Circadian Rhythm

The circadian rhythm is like a biological clock that is built into each and every individual. It is what controls three of your major biological processes: sleeping, eating, and mating. Circadian comes from the latin words "circa" and "diem" which translates to "about a day," which is actually quite fitting since the circadian rhythm is in fact how your body keeps in time with day and night.

So, how does this all work? Your circadian rhythm is sinked to the rising and setting of the sun. It is run by the hypothalamus, or more specifically, a bundle of nerves in the hypothalamus known as the Suprachiasmatic  Nucleus (SCN). The SCN is attached to your optic nerve which is why it responds so well to changes in light. When light appears, hormones are released, which in turn, causes your body begin ramping up its biological processes. Body temperature increases, heart rate increases, blood pressure increases, bowel movements are no longer suppressed (because they are during the night which is why you don't wake up covered in crap) and there is a delay to hormones that aid with sleep, such as melatonin. In relation to this, studies have also shown that through the morning there is an increase to memory, alertness and concentration which results with us being at our cognitive best in the late morning. After that there is a cognitive decline in the early afternoon followed by a second spike in activity. You see, while the urge to sleep is greatest from 2am-4am, the second strongest desire to sleep is actually between 2pm-3pm. What this means (and it is good news for anyone who likes an afternoon nap) is that napping may be an important part of our day. There are a few theories as to why, such as it may have been better for our distant ancestors to rest during the hottest part of the day, but no one really knows for sure exactly why this is.

Where we get into trouble is when we start messing with our internal clocks. As you are probably well aware, our daily routines no longer coincide with sunrise and sunset. The advent of artificial light means we can work, play, and do whatever we want, well into the night (or as early as you want if you are crazy). This can be especially dangerous to shift workers, who should attempt to maintain their internal clock as regulated as possible since disruptions in our natural circadian rhythms have been linked to health issues including: diabetes, obesity, depression, dementia and mood disorders. In other-words, listen to your body as it generally knows what's best when it comes to being asleep and being awake.

Morals, Ethics and Paramedicine

Now before we start talking about morals and ethics in paramedicine, we must first understand the difference between morals and ethics. Morals and ethics both try to determine how one should act in a difficult situation, however; morals refer to social, religious, or personal standards or right and wrong. Ethics, on the other-hand, refers to the rules or standards that govern the conduct of members of a particular group or profession.

It might be tempting to just look at the law for standards of conduct, and though ethics are related to the law, they are not at all the same thing. Whereas the law is mostly concerned with what is wrong, and punishes people for doing things they aren't supposed do, ethics is concerned with doing what is right. As such, the law often has nothing to say on ethical quandaries. Ethics and law do have some related factors though. For instance, both require impartiality, consistency, logic and the balancing conflicting interests.

Religion is another area that may be able to answer our ethical dilemmas. The problem is that there are so many different religions and views, how do we determine which is appropriate? If two people have different religious beliefs, both providing different answers to an ethical dilemma, who is right? Or, are they both right? It is true that religion can enhance and enrich a person's ethical principals and values, but I hope that you can now see why it cannot always be relied on to provide the necessary answers to ethical problems.

Codes of ethics have been developed by a number of organizations (ex. Paramedic Association of Canada) in order to provide their practitioners with guidelines to help with ethical decisions. The PAC has developed a National Code of Ethics for prehospital care. The purpose of this is to:
-Define and clarify ethical principals.
-Identify the basic moral commitments of prehospital emergency medical practitioners.
-Serve as a source for education and reflection.
-Serve as a tool for self-evaluation and peer review.

It is important to note that values are generally the broad ideals for proper prehospital care. The standards refer to moral obligations of the paramedic based on prehospital values. Standards are generally more specific than values.

The National code of ethics from the PAC list three ethical problems faced by paramedics.
-Ethical violations occur when practitioners neglect or fail to meet their moral obligations to their patients.
-Ethical dilemmas arise when reasons both for and against a particular action are present and a decision must be reached.
-Ethical distress occurs when practitioners are in a situation that provokes feelings of guilt, concern or distaste.

Because the guidelines provided by a code are often broad, they very rarely address specific problems or situations. In these cases, it is up to the paramedic to determine the proper action. In order to accomplish this there are a few steps which should be taken:

1. Figure out exactly what the problem is. What are you looking to do, who does it involve, and what are the conditions.

2. List all the implications and consequences of the action, both positive and negative.

3. Compare all the consequences with relevant values that pertain to the case.

Often these values reference the four fundamental principals of bioethics (ethics applied to the human body). These principals are:
-Beneficence - doing good for the patient
-Nonmalfeasence - do no harm to the patient
-Autonomy - the competent adult patient's right to determine what happens to their own body
-Justice - the obligation to treat all patients fairly

Unfortunately, the paramedic in the field does not have time to sit down and go through those steps. In the field, the paramedic may look back on past events and situations to determine whether or not they have already formulated a rule that fits a given situation. If not, there are three tests that can help to quickly solve ethical dilemmas.
-Impartiality Test - Would you be willing to undergo the procedure in the patients place?
-Universalizability Test - Is this the action you would want preformed in all similar circumstances?
-Interpersonal Justifiability Test - Can you appropriately defend and/or justify your actions to others?

Using these, a paramedic can quickly make decisions in difficult situations, enabling the best possible patient care.

Coagulation (Clotting) Cascade

This is just a brief overview concerning how your blood clots and why. It is not all that in depth because I already wrote far more than intended and haven't even really scratched the surface, though it is an extremely fascinating process.

Blood is one of the most amazing substances in existence. It flows around your body in a liquid form, and yet whenever there is a hole somewhere in your circulatory system, it solidifies to plug the hole. It is like those tires that instantly fix a puncture, except that nature did it better and much more eloquently millions of years earlier.

Before we get down to business, there are a few simple terms that we should be aware of and understand.

-Platelet Adhesion: Process by which platelets stick to non-platelet surfaces.
-Platelet Aggregation: Process by which platelets stick to one another.
-Primary Hemostatic (Platelet) Plug: Initial aggregation or clump of platelets before fibrin strands attach.
-Coagulation: Process by which soluble fibrinogen converts to insoluble fibrin strands.
-Secondary Hemostatic (Platelet) Plug: Platelets with overlying layer of fibrin strands.

Before we get down to how the clots form, it may be a good idea to go over why our blood doesn't just solidify.

As you know blood is contained within blood vessels. Now the walls of your blood vessels are exactly like the walls in your house, or would be, if the walls in your house repainted themselves, fixed holes and cracks on their own, and kept themselves in extremely good all around working order, which also means not letting new walls form in the middle (ie. thrombus). The endothelial cells that form the walls of your blood vessels are living, breathing, biologically active cells and as such preform very important functions. One such function is to form a barrier to prevent platelets from binding to collagen which will activate the platelets. They also release Nitric Oxide (NO), Prostocyclin (PGI2) and Endothelial-ADPase, all of which are antiplatelet factors to prevent the platelets from activating and becoming sticky. The endothelial cells also help express heparin sulfate. Heparin sulfate then combines with Antithrombin 3 (which is released from the liver and circulates in the blood). Activated Antithrombin 3 destroys clotting factors Xa and IXa (we will get to those clotting factors a little later) and if attached to a properly sized heparin molecule, it can destroy thrombin. Healthy epithelial cells also express Thrombomodulin which is a devious little protein which takes active thrombin and twists it to its nefarious purpose. Once thrombin is under the control of thrombomodulin it can express protein C and with the help of Vitamin K, it destroys clotting factors Va and VIIIa (I should make a note, though I think that it is fairly obvious by this point, that the clotting factors are expressed as Roman numerals). Healthy epithelium also produces Tissue Plasminogen Activator (t.P.A.) which converts plasminogen to plasmin which then breaks down fibrin into fibrin degradation products (FDP), natural fibrinolysis to prevent clot from floating around your body.  As you can see, a healthy epithelium is very much like a disapproving father sitting on the porch, cleaning his shotgun and generally discouraging any funny business.

Things change however when there is a hole in a blood vessel. The first thing to happen, and it happens faster than a greyhound on cocaine (I bet someone has actually tried that, though I do not condone it), is vasoconstriction. There are different processes by which this occurs. Nervous reflex constriction occurs when damaged nerve endings in the area release tell the smooth muscle to contract. There is myogenic constriction is which damaged smooth muscle contracts. And, then damaged endothelial cell release vasoconstrictors such as Endothelin also causing constriction. All have the same goal however, limit blood loss.

Now when the endothelial cells are injured and interesting thing occurs. Platelets attach to the now exposed collagen and are activated. Von Willebrand Factor (vWF), also attaches to now exposed collagen and helps to grab platelets and stick them to that spot (sort of like Velcro), the fact that these areas are often high shear areas (I can explain it at a later time if you really want to listen to me talk about fluid dynamics) makes the vWF work that much better (remember how clots can often form in turbulent areas like the bifurcation (splitting) of major arteries). This is that platelet adhesion thing from way earlier.

Once platelets are stuck by either collagen or vWF they become activated and change their shape from somewhat disc-like to spiny balls. Activated platelets begin releasing granules. Alpha granules have things like more vWF, enzymes and proteins, and certain clotting factors (particularly V and VIII). Dense (delta) granules contain serotonin, calcium (extremely important in the actual clotting cascade), and ADP. ADP is very important as it helps to activate platelets continuing platelet aggregation and making the plug bigger. Once the platelet is activated, the membrane enzyme phospholipase A2 is also activated which helps release arachidonic acid from phospholipids. Some of the arachidonic acid (I always remember it as spider acid) is converted by cyclooxygenase (COX) into Thromboxin A2 (TxA2) which is another important platelet aggregator as well as a vasoconstrictor.

Now that we have the whole platelet plug thing out of the way. We can actually get to the actual clotting cascade. There are two different pathways: the contact activation (intrinsic) pathway and the tissue factor (extrinsic) pathway. We will start with the intrinsic pathway.

Intrinsic Pathway:
-Clotting factor XII comes into contact with a negatively charged surface and is activated becoming XIIa.
-Factor XIIa reacts with factor XI creating XIa.
-Factor XIa activates factor IX to IXa.
-Factor IXa, with the help of phospholipids, calcium and factor VIIIa, change factor X to Xa.
-Factor Xa, with the help of phopholipids, calcium and factor Va convert Prothrombin to Thrombin.
-Thrombin converts fibrinogen to fibrin which stabilizes the clot.

*It is important to note that thrombin also acts to convert factors V to Va, VII to VIIa, and XI to XIa. It also converts factor XIII to XIIIa which basically causes the cross hatching of fibrin strands, strengthening the clot. Its like you just piled a bunch of empty beer cans in the back of a pick-up truck and are trying to get to the recycling depot. What is going to hold them better? Some rope running back and forth across them or a net?

Fortunately for you the more common pathway is also quite a bit more simple. The extrinsic pathway goes something like this:
-A tissue factor released by injured epithelial cells interacts with factor VII creating VIIa.
-Tissue factor and VIIa then convert factor X to Xa and the rest is the same as the intrinsic pathway.

*Please note that the extrinsic pathway is generally the pathway used in the human body.

There are some important cofactors that were very briefly talked about. The phospholipids provide a place for some of the clotting factors to come together. Calcium is sort of like the seat belt that holds them in place so the reaction can occur. Vitamin K is also extremely important in allowing certain clotting factors to mature (shouldn't be any offspring if they haven't matured). Without enough vitamin K the whole clotting cascade falls apart which is the basis behind how Warfarin and related Coumarins work.

Once the fibrin strands are holding tight to the platelets (and trapping a few red blood cells as well then you have a successful stop to the bleeding, unless you pick at it.

Anyway, I will leave it there because I have already put down much, much more than I originally intended and anyone who has read this far probably hates me for it. I may write some more in the future though on fibrinolysis and also some pharmacology affecting the clotting cascade such as Heparin, Aspirin, Warfarin, etc.

EMS Systems - Medical Direction

Medical direction refers to medical, policies, procedures, and practices available to providers either online or offline. A medical director is a physician who is legally responsible for all clinical and patient care aspects of the system. All that means is anything you do as a paramedic is technically through your medical directors licence since you don't have a medical licence...yet. The medical director carries a plethora of roles in the system including:

-Educate and train personnel
-Participate in personnel and equipment selection
-Develop clinical protocols with the help of expert EMS personnel
-Participate in quality improvement and problem resolution
-Provide direct input into patient care
-Interface between EMS and other healthcare agencies
-Advocate within the medical community
-Serve as the "medical conscience" of the EMS system, including advocating for quality patient care

There is Online Medical Direction which involves actually getting orders for patient care in the pre-hospital setting from a licensed and qualified physician via radio or phone. It allows immediate consultation with a licensed physician to provide instant diagnostic information.

Then there is Offline Medical Direction which refers to the medical policies, procedures and practices that are put in place by medical direction before a call ever happens. This also includes aspects of the systems such as auditing, peer review and quality assurance measures.
Protocols are the policies and procedures of for all components of an EMS system. They provide the standard for patient care, treatment and also provide the baseline for accountability. Protocols for the EMS system are based around the 4 Ts of emergency care:

Triage- Guidelines to address how patients flow through an EMS system. Includes the ways in which system resources should be used to meet patient needs.

Treatment- Guidelines to identify procedures to be performed on direct order from medical direction and procedures that are standing order (preauthorized treatment procedures, a type of treatment protocol)

Transport- Guidelines that address the mode of travel based on patient's injury/illness, the condition of the patient, level of care required and estimated transport time (air vs ground transport).

Transfer- Guidelines to ensure patient is taken to the most appropriate receiving facility for definitive care.

Protocols are also in place for special circumstances such as DNRs, sexual abuse, child or elder abuse, refusal of care, termination of CPR and what to do in the case of intervener physicians. Protocols should standardize field procedures, but still allow the paramedic flexibility to improvise and adapt to unforeseen circumstances.

Information from the Essentials of Paramedic Care Volume 1.

Hyperventilation and its Effects on Brain Perfusion in Presence of ICP

Increasing ICP has a devastating effect on the tissue perfusion of the brain. Because the brain is located in a vault of a fixed size there is little room for an increase in size. There are three components in the cranial vault, with the brain accounting for 80%, the blood and vessels accounting for 12%, and the cerebrospinal fluid accounting for 8%. Any increase in one of these components must be met by an equal decrease in another of the components in order to maintain a constant intracranial pressure. Should this fail to occur due for any reason it will cause a rise in intracranial pressure compressing important brain structures, the spinal column, restricting blood flow to the brain or causing herniation.

In order to understand the effects of an increasing ICP it is important to understand how the brain perfuses its tissues under normal circumstances. Inside the cranial vault there is a special pressure working against the mean arterial pressure (MAP) due to the fixed space. This pressure is known as intracranial pressure (ICP). ICP causes an interstitial hydrostatic pressure working against the intravascular hydrostatic pressure caused by the heart. Think of it as if you were trying to blow up a balloon, except that as you try to inflate it someone else has their hands around it trying to push the air back out, the harder they push the more difficult it becomes to inflate the balloon. Therefore, in order to find the actual cerebral perfusion pressure (CPP) the ICP must be subtracted from the MAP [CPP=MAP-ICP]. Put very simply, what this equation means is that an increase in MAP will result as an increase in CPP, while an increase in ICP will cause a decrease in CPP.

The body, generally, has a very efficient auto-regulatory system when MAP is between 60 mmHg and 160 mmHG and a CPP between 50 mmHg and 150 mmHg, with the ICP in a healthy adult approximately 0-15 mmHg. If CPP drops below an appropriate range, chemoreceptors sense this change and cause vasodilation allowing for increased cerebral blood flow (CBF) and increasing the cerebral blood volume (CBV), rapidly returning the CPP to an acceptable range.

As the ICP rises however, specifically above 35 mmHg (whether due to edema, intracranial bleed, tumour or other pathology) the body's auto-regulatory mechanisms begin to fail and can actually cause greater damage. As mentioned above, when the ICP increases, the CPP decreases. When the CPP decreases, vasodilation occurs in an attempt to increase CBF but also increases CBV in a space that already can't handle anymore volume, which increases ICP, further decreasing CPP and thus the cycle continues. As perfusion in the brain continues to decrease there is an activation of the sympathetic nervous system causing tachycardia and peripheral vascular constriction in an attempt to raise blood pressure and feed the brain as much as possible. This significant increase in blood pressure stimulates the baroreceptors in the aorta which causes an activation of the parasympathetic system which then slows the heart, causing bradycardia. As pressure continues to rise, pressure begins to impede the functions of portions of the brain including the brain stem which includes the respiratory centre. The increase in pressure on the respiratory centres cause irregular respirations. These actions taken by the body are observed as Cushing's Triad (widening pulse pressure, bradycardia, irregular respirations). As ICP continues to increase the brain is eventually pushed out of the skull by the pressure resulting in brain herniation which can quickly cause severe disability or death.

Proper identification and treatment of increased ICP is important to give the patient the best possible chance of a positive outcome, and one of the most widely discussed and fiercely debated treatments for ICP is hyperventilation. The reasoning behind hyperventilation is straightforward. Carbon dioxide (CO2) is a very potent vasodilator. Hyperventilation will decrease the amount of CO2 in the body causing vasoconstriction which should lower the CBV and thus lower ICP. It is also extremely fast acting requiring only seconds of before vasoconstriction begins. There are some serious issues with this simple solution however. Firstly, vasoconstriction can significantly reduce cerebral blood flow to the brain. Not only is the reduction in CBF an issue, but the low levels of CO2 increase the affinity of hemoglobin for oxygen (pushing the oxyhemoglobin dissociation curve to the left). This means that not only is there less blood flow, but the blood that does get through is less likely to supply an adequate amount of oxygen. Hyperventilation of a patient can also lead to an increase in intrathoracic pressure which will lead to a decrease in venous return which can also cause an increase in ICP.

All of that being said, hyperventilation therapy can be a lifesaving tool if used in the proper place, at the proper time and to the proper extent. As was discussed previously, CO2 is a very potent vasodilator, in fact, for every 1 mmHG drop in the PaCO2 there is a 3% decrease in the size of the arterioles. This can decrease the ICP but will also decrease cerebral blood flow, which can lead to ischemia and ultimately necrosis. Increasing ICP, however, can compress the blood vessels, compress vital regions of the brain as well as cause herniation. Under these dire circumstances, the lesser of two evils must be considered, and it may be better to cause ischemia in order to prevent herniation.

Without evidence of herniation, ventilation of a patient with increasing ICP should be maintained at a normal rate, approximately 12 breaths per minute. This will keep the partial pressure of CO2 (PaCO2) at approximately 40 mmHg, with 35-40 mmHg being the goal. In order to manage this, capnography should be used, the more accurate the better, seeing as falling out of this range can lead to poor patient outcomes. The patient should be monitored consistently for signs of cerebral herniation which include headache, one or both pupils dilated and unreactive to light, abnormal posturing (particularly decerebrate posturing), decreased LOC often with a GCS dropping 2 points or more (from a score of eight or less), vomiting, and irregular respirations. If the signs are present, acute hyperventilation may help to prevent severe disabilities or death. Monitor the PaCO2 to prevent it from dropping below 30 mmHg, as a patient who drops below a PaCO2 level of 30 mmHg is statistically more likely to have worse outcomes upon survival. It is also important to remember that hyperventilation is not the only treatment for an increased ICP and should be used as a last resort. Unfortunately, the most effective treatment for ICP is drainage of cerebrospinal fluid from the cavity but that option is not available in the prehospital setting. Fortunately, there are more options for those in the field.

Two of the most essential treatments are also the most simple. Sit the patient up to promote venous return and help prevent as much blood from getting trapped in the cranial vault and provide oxygen to keep the brain oxygenated. A look at the data suggests that there is a serious correlation between a drop in the PaO2 to below 60 mmHg in the arterioles of the brain and worse patient outcomes. A PaO2 of this level, even for a short time, was associated with a 50% mortality rate with approximately 50% of the survivors having severe disabilities. This is due to the fact that as oxygen saturation approaches 50 mmHg, the arterioles dilate increasing blood flow in an attempt to get more oxygen but also increasing ICP.

Intravenous fluids can also be a huge help to a patient suffering from increased ICP. Hypotension, below a systolic pressure of 90 mmHg, can cause significant issues for patients because of the fact that the CPP is decreasing at an exaggerated rate due to a decreasing MAP and increasing ICP. Fluid resuscitation is important, though the right type of fluid is still up for debate. Isotonic solutions are readily available are more than adequate to maintain a blood pressure. New studies, however, have shown that hypertonic solutions may be more beneficial due to their ability to shift fluid out of the tissues of the swelling brain and back to the vasculature (some studies suggest it is nearly as effective as mannitol). This also causes an increase in blood pressure with less solution as compared to an isotonic solution as fluid is pulled into the vasculature from the tissues. One of the issues with the hypertonic solution is the tendency to dilate the arteries. What the net difference is between a fluid shift out of brain tissue and a dilation of the arteries is yet to be determined.

Mannitol is a drug that can be given in the case of ICP. It works to create an osmotic gradient in the blood-brain barrier shifting fluid out of the tissues of the brain thereby lowering ICP. It lowers blood viscosity allowing blood to flow more easily and maintains cerebral blood flow. It has also been shown not to affect brain tissue oxygenation. It should be given as a bolus, as a continuous infusion has been shown to cause an uptake of mannitol into the brain tissue and shift the osmotic gradient in an undesired direction.

Sedatives have also been given to patients with ICP. These are only useful to patients with anxiety issues. Studies have only shown them to be effective at relaxing nervous patients to help prevent an increase in ICP. Giving patients without anxiety sedatives has been correlated with poorer patient outcomes and longer times spent in the intensive care unit. Another technique to controlling ICP involves putting the patient into a hypothermic state. Research has found that for every one degree Celsius that the body's temperature drops, there is a decrease in the cerebral metabolic rate of oxygen by 6%-7%. A lower metabolic rate means that less oxygen is used giving a slightly larger buffer before ischemia occurs. The induced hypothermia was generally maintained for between 24-48 hours in the analysis. Be conscious as to the duration, as some studies have shown that hypothermia in the field followed by rapid rewarming upon admission to the hospital may cause a rebound in ICP leading to problems. One analysis found that patients under 45 years old were 76% more likely to have better ICP control and lower chance of poor outcome if there were kept in a hypothermic state (just less than 35 degrees Celsius) for 48 hours as compared to patient warmed upon admission.

A patient with an increasing ICP is in a very serious predicament. The only definitive treatment is to get them to the hospital, though there are a few things to be done for them. Promote venous return by having the patient sit up if possible. Provide oxygen and prevent hypotension below 90 mmHg. If possible and within your scope, administer mannitol- a hypertonic fluid, or induce hypothermia. Hyperventilation should be used as a last resort against impending herniation of the brain. Understanding the signs and symptoms as well as understanding the benefits and limitations of the treatments is essential in delivering proper patient care.

References

Bouma GJ, Muizelaar JP: Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma 9 (1 Suppl):S333- S348, 1992.

Obrist WD, Langfitt TW, Jaggi JL, Cruz J, Gennarelli TA: Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension. J Neurosurg 61:241-253, 1984

Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, et al: Guidelines for the management of severe traumatic brain injury. XIV. Hyperventilation. J Neurotrauma 24 (1 Suppl):S87-S90, 2007

Di Bartolomeo S, Sanson G, Nardi G, Scian F, Michelutto V, Lattuada L: Effects of 2 patterns of prehospital care on the outcome of patients with severe head injury. Arch Surg 136:1293-1300, 2001

Burke AM, Quest DO, Chien S, Cerri C: The effects of mannitol on blood viscosity. J Neurosurg 55:550-553, 1981