I would like to add a follow up to yesterday’s article (thanks again for the link Tim).  UBC is currently doing a study on PTSD.

In order to be eligible to participate, paramedics must:

1. Be currently employed as a paramedic in Canada.

2. Have a cohabitating spouse or romantic partner who is also interested in participating. (Exception: If your work partner and his/her spouse are interested in participating, you may still participate.)

3. Be working a block of 4 shifts with AT LEAST 1 day off before and AT LEAST 2 days off after in the near future. This means any rotation which contains 4-shift blocks will work!

If you are interested in participating or learning more about this study visit www.medicscope.com

Canadian emergency departments (EDs) annually treat 1.3 million patients who have suffered blunt trauma from falls or motor vehicle collisions and who are at risk for cervical spine (c-spine) injury. Most such cases are alert and stable adults and less than 1% has a c-spine fracture.

The vast majority of these patients are transported to hospital by ambulance and end up in a cervical collar and strapped to a back board.

A group of Ottawa emergency physicians conducted a detailed study of traumatic “neck pain” and their findings were outstanding.  This study resulted in the Canadian C Spine Rules.

This new system is now an international standard as it is incredibly reliable and accurate.  The purpose of the Canadian C Spine Rules is to decide when it is safe to “clear” a patient’s C Spine and when radiography is required.

Prolonged immobilization is often unnecessary and adds considerably to patient discomfort.  Tissue breaks down quickly on the hard boards, even more sore in the elderly.  In attempts to get patient’s off these boards as quickly as possible a group of Ontario hospitals will be training triage nurses to utilize the Canadian C Spine Rules to “clear” your patient’s c spine.

Currently, the following hospitals are participating in the CAHO Canadian C-Spine Rule ARTIC Project: Kingston General Hospital, London Health Sciences Centre, Hôpital Montfort, North York General Hospital, St Michael’s Hospital, Sudbury Regional Hospital, Sunnybrook Health Sciences Centre, Thunder Bay Regional Health Sciences Centre, and University Health Network.

Complete heart block, also referred to as third-degree heart block, or third-degree atrioventricular (AV) block, is a disorder of the cardiac conduction system where there is no conduction through the AV node. Therefore, complete dissociation of the atrial and ventricular activity exists.

The ventricular escape mechanism can occur anywhere from the AV node to the bundle-branch Purkinje system.It is important to realize that not all patients with AV dissociation have complete heart block. For example, patients with ventricular tachycardia have AV dissociation, but not complete heart block. Electrocardiographically, complete heart block is represented by QRS complexes being conducted at their own rate and totally independent of the P waves.

Diagnosing Sepsis

However, the diagnosis of sepsis is difficult and not reliable based on general signs and symptoms such as fever, tachycardia and tachypnea.  In hospital lab values can obtained but how can we as paramedics zero in on the septic patient?

Sepsis is not a simple process to identify.  Early in the cycle, patients can look the all too familiar “Generally Unwell”. Core temperatures can be high or low.  The patient may be aware they’re fighting an infection, but not always.Whether or not your service has a sepsis protocol, recognizing patients transitioning into severe sepsis is an important clinical skill.  Here are some guidelines:

• Identify the high-risk patients: Sepsis is more likely to occur in several high-risk populations.  Have a high index of suspicion when evaluating the elderly or the very young, patients who are bed-confined or immobile, and patients who have had recent surgeries or invasive medical procedures. Be highly suspicious of patients receiving immunosuppressive treatments like chemotherapy or post-organ transplant medications.  Recognize that some disease processes leave the patient naturally immunocompromised.  This is the case with diabetes, liver cirrhosis, autoimmune disease and HIV/AIDS populations.
• Look for a source of infection: In many cases the source of infection is identifiable.  Ask about recent illnesses, surgeries, invasive procedures or trauma.  Has the patient had a respiratory infection or been feeling ill?  Ask about symptoms of gastrointestinal or bladder infections, abdominal discomfort and unusual body or joint pain.  Also ask about current or past prescriptions for antibiotics, steroids or immunosuppressants.
• Pay attention to the patient’s body temperature: We traditionally consider fevers when we envision the body’s response to infection, but septic patients may also be mildly hypothermic.  Ask the patient about recent fever or chills, and if you have a means to take an accurate temperature, take one.  Be suspicious of core temperatures above 38°C  or below 36°C
• Look for changes in vital signs: When an infection is confirmed or highly suspected, changes in vital signs become significant.  Look for a pulse greater than 90 and a respiratory rate above 20 breaths per minute in combination with a blood pressure below 90 systolic or a mean arterial pressure below 65.  Consider these markers tipping points for severe sepsis.
• Assess other subtle physical signs: Patients transitioning into severe sepsis will rapidly become fluid-depleted. Look for signs of dehydration like poor skin turgor, dry mucosa and decreased urine output.

When you think you’ve identified a severe sepsis patient, keep these key points in mind.

• Support the airway: End-organ hypoxia is the enemy of the sepsis patient, so we need to ensure we’re oxygenating appropriately. Place patients with adequate respiratory drive on high-flow oxygen. Monitor the patient’s SpO₂. Keep in mind that sepsis patients are likely candidates for acute lung injury and acute respiratory distress syndrome. When mechanical ventilation is necessary, take care not to overventilate.
• Aggressive fluid resuscitation and hemodynamic stabilization: Septic patients are profoundly dehydrated. Beyond sepsis recognition, aggressive fluid resuscitation may be the single most important intervention we can begin in the prehospital environment. Establish bilateral IV lines. Local protocols will dictate the extent of fluid resuscitation permissible.Call your base physician and consult on appropriate endpoints when your protocols do not specifically address sepsis. Patient age, history, weight, vital signs, medical history and individual physician preferences will all play roles in establishing an initial fluid resuscitation plan. Even patients who are traditionally considered fluid-restricted, such as those with congestive heart failure and renal failure, may still be indicated for well-monitored fluid challenges. Pay close attention to lung sounds and blood pressure during aggressive fluid resuscitation.Prehospital use of vasopressors for sepsis is rare and should be considered only after fluid resuscitation has proven inadequate. Some 40%-60% of severe sepsis patients will eventually receive vasopressors as part of their in-hospital courses, usually dopamine or dobutamine. Seek consultation with your base physician if you’re considering dopamine after unsuccessful fluid administration.
• Prevent hypothermia: Patients transitioning through severe sepsis become highly susceptible to hypothermia. This is especially true in the elderly and young. Abnormally low body temperatures increase mortality in these patients. While we don’t want to bundle febrile patients, resist actively cooling septic patients and protect them from excessive heat loss from the environment and administration of cold fluids.
• Trend the vital signs: Trend heart rate, blood pressure and respiratory rate in septic patients. Calculate the mean arterial pressure if you are trained to do so. Not only are these values excellent warning indicators of early end-organ failure, they are necessary signposts on the journey through sickness and into health.

First take your own pulse.  Then look to mom.

Normal perinatal mortality is 0.04% where as ED perinatal mortality is aprox 8%.

When treating mom always use supplemental oxygen and put mom in left lateral recumbent position.

Establish IV access.  Two large bore IV’s would be appropriate considering the risk of hemorrhage.

Signs of labour include:

Once it is apparent that mom is indeed in labour Signs of Imminent Delivery include Rectal pressure, Strong urge to push, Crowning (sometimes you gotta look) and Multiparity.

To determine the gestation perform a Physical Exam. The fundal height reaches the umbilicus at 20wks.  Add 1cm per week to 36 weeks (costal margin).

DELIVERY

If a prehospital delivery is imminent then Prep the following: Bulb suction, Dry blanket and towels, Cord Clamps and Scissors.

When the baby begins Crowning thin the perineum, support the head with 2 hands and coach mom on pushing.  The Head is Out now Stop pushing!  Suction the mouth and nose and Check for nuchal cord (present in 25% – clamp or reduce).  Next Deliver the Shoulders with gentle downward then upward pressure on the baby’s head.  Have mom push again.  Beware of Shoulder dystocia.

Once the baby has delivered Clamp The Cord.  Use 2 clamps 10cm away from the baby and spaced 4 to 5cm apart.  Cut in between clamps (the umbilical stump can be used for access in hospital).  CAUTION!  The baby is slippery

Now it is time to Deliver the Placenta.  Delivery is proceeded by a gush of fluid or blood.  There is no rush, it may take up to 20 minutes to deliver the placenta.  Do not use too much traction on the cord and make sure to bring the placenta to the hospital.

Postpartum Care

Watch for hemorrhage.  Massage the uterine fundus, this hurts but helps reduce bleeding.  Beware of surprise twins.

Basic Neonatal Resuscitation:

Respiratory
Respiratory
Respiratory
Hypothermia
Hypoglycaemia

Neonatal ABC’s

• Dry
• Warm
• Position
• suction
• Stimulate
• Oxygen
• Ventilation
• Chest compressions
• Meds

Neonatal ACLS

• Perform chest compressions for a HR less than 80 bpm
• Compress at a rate of 120 per min and a depth of ½ to ¼ inch
• Medications (Epinephrine, Narcan, Glucose (administered as D10), Dopamine

Common Complications

Common complications can include Breech presentation, Cord prolapsed, Shoulder dystocia and Bleeding.

Breech Basics

• Only deliver these if necessary
• Do not touch the baby until you can see the umbilicus (you can cause significant intrabdominal injury
• If the head is stuck an episiotomy may be required
• Pull some cord free
• Rotate to deliver the arms
• Finger in the mouth to flex neck and deliver the head

Umbilical Cord Prolapse

• NEVER push it back in!
• Hand in the vagina to push up on baby’s head
• Mom in Trendelenberg
• Drape cord with soaked gauze
• Rapid transport
• Mom needs immediate c-section

Shoulder Dystocia (shoulders trapped behind pubic bone and not entering the birth canal)

• Pull mom’s knees back far
• Put pressure over the bladder
• Twist baby’s torso (not head) intravaginally

Bleeding at Term

• Bloody Show
• Placenta Previa
• Abruptio Placentae (abruption)
• Postpartum: Massage the uterus and Consider retained products

Every paramedic feels a dump of adrenaline when called for “in labour”.  When you arrive on scene consider the possibility of prehospital delivery, calm down and get ready and look for complications.  If the baby is a breech presentation let the body deliver then get the head out.  Once delivered, dry and warm the baby and provide respiratory care if necessary.

Atrial fibrillation describes an irregular and often rapid heart rhythm. The irregular rhythm, or arrhythmia, results from abnormal electrical impulses in the heart. The irregularity can be continuous, or it can come and go.

Normal heart contractions begin as an electrical impulse in the right atrium. This impulse comes from an area of the atrium called the sinoatrial (SA) or sinus node, the “natural pacemaker.”

• As the impulse travels through the atrium, it produces a wave of muscle contractions. This causes the atria to contract.
• The impulse reaches the atrioventricular (AV) node in the muscle wall between the 2 ventricles. There, it pauses, giving blood from the atria time to enter the ventricles.
• The impulse then continues into the ventricles, causing ventricular contraction that pushes the blood out of the heart, completing a single heartbeat.

In a person with a normal heart rate and rhythm the heart beats 50-100 times per minute.

• If the heart beats more than 100 times per minute, the heart rate is considered fast (tachycardia).
• If the heart beats less than 50 times per minute, the heart rate is considered slow (bradycardia).

In atrial fibrillation, multiple impulses travel through the atria at the same time.

• Instead of a coordinated contraction, the atrial contractions are irregular, disorganized, chaotic, and very rapid. The atria may contract at a rate of 400-600 per minute.
• These irregular impulses reach the AV node in rapid succession, but not all of them make it past the AV node. Therefore, the ventricles beat slower, often at rates of 110-180 beats per minute in an irregular rhythm.
• The resulting rapid, irregular heartbeat causes an irregular pulse and sometimes a sensation of fluttering in the chest.

Atrial fibrillation can occur in several different patterns.

• Intermittent (paroxysmal): The heart develops atrial fibrillation and typically converts back again spontaneously to normal (sinus) rhythm. The episodes may last anywhere from seconds to days.
• Persistent: Atrial fibrillation occurs in episodes, but the arrhythmia does not convert back to sinus rhythm spontaneously. Medical treatment is required to end the episode.
• Permanent: The heart is always in atrial fibrillation. Conversion back to sinus rhythm either is not possible or is deemed not appropriate for medical reasons.

Atrial fibrillation, often called A Fib, is a very common heart rhythm disorder.

• It affects about 1% of the population, mostly people older than 50 years. This amounts to more than 2 million people.
• The risk of developing atrial fibrillation increases as we get older. About 5% of people older than 80 years have atrial fibrillation.

For many people, atrial fibrillation may cause symptoms but does no harm.

• Complications can arise, but appropriate treatment reduces these risks.
• If treated properly, atrial fibrillation rarely causes serious or life-threatening problems.

Atrial Fibrillation Causes

Atrial fibrillation may occur without evidence of underlying heart disease. This is more common in younger people, about half of whom have no other heart problems. This is often called lone atrial fibrillation. Some of the causes not involving the heart include the following:

• Hyperthyroidism (overactive thyroid)
• Alcohol use (holiday heart)
• Pulmonary embolism (a blood clot in the lungs)
• Pneumonia

Most commonly, atrial fibrillation occurs as a result of some other cardiac condition (secondary atrial fibrillation).

• Heart valve disease: This can be something you are born with or be caused by infection or degeneration/calcification of valves with age.
• Enlargement of the left ventricle walls (left ventricular hypertrophy)
• Coronary heart disease (or coronary artery disease): This results from atherosclerosis, deposits of fatty material inside the arteries that cause blockage or narrowing of the arteries.
• High blood pressure (hypertension)
• Cardiomyopathy (disease of the heart muscle) leading to congestive heart failure
• Sick sinus syndrome (improper production of electrical impulses because of malfunction of the SA node)
• Pericarditis (inflammation of the sac surrounding the heart)

Atrial fibrillation frequently occurs after cardiothoracic (open heart) surgery, but often resolves in a few days.

For many people with infrequent and brief episodes of atrial fibrillation, the episodes are brought on by a number of triggers. Because some of these involve excessive alcohol intake, this is sometimes called holiday heart. Some of these people are able to avoid episodes or have fewer episodes by avoiding their trigger. Common triggers include alcohol and caffeine in susceptible individuals.

Atrial Fibrillation Symptoms

Symptoms of atrial fibrillation vary from person to person.

• A number of people have no symptoms.
• The most common symptom in people with intermittent atrial fibrillation is palpitations, a sensation of rapid or irregular heartbeat. This may make some people very anxious. Many people also describe an irregular fluttering sensation in their chests.
• Some become light-headed or faint.
• Other symptoms include weakness, lack of energy or shortness of breath with effort, and chest pain.

OntarioMedic is pleased to announce that our filed guide has undergone upgrades and is now available for your Blackberry, iPhone, iPad or Android devices.   Check out our FREE condensed version or order the complete version.

Burns are death and necrosis of a tissue due to heat. Burns may occur due to dry heat, (in form of fire) wet heat (in form of scalds) or electrical burns.

Burns are divided into 3 different types:

(I) First degree or superficial burns:- It is commonly seen with a sunburn. It is usually red and blanches (becomes white) on pressure. It occurs due to damage to only the top (epidermis) layer of the skin. It heals by itself in 3-6 days and generally does not require hospitalization.

(II) Partial thickness burns or second degree burn:- It involves the entire epidermis and some portion of the dermis. They are of 2 types:-

(a) Superficial partial thickness burn:- They are painful and associated with blisters. They heal within 3 weeks without any visible scars. There may be some pigment changes.

(b) Deep partial thickness burns :- They are dry white in color. They may cause scarring and take longer to heal. Skin grafting is usually required for healing.

(III) Full thickness burns:- They involve the entire epidermis and dermis. They are dry and leathery in appearance. They cause scarring and require immediate skin grafting and use of compression garments.

Heat damages the cells of the skin releasing chemicals that stimulate nerves and cause pain. Burn heals when a new layer of skin grows in from the edges of the burn. However, if the burn is very large or very deep, bacteria may invade and cause infection. Also due to evaporation of fluids from the open wound, the patients may get dehydrated.

Hence the 2 major short term complications of burns are infection and dehydration.

SECOND DEGREE BURNS

In most cases, second-degree burns are caused by the following:

• scald injuries
• flames
• skin that briefly comes in contact with a hot object

The following are the most common signs and symptoms of a second-degree burn. However, each child may experience symptoms differently. Symptoms may include:

• blisters
• deep redness
• burned area may appear wet and shiny
• skin that is painful to the touch
• burn may be white or discoloured in an irregular pattern

The symptoms of a second-degree burn may resemble other conditions or medical problems. Consult your child’s physician for a diagnosis.

Superficial second-degree burns usually heal in about three weeks, as long as the wound is kept clean and protected. Deep second-degree burns may take longer than three weeks to heal. Specific treatment for a second-degree burn will be determined, based on the following:

• child’s age, overall health, and medical history
• extent of the burn
• location of the burn
• cause of the burn
• child’s tolerance for specific medications, procedures, or therapies

A second-degree burn that does not cover more than 10 percent of the skin’s surface can usually be treated in an outpatient setting. Treatment depends on the severity of the burn and may include the following:

• antibiotic ointments
• dressing changes one or two times a day depending on the severity of the burn
• daily cleaning of the wound to remove dead skin or ointment
• possibly systemic antibiotics

Wound cleaning and dressing changes may be painful. In these cases, an analgesic (pain reliever) may need to be given. In addition, any blisters that have formed should not be burst.

THIRD DEGREE BURNS

In most cases, third-degree burns are caused by the following:

• a scalding liquid
• skin that comes in contact with a hot object for an extended period of time
• flames from a fire
• an electrical source
• a chemical source

The following are the most common symptoms of a third-degree burn. However, each child may experience symptoms differently. Symptoms may include:

• dry and leathery skin
• black, white, brown, or yellow skin
• swelling
• lack of pain because nerve endings have been destroyed

Large third-degree burns heal slowly and poorly without medical attention. Because the epidermis and hair follicles are destroyed, new skin will not grow.

Specific treatment for a third-degree burn will be determined, based on the following:

• child’s age, overall health, and medical history
• extent of the burn
• location of the burn
• cause of the burn
• child’s tolerance for specific medications, procedures, or therapies

Treatment for third-degree burns will depend on the severity of the burn.  Burn severity is determined by the amount of body surface area that has been affected. Treatment for third-degree burns may include the following:

• early cleaning and debriding (removing dead skin and tissue from the burned area). This procedure can be done in a special bathtub in the hospital or as a surgical procedure.
• intravenous (IV) fluids containing electrolytes
• antibiotics by intravenous (IV) or by mouth
• antibiotic ointments or creams
• a warm, humid environment for the burn
• nutritional supplements and a high-protein diet
• pain medications
• skin grafting (may be required to achieve closure of the wounded area)
• functional and cosmetic reconstruction

PREHOSPITAL / EMS TREATMENT

It goes without question that removal and rapid cooling of the burn is a priority.  By cooling the burn quickly you can arrest the burn’s progress reducing the amount damage and thickness as well as bring relief to the patient.

Clean sterile water will feel extremely cold to your patient, children especially will not like this procedure.  They have already undergone a painful traumatic event and it is hard to do something that seems to be inflicting more discomfort on them.  It is important to realize that removal from the source is not enough to stop the burning process.  Burns continue to spread across the skin and deeper into the tissue destroying more the longer they are allowed to cool by mere convection.  The momentary discomfort caused by water is far outweighed by the cessation of the burning process.

Cooling must be performed judiciously as your patient is subject to hypothermia.  The damaged skin can no longer regulate body temperature and the cooling of the burn will plunge your patient into hypothermia very quickly.  Hypothermia will put your patient at greater risk for V-Fib and Asystole.

Burns are extremely painful and if possible analgesia should be considered.  Clothing should be cut away and jewelry removed.  As the body attempts to compensate by sending plasma to damaged tissue, via 3rd space fluid shift, extremities will swell (jewelry could potentially act as a tourniquet stopping perfusion to digits).  Be sure to monitor your patient’s blood pressure as they may become hypotensive following the fluid shift.  Keep in mind that swelling extremities may give you misleading results.

The paramedic’s largest concern will be to arrest the burning process and rapid transport.  Monitor for dysrhythmias secondary to hypothermia, administer pain relief and oxygen.  The patient’s largest challenge will be infection so be sure to use sterile water and burn dressings.

GENERAL TREATMENT & HEALING

Long-term, during healing, the wound may start shrinking or becoming smaller leading to contractures. Contracted tissue may lead to a loss of normal motion if present in the limbs and can also cause a distorted appearance due to pull on the surrounding healthy tissue. In a burn patient, sensations of hot, cold, wetness, dryness, touch and pain may change even permanently. A patient post-burn will not to be able to sweat properly due to damaged sweat glands. Hence appropriate clothing as per the season is required (cotton in summer and warm clothing in winter)

Skin color is determined from the melanin and carotene pigments in the epidermis. Melanin protects the skin from sunburn. After a burn, the burnt skin may not be able to produce melanin, hence leading to sun burn. Also the skin may become lighter(depigmented or hypopigmented ) as compared to the normal skin or darker (hyperpigmented).

First degree or superficial burns heat naturally. Deep second degree and full thickness burns require skin grafting for rapid healing and minimum scarring and generally require hospital care.

In addition supportive therapy like fluids, blood infusion and pain medication is required. In some patients, the burn may lead to intolerable and excruciating pain for which even lV morphine may be required.

For first degree burns and open wounds, topical creams like silver sulfadiazine and bacitracin may be applied. Often dressings may be applied.

Skin grafting consists of excision or removal of burnt devitalised tissue, removal of healthy skin from a donor site to cover the cleaned burnt area. An instrument (dermatome) gently shaves a piece of skin about 1/100 of an inch thick from the healthy skin and that skin is grafted over the burnt area. Skin can also be used from dead people (cadavers).To help the graft become secure, the area of the graft is immobilized for at least 5 days and later normal daily activity is started. Skin grafting is usually done under anesthesia.

There are other types of artificial skin grafts available which can temporarily cover the wounds:-

(1) Xenograft or Heterograft:- Skin is taken from animals.
(2) Collagen

Meshing is a process by which the donor skin is enlarged to cover a large burnt area when there is not enough healthy skin available. The disadvantage is that it is a less durable graft and leads to more scarring. However, it helps by allowing the blood and body fluids to drain under the graft and thus preventing graft loss and it allows the donor skin to cover a great burnt area.

Grafts are held in place with surgical staples or stitches. Once the graft usually becomes stable within 4-5 days, the staple/stitches are removed.

Although the skin taken from the donor site is very thin, it can cause scarring and pigmentary changes at the donor site.

Contractures usually occur due to extension of burns over a joint limiting movement. Skin tightness may be the first sign of a contracture and anti contracture positioning may be required for 24 hours a day. Exercises to stretch or elongate the skin are recommended. Sometimes surgical procedures like release of the band area (z-plasty) may be required. Before surgery, casting of the limb may be required as a constant stretch is applied by the cast to elongate the skin.

Compression garments are worn over the burnt area. Compression can also be given by splints, orthoses and casts. Compression garments help the burn heal with minimum amount of scarring by pressing and flattening the scars. Compression is given for 22-23 hours a day. It is required until almost 12-18 months post- burn or till the burn completely heals (matures).

ANATOMY OF THE SKIN

Facts about the skin:

The skin is the body’s largest organ, covering the entire body. In addition to serving as a protective shield against heat, light, injury, and infection, the skin also:

• regulates body temperature.
• stores water and fat.
• is a sensory organ.
• prevents water loss.
• prevents entry of bacteria.

Throughout the body, the skin’s characteristics vary (i.e., thickness, color, texture). For instance, the head contains more hair follicles than anywhere else, while the soles of the feet contain none. In addition, the soles of the feet and the palms of the hands are much thicker.

The skin is made up of the following layers, with each layer performing specific functions:

• epidermis
• dermis
• subcutaneous fat layer

How often do auscultate a chest?

Most paramedics would answer almost always.

We all listen for breath sounds and air entry but end there.  You are already at your patient’s chest so why are you not listening to the heart sounds.  It is reasonable to to state that for the most part the reason is comfort: “I hear something but what is it and what does it mean?”

1st & 2nd Heart Sounds

The first heart sound can usually be heard easily with both the bell and the diaphragm but the diaphragm is invaluable for analyzing the second heart sound, with the stethoscope usually best placed at the midleft sternal edge.

First Heart Sound

Loud Heart Sound

• Hyperdynamic (fever, exercise)
• Mitral stenosis
• Atrial myxoma (rare)

Soft First Sound

• Low cardiac output (rest, heart failure)
• Tachycardia
• Severe mitral reflux (caused by destruction of valve)

Variable Intensity of First Sound

• Atrial fibrillation
• Complete heart block

Second Heart Sound

Audible expiratory splitting means > 30 msec difference in the timing of the aortic (A₂) and pulmonic (P₂) components of the second heart sound.

• Splitting of S₂ is best heard over the 2nd left intercostal space
• The normal P₂ is often softer than A₂ and rarely audible at apex
  • Differential Diagnosis of P₂ audible at apex
    • Significant pulmonary hypertension
    • Atrial septal defect
• Findings should be present in both upright and supine positions: normal subjects may have expiratory splitting when recumbent that disappears when upright.

Split S2

Loud Aortic Component of Second Sound

• Systemic hypertension
• Dilated aortic root

Soft Aortic Component of Second Sound

• Calcific aortic stenosis

Loud Pulmonary Component of Second Sound

• Pulmonary hypertension

Third & Fourth Heart Sounds

A triple rhythm in diastole is called a gallop and results from the presence of a S3, S4 or both.

Description:
Both sounds are low frequency and thus best heard with the bell of the stethoscope.

Location:
If originating from LV

• Usually best heard over apex with patient in the left lateral position
• Softer during inspiration

If originating from RV

• Usually best heard over left lower sternal border
• Louder during inspiration

Third Heart Sound S3

Description:
Low frequency sound in early diastole, 120 to 180 ms after S2

Sounds like:
Lub du bub S1S3S2 cadence similar to “Kentucky”

Clinical Significance:
Results from increased atrial pressure leading to increased flow rates, as seen in congestive heart failure, which is the most common cause of a S3. Associated dilated cardiomyopathy with dilated ventricles also contribute to the sound. See Accuracy in Diagnosis of CHF .

Less commonly, valvular regurgitation and left to right shunts may also result in a S3 due to increased flow.

May be normal physiological finding in patients less than age 40.

Fourth Heart Sound S4

Description:
Low frequency sound in presystolic portion of diastole,

Sounds like:
Belub dup S1S4S2 cadence similar to “Tennessee”
Clinical significance:
Seen in patients with stiffened left ventricles, resulting from conditions such as hypertension, aortic stenosis, ischemic or hypertrophic cardiomyopathy.

In patient with mitral regurgitation, suggestive of acute onset of regurgitation due to the rupture of the chorda tendinae that anchor the Valvular leaflets.

Clicks and Snaps

Clicks

EC=ejection click :: OS=opening snap

Ejection click:

Most common early systolic sound; Results from abrupt halting of semilunar valves

Aortic ejection click:

Description:
Loud high frequency sound, associated with murmur due to same etiology
Does not vary with respiration

Location:
Best heard at apex

Clinical significance:
Causes associated with aortic valve with decreased but some residual mobility: i.e., aortic stenosis, bicuspid aortic valves and dilated aortic root; not generally heard with calcific aortic stenosis due to non-mobile valve

Pulmonic ejection click:

Description:
Early systolic ejection sound with associated murmur. Often diminishes with inspiration.

Location:
Sternal edge 2nd or 3rd ICS

Clinical significance:
Causes associated with pulmonic valve: pulmonic stenosis, pulmonary hypertension and dilated pulmonary trunk

Opening snap

Description:
High-frequency early diastolic sound (occurs 50-100 msec after A2) associated with mitral stenosis; sound due to abrupt deceleration of mitral leaflets sound with associated murmur. Often diminishes with inspiration’ accentuated in left lateral position.

Location:
Between apex and left lower sternal border

Sounds like:
RUP bu Dup rrrrrrRup Bu Dup
Correlating to s1, s2, OS, murmur of mitral stenosis,

Clinical significance:
The OS plus typical murmur indicates the murmur is due to mitral stenosis and not a flow rumble across a non-stenotic valve. The timing of the OS has been suggested as a gauge of the severity of the stenosis but has not been found to be reliable for this.

Mid-systolic click (plus late systolic murmur of mitral valve prolapse)

Others:

Prosthetic valves
Prosthetic mitral valve sounds:

• opening sound analogous to opening snap
• closing sound coincides with S1

Prosthetic aortic valve sounds:

• opening sound analogous to ejection click
• closing sound coincides with S2

Murmurs

Cardiac murmurs can be divided into three categories based on where they occur in the cardiac cycle.

Note: Short, quiet systolic murmurs are generally benign. Long systolic murmurs, diastolic murmurs and continuous murmurs are generally pathologic. (Two continuous murmurs that are benign are mammary soufflé and cervical venous hum.)

Intensity of Murmur

University of Washington Department of Medicine

Selective serotonin reuptake inhibitors (SSRIs) are a class of anti-depressant commonly prescribed in Canada.  With the prevalence of SSRI use increasing, so too has the risk for interaction with other prescribed medications.

One of the most dangerous, and rare, interactions is a condition referred to as “serotonin syndrome” or “serotonin toxicity”. Serotonin syndrome refers to the symptoms associated with an increase in the presence of the neurotransmitter 5-hydroxytryptamine (5-HT).

Serotonin syndrome presents within hours to days of an initial dose, an increase in dose or an intentional overdose of an SSRI. Intentional overdoses causing serotonin syndrome can result from a single medication but are generally limited to poly-pharmacy overdoses. Serotonin syndrome itself results from increased serotonergic neurotransmission.

SSRIs work by decreasing the pre-synaptic uptake of serotonin (a neurotransmitter involved in the regulation of aggression, pain, sleep, depression and anxiety). Serotonin syndrome most often occurs as a result of mixing an SSRI with another form of anti-depressant, such as monoamine oxidase inhibitor (MAOI).

MAOIs work by decreasing the action of the enzyme responsible for breaking down synaptic serotonin. The combination of an SSRI and an MAOI would result in an unchecked flood of serotonin into the brain.

Serotonin syndrome can be defined by a collection of symptoms resulting from an increase in serotonin.  Symptoms noted fall into one of three categories:

1. Alteration Of Mental Status: Altered mental status can range from confusion to coma and can include agitation, anxiety, delirium, hallucinations and drowsiness.
2. Neuromuscular Hyperactivity: Neuromuscular hyperactivity includes myoclonus (irregular involuntary contraction of a muscle), hyper-reflexia (overactivity of physiological reflexes), muscle rigidity, shivering and tremors
3. Autonomic Instability: Potentially the most serious, autonomic instability can present as hyperthermia, diaphoresis, sinus tachycardia, hypertension/hypotension, flushing of the skin, diarrhea and vomiting. Indications of a life-threatening presentation include coma, seizures, rhabdomyolysis and disseminated intravascular coagulation.

The two most common differential diagnoses for serotonin syndrome are neuroleptic malignant syndrome (NMS) and malignant hyperthermia. NMS results from ingestion of dopamenergic drugs and symptoms develop over a period of days rather than hours. Given this limited pool of drugs from which to draw, a good history and assessment on scene, as well as determining the times of ingestion and onset of symptoms will effectively rule out NMS.

Malignant hyperthermia, a potentially life-threatening reaction to anesthetic gasses and certain paralytics used in rapid-sequence induction, can be easily ruled out by responders assuming that none of these medications has been given.

In an emergency room setting, serotonin syndrome is treated by discontinuing the medications in question and by providing supportive care to the patient. In the pre-hospital setting, the care is the same.

In order to discontinue the ingestion of medication, activated charcoal is considered indicated if given within 60 minutes of ingestion. Supportive care consists of administration of intravenous fluids to combat dehydration from hyperthermia, benzodiazepines to control tremors and delirium, cooling measures to manage hyperthermia, and intubation and respiratory management as appropriate.

Early recognition is by far the most important measure that can be taken by paramedics. A thorough history and physical examination will offer a patient the best opportunity to receive timely treatment.

Similarly to in-hospital care, treatment for serotonin syndrome is largely supportive. Airway management and ventilatory support including OPA/NPA, intubation or use of a rescue airway such as a King LTD, administration of supplemental oxygen and positive pressure ventilation may all be utilized as appropriate.

Fluid resuscitation can help to combat dehydration and active cooling measures can help to manage hyperthermia.

Methods of active cooling can include, but are not limited to ice packs in the groin, axillae and behind the neck, moistening the patient’s skin with sterile water or saline and turning the air conditioner on in the back of the ambulance. Care must be taken to reduce shivering which will increase core temperature.

Finally, the patient should be rapidly transported to the appropriate receiving facility.