dependent action potentials, all requiring a longer time for depolarization to occur and thus slowing down conduction within these cells, which is useful in SVT. This is basically what the vagus nerve does, but it bypasses the whole acetylcholine business.

Adenosine has a role in slowing down the heart rate enough to assist in diagnosis. It can also terminate specific reentrant tachycardia involving the AV node, including AV nodal reentrant tachycardia (AVNRT), orthodromic AV reentrant tachycardia (AVRT), and antidromic AVRT.

Inverse Ratio Ventilation ( just feel like we need to know it)

normal i:e ratio- 1:2

prolonged inspiratory time with decreased expiratory. decelerating insp flow pattern. use pressure control

increased oxygenation by increasing mean airway pressure(MAP). The primary determinants of MAP are PEEP, inspiratory pressure, and time spent on each phase.MAP correlates with mean alveolar pressure and thus transpulmonary pressure. Though multiple factors are involved, increased transpulmonary pressure increases gas exchange, notionally improving oxygenation. The primary purpose of IRV is to increase mean airway pressure by increasing the time spent on the higher pressure portion of the cycle. This allows the increase of MAP while minimizing the risk for pulmonary injury relative to other aggressive oxygenation strategies.

complications-
Though IRV requires lower peak pressures to achieve the same MAP compared to conventional ventilation, the average pressure in the lungs is increased overall. Thus the patient remains at increased risk for barotrauma. Volume trauma may also occur if there is a high gradient between the P-high and P-low.

Auto-PEEP (also called breath stacking or air trapping) occurs when a patient cannot wholly exhale a breath before the next inspiratory phase begins, resulting in elevated airway pressures. IRV may potentiate this process due to the relatively short expiratory phase or P-low time. There are indications that this auto-PEEP effect may benefit oxygenation in IRV; however, the increased pressures may exacerbate lung trauma and hemodynamic stress. Patients with preexisting obstructive disease (COPD/asthma) who rely on prolonged expiratory times are at increased risk.

IRV increases oxygenation by increasing MAP, which has the additional consequence of increasing the average intrathoracic pressure. Similar to the hemodynamic effects seen with high PEEP, increas

purpose of surfactant

secreted by epithelial cells type 2
1.lowering surface tension at the air-liquid interface and thus preventing alveolar collapse at end-expiration, (2) interacting with and subsequent killing of pathogens or preventing their dissemination, and (3) modulating immune responses.

part 2 and 3 are very dense and beyond worth diving into for this. in summary there are 4 surface proteins and they each play a role in function on point 2&3.

high peak pressure vs low peak pressure

High peak/ low plat - Airway resistance, not compliance problem
Kinked tube- pass suction catheter
Mucus plug- pass suction catheter and suction
Bronchospasm- inhaled bronchodilators
Tube too small- swap tube

High peak/high plat- Suggests decreased compliance, not an isolated resistance problem
Mainstem bronchus- pull back ETT, CXR
Atelectasis- bronchoscopy
Cardiogenic pulmonary edema-diuretics vs inotropes
ARDS- lower V
tPneumothorax- Chest tube
Pneumonia- Antibiotics

low peak- meaning theres a disconnect between vent and patient
work from vent to patient to find it.
ET balloon might have ruptured
if cannot remedy solution quickly ambu bag pt

Amiodarone keep

• Class III anti-arrhythmic.

• Works by blocking potassium rectifier currents responsible for the repolarization of the heart during phase 3 of the cardiac action potential. This potassium channel-blocking effect results in increased action potential duration and a prolonged effective refractory period in cardiac myocytes. Myocyte excitability is decreased, preventing reentry mechanisms and ectopic foci from perpetuating tachyarrhythmias. Electrocardiographic evidence of these effects is evident as prolongation of the QRS duration and QTc interval.
  
  Class 2-beta adrenergeric receptors. Amiodarone is described as a beta-blocker, but it does not "block" the beta-receptor per se. In fact it also has alpha-"blocker" effects. it is a non-comptetitive blocker, which also happens to markedly reduce the number of catecholamine receptors on the myocardial muscle, as well as interfering with the intracellular regulatory unit of adenylate cyclase.
  class 4-calcium channels-Amiodarone appears to have a nonselective L-type calcium channel blocker effect, analogous to that of verapamil and diltiazem. mild peripheral vasodilator effect in high doses.
  class 1- sodium channels- voltage-gated sodium channels are blocked by amiodarone. it markedly decreases the upstroke velocity of Phase 0
  
  side effects:

peak vs plat pressures

peak-this is the pressure that is generated by the ventilator to overcome BOTH airway resistance AND alveolar resistance. The goal of the pressure is to obtain the set inspiratory flow and the tidal volume goal that is set by the provider.
Peak inspiratory pressure = (Resistance x Flow) + (Elastance of respiratory system x Tidal volume) + PEEP

if it is a high peak but normal plat these are causes:
-Kink in the circuit: examine ventilator tubing
-Fluid accumulation: clear the fluid from the circuit
-Biting the ETT: increase sedation or insert bite block
-A small ETT with biofilm forming: consider changing out the tube
-High flow rate or tidal volume: adjust ventilator settings
-Ventilatory asynchrony: increase sedation
-Laryngospasm or bronchospasm: consider steroids, epinephrine
-Mucous plugging: clear out ETT
-Foreign body: removal

plat-This is the pressure that is essentially left over in the lung after the tidal volume has been delivered.
Plateau pressure = Tidal Volume/Compliance at zero flow.

to measure plats n inspiratory hold has to be done on the ventilator. This is where the ventilator pauses for several seconds after the tidal volume has been delivered, which eliminates flow, and thus, airway resistance.

This number is a reflection of the compliance of the lung. If the lung is very compliant as in patients with COPD, the plateau pressure is lower. If the lung is not compliant, as in patients with ARDS or fibrotic lung disease, the plateau pressure will be high.

high peak and high plat= issue with complaince
-Pneumonia
-Pulmonary edema
-Auto PEEP: this is seen in breath stacking where the patient does not have a full exhalation. It is common in COPD and reactive airway diseases.
-Right main stem intubation
-Pneumothorax
-Atelectasis, pulmonary fibrosis, and even abdominal issues like abdominal compartmen

H's&T's

important to eliminate reversible causes of cardiac arrest

5 H's
H ypoxia
H ypovolemia
H ydrogen ion (acidosis)
H ypo / H yper kalemia
H ypothermia

5 T's
T ension pneumothorax
T amponade
T oxins
T hrombosis (pulmonary)
T hrombosis (coronary)

Lasix

mechanism- loop diuretics in general, are so called because they act on the thick ascending limb of the loop of Henle. There, furosemide competes with chloride for the chloride pore of the main transport protein (NKCC2). The result is a failure to transport anything (as the co-transported only works when all the ions are available). Blockade of the NKCC2 transporter decreases the reabsorption of sodium potassium and chloride in the thick ascending limb
This increases the delivery of sodium potassium and chloride to the distal nephron.There, sodium is reabsorbed by aldosterone-regulated ENaC channels.As body water volume decreases with frusemide therapy, so the reabsorption of sodium here escalates, as aldosterone is released in response to hypovolemia.Potassium removal via the urine is also increased because of sodium and potassium being exchanged with the tubular fluid
Chloride and ammonium elimination is also increased, as ammonium is an alternative substrate for NKCC2

mechanism of hypokalemia-
The ENaC channel reabsorbs sodium in the collecting duct.This generates an apical transmembrane potential, as positively charged ions are being removed from the lumen of the duct.This negative apical membrane charge produces a movement of potassium out of the cells via the ROMK channel.In this fashion, sodium is exchanged for potassium in the collecting duct
Thus, increasing the delivery of sodium to the distal nephron creates an increased potassium excretion.

side effects-
Metabolic alkalosis (hypochloraemia)
Hypernatremia (as sodium is retained)
Hypokalemia (as potassium excretion is increased by the increased sodium delivery to the distal nephron)
The increased delivery of chloride to the distal nephron results in urinary acidification.

time- Effect lasts for six hours; half life is about 30-120 minutes
elimination-

Diuril (Chlorothiazide) keep

Target receptor- NCC sodium/chloride cotransporter in the distal convoluted tubule
mechansim- By decreasing the reabsorption of sodium and chloride in the distal convoluted tubule, thiazides block the reabsorption of up to 5% of the total filtered sodium. This increases the delivery of sodium and chloride to the distal nephron. The increased solutes in the collecting duct lumen decrease the osmotic gradient between the duct and inner medulla, preventing water reabsorption in the collecting duct, resulting in diuresis.
Thiazides inhibit sodium reabsorption in the distal convoluted tubule.Thiazide monotherapy has a relatively weak diuretic effect (because not much sodium is generally reabsorbed in the distal convoluted tubule).Patients being treated with loop diuretics will tend to reabsorb more sodium in the distal convoluted tubule due to it not being reabsorbed earlier. Thus, adding a thiazide in combination with a loop diuretic may substantially augment the efficacy of the loop diuretic.

the physiologic problem that drives occult diuretic resistance is avid sodium retention by the remainder of the nephron (especially the distal convoluted tubule). Addition of a thiazide diuretic blocks this, preventing sodium absorption in the distal convoluted tubule and thereby increasing urinary sodium excretion (natriuresis). This promotes balanced excretion of both sodium and water, causing effective volume loss without hypernatremia.

elimination- Virtually all of the dose is eliminated renally; half life is 6-9 hours

Heparin keep

Mechansim-Heparin is present in the body in the secretory granules of mast cells in humans, heparin enhances the activity of antithrombin-III by a factor 1000. It does this by binding to antithrombin III and causing the active site to undergo a conformational change.By binding to antithrombin III and causing the active site to undergo a conformational change, heparin increases its availability to its normal ligands, including factor Xa and thrombin. The result is an increase in the activity of antithrombin, which manifests in the form of the anticoagulant effect

Being a huge molecule, unfractionated heparin does not penetrate the placenta, anticoagulant of choice in pregnancy.

can cause hyperkalemia due to aldosterone suppression

difference between heparin and LMH (lovenox)- The inactivation of thrombin depends on heparin molecule length. On the other hand, inactivation of Xa is independent of length: so long as any sort of heparin is bound to it, antithrombin-III will inactivate Xa. This underlies the difference in pharmacodynamic of low molecular weight heparin and unfractionated heparin.Thus, in summary, unfractionated heparin affects thrombin, whereas low molecular weight heparin only affect

Heparin Antidote

Protamine Sulfate
strongly alkaline polypeptide which binds to strongly acidic heparin irreversibly, and thereby decreases its anticoagulant effect on antithrombin-3.

adverse effects-
-Catastrophic hypotension due to vasodilation, which is thankfully brief (only about 3-4 min) - this seems to be the result of systemic histamine release, triggered in some sort of directly-complement-activating way by the circulation heparin-protamine complexes
-Pulmonary hypertension due to the localised vasoconstrictor activity of thromboxane, activated by an anaphylactoid reaction to protamine
-Anaphylaxis (it is after all a fish product)

1mg reverses 100 units
No more than 50mg at any one time

Cisatracurium (Nimbex) keep

Class: Neuromuscular blocking agent, non depolarizing.

MOA: Binds competitively to cholinergic receptors on the motor end plate, antagonizing acetycholine, resulting in neuromuscular transmission blockade. Action is antagonized by acetylcholinesterase inhibitors such as neostigmine.

Adult IV Push: 0.12- 0.2mg/kg

Adult Drip Rate: Initial 2-5 mcg/kg/min (range 0.5-10.2mcg/kg/min).

Onset Duration: 1.5-3.3 minutes/ 40-90 minutes

Metabolism: Hofmans elimination (pH and temp dependent), metabolites cleared renal/hepatically. Laudanosine and monoquarternary alcrylate (hofmans, MQ alcohol, hepatic, conjugated and excreted).

Esmolol (Brevibloc) keep

Class: Beta blocker, B1 selective.

MOA: directly inhibits cardiac b1 receptors. Decrease HR, increase in sinus cycle length,

Loading Dose: 250-500mcg/kg over 1 minute

Maintenance Dose: 15-300mcg/kg/min

Onset/ Duration: 5-10 minutes, half life 9 minutes, duration 20-30 minutes

Considerations: caution in pts with inadequate myocardial fx since CHF may be precipitated by B-adrenergic blockade

Isoproterenol (isuprel) keep

Class: Nonselective beta-adrenergic agonist.

MOA: Stimulates b1-2 receptors, relaxes bronchial, GI and uterine SM. Increases HR, contractility and vasodilation of peripheral vasculature

Dose: 0.5-20 mcg/min

Onset/duration: Immediate/ 10-15 minutes.

Generally titrated to a specific HR

Ketamine keep

Class: dissociative agent, NMDA- receptor blocker

MOA: NMDA- receptor blocker

Pain dosing: 0.1-0.3 mg/kg/hr

Onset : <30 seconds, bolus 1-4.5 mg/kg over 1-2 minutes (usual dose ~100mg)

Misc: Pre-medicating with benzos (versed) can help reduce hallucinations

Lidocaine keep

Class: 1b antiarrythmic, Na channel blocker.

MOA: Block sodium channels, limit electrical conductance over the cell membrane and reduce the rate of depolarization. class 1b decrease duration ofaction potential.

Loading dose: 1-1.5mg/kg, can repeat with 0.5-0.75mg/kg if needed.

Maintenance: 1-4mg/min

Onset/duration: 45-90 seconds/ 10-20 minutes

Toxicity: normal serum 1.5-5. >5, tox. seizures, coma, etc.
drowsiness, impending doom, HA, tongue paresthesia, etc., methemoglobinemia

Nicardipine (Cardene) keep

Tirofiban (Aggrastat)

Class: glycoprotein IIb/IIIa inhibitor

MOA: inhibits platelet fx by binding GP 2b/3a receptor (primary platelet surface receptor responsible for aggregation)

Mixture: 25mg/500mL [50mcg/mL]

Loading dose: 25mcg/kg over 5 min

Dose: 0.15mcg/kg/min

Onset/ Duration: <10 min/ 4-8 hrs

Cosiderations: renal imp. dose is 0.075 mcg/kg/min

Vasopressin (Vasostrict) keep

Carvidilol keep

Lisinopril kep

What is the reversal for narcotics

narcan 0.3mg/ 0.4-2 mg IV/IM/SC; repeat q2-3min PRN; not to exceed 10 mg (0.01 mg/kg)

SE:V-fib/ SVT, r/t pain SNS surge

Whats the reversal for benzos

Flumanizel

0.2 mg IV over 15 sec
IF after 45 sec no response, administer 0.2 mg again over 1 min; may repeat at 1 min intervals; not to exceed 4 doses (1 mg)

Antidote for heparin

protamine sulfate

Cranial Nerves

I. Olfactory
II. Optic
III. Oculomotor
IV. Trochlear
V. Trigeminal
VI. Abducens
VII. Facial
VIII. Vestibulocochlear
IX. Glossopharyngeal
X. Vagus
XI. Accessory
XII. Hypoglossal

Normal values of ICP
CO
CI
MAP
Cerebral perfusion pressure
Coronary Perfusion Pressure
SVR and PVR

• ICP-normal is 0-10mmHg, 11-20 is moderately high, increased is >20mmHg.

• Coronary Perfusion Pressure- is the difference between the aortic diastolic pressure and left ventricular end-diastolic pressure (LVEDP) normal is 60-80mmHg.

• CO=HRxSV normal is 4L-8L/min, the amount of blood pumped through the body in one minute

• CI-takes into account body surface area and is more meaningful than CO normal is 2.5-4 L/min/m2MAP- the average pressure in a patient's arteries during one cardiac cycle. ((2xDBP) + SBP)/3
  Cerebral Perfusion Pressure-=MAP-ICP average is 80-100mmHg minimum for perfusion is 50 and brain death is <30mmHg,
  SVR-systemic vascular resistance & PVR-pulmonary vascular resistance-afterload of the right ventricle

Review clotting factors both intrinsic and extrinsic

intrinsic coagulation pathway is stimulated by a vascular endothelial injury- cell trauma(valve, IABP), sepsis, shock, ARDS, hypoxemia, acidemia, cardiopulmonary arrest. Extrinsic coagulation pathway is stimulated by tissue injury and releases tissue thromboplastin-extensive trauma, OB emergencies, malignancies, dissecting aortic aneurysm, extensive MI.

What is vitamin K dependent clotting factors

Prothrombin, FVII, FIX, protein C, and protein S

What is the difference between Coumadin and Heparin, which one works on the intrinsic and extrinsic pathway

Coumadin works on conversion of prothrombin and inhibits the vitamin K. Heparin works on the thrombin and inhibits thrombin.

What clotting factors make up Cryo

Fibrinogen.

What lab test are used to monitor Heparin

APPT AntiXA

What lab test is used to monitor Coumadin

INR

What are the pain receptors

mu1, mu2, kappa & delta

How much more potent fentanyl is then morphine

100x

What is protamine sulfate is made from

salmon sperm

PEEP (Positive End Expiratory Pressure)

positive pressure at the end of exhalation, creates more surface area for gas exchange, increases alveolar recruitment. Oxygenation.

What is the percentage of O2 in 2LNC?

Face mask?

Nonrebreather?

2L-28%

5L-40%

Nonrebreather 60-80%

What is the difference between LR and NS

normal saline-154mmols Na+ and 154 of Cl-, isotonic crystalloid, effects las about 40mins then leaves vascular space, large volumes may lead to hyperchloremic acidosis. Do not give with hypernatremia or renal failure. &
LR-Has 130mmols of Na+, 109 Cl-, 4K+, 2.7 Ca++, 28 lactate. Isotonic crystalloid lasts 40 mins then leaves vascular space. Best mimics extracellular fluid minus proteins, recommended resuscitation fluid by the ACS committee on trauma, has the potential to correct lactic acidosis yet in severe hypoperfusion it may promote lactic acidosis due to lactate accumulation. Do not give through a blood product transfusion line or to those who should not get K+ or lactate.

trace a drop of blood through the heart

into the superior and inferior vena cava->right atrium-> tricuspid valve-> right ventricle->pulmonic valve->pulmonary artery-> lungs oxygenated back to the heart through the pulmonary veings-> left atrium-> mitral valve->left ventricle->aorta->rest of the body

What is the difference between: LMA and ETT

Laryngeal mask airways can maintain a patent airway when ETT is neither required or desired-asthmatic pt's- ETT can cause tracheal trauma, laryngeal edema and other negative effects.

What is the autonomic nervous system:

sympathetic-fight or flight vs. parasympathetic-rest and digest

What are the receptors associated with sympathetic

(alpha, beta, dopa)

What are the receptors associated with parasympathetic nervous system

(muscarinic & nicotinic)

Where is renin secreted from? angiotensin 1? angiotensin 2?

What do they do?

Renin-kidneys, Angiotensin-liver
liver makes angiotensinogen and kidney makes renin that turns it to angiotensin 1 then ACE turns it to angiotensin 2. A system to regulate blood pressure, when bp falls kidneys release renin to increase bp. So ace inhibitors lower bp

What size of endotracheal tube for male and female

male (7-8mm) & female (6-7mm)

What is the difference between a pacemaker and AICD

AICD will defibrillate if lethal rhythm detected. Pacemaker has set rate so the patient doesn;t fall below threshold

What is the name of drugs that are ARBS

Angiotensin receptor blockers
(Diovan)