March 29, 2009, Dr Cooper

Pediatric Circulatory Emergencies

PAT

Is he in shock? Volume or Cardiogenic, assess vitals, mentation, etc, (BP last indicator)

Peds, who present with dysrhythmias, present like they are in shock. They won’t tell you that they have palpitations, etc, do not presume that if a child is in shock you always give fluid…must rule out cardiogenic causes.

Shock- failure of circulation to meet the metabolic demands of the tissues (energy)

• Hypoperfusion – inability of circulation to deliver blood to tissues, results in hypoxia
• Hypotension – not enough pressure to deliver blood to core organs
• Compensated shock – inability to meet needs of peripheral tissues
• Decompensated shock – inability to meet metabolic demands of core organs
• Cardiopulmonary failure – moribund state resulting in from total respiratory and/or circulatory collapse

Preload – tension in ventricle wall at end diastole – corresponds with RAP/LAP (potential amount of force that can be generated by the ventricle based upon the amount of stretching by the muscle fibers – determined by end diastolic volume

Afterload- tension in ventricular wall at end systole (covaries with PVR peripheral vascular resistance) (pressure head against which the heart has to squeeze)

Contractility – force developed by the ventricular wall during systole

Pediatric Hemodynamic changes

• Blood Loss Heart rate immediately increases and only drops at around 45% loss
• BP maintains until about 30% loss and then drops severely (soft arteries can constrict much better than adults)
• CO starts dropping immediately and also drops severely of at 30% loss

Shock – A Hydraulic Solution

Pump Failure (cardiogenic)

• Electrical dysrhythmias (defib cardiovert)
• Mechanical – cardiomyopathy (inotrope, vasopressor)

Pipe Failure

• Distributive –(anaphylaxis, neurogenic – decreased vascular tone) (volume resuscitation MAST, Epi, contain the spread)
• Obstructive (Pneumothorax, Tamponade) (decompress tension pneumo)

Prime Failure

• Hypovolmic dehydration, hemorrhage, GI
• Dissociative –CO poisoning (o2 specific antidote)

Kids have proportionally larger blood volume but absolute volume is smaller

Softer more compliant vessels – capable of intense vasoconstriction

Smaller heart ventricles less compliant – less stretch per Starling’s Law – cannot really increase contractility – more dependent on rate to increase CO

Pulse higher than 150 – (5x age in years) is tachycardia, BP <70 +2 x age is lowest BP

Hypovolemic shock most common is peds, then septic, then cardiogenic

Hypovolemic – mostly dehydration, then hemorrhagic, GI

Septic –more common endotoxin vs extotoxin – (results in inability for cells to extract o2)

Cardiogenic – usually electrical (SVT VFIB)

Kids don’t usually get clammy unless cardiogenic, mottled in Hypovolemic

Simultaneous palpation of proximal and distal pulses (eg. femoral vs Pedal) big diff indicates compensated shock

Fluid Doses 20ml/kg of NS or LR – does it help? See study…Bottom line – maybe not be effective in short transport times. Focus on maintaining airway.

2 attempts or 90 sec, AC or saphenous at ankle. Then try IO. IO must be injected under pressure, gravity drip will not work

Pediatric Trauma

• Immature anatomy
• Different mechanisms
• Long term sequela
• Age specific equipment

• Larger heads, softer skulls – will fall head first, will decompensate quickly due to head trauma, soft tissue obstruction due to decrease tone leading to hypoxemia, ICP, cerebral edema,
• Proportionally smaller torso yet larger organs
• Impact – smaller total body mass
• More often hit by cars than unrestrained passengers (abdomen and L spine from improper seat belt position)
  • Waddell’s Triad
  • 1. Femur fracture
    2. Intra-abdominal or intrathoracic injury
    3. Head injury
• Falls from height
• Fall from bike – head – unhelmeted bike riders 2^nd leading cause of head injury death in US kids (#1 MVA)

Normoventilate(30) for resp failure, decomp shock, traumatic coma

Hyperventilate (35)– single dilated pupil, fixed dilated, apneic spells

SCIWORA Syndrome: (Spinal Cord Injury w/o Radiologic Abnormality)

Head Trauma – ….

Neck Trauma ……

Chest Trauma – soft bone structure –

Abdominal Trauma – upper organs are lower, lower organs are higher (liver not well protected), thinner walled, abdominal viscera less protected

MSK Trauma, lose less blood, growth plate involvement, incomplete fractures, vascular injury common

ABCDEF – Airway Breathing Circulation Disability (pupils and GCS), E exposure, (but keep warm) F (focused physical on stable patient)

El Physiocontrol Lifepak 12, así como muchos otros tipos de equipos médicos usados se pueden comprar en línea por mucho más barato que comprar nuevos.

3/25/09 Dr Cooper

Pediatric Airway Management

Bag and drag, get control of lungs and heart will follow – get control of airway and move

Start with PAT – Appearance – example, seesaw respirations – upper airway obstruction. Snoring; soft tissue, gurgling; secretions, stridor; croup FBAO, epiglottis. Hoarseness; laryngeal trauma

• Mandibular block, needs to be moved forward– use OPA or Jaw thrust
• Larynx, higher and more forward in the throat, airway is funnel shaped, particulate matter can get wedged below cords but above cricoid ring.
• Size of Infant airway= drinking straw. Adult=Garden hose

Management

• Non- rebreather
  Pulse Oximeter of 90-95%, GCS 14, AVPU of V , compensated shcok – SBP 70-90 + 2x age
• BVM, Spo2 <90%, SBP <70 + 2x age (decompensated shock), Traumatic Coma, AVPU P or U, GCS 8 or less – disable pop-off valve, watch the chest just rise,
  • Size the mask, completely cover nose and mouth, face mask cannot press against eye, causes profound vagal response in baby
  • EC Clamp
• OPA – teeth to angle of mandible
• NPA – nares to tip of earlobe
• Positioning
  • Medical – Sniffing plus
  • Trauma – Neutral airway position
  • Squeeze – relax, 20 times per minute
  • Do not hyperextend neck in either case
  • Infant – pad entire body (or use a backboard with a hole for head). Head is too high and padding aligns plane of face to be parallel with stretcher. Disproportion ends around 8 years of age. Older child may need a shoulder roll.
  • Steeles rule of three, spinal cord is only one third of spinal canal. Hard to add further injury as long as you keep some degree of caution, a little movement won’t injure,
  • May have to remove C collar in order to intubate

Technique for high pressure ventilation- Sniff plus, jaw thrust up into mask, two thumbs on side of mask

ETT – respiratory failure decompensated shock, traumatic coma

• Miller Blade to lift floppy epiglottis (less than 8 years)
• Uncuffed tube – allows for larger diameter tube, and cuff pressure may cause pressure on tracheal mucosa
• Pass tube just below where black mark disappears
• 4 Ps
  • Prepare – suction o2 scope and tube
  • Position patent and operator – eye level of airway –
  • Preoxygenate
  • Perform intubation _ don’t persist longer than you can hold your own breath
    • Smaller mouth, developing dentition, etc avoid levering, suction avoid prying
  • RSI where used – GCS 5-9
  • Confirm placement primarily and secondary (wave form capnography)
• Neonatal Intubation – very delicate maneuver
• DOPE for common ETT problems
  
  • Displacement – re-auscultate
    
  • Obstruction – suction
    
  • Pneumothorax – absent sounds on one side
  • Equipment failure –
  • Don’t screw around, bad tube – remove
• Nasogastric Intubation
  • Straight back into nares will follow curve of throat, measure from nares, around ears down to xyphoid process

ETT vs BVM – No significant mortality differences, true for medical and trauma patients.

BVM the single most important skill to master

(TUBE TOOLS – CD Rom)

The Physiocontrol Lifepak 12 as well as many other types of used medical equipment can be purchased online for much cheaper than buying new.

___________________

Respiratory Problems

• Respiratory distress – increased effort but enough to compensate for tissue hypoxia – due to mild hypoxemia (days)
• Respiratory failure increased or decreased effort not enough to compensate for tissue hypoxia – due to sever hypoxemia (hours)
• Respiratory arrest – if uncorrected leads to cardiopulmonary arrest (2 minutes)

• Upper airway obstruction – extrathoracic
• Lower airway disease – intrathoracic

Grunting = PEEPing

Peripheral mottling – circulatory problem; central mottling- respiratory problem

Sniffing and tripod – severe distress, head bobbing or grunting – respiratory failure

Oxyhemoglobin dissociation curve – kid won’t turn blue until o2 is dangerously low

Pediatric Respiratory volumes -Kids have smaller oxygen cushion than adults, will deteriorate more quickly. Higher o2 requiements

Upper Airway Obstructions

• Croup
• FBAO
• Bacterial Tracheitis
• Least common.epiglottitis rare due to vaccine

Lower Airway

• Asthma –reactive airway disease
• Bronchiolitis – caused by RSV
• Pneumonia – lung tissue disease
• FB – small FB lodged in lower airway – generally caused resorbtion atelectasis

Pediatric Airway Assessment – determine degree of problem – altered mental status very worrying sign, indicates respiratory failure – BVM – if the baby accepts the mask he needs the mask.

Treatment – o2 always primary – everything else is adjunct

Pediatric Assessment, Dr Cooper

3/23/09

See www.cpem.org

• Planning: Triage & transport – Needs vs. resources – enroute, review and plan
• Arrival: General Impression: Pediatric Assessment Triangle (PAT) – Hands off assessment – ABC Appearance, Work of Breathing, Circulation to skin
• Initial Assessment: Rapid cardiopulmonary assessment – Hands on
• Focused History: pertinent negatives, relevant findings

Pediatric Assessment Triangle

1. Appearance
   

• Alertness
• Distractibility
• Consolibility
• Eye contact
• Quality of cry
• Spontaneous movement
• (All critical to whether brain is perfused properly)

   

1. Work of Breathing
   

• Chest rise
• Rocking motions
• Retractions
• Nasal flailing
• Head bobbing
• Grunting
• Snoring
• Stridor

(C)Circulation

• Pallor
• Mottled
• Blue
• Grey

Initial Assessment: Rapid cardiopulmonary assessment – Hands on

• Airway –clear? Maintainable?, stable?
• Breathing – ventilation, oxygenating, stable? In peds rates and effort are not necessarily related like adults, effort much more important!
• Circulation: Shock? Cardiogenic?, stable? Shock: inability of blood to meet metabolic needs of the tissues- Mental status, pulse rate and character; distal vs. proximal, skin color, BP. Cardiogenic shock: Dysrhythmias, other , compensated, decompensated, cardiopulmonary failure (cardiogenic shock not initially treated with fluid)

Focused History: pertinent negatives, relevant findings

Why peds don’t have heart attacks: no CAD, atherosclerosis, etc –congenital heart diseases are rare. Adults drop dead, kids droop dead (secondary to respiratory arrest, etc)

Anatomic & Physiologic differences

Child airway – funnel shaped, narrowest part is at crichoid ring- adult s cylinder, narrowest at glottis

• Small jaw, large tongue, prone t soft tissue obstruction – reposition
• Immature immune system. lack of specific antibodies, protective mucus layer
• Infants are nasal breathers, keep clear
• Floppy omega shaped epiglottis
• Narrow subglottic area

Remember if suspected C spine injury, stabilize c spine before/while maintaining airway

Breathing anatomy

• Adult – diagonal ribs, stiff cartilage, stronger muscles
• Ped – horizontal ribs, soft cartilage, weaker muscles – diaphragmatic breathers, much less alveoli – faster o2 depletion. Susceptible to barotraumas, high risk of Pneumothorax, bag until chest rise, no more. (head bobbing grunting – near end resp failure)young tissue – high elastin content– shift mediastinum -easily

Breathing assessment requires an open Airway! – ASSESS A, THEN FIX A! THEN GO ON TO B!

• Is ventilation adequate – inspect chest rise – capability    
• Auscultation – air entry
• (Missed slide)

Always consider hypoxia first as cause for AMS

• Auscultate in armpits, small chest, sounds travel
• ETT only of BVM ineffective
• Consider NG/OG if abdominal distention

Circulation

• Adults, big hearts large chambers and thin walls, Starlings Law (like a spring, recoil helps CO)
• peds – small chambers thick walls – can’t vary CO well with heart walls, CO depends only on HR
• Adults – stiff vessels – vigorous response to hypovolemia and hypothermia
• Peds – soft vessels – more compliant vessels
• Smaller blood volume, lose lager percentage compared to adult
• Smaller fat mass – larger relative blood volume

Bleeding control – direct pressure – retain systemic o2

Shock assessment – cause assessment – cardiogenic etc – Simultaneous palpation of central and peripheral pulses – strong central weak peripheral – compensated – everything weak; decompensated shock

• Tachycardia = 150 – 5x age in year
• Kids get mottled – not clammy
• Cap refill – use warm extremities
• Minimum systolic BP: 80 + 2x age

Adrenaline makes you stupid – use a Broselow Tape

Dr Giordano

3/15/09

Chest Pain Lecture

• Coronary artery Diseases (CAD)
  • Ischemia
  • Infarction
• Atherosclerosis – is a hardening of an artery specifically due to an atheromatous plaque
  • Inner lining of aorta, cerebral and coronary blood vessels
  • Streak of fat enlarges
  • Locus for formation of a fixed clot
• Arteriosclerosis
  • Caused by calcium precipitation
  • Reduces elasticity of arteries
• Peripheral Vascular Disorders (PVD)
  • Arterial bruits (swishing) indicate presence of atherosclerosis, no carotid massage!
  • Claudication –severe pain in calf muscle, painful limp, caused by narrowing of vessels to these muscles
  • Phlebitis –inflammation of veins – may lead to PE
    • S&S -Pan, swelling, redness, warmth, tenderness, (only present in half )
• Acute Coronary Syndrome (ACS)
  • Any group of symptoms consistent with AMI
  • Typically presents as chest pain
  • Get a 12 lead
  • Q waves – AMI
  • Unstable angina
  • May not see any EKG changes
• Angina Pectoris
  • Principal symptom of CAD
  • Choking the chest
  • Supply of o2 is insufficient for needs of myocardium
  • Cardiac muscle becomes ischemic
  • Switches to anaerobic metabolism, producing lactic acid, pain
• Stable angina
  • Recurrent pattern
  • Predictable pain after certain exertion, predictable location duration and intensity
  • Chronic
• Unstable Angina
  • Indicates greater degree of obstruction
  • Noticeable changes
  • Occurs without predictable stress
• Prinzmetal’s angina, May
  mimic MI pattern in 12 Lead EKG and reverses with NTG, also known as variant angina or angina inversa, is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in cycles. It is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than directly by atherosclerosis (buildup of fatty plaque and hardening of the arteries).
• Management considerations
  • Not all chest pain is caused by cardiac ischemia or injury.
  • Difficult to differentiate between angina and an MI in the field
  • Better to overtreat angina than to undertreat an MI
• Heart attack
  • Portion of cardiac muscle is deprived of o2 long enough for portions to die
    • Occlusion by clot
    • Spasm of coronary artery
    • Reduction of blood flow from any cause
• Visceral Pain
  • Blood vessels – organs
  • Difficult to describe or pinpoint
  • Heaviness, ache, discomfort
  • Referred pain
• ACS
  • Unstable angina
  • MI
    • Q-wave, transmural
    • Non q wave, sub-endocardial
• Occlusion will result in;
  • 70-80% CP at exertion, 90% CP at rest, 100% CP not relieved with NTG
• Unstable angina – Preinfarction
  • At rest, harbinger of MI, clot forms over disrupted plaque (analogous to TIA vs CVA)
  • Sudden total or near total occlusion
  • TX: decrease o2 demand, rest, NTG, increase o2 supply, decrease clotting with ASA
• AMI
  • Infarct=tissue death
  • May be precipitated by, artery spasm, micoemboli, volume overload, hypotension, resp failure
• Tissue changes
  • Necrotic zone
  • Ischemic zone
    • Viable tissue
    • Dysrhythmias, increased PVCs (multifocal), leading to Vtach, Vfib
  • Ischemia – inverted T waves in 2 related leads
  • Injury –ST elevation >1mm in 2 related leads
  • Infarct – Q waves >.04 sec wide or 1/3 of R, with ST elevation
• To diagnose an MI – need two of the following
  • Good story, usually >20 min of CP
    • Not relived by rest, o2 or NTG
    • May be relieved by MS or NTG drip
    • May be repetitive, relieved by antacids, unrelated to exercise, palpitations, abd pain
    • 1/3 are silent, diabetics, dementia, AMS
  • EKG Evidence
  • Enzymes
• Physical exam
  • Hemodynamic status
  • Abnormal heart sounds
  • CHF
• EKG
  • Used to Rule IN an AMI
  • Higher ST segment elevations, reciprocal changes, worse prognosis
• Cannot rule OUT an MI in the field
• Cardiac enzymes
  • Damaged myocardial cells leak contents
  • No more IM meds in MI
  • CPK, Troponin, LDH, AST, Myoglobin
• Prehospital Management
  • Calm
  • Prevent/treat Dysrhythmias
  • Thrombolytics (?)
  • ABCs, vitals, o2, IV, bloods, EKG
  • Targeted H&P
  • Rapid classification of 12 Lead EKG
  • Listen, ear can pick up slight irregularities better than the eye
  • ECG does not give any information as to strength of contraction – Asses peripheral blood flow (remember PEA)
  • Rapid transport
  • MONA – Morphine, o2, NTG, ASA (OANM)
  • Beta Blockers? Decreases work load on heart, many contraindications, CHF, Bradycardia, Asthma, will decrease CO
• Location and size-which artery is blocked and where
• Majority involve left ventricle
• No typical AMI patient
• Women may present with;
  • Nausea
  • Lightheadedness
  • Epigastric burning
  • Sudden onset of weakness
• Reperfusion techniques for ACS
  • Fibrinolysis
  • Percutaneous intervention ( Balloons, stents, etc)

CHF

• Left Sided – most commonly damaged during AMI, and chronic HTN
  • Advanced – cyanosis, Cheyne-stokes breathing
  • Wheezing, crackles due interstitial spaces filling with fluid
  • Peripheral vasoconstriction
  • Increased peripheral resistance
  • weakened hypoxic heart
  • S&S
    • Agitation
    • Severe dyspnea
    • Tachypnea
    • Tachycardia
    • Elevated BP
    • Crackles, wheezes
    • Frothy pink sputum
  • Management
    • Improve o2 (CPAP)
    • Reduce volume of venous blood (diuretic?)
    • Sit upright, feet down
    • Saline lock for Medication access
    • NTG, MS, Lasix
• Right Sided
  • Result of left sided chf
  • PE or COPD (cor pulmonale)
  • Blood backs up behind right ventricle
  • S&S
    • Visible distention
    • edema
    • may reverse left sided
    • seldom life threatening
    • requires days to weeks to reverse
    • tx in field

Wikipedia on Myocardial Infarction

3/11/09

Heart Disease

• 600k deaths
• 37% of all deaths

Risk factors

• Age
• Family history
• Hypertension
• Elevated cholesterol level
• Smoking
• Carbohydrate intolerance
• More women die of a cardiac event
• Other factors include
  • Diet
  • Obesity
  • Oral contraceptive use
  • Sedentary lifestyle
  • Stress
  • Personality type

Some more notes about the heart

• Point of maximal impulse -Normally located on the left anterior part of the chest, in the midclavicular line, at the fifth intercostal space
• The cardiac cycle
  • Comprises one complete phase of atrial and ventricular relaxation, followed by one atrial and ventricular contraction
  • During the relaxation phase, the left atrium fills passively with blood.
• Two pumps in one
  • Right side is a low-pressure pump.
  • Left side is a high-pressure pump.
• Preload
  • Pressure under which a ventricle fills
  • Influenced by the volume of blood returned by the veins to the heart
  • Afterload – pressure the heart has to overcome to generate a blood pressure (Peripheral Vascular Resistance) Chronically high afterload (arteriosclerosis)
• Automaticity – Generates its own electrical impulses without stimulation from nerves
• Contractility
  • Heart varies the degree of contraction of its muscle.
  • Changes may be induced by medications.
  • Ventricles are never completely emptied of blood.
  • Nervous controls regulate the contractility of the heart.
• SA Node – dominant pacemaker – located in right atrium
• Depolarization
• Repolarization
  • Closing of the sodium and calcium channels
  • Restores the negative charge
  • Sodium-potassium pump
  • Refractory period
  • Absolute refractory period
  • Relative refractory period

Levine’s Sign
is a clenched fist held over the chest to describe ischemic chest pain.^[1] As the referred pain associated with ischemia radiates to the area of the left proximal forelimb, the right, unaffected arm is used to produce the gesture.

It is named for Dr. Sam Levine who first observed that many patients suffering from chest pain made this same sign to describe their symptoms. This clenched fist signal may be seen in patients with myocardial infarction and angina pectoris.

John Clappin

3/8/09

Cardiovascular System

Heart

• Two Sided pump – each side contracts together (atria and ventricles)
  • Systemic circuit
  • Pulmonary Circuit
• Landmarks:
  • Angle of Louis (or Sternal Angle – formed at bottom of Manubrium where meets the sternum) – 2^nd rib to the left base of heart, major vessels
  • 6^th Rib – Apex of heart in 5^th intercostal space – left midclavicular line
  • Right border of sternum
• Heart Sounds – S1 – when AV valves shut (5^th intercostal space –tricuspid valve right sternal border, mitral valve(bicuspid)– 5^th intercostal space left midclavicular line), S2 when semilunar valves shut (2^nd intercostal space right and left)(vibrations of blood not actual valve sounds)
  • Abnormal Sounds –
    • S3 is a rare extra heart sound that occurs soon after the normal two “lub-dub” heart sounds (S₁ and S₂)- sign of Left Sided CHF or Mitral regurgitation – (sounds like Kentucky?)
    • S4, atrial kick (Tennessee?) S₄ is a rare extra heart sound that occurs immediately before the normal two “lub-dub” heart sounds (S₁ and S₂). It occurs just after atrial contraction and immediately before the systolic S₁. S₄ is caused by the atria contracting forcefully in an effort to overcome an abnormally stiff or hypertrophic ventricle.
• Blood flow
  • Vena Cava to R atrium
  • Through R AV Valve (tricuspid) into R Ventricle
  • Through pulmonary (pulmonic) semilunar valve to pulmonary arteries and lungs (pulmonary circuit)
  • Back from lungs through pulmonary veins into left atrium
  • Through L AV valve (bicuspid or mitral) into left ventricle
  • Through aortic semilunar valve out to aorta and systemic circuit
  • Structures of valves
    • Chordae tendinea – tendons (attached to ventricular wall by papillary muscles) that attach to the cusps of the AV valves, during contraction these tendons pull the cusps shut, thereby preventing backflow or regurgitation (regurgitation will cause a heart murmur)
    • Coronary sulcus – separates atria from ventricles
    • Coronary sinus – is a collection of veins joined together to form a large vessel that collects blood from the myocardium of the heart.
    • The trabeculae carneae are rounded or irregular muscular columns which project from the whole of the inner surface of the ventricle, the purpose of the trabeculae carnae is most likely to prevent suction that would occur with a flat surfaced membrane and thus impair the heart’s ability to pump efficiently. The trabeculae carnae also serve a similar function to papillary muscles in that their contraction pulls on the chordae tendinae, preventing inversion of the mitral (bicuspid) and tricuspid valves. This prevents backflow of blood from the ventricles into the atriums.

Anatomy of thoracic cavity and Heart

• Left pleural cavity, right pleural cavity, and mediastinum (each made of a serous membrane)
  • Endocardium –inner layer of heart – smooth muscle
  • Myocardium – middle muscular layer
  • Epicardium aka visceral pericardium – outer layer
  • Pericardium – Cavity that surrounds the heart, visceral pericardium (inside) and parietal pericardium (surrounded by dense fibrous layer -attached to chest wall) filled with pericardial fluid – purpose is to protect heart and provides a degree of lubrication for heart to beat. Normally contains about 30 mL of serous fluid

Becks Triad – The result is the triad of 1. Low arterial blood pressure (reducing stroke volume and CO) 2. Increased central venous pressure (evidenced by JVD), and; 3. Distant heart sounds. Narrowing pulse pressure may also be observed.

• Cardiac Tamponade – sudden due to trauma
• Pericarditis – slower, due to infection

Electrical conductivity of the heart (basically – to be discussed in further detail in later lectures) Monitored by using an EKG Machine

• Starts in SA node
  (Pacemaker at 60-100 beats per minute)
• Slows in AV node so AV valve can effectively allow the blood to pass (100 msec delay) atrial contraction begins
• AV junction (includes AV node, surrounding tissue, and Bundle of His)
• AV Bundle (Bundle of His)(Pacemaker at 40-60 beat per minute)-then to Bundle Branches (Left and Right)
• Purkinje Fibers – distributes throughout the ventricular myocardium – ventricular contraction begins (Pacemaker at 20-40 beat per minute)

(See Palpitations)

Some random points

• Antiarrthymic drugs – act specifically on cell membranes of ectopic sites and blocks sodium from entering cell –
• Vasovagal response – stimulating the vagus nerve will cause overstimulation of parasympathetic nervous system, causing bradycardia – Valsalva
  maneuver

Cardiac Output (CO) Stroke volume x pulse rate

Dr Hernandez

3/1/09

Pulmonary Embolism

• Pulmonary artery blockage
• Risk factors 5 Fs – female, fat, forty, fertile, fair
• Usually present in the acute with normal lung sounds
• After that area of lung becomes ischemic it may start wheezing and then after a while – alveolar collapse and absent lung sounds
• Saddle embolism – immediately fatal
• Pain with walking , diameter of one leg bigger than other
• Usually will not travel far enough to cause CVA as gets trapped in lungs

Contributing factors

• Venous injury, venostasis, increased coagulability (triad)
• Pregnancy (blood loss, tearing of placenta, hypercoagulability)
• Disease (cancer, tumors,
• Multiple trauma, hemostasis
• Immobility after surgery, other prolonged immobility

PE Assessment

• Cough
• Hemoptysis (rare)
• Pain
• Anxiety
• Syncope
• Hypotension
• Pleural rub
• Tachycardia
• Tachypnea
• Fever (rare)
• JVD
• Localized crackles, wheezing

PE Management

• O2
• EKG Monitoring
• Pulse Oximeter
• IV NS or LR
• Rapid Transport

URI

• Nose throat sinuses larynx
  
• Cold pharyngitis tonsillitis sinusitis laryngitis croup
  
• Rarely life threatening
  
• hand washing – key
  
• beware if immunocompromised, transplant patent, infants
  

Some other pediatric lower respiratory infections

• Bronchiolitis
  also see
  AAP Policy
  
• RSV – Respiratory Syncytial Virus
  

Spontaneous Pneumothorax

• dyspnea , chest pain, pallor, diaphoresis, tachypnea

Tension Pneumothorax

• Absent one side , greatly diminished on other
• JVD, muffled heart tones, tracheal deviation

Pharmacological Management

• Oxygen
• Albuterol – asthma, copd, anaphylaxis
• Epinephrine
• ipratropium – Anticholinergic – caution with peanut allergies
• Isoetharine
• Alupent -
  metaproterenol
  
• Racemic epinephrine – upper airway – nebulized – croup
  
• Terbutaline
• Magnesium sulfate
• Corticosteroids

ARDS – common causes

• Always a precipitating event
• Sepsis
• Bronchial aspiration of gastric contents
• Multiple trauma
• Inhalation – fires
• 12-48 hours for S&S
• Young people with no medical Hx
• Can occur in peds

Cystic Fibrosis

• Thick secretions
• Can lead to many other respiratory problems

More discussion about EKG machines and ECG monitoring will be discussed in future lectures.