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I am a Southern American RN BSN working nights in cardiothoracic ICU with an adult ECMO and MCS specialty.

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got into NP school. start august 23. been busy gettin things in order!

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NP school

i am ACTUALLY applying for fall 2018 start in a dual FNP/AGACNP program. here is hoping

[hansonsanatomy]

The dreaded PE

[caringintensely]

No.

Talk about setting an impossible standard. Talk about empty words that set new nurses up for disappointment.

New nurses, hear me.

YOU WILL have days when your compassion runs dry and you take care of your patient simply because it’s your job, and you have to, not because you are some kind of angel.

YOU WILL pull another nurse into the med room to chew out the family member who is driving you insane.

YOU WILL cause your patient pain. With just about everything you go into the room to do. Heparin shots, enemas, dressing changes, repositioning patients in pain, making them get out of bed after surgery when all they want to do is rest. You will do these things because it is for their good, and because recovery is painful and they need someone to lead them through it.

And you will have a day when you drive home from the hospital and cry and come to the conclusion that nursing was a huge mistake, you can’t do it, it’s too hard.

If we don’t tell you to expect it, you may not realize that you are incorrect and that you’re simply coming to grips with the reality of a profession that can push you to your limits in every way.

We have a high calling as nurses, but don’t romanticize it too much in your mind. We’re just people.

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Pre-renal: decreased perfusion

decreased volume

decreased albumin

restrictive cardiac disease

Intra-renal: tubular or glomerular defect

Post-renal: outflow obstruction

[sarcasticbabywhispererjess]

The fastest way to stabilize your patient that won’t stop coding... make them a DNR. Works every time.

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[thefuturern]

Increased Intracranial Pressure

(>20 mm Hg) Due to a rigid and fixed skull, there is no room for any additional fluid, blood, or lesions. Additional matter without an expansion of volume, especially, creates increased pressure. Increased intracranial pressure is very serious and could lead to brain herniation and subsequent death.

Causes

Brain tumors

CNS infections

Cerebral edema

Intracranial bleeding

Excess CSF

Manifestations

Changes in level of consciousness (LOC) ***often the first indication***

Glasgow Coma Scale measures LOC via eye, motor, and verbal responses to stimulus from the environment. It scores from 3-15 w/ 8 being the “magic number” - think magic 8 ball. If you shake it up, or stimulate it, and a number < 8 appears a severe coma is present. 9-12 represents a moderate coma. 13-14 represents a mild coma.

Blurred vision

Coma

Decerebrate posture (extension of arms indicative of brain stem involvement)

Diplopia

Doll’s eye phenomena

Headache

Projectile vomiting

Behavior changes

Seizures

Cushing’s reflex (as manifested by Cushing’s triad):  increased BP w/ widening PP (peripheral resistance increased to shunt blood towards the oxygen-needy brain), decreased pulse rate (in a vagal-induced response to rising BP), decreased/irregular (Cheyne Stokes) respirations

Indicative of impending herniation - emergent medical response necessary.

Treatment of ICP

Keep HOB elevated at 30 degrees

Keep patient well hydrated

Frequent neuro-checks needed

Strict I&O

Anticonvulsants for seizure prevention (phenytoin)

Mannitol (osmotic diuretic used to reduce cerebral edema)

Loop diuretics

Avoid aspirin, narcotics, or meds that depress respirations (as they are already at risk for being low)

Hyperventilate patient (blow off CO2 [hypocapnia]) to decrease cerebral blood flow (cerebral vasoconstriction in response to low CO2 levels)

Decrease environmental stimuli

initiate seizure and safety precautions (padded side rails up, call light w/in reach)

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the Monro-Kellie hypothesis

The Monro-Kellie doctrine states that three things exist within the fixed dimensions of the skull: blood, cerebrospinal fluid, and brain. An increase in any one component must necessarily lead to a decrease in one (or both) of the other components, otherwise intracranial pressure will increase.

Increases in one of the three components can take many different shapes and sizes. For example, abnormal bleeding within the cranium such as in epidural and subdural hematomas are common examples, which typically occur after traumatic events (think car accidents, falls, etc). Bleeding within the brain tissue itself - known as an intraparenchymal or intracerebral hematoma - can also occur, especially in patients with untreated high blood pressure. Brain tumors of any type effectively increase the amount of brain tissue. And last, but not least, the cerebrospinal fluid can back up in a condition known as "hydrocephalus".

Regardless of the cause, the end result is an abnormal increase in either blood, brain, or cerebrospinal fluid within the confines of the skull.

So what's the big deal? If the abnormality becomes large enough, the pressure within the skull can increase rapidly. Eventually the pressure can become so great that the brain gets squished, and will pop over rigid boundaries and out the small holes within the skull.

This is known as "herniating" the brain tissue. It can occur in numerous places within the skull depending on where the pressure is greatest. However, the most important herniation clinically occurs at the base of the skull where a hole known as the foramen magnum exists.

When the brain herniates here it really pisses off a vital structure known as the brainstem. The brainstem is responsible for all the stuff we don't consciously think about (heart rate, breathing, etc.), which ultimately keeps us alive. When herniation of the brainstem through the foramen magnum occurs it stretches all the "wires" that allow our brainstem to function properly. If severe enough, all those autopilot functions (ie: breathing, beating of the heart, etc.) stop working and brain death occurs.

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me: say it— i need to hear those three words

library database: Full Text Online

me, shedding tears: i love you too

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Valve Disorders

Right Heart

tricuspid stenosis: ↓ blood flow to RV

pulmonic insufficiency: blood back flows to RV

tricuspid insufficiency: backflow to RA

pulmonic stenosis: ↓ flow to PA

Left Heart

mitral stenosis: ↓ blood flow to LV

aortic insufficiency: blood back flows to LV

mitral insufficiency: backflow to LA

aortic stenosis: ↓ flow to aorta

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parasympathetic receptors

Now let's switch to the parasympathetic or cholinergic receptors. These are easier since there are only two types, muscarinic receptors and nicotinic receptors. And I will make it even easier by getting rid of the nicotinic receptors after I tell you they are involved in muscle contraction and are affected by substances such as curare (used on those poison tipped arrows) that cause muscle paralysis by blocking these nicotinic receptors.

Medications such as succinlycholine are available to block the nicotinic receptors and induce paralysis necessary for certain medical procedures.

We are left with the one parasympathetic receptor you must learn, the muscarinic receptor. When this receptor is stimulated, it causes a decrease in the heart rate, a decrease in heart contractility and a decrease in the size of the bronchioles. When we are at rest, we can slow down and conserve energy.

The parasympathetic nervous system helps us do this. What would happen if we block the muscarinic receptors? That would cause the heart rate and contractility to increase, dilation of the bronchioles and less production of secretions in the body.

This is the exact effect of atropine, a drug we use to counteract too much parasympathetic activity such as from over-stimulation of the vagus nerve or the effects of certain chemical warfare nerve agents and organophosphate poisoning. Atropine is a parasympatholytic, we can also call it a parasympathetic antagonist or parasympathetic blocker or an anticholinergic medication.

All these terms mean the same; it means they block the action of acetylcholine at the parasympathetic receptors. The effect of blocking any receptor causes the opposite effect we would expect from stimulating the receptor.

Ipratroprium is another example of a parasympathetic blocker medication but this one is inhaled so most of the effect occurs in the lungs, and when we block parasympathetic receptors in the lungs we cause the bronchioles to dilate and decrease production of secretions like mucus. That makes ipratroprium useful in the patient with COPD who produces excessive pulmonary mucous and in combination with albuterol for any wheezing patient.

But remember that the primary rescue medication for bronchospasm is a beta 2 agoinist such as albuterol although ipratrorium is often added and is available as a combination inhaler with albuterol called Combivent.

It is important to remember that it is the balance between the sympathetic and parasympathetic nervous system that keeps our automated body functions in balance and working properly. Outside forces, including drugs, medications or poisons can change the functioning of the autonomic nervous system. And it is wise to keep in mind that all medications are potential toxins that have some beneficial side effects.

In summary, if you are familiar with the actions of the autonomic nervous system receptors then you can easily recall the therapeutic actions of many commonly used medications and their overdose presentation as well as certain poisons and frequently abused drugs.

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sympathetic receptors

The types of sympathetic or adrenergic receptors are alpha, beta 1 and beta 2. Alpha-receptors are located on the arteries. When the alpha receptor is stimulated by epinephrine or norepinephrine, the arteries constrict. This increases the blood pressure and the blood flow returning to the heart. The blood vessels in skeletal muscles lack alpha-receptors because they need to stay open to utilize the increased blood pumped by the heart.

Fight or flight Remember the fight or flight response? It would not make sense to take blood from other parts of the body and pump it to the muscles so we can run away or defend ourselves if the blood vessels in the skeletal muscles are also constricted and cannot benefit from the increased blood circulation providing extra oxygen and nutrients.

So what do you think happens if we block these alpha-receptors? Right, the arteries dilate. Thus an alpha-blocker medication causes vasodilation and can be used to treat hypertension.

Next are the beta receptors. Beta 1 receptors are located in the heart. When Beta 1 receptors are stimulated they increase the heart rate and increase the heart's strength of contraction or contractility.

The beta 2 receptors are located in the bronchioles of the lungs and the arteries of the skeletal muscles. When these receptors are stimulated, they increase the diameter of the bronchioles to let more air in and out during breathing and they dilate the vessels of the skeletal muscles so they can receive the increased blood flow produced by stimulating the alpha and beta 1 receptors.

So reflect for a moment: If norepinephrine or epinephrine is the neurotransmitter of the sympathetic nervous system and it interacts with all the receptors we just described, then we know that norepinephrine or epinephrine stimulates the alpha, beta 1 and beta 2 receptors and thus it is an alpha agonist, a beta 1 agonist and a beta 2 agonist.

When we administer epinephrine or adrenaline to a patient, we expect alpha, beta 1 and beta 2 agonist effects; we expect an:

Increase in blood pressure

Increased heart rate

Increased cardiac contractility

Dilation of the bronchioles in the lungs

Dilation of the vessels in the skeletal muscles

We can also stimulate a single receptor site such as a beta 2 agonist medication like an albuterol inhaler that stimulates beta 2 receptors in the lungs then we can dilate the bronchioles in the patient with bronchospasm without causing excessive stimulation of the heart.

Or we can use a beta 1 antagonist medication more commonly called a beta blocker such as metoprolol (or other drugs ending in ‘olol') which blocks Beta 1 receptors thus decreasing heart rate and contractility which decreases blood pressure for the hypertensive patient and decreases the chance of a dysrhythmia after a heart attack by controlling the heart rate.

The sympathetic receptors can be over-stimulated by the non-therapeutic use of substances like cocaine and methamphetamines. Or the excessive use or overdose of sympathomimetic medication like pseudoephedrine or those used to treat attention deficit disorders.

Severe alcohol withdrawal may also induce sympathetic overdrive. Excessive stimulation of the sympathetic receptors can result in dangerously high blood pressure, tachycardia, dysrhythmias and hyperthermia, any one of which may cause organ damage with the real potential for organism death.

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Remember the following: Rise In 2,3-DPG H+ (acidosis) Temperature (hyperthermia) to help you remember which factors shift the curve right and the opposites to the left. The issue here is affinity. A shift to the right decreases affinity, and a shift to the left increases affinity. This is why the saturation is lower for a given PaO2 when the curve is shifted to the right. Acidosis, hyperthermia, and increased 2,3-DPG (2,3-diphophoglycerate) shift the curve to the right. Envision the curve with oxygen saturation on the vertical axis and PaO2 on the horizontal axis. A shift right would result in a lower saturation for a given PaO2, whereas a shift left would result in a higher saturation for a given PaO2.

Acidosis and hyperthermia shift the oxyhemoglobin dissociation curve to the right. This decreases affinity between hemoglobin and oxygen and results in a lower oxygen saturation for a given PaO2. The shift of the curve to the right, decreasing affinity, means it is more difficult for the hemoglobin to pick up oxygen at the lung, but it gives up oxygen easily at the tissue. In addition, remember that with a normal midline curve, a PaO2 of 60 mm Hg correlates with an SaO2 of 90%.

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CaO2 is the content of oxygen in the arterial blood. CaO2 is calculated using the hemoglobin level and saturation level of the hemoglobin (SaO2). DO2 is the delivery of oxygen to the tissue. DO2 adds the cardiac output to the picture and is calculated using hemoglobin level, SaO2, and either the cardiac output (DO2) or cardiac index (DO2I). VO2 is the consumption of oxygen by the tissue. VO2 uses venous oxygen saturation (SvO2) as a reflection of venous reserve and is calculated using the difference between SaO2 and SvO2. A:a gradient is a reflection of the process of diffusion across the alveolar-capillary membrane. This gradient is calculated by subtracting the PaO2 (arterial) from the PAO2(alveolar).