Medical Review Flashcards
What are the general steps for administering a medication?
Obtain an order from medical direction- every medication we assist with, or administer, requires an order from our medical director.
Select the proper medication- Once the order is approved, it is our responsibility to ensure we select the proper medication.
Verify the patient’s prescription for patient-assisted administration- Make sure the medication is ACTUALLY prescribed for the patient.
Check the expiration date
Check for discoloration or impurities- if it appears cloudy or discolored do not administer the medicine.
Verify the form, route, and dose
ALWAYS remember your five rights of medication administration:
Right patient
Right medication
Right route
Right dose
Right date ( and time)
Can too much oxygen be harmful? How so?
In some conditions, such as an ischemic stroke, administering oxygen when not indicated may actually worsen the tissue damage (cause reperfusion injury) by an increase in free radical production when the artery is reopened and blood supply reestablished to the once ischemic tissue.
Some studies have also shown an increase in tissue damage to the heart when oxygen was administered to a patient experiencing an acute myocardial infarction who had an SpO2 of 94% or greater and no signs of hypoxia.
In general what is your target SpO2 for medical patients? For trauma patients?
Medical patients: SpO2 94% or greater
Trauma patients: SpO2 95% or greater
What do the following receptors do: beta 1, beta 2, alpha 1, alpha 2?
Alpha 1- Vasoconstriction: blood moves to the core of the body & organs, the skin becomes pale/cool. Sweat glands: diaphoresis occurs
Alpha 2- Inhibits Alpha 1 response.
Beta 1-Heart: rate and force of contraction increased.
Beta 2- Lungs: causes smooth muscles to dilate to provide more oxygen for the body.
What medication stimulates all of the above receptors?
Epinephrine
What is the mechanism of action of a beta 2 agonist? What is an example of a beta 2 agonist?
Mechanism of action for Beta 2 agonist- Focused on vasculature and smooth muscles (bronchioles) when stimulated, they cause bronchodilation, vasodilation, decrease BP, decrease peripheral resistance, decreased diastolic pressure, and insulin release.
What is the liter flow for a SVN?
SVN Liter flow: 6-10 lpm
What two EMT medications can be given IN?
Glucagon
Naloxone Hydrochloride ( Narcan)
When giving a medication IN, what is the max volume (ml) that can be given at one time in one nare?
1 mg per nostril with max volume 0.5mg per spray
What EMT medication is given IM?
Epinephrine
What information must be obtained before giving NTG to a patient?
It is important to measure the patient’s blood pressure both before and after administration as it lowers the BP tremendously.
You also must ensure they were not given any ED medication within the last 48 hours.
How many times should you check your medication prior to administering it?
3 times
What are the “five rights” of medication administration?
Right patient
Right medication
Right route
Right dose
Right date (time)
Trace the path of blood through the heart and body.
Right Atrium
Tricuspid Valve
Right Ventricle
Pulmonic Valve
Pulmonary Arteries
Pulmonary Arterioles
Pulmonary Capillaries
Pulmonary Venules
Pulmonary Veins
Left Atrium
Bicuspid/ Mitral Valve
Left Ventricle
Aortic Valve
Aorta
Arteries
Arterioles
Capillaries
Venules
Veins
Inferior/Superior Vena Cava (and then back to the right atrium)
What are three lethal cardiac dysrhythmias?
Ventricular Fibrillation (V-Fib)
Asystole
Pulseless Electrical Activity (PEA)
What factors contribute to thrombus formation?
Several components are involved in the clot formation system, the most important of which are platelets (disk shaped elements in the blood that are fragments of cells from the bone marrow), a thrombin (a protein responsible for activating the formation of a clot), and fibrin (protein strands that form a mesh that strengthens a clot).
A thrombus can form within a coronary artery at a site where plaque (a fatty deposit) has built up. The thrombus formation develops in the following way: A plaque deposit inside the coronary artery can weaken over time and rupture. The body views the plaque rupture as an injury and sends out a cascade of substances to form a clot to stop the bleeding at the injury site. Platelets begin to cover the site and thrombin is activated to form a clot. The clot may partially or completely occlude the coronary artery, cutting off or reducing the supply of oxygenated blood to the heart muscle. The heart muscle becomes deprived of oxygen and may eventually begin to die. This is what leads to a heart attack and subsequent heart failure or serious cardiac rhythm dysrhythmias.
What is coronary artery disease (CAD)?
Coronary artery disease is the narrowing and hardening of the coronary arteries that supply the heart muscle.
What is atherosclerosis? How does it contribute to CAD? How does it contribute to ACS?
Atherosclerosis- A systemic artery disease in which plaque builds up inside the arteries; a form of arteriosclerosis.
Relation to CAD- Coronary artery disease is a condition which affects the arteries that supply the heart with blood. It is usually caused by atherosclerosis which is a buildup of plaque inside the artery walls. This buildup causes the inside of the arteries to become narrower and slows down the flow of blood.
Contribute to ACS- Sometimes, a gradual buildup of fat and cholesterol (plaque) hardens and narrows your arteries (atherosclerosis). Acute coronary syndrome can occur suddenly when this plaque tears or splits open. A blood clot forms over the opening, narrowing or blocking blood flow to a part of your heart called the myocardium.
What is the difference between atherosclerosis and arteriosclerosis?
Atherosclerosis is a specific type of arteriosclerosis. Atherosclerosis is the buildup of fats, cholesterol, and other substances in and on the artery walls. That buildup is called plaque. This then leads to them blocking the blood flow.
Arteriosclerosis is a disease that blocks the wall of arteries due to aging
What are the two forms of ACS?
Angina Pectoris - “pain in the chest”
Myocardial Infarction
What are the “classic” s/s of AMI/ACS?
S/S of AMI-
Chest discomfort radiating to jaw,arms, shoulders, or back
Anxiety
Dyspnea
Sense of impending doom
Diaphoresis
Nausea and vomiting
Light-headness or dizziness
Weakness
S/S of ACS-
Steady discomfort, usually located in the center of the chest but can be more diffuse throughout the front of the chest.
discomfort that is usually described as pressure, tightness, aching, crushing, or heavy
Discomfort that might radiate to the shoulders, arms, neck, jaw, back, or epigastric region
cool, clammy skin
anxiety
dyspnea
diaphoresis
Nausea & vomiting
complaint of indigestion pain
How might the s/s of AMI be different in males vs. females?
Remember that diabetics, the elderly, and women are prone to an atypical presentation of symptoms when experiencing an AMI. Many might suffer a “silent MI” in which no chest discomfort is experienced. They might complain only of shortness of breath, nausea, light-headness, or weakness.
What three types of patients are most likely to have an “atypical” presentation of ACS?
Woman
Diabetics
the elderly
How has the patriarchy contributed to labeling “atypical” presentations of ACS as such?
Classic Angina- is typically relieved with rest and nitroglycerin.
If the classic angina following exertion is not relieved after rest or after three nitroglycerin tablets or sprays over a 10-minute period, you should recognize this as ACS and treat it as an emergency.
Unstable Angina- Is typically including pain or discomfort that occurs at rest, continues without relief, or is prolonged.
If the patient experiences angina that occurs at rest and lasts for more than 20minutes, angina with a recent onset that progressively worsens, or angina that wakes the patient at night, you should recognize this as ACS and treat it as an emergency.
What is the harm in this labeling?
Emergency care for the patient suffering from angina should be provided regardless if signs and symptoms of ACS exist.
What is myocardial ischemia? Stable angina? What are its s/s?
Myocardial ischemia- occurs when a portion of the heart muscles dies because of the lack of an adequate supply of oxygenated blood.
Stable angina- Occurs when the heart muscle itself needs more blood then it’s getting.
S/S of stable angina-
Steady discomfort, usually located in the center of the chest but can be more diffuse throughout the front of the chest.
discomfort that is usually described as pressure, tightness, aching, crushing, or heavy
Discomfort that might radiate to the shoulders, arms, neck, jaw, back, or epigastric region
cool, clammy skin
anxiety
dyspnea
diaphoresis
Nausea & vomiting
complaint of indigestion pain
What is the difference between stable vs. unstable angina?
Stable- Occurs during physical activity or exertion and goes away with rest.
Unstable- Occurs during rest or with little physical activity.
What is the difference in the description of pain between ACS vs. stable angina?
Pain with ACS will be nearly the same but maybe more intense, and will usually last longer. Nitroglycerin will give little, if any, relief for ACS.
What is the EMT treatment for ACS?
Establish an open airway
If pt. respirations become inadequate, begin positive pressure ventilations.
Apply the pulse oximetry- if drops below 94% provide oxygen
If pt. has prescribed Nitro and has a SBP of greater than 90 mmHg, place them in a sitting, or lying position and administer nitroglycerin tablets or spray.
If pt. is suspected of having coronary artery occlusion, administer 160-325 mg of Aspirin if local protocols allow.
Contact ALS
Continue to monitor patients and be prepared to manage a cardiac arrest patient.
What is the target SpO2 for a patient with ACS?
94% or above
What are two ways that too much oxygen can harm an ACS patient?
In ACS the coronary artery is occluded and cuts of blood supply to a dsital area of heart tissue. This area of tissue becomes ischemic from the lack of oxygenated blood. During this period, there is an inflammatory response and the release of damaging molecules made from oxygen are called free radicals. The restoration of blood to an area of tissue that was ischemic from low blood flow or occlusion of a vessel is called reperfusion. The oxygen in the blood flowing to the reperfused tissue increases the production of oxygen free radicals. The free radicals directly damage cell membranes and other cellular components and result in cells death. This is called reperfusion injury.
In other words: free radicals damage other cells = cell death & by the artery being so inflamed it causes damage.
What is the etiology of reperfusion injury? What can an EMT do to minimize the risk of this?
Higher oxygen levels in the blood result in an increase in the production of damaging free radicals & potentially greater call & tissue death. This occurs after the hypoxic state due tto the blood flow being restored and the cells are receiving oxygen again. The heart along with the brain,kidneys, liver, lungs, and intestines are highly sensitive organs affected by the production of free radicals during reperfusion. Keeping in mind the injurious process that occur to tissues undergoing reperfusion, it makes sense that supplying more oxygen causes greater tissue damage. Also, higher levels of oxygen in the blood causes coronary artery vasoconstriction and can reduce blood flow to the cardiac tissue.
We only administer oxygen if the SpO2 is 93% or less. We use a NC starting at 2 lpm with just enough administered to reverse the hypoxia. When we reach our goal of 94%, or above, we need to maintain it so we do not raise the oxygen level if it is not necessary.
What is the mechanism of action of aspirin? How does this help a patient with ACS?
MOA: Aspirin is a medication that produces a rapid antiplatelet effect.
Helps ACS? : The effect, listed above, decreases the ability of platelets to clump together during the clotting cascade and reduces the formation of a clot in the coronary artery at the site of the blockage. It also reduces the incidence of coronary reocclusion and recurrent ischemic events following in-hospital therapy with fibrinolytic agents.
What is the mechanism of action of nitroglycerin? How does this help a patient with ACS?
MOA: Dilates blood vessels, decreases workload of the heart, and decreases cardiac oxygen demand.
Help pt. w/ ACS? : Nitroglycerin causes venous and arterial vasodilation, resulting in preload and afterload reduction. The end result is a decrease in myocardial oxygen demand which lessens ischemia.
What are the contraindications for nitroglycerin?
Pt. has a SBP of 90mmHg or patients SBP drops more than 30 mmHg from the baseline.
Heart rate is less than 50 bpm or greater than 100 bpm.
Patient has a suspected head injury.
Patient is a child or infant.
3 doses have already been consumed by the patient.
Patient has taken ED medication within the past 48 hours.
What are the s/s of heart failure? How does heart failure differ from heart attack?
S/S of Heart Failure: See below
Marked or severe dyspnea
tachycardia
difficulty breathing while supine
suddenly waking at night with dyspnea
fatigue on any type of exertion
anxiety
tachypnea
Diaphoresis
Upright position with upper/lower extremities dangling
cool, clammy, pale skin
chest discomfort
edema
cyanosis
JVD or Distended neck veins
distended and soft spongy abdomen
What are the s/s of right- vs. left-sided heart failure? Which causes pulmonary edema? Which causes pedal edema? Which causes JVD? Which causes ascites (abdominal distention)?
S/S of Right sided HF:
SBP low to normal range
Breath sounds should be clear
JVD & Peripheral edema
S/S of Left sided HF:
Normal to high range of SBP
inspiratory rales upon breath sound auscultation
No JVD or peripheral edema present
Pulmonary edema is caused: Both but more often than not left-sided
Pedal edema is caused: Right-sided heart failure
JVD is caused by: Right-sided heart failure BUT it can be a sign of late left-sided heart failure.
Ascites abdominal distention is caused by: Right-sided heart failure
What is the EMT treatment for CHF?
Ensure patient airway is patent. If inadequate, provide positive-pressure ventilations.
If a patient has an adequate respiratory rate, deliver supplemental oxygen with the same indications as listed by the pharmacology quiz review.
If a patient experiences chest discomfort and has prescribed Nitro, give one tablet every 3-5 minutes until the 3 max dose is met.
Continuously reassess the patient and be prepared for respiratory failure and cardiac arrest.
Be sure to allow the patient to lay in a position of comfort.
How can CPAP help a CHF patient?
The heart failure patient with pulmonary edema will benefit greatly from positive pressure ventilations. It will increase the effectiveness of gas exchange by forcing oxygen to cross over the alveoli and the space between the alveoli and the capillary. If the patient can withstand it and medical direction allows this positive pressure ventilation as early as possible.
What is an aortic aneurysm? Aortic dissection? What are their s/s? What is the EMT treatment?
Aortic Aneurysm- Occurs when a weakened section of the aortic wall, usually resulting from atherosclerosis, begins to dilate or balloon outward from the pressure exerted by the blood flowing throughout the vessel.
S/S of Aortic Aneurysm: see below
difficulty or painful swallowing
difficulty breathing
feeling full
hoarseness
pain
a pulsating or throbbing feeling in your stomach
Shortness of breath
swelling in your neck, face, or arms
Treatment: If a pulsating mass is felt and aortic aneurysm is suspected, administer oxygen and transport the patient immediately as only surgery can prevent the rupture from occurring.
Aortic Dissection-Occurs when there is a tear in the inner lining of the aorta and blood enters the opening and causes separation of the layers of the aortic wall.
S/S of Aortic Dissection: see below
sudden severe chest or upper back pain or stomach pain
Loss of consciousness
shortness of breath
symptoms similar to a stroke such as vision problems or difficulty speaking/ weakness
weak pulse in one arm or thigh compared to the other
leg pain
difficulty walking
Treatment: For chest pain or back pain that can result from an aortic dissection, administer supplemental oxygen and assist the patient with their prescribed Nitroglycerin if the SBP is more than 90mmHg and no signs of hypovolemia are present. If aortic dissection is suspected DO NOT give them aspirin.
What is the most common cause of cardiac arrest in children?
Respiratory compromise
What is the most common ED treatment for confirmed ACS? How is this done?
Percutaneous Coronary Intervention (angioplasty)
This is done by rapidly removing the clot by percutaneous intervention or fibrinolytics, distal perfusion can be restored, and the extent of myocardial damage can be minimized.
Why should you request ALS for a patient with ACS? What can ALS do to help?
It is important to request ALS for patients with suspected ACS so we can obtain vital information to pass along to the receiving hospital as a warning of the incoming patient. This helps the hospital prepare to receive and treat the patient as the emergency they are.
ALS can do more than we can as EMTBs. They can help prep the patient for surgery more so than we can and start IV therapy as well as begin incubation.
What is the difference between a seizure and convulsions?
Convulsion- Unresponsiveness accompanied by a generalized jerky muscle movement affecting the entire body.
Seizure- A sudden temporary alteration in the mental status caused by a massive electrical discharge in a group of nerve cells in the brain.
The difference is that a convulsion occurs in only one type of seizure and is a sign of abnormal electrical activity occurring in that seizure.
What is the difference between a primary vs. secondary seizure?
Primary seizures, also called unprovoked seizures, in adults are usually due to a genetic or unknown cause. (most common disease being epilepsy)
Whereas secondary seizures, or provoked seizures, do not result from a genetic cause but occur as the result of an insult to the body, such as a fever, infection, hypoxia, hypo/hyperglycemia, drug intoxication, drug withdrawal, etc.
Describe the different types of seizures. What are the s/s of each?
Tonic-clonic- loss of consciousness; muscle rigidity; convulsions, incontinence; postical
Absence- Brief loss of consciousness; no loss of muscle tone; eyes flutter; more common in children
Myoclonic- Sporadic jerking isolated muscle groups on both sides of the body; more common in children;occur often; associated with sleep
Tonic- muscle stiffness and rigidity
Atonic- Loss of muscle tone and strength; patient suddenly drops to the ground; often called “drop attack or drop seizure”
Febrile- Tonic-clonic seizure due to a high fever; most common in children
Partial Seizures ( Involve only one part of the brain) : see below
Simple partial- awake and aware
Simple partial Motor- jerking or stiffening motor activity to a focal area on one side of body
Simple partial sensory- unusual sensations of visions, hearing, smell, taste or touch
Simple partial autonomic- strange or unpleasant sensations in the stomach, head or chest; changes in HR and RR; goosebumps
Simple partial psychic- Memory or emotional disturbances; garbled speech; trouble understanding; fear; depression; happiness for no reason; deja vu
Complex Partial- awake but not aware; lip smacking,hand clapping, wringing of the hands, picking of clothes,patient can maintain activity during seizure such as riding a bike; auditory, visual, or smell hallucinations; blank vacant stare
Partial seizure with secondary generalization- awake state with partial seizure activity that progresses to loss of consciousness and generalized tonic-clonic seizure
What is the difference between a generalized vs. partial seizure?
Generalized involves the whole brain
Partial involves only part of the brain
What are the risks/dangers associated with a generalized seizure?
This type of seizure usually begins with abnormal electrical activity low in the cerebral cortex that spreads upwards, affecting both the cerebral hemispheres, and downward, affecting the reticular activating system (RAS). Because of the involvement of both cerebral hemispheres and the RAS, the patient does not remain awake or aware.
What are the stages of a grand mal seizure?
Aura- this serves as a warning that a seizure is going to begin and involves some type of sensory perception by the patient.
Loss of consciousness- the patient loses consciousness after the aura.
Tonic phase (muscle rigidity)- The patient’s muscles become contracted & tense, and the patient exhibits muscular rigidty.
Clonic phase (convulsion)- Muscle spasms then alternate with relaxation, producing the typical violent and jerky seizure activity of the clonic phase.
Postictal state- The patients recovery phase
What is an aura?
Aura- this serves as a warning that a seizure is going to begin and involves some type of sensory perception by the patient.
What are s/s of a postictal state?
S/S of postictal state: see below
mental status gradually improves over time
patient is exhausted and weak on one side of the body
headaches are very common
Usually last from 10-30 minutes but can lasts hours
What distinguishes a simple partial seizure from a complex partial seizure?
Simple partial seizures- The patient is awake and alert that the seizure activity is occurring because the RAS is not involved & only one cerebral hemisphere is involved.
Whereas complex partial seizures, the patient is not aware of their surroundings. This is because while it starts in one small area in the temporal lobe or frontal lobe, it begins as a simple partial seizure, then; the electrical discharge quickly spreads to other areas of the brain leading to the unaware state. The RAS is not involved; therefore the patient remains in an awake state, however, the specific area of the brain involved in the seizure, typically the temporal lobe, causes them to lose awareness.
What other conditions might mimic a complex partial seizure?
Daydreaming
Suspected intoxication
drug use
mental illness
disorderly conduct
What is the difference between primary/unprovoked vs. secondary/provoked seizures?
Primary seizures, also known as unprovoked, are due to a genetic or unknown cause. Whereas secondary, or provoked, seizures are a direct result from an insult to the body, such as fever or infection as two examples.
What is a prolonged seizure? What is status epilepticus? What is the EMT treatment?
Prolonged seizure- A seizure that lasts between 5 and 30 minutes.
Status epilepticus is defined as a continuous seizure lasting longer than 30 minutes or two or more sequential seizures.
When this occurs treatment is required to avoid adverse and possible life-threatening consequences including aggressive airway management, positive pressure ventilation with supplemental oxygen, and immediate transport to a medical facility.
During a prolonged seizure would you expect the SpO2 to increase or decrease?
decrease
During a prolonged seizure would you expect the EtCO2 to increase or decrease?
increase
What physical signs might you look for as evidence that a patient had a generalized seizure?
Loss of consciousness
Aura
muscle rigidity
convulsions
postictal state
What is the EMT treatment for a seizure?
Prevent injury to the patient
Position the patient in a lateral recumbent position
Maintain a patent airway
Suction
Assist ventilation if needed
maintain adequate oxygenation
transport
What questions should you ask bystanders who witnessed a person seizing?
Was the patient awake during the seizure?
Was the muscle activity a twitching or jerking motion?
When did the seizure start?
How long did the seizure last? (keep in mind bystanders tend to overestimate)
Did the patient hit his head or fall?
Does the patient have a hx of seizures?
What was the patient doing exactly before the seizure?
What causes a febrile seizure? What is the most common age range for febrile seizures?
Febrile seizures are caused by a high fever.
Most common in infants from 3-6 months of age all the way up to 5-6 years of age.
What should you do if a patient in SMR on a LBB starts seizing?
loosen the straps on the LBB
What is the etiology of a vasovagal faint?
An overwhelming influence of the parasympathetic NS that causes blood vessels to dilate throughout the body. Gravity causes the blood to pool in the lower extremities, decreasing blood flow and perfusion to the brain and in turn, causing a syncopal episode.
What are some s/s that distinguish seizure vs. syncope?
Syncope differences are listed below:
The episode usually begins in a standing positon.
The patient remembers feeling faint or light-headed.
The patient becomes responsive almost immediately after becoming supine.
The skin is usually pale and moist.
What is the difference between an allergic reaction and anaphylaxis?
An allergic reaction is a misdirected and excessive response by the immune system to an allergen by releasing antibodies to fight the allergen causing signs and symptoms like a mild rash, etc. Anaphylaxis is caused when a certain antibody called immunoglobulin E (IgE) is produced, IgE antibodies stimulate a release of chemical substances that cause life-threatening reactions in the airway, lungs, heart and blood vessels.
What is the etiology/pathophysiology of anaphylaxis?
Anaphylaxis is caused when a certain antibody called immunoglobulin E (IgE) is produced, IgE antibodies stimulate a release of chemical substances that cause life-threatening reactions in the airway, lungs, heart and blood vessels.
What are the s/s of anaphylaxis?
S/S of anaphylaxis: see below
Respiratory distress
decreasing BP
itchy/watery eyes
runny or stuffy nose
sense of impending doom
general discomfort
swelling of face
What are some common causes of anaphylaxis?
Causes of anaphylaxis: see below
food
latex
vaccines
perfumes
bee/wasps stings
antibiotics
What is the EMT treatment for anaphylaxis?
Maintain a patent airway
Suction PRN
Maintain adequate oxygen / be prepared to assist with ventilations
Administer epi
Consider ALS
Immediate transport
What is the difference between an anaphylactic reaction and an anaphylactoid reaction?
Anaphylactoid reactions happen when the pt has had no previous exposure to the certain antigen so IgE antibodies were not produced and the antigen just causes the chemical substances to release on its own unlike anaphylaxis reactions.
What is meant by a biphasic anaphylactic reaction? How often does this occur? What is its treatment?
A biphasic anaphylactic reaction is a secondary reaction that happens in 20% of people who had an anaphylactic reaction.
4-6 hours after the first reaction they have a second one that can sometimes be more severe than the first, its treatment is the same as the initial reaction.
What receptors does epinephrine activate? What does each of these receptors do?
Alpha 1- causes vessels to constrict
Alpha 2- checks on Alpha 1 and regulates the amount of vasoconstriction
Beta 1-Increases HR, force of contraction, and speed of electrical impulses carried through the heart
Beta 2- Causes the bronchiole smooth muscle to dilate
How is epinephrine administered? What is the adult dose? What is the pedi dose?
Administered through intramuscular
Adult dose: 0.3mg
Child dose: 0.15mg
What should you do with an auto-injector after you have used it?
Place it in the biohazard puncture-resistant container
What are the hollow vs. solid vs. vascular organs in the abdomen?
Hollow- Hollow: appendix, bladder, common bile duct, fallopian tubes, gallbladder, intestines, stomach, uterus, ureters.
Solid- kidney, liver, ovaries, pancreas, spleen.
Vascular- abdominal aorta, inferior vena cava.
What are the different types of abdominal pain?
Visceral: pain from an organ, usually poorly localized and less severe pain, dull or aching feeling and can be intermittent or constant.
Parietal (Somatic): associated with inflammation of peritoneal lining, pain is more severe, usually found on one side or the other, typically constant.
Referred: a type of visceral (organ) pain that is felt somewhere else and not felt in the organ that is causing the pain.
What are the most common sites of referred pain from abdominal conditions?
Neck
upper back
lower abdominal/back area
down the arm
etc.
What is peritonitis? How can an EMT assess for this?
Peritonitis- It is irritation and inflammation of the peritoneum.
EMT Assessment- You can assess it by doing the Markle test where you have the patient stand upright, go up on their toes, and drop down onto their heels, if they grimace or moan/complain of pain, the test is positive.
Where should you start with palpation of the abdomen?
The area of the abdomen that is least painful and farthest from the site of the pain.
What is appendicitis? What are its s/s? What are its risks? How does the pain of appendicitis progress?
Appendicitis- Inflammation of the appendix.
S/S: see below:
abdominal pain
fever
chilis
anorexia
abdominal guarding
How does pancreatitis most often present?
Severe pain in the middle of upper quadrants that sometimes radiates to the mid to lower back.
What are some common causes of pancreatitis?
long term alcohol use
gallstones
infection
What is cholecystitis? What are its s/s? Where might this be felt as referred pain?
Cholecystitis- Inflammation of the gallbladder is commonly associated with the presence of gallstones.
S/s of Cholecystitis: see below
tenderness of palpation of the RUQ
belching or heartburn
nausea and vomiting
sudden onset of abdominal pain located in middle of the upper quadrants
Referred pain: in the right scapula.
What are the s/s of a GI bleed?
abdominal pain or tenderness
Hematemesis (vomiting blood)
Hematochezia ( bright red blood in the stool)
Melena (dark tarry stools)
Altered mental status
tachycardia
signs of shock
What is hematemesis vs. hematochezia vs. melena? Which of these supports an upper vs. a lower GI bleed?
Hematemesis: vomiting blood which can be bright red or look like coffee grounds.
Hematochezia: bright red blood in the stool normally signifying a rapid onset.
Melena: dark tarry stools containing decomposting blood normally from the upper GI tract.
Upper GI Bleed- Melena
Lower GI Bleed- Hematemesis & hematochezia
What is voluntary vs. involuntary guarding?
Involuntary- a contraction of the abdominal wall muscles that the patient cannot control.
Voluntary- when a patient contracts the abdominal wall muscles usually in anticipation of pain or discomfort.
What causes esophageal varices? What are its s/s?
Esophageal varices- are a bulging, engorgement, or weakening of the blood vessels in the lining of the lower part of the esophagus.
S/S of Esophageal Varices: see below
large amounts of bright red hematemesis
absence of pain or tenderness in the abdomen
rapid pulse
breathing difficulty
pale, cool, clammy skin
other s/s of shock
jaundice- yellowing of the skin
What is anemia?
A deficiency of healthy red blood cells in the blood.
What is hemophilia?
A clotting disorder in which the patient’s body cannot form clots properly, resulting in the body taking longer to stop bleeding.
What is deep vein thrombosis (DVT)? How might this cause a PE?
DVT is when blood clots form in the deep veins of the body, most commonly in the deep veins of the legs.
A DVT can cause a VTE that is a clot that breaks off and travels to the right side of the heart and into the lungs where it blocks a pulmonary artery causing a pulmonary embolism (PE).
What is endometriosis?
A condition in which the endometrial tissue grows outside of the uterus.
What is pelvic inflammatory disease (PID)? What are its s/s?
An infection of the female reproductive tract caused by bacteria, fungi or viruses.
S/S of PID: see below
abdomen/pelvic pain or tenderness
vaginal discharge with abnormal color/ smell
fever or chills
irregular bleeding/ cramping
What are the s/s of a UTI?
S/S of UTI: see below
abdominal/pelvic pain or tenderness
hematuria
urine with cloudiness or a flou/strong odor
pain or burning with sexual intercourse
frequent or urgent need to urinate
flank pain
fever or chills
AMS
What are the s/s of kidney stones?
S/S of Kidney stones: see below
abdominal/ pelvic pain or tenderness
flank or back pain that is colicky/ severe
groin pain
abnormal urine color
pain with urination
frequent or urgent need to urinate
fever or chills
What are the two different kinds of dialysis? What are the advantages/disadvantages/risks of each?
2 different kinds: Hemodialysis & Peritoneal dialysis.
Hemodialysis a dialysis machine containing the dialysate is connected to an access site on the patient. This is usually done at an outpatient treatment center but can be performed elsewhere. The EMT should NOT obtain a BP of a dialysis patient on the side of the patient’s access site.
Peritoneal dialysis is run through a tube into the patient’s abdomen. The fluid remmains there for several hours so it can be absorbed through wastes and then drained out of the body through a different tube. This usually occurs while the patient is asleep at night.
Disadvantages to both: see below
Hypotension
muscle cramps
peritonitis
nausea/ vomiting
hemorrhage (usually around the access site)
infection at the access site
irregular pulse or cardiac arrest
sepsis
difficulty breathing
Treatment: see below
1. Maintain the airway, breathing, and circulation
2. Support ventilation- as needed.
3. Provide high-concentration oxygen
4. Stop any bleeding- from the shunt or access site as needed.
5. Position the patient- if the patient has signs of shock, place them in a supine position. If the patient has pulmonary edema, place them upright.
6. Transport
How does a patient usually present when they have an acute abdomen?
Appears generally ill and assumes a guarded position with knees drawn up and hands clenched over the abdomen.
In what position should a person with an acute abdomen be transported?
position of comfort
What are your treatment priorities for a drowning victim?
- Establish and maintain spine motion restriction if spinal injury is suspected.
- Begin positive pressure ventilation with a pocket mask in the water, if possible.
- Float a backboard under the patient and move to shore. Remove the patient on the backboard while maintaining spine mobilization.
- Establish and maintain an open airway, insert a nasopharyngeal airway if the patient is unresponsive and has no gag or cough reflex.
- Suction secretions as necessary.
- If breathing is inadequate, provide positive pressure ventilation with supplemental oxygen at a rate of 10-12 ventilations/minute for an adult and 12-20 ventilations/minute for a child/infant.
- If breathing is adequate, administer oxygen by NRB mask at 15lpm. If possible deliver warm, humidified oxygen if hypothermia is suspected.
- If no pulse, begin CPR and follow AED protocols
- If hypothermia is suspected, follow the generalized protocol.
- Place the patient in a lateral recumbent position only if spinal injury is not suspected.
- Always transport a submersion patient.
- Perform reassessment every 5 minutes.
What is the mammalian diving reflex? What changes does this reflex cause in the body? What is its significance for drowning victims?
Mammalian diving reflex: The body’s natural response to submersion in cold water in which breathing is inhibited, the heart rate decreases, and blood vessels constrict to maintain cerebral and cardiac blood flow.
Changes in the body: When the body is submerged in cold water the larynx spasms, the breathing is inhibited, the heart rate slows down, and the blood vessels throughout most of the body constrict.
The significant difference between warm-water and cold-water drowning: when a person dives into cold water (below 70 degrees F) the mammalian diving reflex drastically slows down metabolism and makes the patient more likely to be resuscitated, even after prolonged submersion.
What is the etiology for barotrauma in a patient who has been scuba diving?
Barotrauma: sometimes called the “squeeze” occurs during ascent and descent when air pressure in the body’s air cavities become too great. As a result, tissues in the air cavities are injured.
What are the s/s of barotrauma?
S/S:
mild to severe pain in the affected area
clear to bloody discharge from the nose or ears
extreme dizziness
nausea
disorientation
What types of organs are most likely to be harmed with barotrauma?
middle or inner ears
lungs
eyes
What is the etiology of decompression sickness (DCS)?
Decompression sickness is caused by dissolved gasses coming out of solution to form bubbles inside the body on depressurization.
What are the s/s of DCS?
S/S Of Type I DCS:
Pain
Pruritus (itching) and burning sensation of the skin
skin rash
skin has orange-peel appearance (rare)
Painless pitting edema (uncommon)
S/S Of Type II DCS:
Low back pain that progresses to paresis, paralysis, or numbness
Headache, visual disturbances, dizziness, tunnel- vision
Altered mental status
Nausea, vomiting, vertigo, tinnitus partial deafness
What is the treatment for DCS? Where does a patient suffering from DCS need to go?
Treatment steps: see below
1. take spine motion restriction precautions if spinal injury is suspected.
2. Open the airway and assess for adequate breathing
3. initiate CPR and apply the AED if indicated
4. Transport immediately
*****DCS patients need to go to a facility with a hyperbaric oxygen chamber if possible.
What might cause an air gas embolism (AGE) in a patient who has been scuba diving? What are its s/s?
Air Gas Embolism: is a blocking of blood vessels by an air bubble or clusters of air bubbles. This blockage interferes with perfusion of the body tissues with oxygen and nutrients normally supplied in the blood.
Causes: During a dive, pressure on the diver’s body increases and the volume of a gas decreases as he descends. Conversely, that pressure is lessened as the diver ascends.
S/S: See below
Itchy; blotchy, or mottled skin
difficulty breathing
dizziness
chest pain
severe, deep aching pain in the muscles, joints, & tendons
blurred or distorted vision
partial deafness
nausea or vomiting
numbness or weakness on one side of the body
lack of coordination
swelling and crepitus in the neck
loss or distortion of memory
coma
cardiac or respiratory arrest
behavioral changes ( sometimes the only sign)
What is the sound and etiology of wheezing? Stridor? Rhonchi? Rales?
Wheezing is a high-pitched, musical, whistling sound that is best heard initially on exhalation but can also be heard during inhalation in more severe cases. It is an indication of swelling and constriction of the inner lining of the lower airways, primarily the bronchioles.
Rhonchi, which can also be referred to as coarse crackles, is snoring or rattling noises heard on auscultation. They indicate obstruction of the larger conducting airways of the respiratory tract by thick secretions of mucus.
Why is it important to always auscultate BBS on bare skin?
To achieve the most accurate interpretation of breath sounds, it is important to auscultate in the appropriate fashion. Whenever feasible, have the patient sit upright and, while using the diaphragm end of your stethoscope over bare skin (never auscultate over clothing), instruct the patient to take a deep breath (inhale) through the mouth and breathe out (exhale) passively through the mouth.
What is the tripod position? What does it indicate?
Leaning forward, braced with arms and elbows locked and hands on a hard surface)
Indicative of respiratory distress
What are the s/s of respiratory distress vs. respiratory failure vs. respiratory failure?
Respiratory distress: Typically, a patient in respiratory distress has a normal minute ventilation from compensation in the tidal volume (breathing deeper) and/or the respiratory rate (breathing faster). Because the tidal volume and respiratory rate are still adequate, the patient is compensating.
Respiratory failure: Inadequate tidal volume or an inadequate respiratory rate or both
Respiratory arrest: Respiratory arrest is the complete cessation of breathing effort or the patient experiences agonal breathing. Agonal breathing occurs when the brainstem reflex causes a gasping breath in an otherwise apneic patient.
No tidal volume or respiratory rate
What is the difference between ventilation vs. oxygenation vs. respiration?
Respiration is the exchange of oxygen and carbon dioxide
Ventilation is the act or process of inhaling and exhaling
Oxygenation refers to the process of adding oxygen to the body system; specifically, this is the process of loading oxygen molecules onto hemoglobin molecules in the bloodstream.
What are the indicators that a respiratory condition is getting better/worse?
Subjective complaint of shortness of breath
Restlessness and anxiety
Tachycardia (early finding) or bradycardia (later finding)
Tachypnea
Pale, cool, clammy skin (early finding) or cyanosis (later finding)
Abnormal respiratory pattern
Wheezing, rhonchi, or crackles
Difficulty or inability to speak
Muscle retractions (Suprasternal, supraclavicular, sub-clavicular, intercostal retractions indicate difficulty in inhaling through constricted airways or difficulty in expanding lungs against poor compliance )
Altered mental status (Anxiety and confusion is an early finding; aggressive or complacent behavior and sleepiness is a later finding.)
Abdominal breathing (Excessive use of abdominal muscles indicates difficulty in exhaling through constricted airways)
Excessive coughing (with or without expectorating material)
Tripod position (leaning forward, braced with arms and elbows locked and hands on a hard surface)
Pulse oximeter reading <94%
What are the etiology and pathophysiology of emphysema? Chronic bronchitis? Pneumonia? PE? Pulmonary edema? Asthma? Pneumothorax? Hyperventilation syndrome?
Emphysema is a permanent disease process distal to the terminal bronchioles that is characterized by the destruction of the alveolar walls and the distention of the alveolar sacs, and a gradual destruction of the pulmonary capillary beds with a severe reduction in the alveolar/capillary area in which gas exchange can occur.
Pathophysiology - In emphysema, the lung tissue loses its elasticity, the alveoli become distended with trapped air, and the walls of the alveoli are destroyed. Loss of the alveolar wall reduces the surface area in contact with pulmonary capillaries. Therefore, a drastic disruption in gas exchange occurs, and the patient becomes progressively hypoxemic and begins to retain carbon dioxide.
Chronic bronchitis is a disease process that primarily affects the bronchi and bronchioles. Like emphysema, chronic bronchitis is associated with cigarette smoking. By definition, chronic bronchitis is characterized by a productive cough that persists for at least three consecutive months a year for at least two consecutive years.
Pathophysiology - Chronic bronchitis involves inflammation, swelling, and thickening of the lining of the bronchi and bronchioles and excessive mucus production. The alveoli remain unaffected by the disease; however, the inflamed and swollen bronchioles and thick mucus restrict airflow to the alveoli so that they do not expand fully, causing respiratory distress and possible hypoxia.
Patients infected with the human immunodeficiency virus CHIV) and others who are on immunosuppressive drugs, such as cancer or transplant patients, are also prone to pneumonia. Additional risk factors include cigarette smoking, alcoholism, and exposure to cold temperatures.
Pathophysiology - Pneumonia is primarily an acute infectious disease caused by a bacterium or a virus that affects the lower respiratory tract and causes lung inflammation and fluid or pus-filled alveoli. This leads to a ventilation disturbance in the alveoli with poor gas exchange.
In pulmonary embolism, an obstruction of blood flow in the pulmonary arteries leads to hypoxia. Patients at risk for suffering a pulmonary embolism are those who experience long periods of immobility (such as bedridden individuals, those who travel for a long period confined in one position, those with splints to extremities) as well as those with heart disease, recent surgery, long-bone fractures, venous pooling associated with pregnancy, cancer, deep vein thrombosis (development of clots in the veins, most commonly in the legs), estrogen therapy, clotting disorders, history of previous pulmonary embolism, and those who smoke.
Pathophysiology - Pulmonary embolism is a sudden blockage of blood flow through a pulmonary artery or one of its branches. The embolism is usually caused by a blood clot, but it can also be caused by an air bubble, a fat particle, a foreign body, or amniotic fluid
Pulmonary edema: The two kinds of pulmonary edema are cardiogenic and noncardiogenic.
Cardiogenic pulmonary edema is typically related to an inadequate pumping function of the left ventricle that drastically increases the pressure in the pulmonary capillaries, which forces fluid to leak into the space between the alveoli and capillaries and, eventually, into the alveoli.
Noncardiogenic pulmonary edema, also known as acute respiratory distress syndrome (ARDS), results from the destruction of the capillary bed that allows fluid to leak out. Common causes of noncardiogenic pulmonary edema are severe pneumonia, aspiration of vomitus, submersion, narcotic overdose, inhalation of smoke or other toxic gases, the ascent to a high altitude, sepsis, and trauma.
Acute pulmonary edema, usually caused by a cardiogenic etiology, occurs when an excessive amount of fluid collects in the spaces between the alveoli and the capillaries (Figure 16-7™). This intrusion of fluid disturbs normal gas exchange by reducing the capability of oxygen and carbon dioxide to diffuse across the alveolar-capillary surface because of the collection of water both in the alveoli and between the alveoli and capillaries (ventilation side of the ventilation/perfusion ratio), which makes less oxygen available to the blood flowing through the capillaries (perfusion). This leads to hypoxemia and cellular hypoxia. Off-loading of carbon dioxide from the capillaries into the alveoli is also impeded, leading to hypercarbia.
What is COPD? What are its different forms? What are its s/s? What are its treatments?
The three most commonly encountered obstructive pulmonary diseases are emphysema, chronic bronchitis, and asthma.
Emphysema and chronic bronchitis are chronic disease conditions that continue to progress. These patients are typically older and exhibit abnormal lung function and signs and symptoms of the disease continuously (chronically). Thus, emphysema and chronic bronchitis are referred to as chronic obstructive pulmonary disease (COPD).
Many patients have a combination of chronic bronchitis and emphysema and present with a mixture of signs and symptoms associated with both conditions.
Emphysema
S/S
Anxious, alert, and oriented
Dyspneic
Uses accessory muscles
Thin. barrel-chest appearance from chronic air trapping in the alveoli causing the anterior-posterior diameter of the chest to increase
Coughing, but with little sputum (the material that is coughed up
Prolonged exhalation
Diminished breath sounds (indicating poor air movement)
Wheezing and rhonchi on auscultation
Pursed-lip breathing (physiologic PEEP)
Extreme difficulty of breathing on minimal exertion
Tachypnea-breathing rate usually greater than 20 per minute at rest
Tachycardia (increased heart rate)
Diaphoresis (sweating; moist skin)
SpO2 of 94% or greater unless in respiratory failure
Tripod position
May be on home oxygen
Treatments
Administer oxygen, bronchodilators, corticosteroids and CPAP
Chronic bronchitis
S/S
Cough (hallmark sign) is prominent, vigorous cough- ing produces sputum
Typically, overweight, with prominent peripheral edema and chronic jugular vein distention
Chronically cyanotic complexion (As already noted, chronic bronchitis patients were often called “blue bloaters,” but this is outdated because many COPD patients don’t conform to the description.)
Minimal difficulty in breathing and anxiety, unless in respiratory failure
SpO2, reading of <94%, indicating chronic hypoxemia
Scattered rales (crackles) and coarse rhonchi usually heard upon auscultation of the lungs
Wheezes and, possible, crackles at the based of the lungs
Asterixis (flapping of extended wrists)
Treatment
Administer oxygen, bronchodilators, corticosteroids and CPAP
What is the target SpO2 for patients with known COPD?
88-92%
What are the two most common causes of emphysema?
Cigarette smoking
Persons continuously exposed to environmental toxins are also predisposed
What is the relationship between PE and DVT? How might one cause the other?
Include an assessment of the lower legs in any patient with respiratory distress or a complaint of dyspnea, especially if it has a sudden onset. Swelling, pain, and redness in one limb are typically indicative of a deep vein thrombosis (DVT), which is a common source of the pulmonary embolism that travels and becomes lodged in the pulmonary vessels.
In any patient complaining of shortness of breath, assess for pain, redness, increased warmth and swelling to the lower leg, especially at the calf. These are signs of deep vein thrombosis (DVT), a blood clot in a vein of the lower leg that ‘might have broken free, traveled to the lungs and caused a pulmonary embolism.
What is the relationship between PE and right-sided heart failure?
Pulmonary embolism results in a rapid increase in pulmonary vascular resistance, leading to pulmonary hypertension in arteries of the lungs
What is the treatment for pulmonary edema caused by CHF?
Nitrogen and CPAP
What are the s/s of a pneumothorax? What is the treatment for pneumothorax? What is contraindicated for a pneumothorax?
S/S
Sudden onset of shortness of breath
Sudden onset of sharp chest pain or shoulder pain
Decreased breath sounds to one side of the chest (most often heard first at the apex, or top, of the lung)
Subcutaneous emphysema
Tachyonea
Diaphoresis
Pallor
Cyanoisis (can be seen late and in a large or tension pneumothorax)
SpO2 <94%
Treatment
Administer oxygen to maintain a SpO2, of 94% or greater if the patient presents with signs of respiratory distress, chest pain, or any other indicators for oxygen administration.
If inadequate breathing is present, provide positive pressure ventilation.
Contraindication
CPAP is contraindicated in a patient with a suspected » pneumothorax regardless of the complaint of dyspnea and evidence of respiratory distress. The positive pressure can increase the size of the pneumothorax and worsen the hypoxia.
What causes carpal pedal spasms?
hyperventilation
What is cystic fibrosis? What causes this? How do people with this most often die?
Cystic fibrosis (also known as CF, mucoviscidosis, or mucoviscidosis) is a hereditary disease. Although it commonly causes pulmonary dysfunction because of changes in the mucus-secreting glands of the lungs, it also affects the sweat glands, the pancreas, the liver, and the intestines.
In cystic fibrosis, however, an abnormal gene alters the functioning of the mucous glands lining the respiratory system, and there is an overabundant production of mucus, which is thick and sticky. As this thick mucus layer develops, there is blockage of the airways as well as an increase in the incidence of lung infections because bacteria can readily grow in the thick mucus. Repeated lung infections cause scarring of the lung tissue and promote ongoing pulmonary damage. As a result, there is a progressive diminishment in respiratory function, leading to respiratory failure and death
What is the difference between croup and epiglottitis? What are their s/s?
Croup (laryngotracheobronchitis), commonly seen in children, involves the swelling of the larynx, trachea, and bronchi, causing breathing difficulty. The child typically does not feel well, has a sore or hoarse throat, and has a fever. At night, the condition usually worsens.
S/S
You might hear a hallmark sign of croup, a cough that sounds like a barking seal.
Epiglottitis, an inflammation affecting the upper airway, can be an acute, severe, life-threatening condition if left untreated.
S/S
Upper respiratory tract infection
Dyspnea, usually with more rapid onset
High fever
Sore throat and pharyngeal pain
Inability to swallow with drooling
How do the s/s of respiratory distress differ between a child and an adult? For which age group will retractions be an early vs. late sign? Why?
Child (early)
Increased use of accessory muscles to breathe
Sternal and intercostal retractions during inspirations
Tachypnea (increased breathing rate)
Tachycardia (increased heart rate)
Nasal flaring
Prolonged exhalation
Frequent coughing (can be present instead of wheezing in some children)
Cyanosis to the extremities
Anxiety
Retraction (this is a late sign in adults and sign of severe respiratory distress)
Adult
Internal use of accessory muscles to breath
Sternal and intercostal retractions during inspirations
Tachypnea (increased breathing rate)
Tachycardia (increased heart rate)
Nasal flaring, breathing with the mouth open
Prolonged exhalation (with pursed lips)
Frequent coughing
Cyanosis to the extremities
Anxiety
Confusion
Inability to speak in full sentences
What is subcutaneous emphysema? How and where is it most often detected?
Subcutaneous emphysema is a common result of trauma to the neck and chest, indicating a hole in the lung, trachea, bronchus, or esophagus. Inspect for any evidence of trauma.
Subcutaneous emphysema can be felt much more easily than it can be seen on inspection
Crepitus on palpation
Distention or bloating may be present in the abdomen, chest, neck, and face
What are the s/s of pediatric respiratory distress vs. failure?
Distress
Increased use of accessory muscles to breathe
Sternal and intercostal retractions during inspirations
Tachypnea (increased breathing rate)
Tachycardia (increased heart rate)
Nasal flaring
Prolonged exhalation
Frequent coughing (can be present instead of wheezing in some children)
Cyanosis to the extremities
Anxiety
Retraction (this is a late sign in adults and sign of severe respiratory distress)
Failure
AMS
Bradycardia
Hypotension
Extremely fast, slow, or irregular breathing pattern
Cyanoisis to the core of the body and mucous membrane
Loss of muscle tone
Diminished or absent breath sounds
Head bobbing
Grunting
Seesaw or rocky breathing
Decreased response to pain
Inadequate tidal volume
What is seesaw breathing? What does it indicate?
The chest is drawn inward, and the abdomen moves outward, indicating extreme inspiratory efforts
Indication of respiratory failure (in children)
What is the reticular activating system? What does this have to do with a patient’s level of responsiveness?
The reticular activating system (RAS) is not a structure but a network of nerve cells in the brain- stem that constantly transmit environmental and sensory stimuli to and from the cerebrum. If this network is damaged or becomes dysfunctional, the patient loses consciousness.
Similarly, if both cerebral hemispheres are damaged or become dysfunctional, the patient can no longer remain conscious. Thus, for the patient to remain in an awake and alert state, the reticular activating system and at least one cerebral hemisphere must be intact.
What is a neurological deficit? What is a stroke?
The ability to be alert and aware of your surroundings, to speak, to feel sensations, and to move are all functions of the brain and nervous system. When the patient loses some or all these abilities, he experiences a neurologic deficit. A neurologic deficit is defined as any deficiency in the functioning of the brain or nervous system. Altered mental status, slurred or absent speech, paralysis, weakness, and numbness are all signs and symptoms of a neurologic deficit. A neurologic deficit alerts you to the possibility of a condition that is affecting the patient’s central nervous system, which is composed of the brain and spinal cord.
Stroke - Due to the inadequate delivery of oxygen and glucose to a portion of the brain caused by a blood clot obstructing a cerebral artery or from a rupture of a cerebral artery.
What are the two general types of stroke?
Ischemic and hemorrhagic
What is the difference between an embolic vs. a thrombotic stroke?
A stroke resulting from thrombus formation is called a thrombotic stroke. A clot or other matter that has traveled from another area of the body is called an embolus.
An embolic stroke occurs most often when the patient is awake and active. The onset of signs and symptoms is usually more sudden than in a thrombotic stroke.
Because the narrowing and eventual occlusion of the artery occur over a longer period than an embolic-type occlusion, the onset of signs and symptoms of a thrombotic-type stroke is slower. This is the most common type of stroke. A severe headache is not a common symptom of a thrombotic stroke.
What are the etiology and pathophysiology of an ischemic vs. hemorrhagic stroke?
Stroke caused by a blockage is referred to as an ischemic stroke, and a stroke caused by rupture and bleeding is referred to as a hemorrhagic stroke.
Ischemic strokes, which account for approximately 87 percent of all strokes, occur when the cerebral artery is blocked by a clot or other foreign matter.
An ischemic stroke occurs when a thrombus is formed on the wall of an artery or when an embolus travels from another area until it lodges in and blocks an arterial branch.
Hemorrhagic strokes are usually caused by either of two types of weakened blood vessels: an aneurysm or an arteriovenous malformation (AVM).
An aneurysm is a ballooning of a weakened area within an artery wall. If left untreated, the area continues to weaken and balloon until it ruptures. The weakened area can be a congenital defect that has been present since birth. This is a common cause of strokes in younger, healthy adults.
Why do strokes, as opposed to spinal cord injuries, generally affect only one side of the body?
When a stroke damages the areas of the brain that control muscle movement, the signals between the brain and the muscles can become weakened or lost
It is rare that paralysis from a stroke affects both extremities on both sides of the body. Usually, the face is paralyzed on one side, and the extremities are weak or paralyzed on the opposite side. The pattern of paralysis is one factor that helps you distinguish a stroke from a spinal injury, which, unlike a stroke, frequently causes paralysis to both legs (paraplegia) or to all four extremities (quadriplegia).
What is a cryptogenic stroke?
A cryptogenic stroke is defined as one that cannot be conclusively attributed to an embolism originating from the heart, thrombosis in an artery, or small artery disease despite extensive medical diagnostic testing. Cardiac embolism secondary to atrial fibrillation is thought to be a common cause. Other possible causes include a defect between the walls of the atria, thrombophilia (an abnormal tendency to form clots), a nonbacterial infection to the inner lining of the heart (endocarditis), and cerebrovascular disease that is sub-clinical (not yet producing any signs or symptoms). The main problem with cryptogenic stroke is the inability to identify the cause, which leads to the inability to effectively treat it to prevent a stroke from occurring or recurring.
What is an aneurysm? What is an arteriovenous malformation (AVM)?
An aneurysm is a ballooning of a weakened area within an artery wall.
An arteriovenous malformation (AVM) is a tangle of abnormally formed blood vessels in the brain or on its surface, which divert blood directly from the artery to the vein, bypassing the capillaries
What is meant by the ischemic penumbra vs. infarct zone of a stroke?
The area of ischemia during the stroke, where the brain cells are electrically silent from a lack of ATP but are still alive, is referred to as the ischemic penumbra or the ischemic shadow. As already noted, it is possible to salvage this tissue by restoring the blood flow because the cells’ membranes are still intact and the cells aren’t.
A large clot can cause immediate infarction and death to some brain cells from a complete cessation of blood flow to that area. With a complete absence of blood flow, there is no reversible ischemic penumbra. Instead, the area of dead tissue is referred to as the infarct zone.
How do you assess a patient for a stroke?
Listen for garbled sounds or slurring when the patient speaks, Have the patient say the following phrase to assess his speech capability: “You can’t teach an old dog new tricks.” An abnormal finding would be if the patient said the wrong words, slurred words, could not say the phrase at all, uttered a completely unrelated phrase, or didn’t understand your directions.
When assessing the extremities, you may find a reduction in the sensory and motor function on one side of the body. The patient may lack the ability to feel your touch or to feel pain and may display weakness or paralysis. Check the grip strength in the upper extremities by having the patient grasp and squeeze patient fingers. Have the patient push and pull up against your hands with his feet to assess for equality of strength in the lower extremities. Note any differences in strength between the right and left sides and the upper and lower extremities. Assess for arm drift by instructing the patient to extend his arms, palms up, with eyes closed for 10 seconds. Note a downward drift or drop of one extremity. It is important to perform the assessment as quickly as possible and not delay transport to do a detailed neurologic examination. Time is brain! That is, a delay in getting the patient to an appropriate stroke care facility could lead to greater brain ischemia and more extensive permanent damage.
What is the Cincinnati Pre-hospital Stroke Scale (CPSS)? What are its components?
Used to diagnose stroke inpatient
CPSS tests for
Facial droop by having the patient show his teeth or make a smile; Normal – Symmetry to both sides; Abnormal: One side of the face droops or does not move symmetrically
Arm drift by having the patient close his eyes with both for 10 seconds. Normal – Symmetric movement in both arms. Abnormal: One arm drifts down or asymmetric movement of the arms
Abnormal Speech: Have the patient say, “You can’t teach an old dog new tricks”. Normal: The correct words are used, and no slurring of words is noted. Abnormal: The words are slurred, the wrong words are used, or the patient is aphasic
How do you test pronator drift? What does this indicate?
A patient who has not suffered a stroke can generally hold arms in an extended position with eyes closed.
A stroke patient will often display “arm drift” or “pronator drift”; that is, one arm will remain extended when held outward with eyes closed, but the other arm will drift or drop downward and pronate (turn palm downward)
What conditions might sometimes mimic a stroke?
The patient’s movements should always be guided rather than restrained to prevent further injury. It may also be necessary to move objects away from the patient. Some people place spoons or other hard objects in the patient’s mouth to prevent him from “swallowing his tongue,” which is anatomically impossible. Remove these objects immediately because they can easily cause injury to the mouth, tongue, teeth, and jaw, or they can break and cause airway obstruction. It is common for the patient to bite his tongue during the seizure; therefore, you may notice small amounts of blood around his mouth. The smell or sight of urine and feces might also be noted, as loss of bowel and bladder control is common during seizures. Because seizure activity can mimic a heart attack and can result in short periods of apnea (absence of breathing), you might find a bystander performing CPR on the patient on your arrival.
What is a TIA?
Patients who experience a transient ischemic attack (TIA) develop many of the same signs and symptoms as those who are experiencing a stroke. Many people refer to these as mini-strokes. The key difference between a stroke and a TIA is that the cerebral artery blockage is transient or temporary in a TIA and the signs and symptoms disappear without any obvious permanent neurologic deficits.
What is the significance of getting the exact time when the s/s of a stroke began?
Because the drugs used to dissolve the clot are typically administered within 3 to 4.5 hours of the onset of the stroke, passing this information on to the hospital is critical. The hospital staff can then gauge how much time has expired and the course of treatment. Time is precious, and the transport must occur rapidly to a medical facility that can manage a stroke patient.
What are fibrinolytic? What are the indications for fibrinolytic?
Percutaneous Intervention or Fibrinolytic Therapy and the EMT’s Role. One advantage of interviewing the patient in the prehospital setting is the ability to gather the information that is important to the ongoing management of the patient in the hospital setting. Patient care for myocardial infarction can be greatly enhanced if the hospital receives certain patient information necessary to make patient care decisions. With rapid removal of the clot by the percutaneous intervention (also known as coronary angioplasty) or fibrinolytic, distal perfusion can be restored, and the extent of myocardial damage can be minimized or even inhibited. One concern with fibrinolytic, however, is that they don’t just selectively dissolve clots in the heart; they can dissolve clots no matter where they are in the vessels of the body. For this reason, recent stroke patients, patients with a history of recent surgery, and similar patients cannot receive fibrinolytic drugs because of the risk that they may cause internal hemorrhage or other life-threatening complications. Therefore, percutaneous intervention (angioplasty) has become the most important consideration in the ST elevation MI patient. Patients with an ACS are preferably transported to a medical facility with percutaneous intervention capabilities.
Fibrinolytic drugs and invasive mechanical devices and procedures are now available that can be used on certain stroke patients to reduce or even reverse the consequences of the stroke by breaking up or removing the clot causing the obstruction. The fibrinolytic drugs must be administered within 3 hours from the first sign or symptom of the onset of the stroke or 4.5 hours for selected patients.
What is the target SpO2 for a stroke patient? Can you give a stroke patient too much O2?
94% or greater
High levels of oxygen can also be harmful – causing constriction of the blood vessels, reduced blood flow to the brain, damage to the lungs, and restricting people’s mobility
What is the difference between vascular vs. tension vs. organic HA? Which type of HA is a migraine?
Tension headaches. These are thought to be caused by the contraction of the muscles of the neck and scalp. The pain is usually described as “tight” or “viselike.” This is the most common type of recurring headache found in children, adolescents, and adults
Organic headaches. Also called traction or inflammatory headaches, these are not simply headache conditions but rather are symptoms of another condition. They may be a result of tumors, infection, stroke, or inflammatory disorders within the cranium such as a hemorrhage or meningitis.
Vascular headaches. These occur because of dilation or distention of vessels or inflammation within the cranium. Migraine headaches are thought to be caused by spasms of vessels followed by vasodilation and a change in the chemicals that transmit nerve impulses in the brain. Migraines are often described as throbbing and can be generalized or localized to one side of the head. The patient also commonly experiences sensitivity to light (photosensitivity), nausea, vomiting, and sweating.
Migraines can be preceded by an aura, such as blind spots, bright shimmering lights, weakness to one side of the body, numbness or tingling to one side of the body, visual or hearing hallucinations, double vision, incoordination, or syncope. A vascular headache can also be caused by hypertension (high blood pressure), typically reaching a diastolic pressure of 120 mmHg for a headache to occur.
What is the role of glucose in the body?
Glucose is a major source of fuel for cells. Maintenance of the glucose level in the blood is crucial to the normal function of cells.
What body organ can use nothing but glucose for energy?
The brain cells cannot use anything but glucose. Thus, cells in the rest of the body can continue to function by using other energy sources, whereas the brain cells (which do not store glucose), when deprived of glucose, dysfunction, shut down, and eventually begin to die.
What is the function of insulin? Is it a hormone or an electrolyte? What organ produces insulin? Does insulin raise or lower the BGL?
Insulin, a hormone that is secreted by the pancreas, lowers the blood glucose level (BGL). Insulin attaches to the cell at a specific (receptor) site and causes another channel on the cell membrane to open. A protein then carries the glucose into the cell through this channel. Thus, insulin facilitates the movement of glucose into the cell. If insulin is not available, glucose moves into the cell at a rate approximately 10 times slower. This causes glucose to build up in the blood- stream, causing the blood glucose level to increase.It has three main functions:
It increases the movement of glucose out of the blood and into the cells.
It causes the liver to take glucose out of the blood and convert it into glycogen, the stored form of glucose.
It decreases the blood glucose level by the actions just listed: facilitating the movement of the glucose out of the blood and into the cells and the liver.
What is the function of glucagon? Is it a hormone or an electrolyte? What organ produces glucagon? Does glucagon raise or lower the BGL?
Glucagon, a hormone that is secreted by the pancreas, increases the Blood Glucose Level (BGL). The function of glucagon is exactly the opposite of insulin’s function. Glucagon, however, is secreted when the blood glucose level is low and works to increase the blood glucose level. Glucagon raises the blood glucose level by converting the glycogen stored in the liver back into glucose to be released into the blood, as well as converting noncarbohydrates into glucose. It has three main functions:
It converts glycogen stored in the liver back into glu- cose and releases it into the blood.
It converts other, non carbohydrate substances into glucose in the liver.
It increases and maintains the blood glucose level by the actions just listed: converting glycogen and other substances into glucose.
What role does epinephrine (adrenalin) play in helping maintain a person’s blood glucose level? When is it released? What are the s/s of its release?
Many other hormones are also released to help main- tain the blood glucose level. One of these hormones is epinephrine (adrenaline). Epinephrine is released by the adrenal glands when the blood glucose level decreases to a dangerously low level. Epinephrine stops the secretion of insulin and promotes the release of stored glu- cose from the liver as well as the conversion of other substances into glucose. Many of the signs you see in a patient with a low blood glucose level are caused by epi- nephrine. These signs and symptoms are discussed later in the section on hypoglycemia (low blood glucose).
What is the normal blood glucose level in a non-fasting patient?
The blood glucose level of a person who has fasted for 8-12 hours would normally read 80-90 mg/dL. Because patients are not always in a fasting state when you test their blood glucose level, many sources use much wider ranges of 70-140 mg/dL as a normal blood glucose level.
What is the difference between type 1 vs. type 2 diabetes?
There are four types of diabetes mellitus. The two that you most often find in the prehospital environment are type 1 diabetes and type 2 diabetes. Type 1, was once known as insulin-dependent diabetes mellitus (IDDM) because these patients are required to inject insulin to regulate their blood glucose levels. The type 1 patient’s pancreas usually does not secrete any insulin. These patients are typically younger when the diabetes occurs, most commonly under the age of 40. The peak ages for onset of type 1 diabetes mellitus are 4-6 years and again at 10-14 years. The patients are typically lean from weight loss. Their blood glucose levels are extremely high if untreated. These patients suffer from the three Ps. Type 1 diabetics often have difficulty keeping their blood glucose level within the normal range, with the possibility of hav- ing too high or too low a blood glucose level. Therefore, they are prone to suffering from a hyperglycemic condition called diabetic ketoacidosis (DKA). They can also suffer from hypoglycemia (low blood glucose). Type 1 diabetes is much less common than type 2 diabetes. Type 2 diabetes was once known as non-insulin- dependent diabetes mellitus (NIDDM) because type 2 patients usually do not need to take insulin. However, they do have to regulate their diet and exercise and take oral drugs to help the pancreas secrete more insulin or to make the insulin that is secreted more effective in facilitating movement of glucose into the cells. Type 2 diabetic patients are usually middle-aged or older. They are typically overweight. Like type 1 diabetics, they suffer from high blood glucose levels if untreated and can also present with a history of the three Ps. These patients are prone to a hyperglycemic condition called hyperglycemic hyperosmolar syndrome (HHS) or nonketotic hyperosmolar state (NKHS).It is estimated that 1-2 percent of the population has a true form of diabetes mellitus. Of these, approximately 25 percent suffer from type 1 and the remaining 75 percent suffer from type 2. Diabetes mellitus is more common in Caucasians than in non-Caucasians.
What are the s/s of hypoglycemia? What BGL defines hypoglycemia?
Hypoglycemia is the term for a low blood glucose level (hypo = low, glyco = glucose, emia = blood). It is usually defined as a blood glucose concentration less than 70 mg/dL and is the most common type of endocrine emergency. It is more common in type 1 patients than in type 2 patients. Hypoglycemia is the most dangerous acute complication of diabetes mellitus. It is estimated that most diabetics experience mild episodes of hypoglycemia one to two times per week that are self-treated, and 30 percent experience a severe hypoglycemic episode annually. Hypoglycemia occurs when the amount of glucose in the blood falls below the normal lower limit. As noted earlier, it is typically defined as a blood glucose level less than 70 mg/dL with signs and symptoms of hypoglycemia. The most common sign of hypoglycemia is an altered mental status. This is due to the sensitivity of the brain to a drop in the blood glucose level. As already discussed, the brain cells can use only glucose as an energy source, unlike other cells that can burn fat and protein for energy. As the blood glucose level continues to drop, the mental status of the patient continues to deteriorate. If the blood glucose level is not restored, the brain cells will begin to die. Hypoglycemia usually occurs in type 1 diabetes mel- litus in which the patient must take insulin to regulate his blood glucose levels. This patient takes his insulin, but with excessive results (blood glucose levels decrease too much), for one of the following reasons:
The patient takes his insulin and does not eat a meal
The patient takes his insulin, eats a meal, but drastically his activity beyond normal
The patient takes too much insulin, either forgets and takes an extra dose or takes takes too much at one time
What are the s/s of hyperglycemia? What BGL defines hyperglycemia?
Hyperglycemia is the term for a high blood glucose level (hyper = high, glyco = glucose, emia = blood) and is defined as a blood glucose level greater than 200 mg/dL. Any hyperglycemic episode in a diabetic patient should prompt the EMT to assess for an infection, acute medical illness, recent cocaine use, or medication noncompliance. Unlike hypoglycemia, which is characterized by the presence of insulin and a lack of glucose in the blood, in hyperglycemic conditions there is a lack of insulin and an excessive amount of glucose in the blood. In hypoglycemic conditions, the brain is starved of glucose. In hyperglycemic conditions, the brain has more glucose than it knows what to do with.
What are the 3 (or 4) Ps? Do they point to hyperglycemia or hypoglycemia?
Because of the higher-than-normal loss of body water, diabetes mellitus patients typically complain of frequent thirst (polydipsia) and frequent urination (polyuria). Also, because the cells are starving for energy, the patient is typically hungry (polyphagia). Polydipsia, polyuria, and polyphagia are referred to as the three Ps—signs that commonly alert physicians to a possible diagnosis of diabetes mellitus.
The first sign of the patient’s diabetes mellitus might be one of the severe hyperglycemia conditions discussed later in the section.
What is DKA? What is HHS? How do the pathophysiologies of these differ? How do their s/s differ? What is the blood glucose range for each?
As noted earlier, two conditions that may result from extreme hyperglycemia are diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). HHS is also known as nonketotic hyperosmolar state (NKHS) or hyper- glycemic hyperosmolar nonketotic syndrome (HHNS). DKA is more commonly seen in the type 1 diabetic, whereas HHS is more common in the type 2 diabetic. In both conditions, the blood glucose level increases drastically.
The name diabetic ketoacidosis indicates what occurs in the condition. The blood glucose level is elevated, typically greater than 350 mg/dL because of an inadequate amount of insulin. The brain has an excess amount of glucose; therefore, it is not suffering from low blood glucose. However, the other cells in the body are starving for glucose because there is an inadequate amount of insulin to help move the glucose out of the blood and into the cells at a fast-enough rate. The cells begin to burn fat for energy as the glucose collects in the blood. This causes two problems: dehydration and acidosis. First, consider how dehydration occurs. The excess glucose from the blood begins to spill into the urine, drawing large amounts of water with it. The patient begins to urinate frequently because of the excessive glucose, simultaneously eliminating large amounts of water attracted to the glucose. This leads to dehydration in the patient. Additionally, because all cells (those other than brain cells) that rely on insulin to move glucose across their cell membrane receive little glu- cose from the blood, they think that they are starving and signal the brain to produce more glucose. The pancreas secretes glucagon in response to the cells’ request for more glucose, although the blood glucose level is already excessively high. In response to the request for more glucose, the liver converts glycogen into glucose and releases it into the blood, which exacerbates the spillage of glucose into the urine and the consequent dehydration. Second, consider how acidosis develops. Because the liver cells are not taking in glucose, the liver begins to metabolize fats for energy, which produces a by- product called ketones. The ketones produce a form of a strong acid. As the liver metabolizes more fat, acid levels in the body begin to increase to dangerous levels (acidosis). These two problems, dehydration and acidosis, lead to many of the signs and symptoms seen in DKA and can eventually cause the brain to fail. In addition to dehydration and acidosis, an electrolyte imbalance develops, which can lead to cardiac disturbances. Because it takes quite a bit of time for the effects of the acid and dehydration to occur, the signs and symptoms of DKA usually do not occur for up to several days.
Do fruity breath and Kussmaul respirations point to DKA or HHS? Why?
As mentioned previously, DKA progresses slowly over a few days. The signs or symptoms related to dehydration are polyuria, polydipsia, poor skin turgor, tachycardia, and positive orthostatic tilt test. Nausea, vomiting, and muscle cramps are typically due to electrolyte disturbances from the loss of sodium, potassium, and magnesium. The acid in the body produces Kussmaul respirations, warm and dry skin, and a fruity odor on the breath. Kussmaul respirations are a pattern of deep and rapid breathing that is commonly seen in patients with DKA. It is an attempt by the body to blow off carbon dioxide to reduce the acid load in the body. Carbon dioxide produces another form of acid called carbonic acid. If the patient can blow off large amounts of carbon dioxide by hyperventilating (deep and rapid breathing), he can then reduce the amount of carbonic acid and thus reduce the total amount of acid in the body. As the ketone acid in the body increases, the patient will breathe deeper and faster to keep the acid load under control. The fruity odor, which smells like Juicy Fruit gum or acetone, is from the ketones building up in the body.
Why is HHS most often associated with type 2 DM?
This is because the type 2 patient’s pancreas can continue to produce and secrete some insulin, so some glucose is still getting into the cells (Figure 20-8 ®). The glucose entering the cells keeps the amount of fat being metabolized by the liver to a lesser amount than is seen in DKA. If there is not a significant amount of fat being metabolized, there will be a lesser production of ketones as a by-product of fat breakdown. Therefore, unlike DKA, in HHS there is not a collection of a large amount of ketones that would cause an acid load in the body, thus the non- ketotic reference in the name.
What is the EMT treatment for hypoglycemia?
The patient suffering from hypoglycemia must be given sugar to increase the blood glucose level as quickly as possible to prevent the brain cells from dying. You would provide the same treatment as outlined earlier in the chapter for an altered mental status or unknown history.
What are the contraindications for oral glucose? How do you administer it?
Oral glucose shouldn’t be administered to patients who are unresponsive, unable to swallow the medication, or has a confirmed BGL greater than 70 mg/dl.
What are the 4 ways poisons can enter the body? Which is the most common route?
Ingestion. A drug or substance can be swallowed with absorption occurring through the gastrointestinal tract (stomach and intestines). This is the most common route of poisoning. Most of the poison is absorbed from the small intestine and not from the stomach.
Inhalation. Breathing a poison—typically a gas, vapor, fume, or aerosol—into the lungs enables rapid absorption into the body. The poison is transported down the respiratory tract with each inhalation until it reaches the alveoli. When in the alveoli, the poison can cross the alveolar-capillary membrane and enter the bloodstream, where it is then transported widely throughout the body. This not only produces a more immediate effect than ingestion but also typically causes signs and symptoms to appear earlier, with a tendency to be more systemic (throughout the body) in nature.
Injection. A poison can be injected under the skin, into the muscle, or directly into a blood vessel. This can result in a local reaction to the poison, which is usually immediate.
Absorption. A poisonous substance can enter the body when it contacts the skin or mucous membrane. The poisonous powder can be a dry powder or a liquid.
What are the most common causes of death for a person who has been trapped in a fire?
Patients who are trapped in a fire are typically exposed to large amounts of toxic substances. The incomplete combustion of products releases toxic fumes, many of which are lethal. Most people who die in a fire do so from inhalation of toxic fumes and not from burns. The second most common cause of death in a fire is from airway injuries secondary to breathing in superheated air. The third most common cause of death in a fire is trauma.
What are the s/s of toxic ingestion?
The signs and symptoms of poisoning by ingestion vary, depending on what was ingested and the route of entry into the body
What is the etiology of CO poisoning? What are its s/s? What is the EMT treatment?
Carbon monoxide displaces oxygen as it attaches to hemoglobin molecules in the blood. The attached CO turns the color of the hemoglobin extremely red. A pulse oximeter works by reading the color of the hemoglobin. Under normal circumstances, red hemoglobin indicates that oxygen is attached to it. Because CO also turns the hemoglobin red, the pulse oximeter reads the red color and provides an extremely high but false SpOz reading. The cells are truly hypoxic even though the SpOs can be 100%. Thus, guiding oxygen therapy by the SpO> does not apply to CO poisoning. Signs and symptoms include: headache, Tachypnea, Dizziness, Nausea and vomiting, altered mental status, and high pulse oximeter reading.
EMT Treatment: Assess the breathing status. If the rate and tidal volume are adequate, administer a high concentration of oxygen via a nonrebreather mask at 15 Ipm, regardless of the SpO2 reading. The half-life of carboxyhemoglobin decreases from 240 to 320 minutes in a patient breathing ambient air to 50 to 100 minutes in a patient on a high concentration of oxygen. Do not rely on the pulse oximeter to guide oxygen therapy. Carbon monoxide monitors (CO-oximeters) are available that can indicate the amount of carbon monoxide in the blood.
What is the etiology of cyanide poisoning? What is the EMT treatment?
The patient may be breathing in an adequate percentage of oxygen, and the oxygen is adequately transported to the cells, but the cyanide prevents the oxygen from being used effectively by the cells. In this case, the alveoli and blood have adequate amounts of oxygen; nevertheless, the cells become severely hypoxic.
EMT Treatment:
1.remove the patient from the toxic environment.
2.Establish and maintain a patent airway
3.Assess the breathing status
4.Consider ALS for cyanide meds
5.rapid transport
When do the s/s of withdrawal usually begin? What causes these s/s?
A habitual drug user can develop a tolerance to a drug in which larger doses are required to produce the same desired effects. This quite often leads to a physical or psychological dependence, in which the patient experiences a strong need to use the drug repeatedly. The psychologically dependent person is completely preoccupied with the procurement of the drug. His behavior can be compulsive or neurotic and is geared toward acquiring another dose of the drug. There are, however, no physiological consequences of drug withdrawal for this patient. The physically dependent drug user, however, undergoes physiological changes within the body that require the drug to be present in his system to prevent withdrawal consequences from occurring. Drugs that commonly produce physical drug dependence are narcotics, sedatives, hypnotics, barbiturates, cocaine, and marijuana.
The following signs and symptoms of drug withdrawal usually begin to occur at about the time when the next drug dose is required, and they usually peak at 48 to 72 hours after the person has stopped taking the drug
Anxiety
Agitation
Tremors
Profuse sweating
Elevated heart rate and blood pressure
Hallucinations
Feeling things on the body that is not there
Nausea
Abdominal cramping
What are the s/s associated with the stages of alcohol withdrawal?
Withdrawal syndrome occurs after a period of abstinence from the drug or alcohol to which a person’s body has become accustomed. However, it does not require that the alcoholic or drug abuser stop drinking or taking the drug completely. The withdrawal syndrome can also occur when an alcoholic’s alcohol intake falls below the amount usually ingested. Alcohol withdrawal is dose-dependent: The more the alcoholic drinking, the more severe the syndrome will be. Alcohol withdrawal syndrome, which can mimic many psychiatric disorders, is characterized by the following signs and symptoms:
Stage 1. This occurs within approximately 8 hours and is characterized by nausea, insomnia, sweating, and tremors.
Stage 2. This occurs within 8 to 72 hours and is characterized by a worsening of stage 1 symptoms plus hallucinations.
Stage 3. This can occur as early as 48 hours following the last alcoholic beverage and is characterized by major seizures.
Stage 4. This is characterized by delirium tremens, which can occur 1 to 14 days after the last dring.
What are the s/s of DTs?
The last stage of alcohol withdrawal, delirium tremens (DTs), is a severe, life-threatening condition with a mortality rate of approximately 5 to 15 percent. DTs can occur between 1 and 14 days after the patient’s last drink, most commonly within 2 to 5 days. A single episode of DTs lasts between 1 and 3 days. Multiple episodes can last as long as a month. DTs should be suspected in any patient with delirium (mental confusion) of unknown cause. Signs and symptoms of DTs follow:
Severe confusion
Loss of memory
Tremors
Restlessness and irritability
Dilated pupils
Profuse sweating
Insomnia
Elevated blood pressure
Tachycardia
Nausea and vomiting
Diarrhea
Hallucinations, mostly of frightening nature
Seizures are common in alcoholic withdrawal but not in DTs. However, approximately a third of those who have seizures in early withdrawal progress to DTs if left untreated or if treated inadequately. The treatment goals for a patient who experiences DTsinclude psychological as well as physical support. (DTs can be a frightening experience.)
What are the s/s of narcotic or heroin or morphine, or opioid overdose? What is the EMT treatment?
CNS depression
Respiratory depression
Miosis (constricted pupils)
Seizure that can occur due to the hypoxia associated with the respiratory depression
Psychomotor delay and disabilities from hypoxia and cell injury
Dysarthria (speech disturbance from paralysis of facial muscles) from hypoxia and cell injury
Ataxia (incoordination from hypoxia and cell injury
Tremors from hypoxia and cell injury
Crackles from acute pulmonary edema associated with leaking pulmonary capillaries thought to be from the related hypoxia
Hearing loss from altered metabolism or direct effect on the car
Hypotension from CNS depression
Braciycanlia from CNS depression
Nausea and vomiting from decreased gastrointestinal motility
Urinary retention from urethral sphincter spasm
Pruritus (itching), flushing and urticaria (hives) from histamine release
Hypoglycemia (the mechanism is unclear)
Hypothermia (the mechanism is unclear)
Treatment
Establish and maintain an open airway. Be prepared to suction the airway or place the patient in a lateral recumbent position due to an increased risk of vomiting
Assess the breathing status. If the respiratory rate or tidal volume is inadequate, immediately provide positive pressure ventilation while maximizing oxygen delivery through the ventilation device.
Maintain adequate oxygenation. If the SpO2 is <94% or signs of respiratory distress, hypoxia, hypoxemia, or poor perfusion are present, administer oxygen via a nasal cannula to achieve and maintain a SpO2 of 94% or greater.
Administer naloxone. If the patient has respiratory depression, hypotension, or bradycardia, administer naloxone to block the opioid receptors and reverse the effects of the heroin or other opioid drug that has been abused. Naloxone can be administered intranasally (Figure 22-20 ) using a mucosal atomizer device or it can be administered as an intramuscular injection. Follow your local protocol. With naloxone administration, you can completely reverse the opioid effects in some patients who become combative upon regaining consciousness (Figure 22-21 ). Take precautions to ensure your safety prior to administration of the naloxone. Also, some drugs, such as carfentanyl require much higher doses of naloxone administration. The amount that you carry and route might not be adequate to reverse the physiologic instability in these patients. You might need to request an ALS unit for intravenous administration of much larger doses of naloxone.
Naloxone is a pure opioid antagonist with a rapid onset of action. It competitively binds opioid receptors and can reverse all of the receptor actions of the opioid by effectively blocking the ability of the drug to bind with the receptor site.
The typical dose is 0.4 mg to 2 mg when given by various routes. When administered by an intranasal route, the typical dose is 2 mg—1 mg is administered via a mucosal atomization device (MAD) in each nostril.
Following the administration of naloxone, it is important to reassess the airway, respirations, oxygenation, pulse, and blood pressure. You are primarily looking for the reversal of any respiratory depression, hypotension, and bradycardia. If the patient continues with respiratory depression, hypotension, or bradycardia after the initial administration, it may be necessary to redo the patient. Follow the same steps 5 through 9 until the desired effect is achieved. Your intention is not to completely reverse the mental status of depression but to reverse any respiratory depression, hypotension, and bradycardia. The opioid the patient took may outlast the effects of the naloxone, which will cause the patient to deteriorate. lf this occurs, it is necessary to redo the patient.
What are the s/s of methamphetamine use? How would this affect a patient’s vital signs?
Hyperthermia, muscle rigidity, or severe excitation can occur, leading to long periods of an awake and excited state. The resulting 1 hypertension, hyperthermia, and increased muscle tone can be life-threatening. Methamphetamine use is associated with the sensation of ants or bugs crawling under the skin. The patient often picks at his skin or mutilates himself. Panic attacks and visual and auditory hallucinations can also occur.
What are the s/s of a cocaine overdose?
Alcohol ingestion, local inflammation, cold exposure, or a severe heat emergency (heat stroke) can also turn the skin red.
What is the talk-down technique? When should you not try to use this on a patient?
The talk-down technique, discussed next, is useful with a patient who is experiencing a “bad trip.” The Talk-Down Technique - The talk-down technique can help you reduce the patient’s anxiety, panic, depression, or confusion, as follows:
Never use the talk-down technique for patients who you know have used the hallucinogen phencyclidine (PCP) because it can further agitate them.
What is a synthetic cannabinoid? How is it taken? What are its dangers?
Synthetic cannabinoid: A synthetic cannabinoid, often categorized as a new psychoactive substance (NPS), is a manufactured chemical that has similar effects as THC found in cannabis. It is an unregulated substance that is sold as a mind-altering chemical. It is sprayed on dried or shredded plants to be smoked (herbal incense), or can be used as a liquid that can be vaporized and inhaled in e-cigarettes or other similar devices. It can also be brewed as tea. It is often referred to as synthetic marijuana or “fake weed” and labeled as a safe alternative to natural marijuana that is legal even in states where natural marijuana is illegal. It is often sold as herbal incense and comes in colorful foil packages or bottles similar to e-cigarette liquids. They are often labeled as “not for human consumption” but are still smoked or inhaled by many users.
Dangers
Synthetic cannabinoids can affect the brain more powerfully than marijuana and can produce unpredictable and life-threatening effects. This occurs because synthetic cannabinoids bind more strongly to the cell receptors affected by THC. Users report that the substance produces similar effects as marijuana, such as elevated mood, relaxation, altered perception, and psychosis, in which there is disordered thinking and detachment from reality.
What is tolerance vs. dependence vs. addiction?
Tolerance: A habitual drug user can develop a tolerance to a drug in which larger doses are required to produce the same desired effects. This quite often leads to physical or psychological dependence, in which the patient experiences.
Dependence: Drugs that commonly produce physical drug dependence are narcotics, sedatives, hypnotics, barbiturates, cocaine, and marijuana.
Addiction: This is an illness; sudden withdrawal can cause apathy, long periods of sleep, irritability, depression, and disorientation.
