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Transcript for:
Overview of Cardiology Concepts

Erik Mack CARDIOLOGY

  1. Rhythms
    1. How to approach dysrhythmia interpretation
    2. Rhythms Originating in the SA Node*
      1. Normal Sinus Rhythm
      2. Sinus Bradycardia
      3. Sinus Tachycardia
      4. Sinus Dysrhythmia
      5. Sinus Arrest
      6. Sick Sinus Syndrome
    3. Rhythms Originating in the Atria*
      1. Premature Atrial Complex (PAC)
      2. Supraventricular Tachycardia (SVT)
      3. Preexcitation (WPW & Lown-Ganong-Levine Syndrome)
      4. Atrial Fibrillation (AFib)
      5. Atrial Flutter (AFlutter)
      6. Wandering Atrial Pacemaker (WAP)
      7. Multifocal Atrial Tachycardia (MAT)
    4. Rhythms Originating at the AV Junction*
      1. Premature Junctional Complex (PJC)
      2. Junctional Escape Rhythm
        1. Accelerated Junctional Rhythm
        2. Junctional Tachycardia
    5. Rhythms Originating in the Ventricles*
      1. Premature Ventricular Complex (PVC)
      2. Idioventricular Rhythm (IVR)
      3. Accelerated IVR
      4. Ventricular Tachycardia
      5. Ventricular Fibrillation (VFib)
    6. Other*
      1. Pulseless Electrical Activity (PEA)
      2. Asystole
  2. 12-Lead ECGs
    1. Bundle Branch Blocks
    2. Pulmonary Embolisms (S1Q3T3
    3. STEMI/MI
  3. Congestive Heart Failure
    1. Left Ventricular Failure
    2. Right Ventricular Failure

Cardiac Rhythms

Cardiac Rhythms How to approach dysrhythmia interpretation

  1. Identify the waves (P-QRS-T)
    1. P Wave: Atrial Depolarization; should be less than .11 seconds (less than three .04 small boxes) in duration, and amplitude less than 2.5mm tall (2.5 small boxes)
    2. QRS Complex: Ventricular Depolarization; should be narrow and less than .11 seconds in duration (less than three small .04 boxes wide). The QRS indicates that the impulse conduction has traveled through the AV Junction, through the Bundle of His, through the left and right bundles, and out to the Purkinje system.
      1. Q-wave: Represents conduction through the interventricular septum. Should last no longer than .04 seconds (one small box), and no more than ⅓ the total height of the QRS complex.
        1. Pathological Q
      2. R and S wave: Represent depolarization of the right and left ventricles.
      3. T- wave: Represents ventricular repolarization. Should be asymmetric, less than ½ the the overall height of the QRS complex, and oriented in the same direction (Upwards T-wave if QRS is positive, and vice versa).
        1. During Myocardial ischemia, injury, and infarction, the T-wave becomes very large (hyperacute), peaked or tented in shape, symmetric, and broad.
          1. Tall, pointed (peaked) T-waves indicate hyperkalemia.
          2. Deeply inverted T waves may be seen with acute CNS events i.e massive stroke or intracranial hemorrhage.
      4. **U-wave: Likely represents the final stage of ventricular repolarization. May be seen after the T-wave and before the P-wave. U-wave direction is usually the same as T-wave in Lead Ⅱ. A U-wave taller than 2mm (two small boxes height) is pathological and may indicate hypokalemia or cardiomyopathy.

ECG Representation Cardiac Event Normal Duration P-wave Depolarization of the Atria <0.11 seconds PR Interval Depolarization of the atria and delay at the AV junction 0.12 to 0.20 seconds QRS Complex Depolarization of the ventricles <0.11 seconds ST Segment Period between ventricular depolarization and beginning of repolarization

T wave
Ventricular repolarization


R-R Interval
Time between successive ventricular depolarizations

2. Measure the PRI

  1. PRI: the distance represents the time required for an impulse to traverse the atria and AV junction. This should be between 0.12-0.20 seconds (3-5 small boxes) in length.

**Note, this example has an elongated PRI

  1. Determine the QRS complex duration

    1. Should be narrow, and less than 0.11 seconds in duration (less than three small boxes wide).

  2. Determine Rhythm Regularity

    1. March out R waves.

  3. Measure the Heart Rate

    1. For Regular Rhythms: Use 300, 150, 100 // 75, 60, 50 methods. Find an R-wave that lands on a solid box, move over one, and begin counting down until your next R-wave (Figure 1)
    2. For irregular or regular rhythms: Use the “6-Second Method”. Count the number of QRS complexes in a 6 second strip and multiply by 10.

(Figure 1)

(Figure 2)

Rhythms Originating in the SA Node* Normal Sinus*

The SA is the primary pacemaker and is conducting as it should. Hence the following features

  • Intrinsic rate of 60-100 BPM
  • Regular Rhythm
  • An upright P-wave before every QRS
  • PRI of 0.12 to 0.20 seconds
  • QRS of less than 0.11 seconds Treatment: Not needed.

Sinus Bradycardia*

The SA is still the primary pacemaker here but the rate is simply below 60.

  • Rate of <60 BPM
  • Regular Rhythm
  • An upright P-wave before every QRS
  • PRI of 0.12 to 0.20 seconds
  • QRS of less than 0.11 seconds Treatment (per ACLS): Rarely needed. Look to other causes. However, utilize the bradycardic algorithm PRN.

Sinus Tachycardia*

The SA is still the primary pacemaker here but the rate is simply above 100.

  • Rate of >100 BPM
  • Regular Rhythm
  • An upright P-wave before every QRS
  • PRI of 0.12 to 0.20 seconds
  • QRS of less than 0.11 seconds Treatment (per ACLS): Rarely needed. Look to other causes. However, utilize the tachycardic algorithm PRN.

Sinus Dysrhythmia* The SA is still the primary pacemaker here but there is a slight variation in the cycling of a sinus rhythm, usually exceeding 0.12 seconds between the longest and shortest cycles. This is often benign and associated with respiratory cycles. Specifically, the rate increases during inspiration, and decreases during expiration. This is more common in children and young adults.

The SA is still the primary pacemaker here but the regularity differs upon respiratory patterns.

  • Rate of 60-100 BPM
  • Regular Rhythm
  • An upright P-wave before every QRS
  • PRI of 0.12 to 0.20 seconds
  • QRS of less than 0.11 seconds

Sinus Arrest* Sinus arrest occurs when the SA node fails to send an impulse. This eliminates the presence of a P-QRS-T complex to occur (essentially a skipped beat). The SA node resumes function immediately as if nothing happened.

The SA is still the primary pacemaker here but there are missed beats.

  • Rate of 60-100 BPM
  • Regular Rhythm
  • An upright P-wave before every QRS
  • PRI of 0.12 to 0.20 seconds
  • QRS of less than 0.11 seconds

Causes: SA node ischemia, increased vagal tone, carotid sinus massage, and medications such as digitalis (a positive inotropic and negative chronotropic drug, meaning that it increases the force of the heartbeat and decreases the heart rate. Used for CHF and AFib) and quinidine (a class Ia antiarrhythmic agent used to interrupt or prevent reentrant arrhythmias and arrhythmias due to increased automaticity, such as atrial flutter, atrial fibrillation, and paroxysmal supraventricular tachycardia.)

Treatment: Should heart rate decrease below 60 bpm (and the patient becomes unstable, consider TCP). Note: at a HR of less than 60, an ectopic focus may take over from either the AV junction or the ventricles.

Sick Sinus Syndrome (SSS)* SSS encompasses a plethora of rhythms characterized by a poorly functioning SA node. May be noted by sinus bradycardia, sinus arrest, SA block, and the alternating of extreme bradycardia and tachycardia (known as bradycardia-tachycardia syndrome).

Rhythms Originating in the Atria* How does this happen? Although the SA node is usually the primary pacemaker of the heart, any foci within the atria can act as the pacemaker (should it supersede the SA node in overdrive suppression). This is typically presented normally as upright P-waves before every QRS complex, but are not the same morphology as the SA node.

Premature Atrial Complex (PAC)* A PAC is not a dysrhythmia, but is, however, an ectopic (changes in a heartbeat that aren’t normal) complex that appears within another rhythm. A PAC will occur earlier than expected for the next normal sinus complex which produces a short R-R interval between it and the previous R wave (from the preceding QRS complex).

Note a PAC as follows:

  • Rate depends on underlying rhythm
  • Irregular Rhythm
  • An upright P-wave before every QRS, however, the shape differs from other P-waves
  • PRI of 0.12 to 0.20 seconds (may vary slightly depending on location of of PAC)
  • QRS of less than 0.11 seconds Note: A PAC is NOT always conducted to the ventricles, thus, a P-wave that shows up early on the ECG and is not followed by a QRS complex is called a nonconducted PAC. Unlike an AV block, nonconducted PACs occur infrequently, randomly, and the P-P interval associated with a nonconducted PAC will be shorter than the other P-P intervals. In an AV block, the P-P interval will stay the same.

Causes: PAC’s are common and can be caused by stress, caffeine/stimulants, or conditions such as heart failure, or electrolyte imbalance. Treatment is only necessary when PAC’s become frequent and consists of addressing the underlying cause of the PACs.

Supraventricular Tachycardia (SVT)* SVT is a rhythm that originates from above the ventricles with a ventricular rate faster than 150 bpm at rest. This reduces the amount of time available for ventricular filling, and in turn, decreases cardiac output (CO). At a rate of 150+, P-waves will be absent on ECG due to them being completely obscured by the T-wave.

SVT presents as follows:

  • Rate typically 150+ bpm
  • Regular Rhythm
  • P-Wave unable to be seen
  • PRI unable to be obtained (P-waves are obscured)
  • QRS of less than 0.11 seconds (narrow complex)

Note: the most common type of SVT is called AV Nodal Reentrant Tachycardia (AVNRT), and is associated with reentry. Think of this as the spread of an impulse through tissue that has already been stimulated by that same impulse. AV nodal reentrant tachycardia (AVNRT) is like a traffic jam in the heart's electrical system. Imagine there's a loop (reentrant circuit) formed in the AV node, which is like a junction box controlling the traffic between the heart's upper and lower chambers. Sometimes, an extra electrical pathway develops in this junction, creating a shortcut. When the heart's electrical signals get caught up in this loop and keep circulating, it causes the heart to beat too fast (tachycardia), like cars stuck in a roundabout with no exit. SVT can also be referred to as Paroxysmal SVT (PSVT), and is when the SVT surges and returns to normal.

Treatment: Follow the ACLS Tachycardia algorithm. Stable/Unstable: defined by CHADS- C- chest pain H- hypotension A- altered mental status D- dyspnea S- skin signs poor Unstable = two or more signs of instability PLACE DEFIBRILLATION PADS REGARDLESS OF STABILITY

IF STABLE: Vagal Maneuvers: Have patient attempt to blow out syringe off of a 10cc syringe (with as much effort as possible) If vagal maneuvers fail ⇩ Adenosine: 6 mg rapid IVP immediately followed by 10cc normal saline. If unsuccessful, attempt a following 12 mg rapid IVP immediately followed by 10cc normal saline If Adenosine fails or patient becomes unstable ⇩ Synchronized Cardioversion: Synchronized, then adjust joules to following Zoll: 100, 120, 150, 200J or LifePak: 100, 200, 300, 360J

Treatment (per ACLS): the bradycardic algorithm is as follows:

  • Atropine: 1 mg bolus, repeat every 3-5 minutes (max 3mg total) If Atropine is Ineffective⇩
  • Transcutaneous Pacing (TCP): Start with rate of 70, and mA of 40. Adjust amperage until both electrical and mechanical capture (radial pulse) is achieved. and/or⇩
  • Dopamine infusion or Epinephrine infusion
    • Dopamine: 5-20 mcg per minute (titrate to patient response)
    • Push-Dose Epinephrine: 2-10 mcg per minute (titrate to patient response)
    • Epi
    • Epi

Preexcitation Disorders* Preexcitation refers to the early depolarization of ventricular tissue through an accessory pathway (this is a congenital birth defect) between the atria and the ventricles. Think of this accessory pathway as an extra bundle of myocardial tissue that forms another possible route of conduction from the atria to the ventricles. Patients with preexcitation disorders are more susceptible to tachydysrhythmias. Within preexcitation disorders are WPW and LGL syndromes. The most common preexcitation disorder is Wolff-Parkinson-White (WPW) Syndrome.

Wolff-Parkinson-White (WPW) Syndrome*

In patients with WPW, the accessory pathway is the Bundle of Kent.

WPW is characterized by:

  • Rate dependent on patient
  • Regular Rhythm
  • Normal upright P-waves
  • PR segment is absent and slurs immediately into the QRS complex
  • Wide QRS of greater than 0.12 seconds
  • Appearance of a Delta Wave (A delta wave is a slurring of the upstroke of the first part of the QRS complex- indicating an early departure from the PR segment as a result of the impulse taking the In WPW syndrome, there's an extra electrical pathway in the heart called an accessory pathway. This pathway allows electrical signals to travel from the atria (upper chambers) to the ventricles (lower chambers) faster than normal. The "delta wave" on an ECG appears because this accessory pathway causes the ventricles to start activating earlier than they should during each heartbeat.

⚠⚠DO NOT GIVE ADENOSINE, CALCIUM CHANNEL BLOCKERS, BETA BLOCKERS, OR ANY MEDICATION THAT SLOWS CONDUCTION THROUGH THE AV NODE TO A PREEXCITATION DISORDERED PATIENT⚠⚠ Why? Giving a medication that slows conduction through the AV node will accelerate conduction through the accessory pathway which will increase the heart rate.

Lown-Ganong-Levine Syndrome (LGL)* LGL is another preexcitation syndrome where preexcitation of the ventricles occurs due to an accessory pathway. Unlike WPW, the accessory pathway is thought to be within the AV node itself. It is the same as WPW on ECG, however, there is no Delta wave, a short PR interval. WPW is characterized by:

  • Rate dependent on patient
  • Regular Rhythm
  • Normal upright P-waves
  • PR segment is short*
  • Normal QRS of less than 0.11 seconds
  • NO Delta Wave

⚠⚠DO NOT GIVE ADENOSINE, CALCIUM CHANNEL BLOCKERS, BETA BLOCKERS, OR ANY MEDICATION THAT SLOWS CONDUCTION THROUGH THE AV NODE TO A PREEXCITATION DISORDERED PATIENT⚠⚠ Why? Giving a medication that slows conduction through the AV node will accelerate conduction through the accessory pathway which will increase the heart rate.

Atrial Fibrillation (AFib)* Atrial Fibrillation is a rhythm in which the atrium is no longer contracting but instead fibrillates (quivers). AFib occurs when multiple cells in the atria depolarize independent of one another, instead of in response to the SA node firing. This results in a quivering of the ECG baseline, an irregular rhythm (irregularly irregular), and no discernible P-waves.

AFib is characterized by:

  • Rate dependent on patient
  • Irregular Rhythm
  • No upright P-waves
  • PR segment is absent
  • Normal QRS of less than 0.11 seconds Patients with AFIb are typically on a blood thinner (such as Eliquis, Coumadin, etc), a calcium channel blocker, beta-blocker, or digoxin. NOTE: Atrial Fibrillation with Rapid Ventricular Rate (AFib RVR) can occur when the ventricular rate increases above 100 bpm. Treatment includes Beta-blockers, Calcium channel blockers, and cardioversion**. **Use extreme caution with cardioversion as the risk for the patient to experience a thromboembolic event is high.

If the rate is high (above 100 bpm) and the rhythm is irregular, it is AFib RVR

Atrial Flutter (AFlutter)* Atrial Flutter is a rhythm in which the atria fires at a rate too fast for the ventricles to respond. This results in multiple ‘F” waves to be present (looks like multiple P-waves in succession) and resembles a “sawtooth appearance.” In AFlutter, one or more of the F waves is blocked by the AV node, which is the cause for the flutter waves prior to the QRS complexes (usually a 2:1 ratio).

AFlutter can also present as Atrial FLutter with a Rapid Ventricular Rate typically greater than 100 BPM. Unlike AFib RVR, AFlutter RVR is regular. Treatment is the same as with AFib: beta blockers, calcium channel blockers, and synchronized cardioversion. Same risk for throwing a clot as AFib, use extreme caution. AFlutter is characterized by:

  • Rate 60-100, 100+ is AFlutter RVR
  • Regular Rhythm (Usually 2:1; meaning 2 F-waves for every QRS)
  • Upright F-waves
  • Normal QRS of less than 0.11 seconds Multifocal Atrial Tachycardia (MAT)* In Multifocal Atrial Tachycardia (MAT), multiple ectopic sites within the atria depolarize at different, but rapid rates.

MAT is characterized by:

  • Rate 100+ beats per minute
  • Irregular rhythm
  • P-wave before every QRS, except shape differs with each foci
  • PRI 0.12-0.20 seconds
  • Normal QRS of less than 0.11 seconds If you observe a fast heart rate, irregular rhythm, and multiple P-wave morphologies on the ECG, it suggests the presence of multifocal atrial tachycardia. Note: MAT is often seen in COPD patients, pulmonary hypertension coronary disease, Treatment is deferred to ED.

Rhythms Originating at the AV Junction*

    If the SA node fails to initiate an impulse, then the AV junction (also called the AV node) should take over as the heart's pacemaker. A rhythm originating from the AV Junction (referred to as a “junctional rhythm”) has an intrinsic rate of 40 to 60 beats/minute. When a junctional rhythm is generated, the impulse travels into the ventricles as normal (thereby generating a normal QRS) but then traveling back up to the SA node (creating a retrograde, absent, or post QRS retrograde P-wave). 
    There are three ways in which a normal QRS complex can be seen, despite abnormal P-waves:
  1. Inverted P-wave: due to the impulse moving upward through the atria before the other part of it enters the ventricles
  2. Absent/buried P-wave: if the impulse moves through the ventricles and atria at the same time (splits between the two) due to the depolarization of both at the same time
  3. Late + Inverted P-wave: Since the electrical impulse is originating from the AV junction and traveling retrogradely to the atria, it takes longer for the atria to depolarize compared to when the impulse originates from the sinoatrial node. This delayed atrial activation can result in an inverted P-wave that appears after the QRS complex on the electrocardiogram (ECG).

Premature Junctional Complex (PJC)* A PJC (also known as ectopic complexes-meaning they come from a site other than the SA node) is not a dysrhythmia, rather, it is an early complex that occurs within another rhythm. Simply put, a PJC is an early beat.

PJCs are characterized by:

  • Rate dependent on underlying rhythm
  • Irregular rhythm
  • P wave is absent or inverted or inverted and after the QRS
  • PRI, if present, will be less than 0.12 seconds
  • Normal QRS of less than 0.11 seconds Causes: PJC’s are common and can be caused by stress, caffeine/stimulants, or conditions such as heart failure, or electrolyte imbalance. Treatment is only necessary when PJC’s become frequent and consists of addressing the underlying cause of the PJCs.

Junctional Escape Rhythm* A junctional escape rhythm (also known as a junctional rhythm) occurs when the SA node fails to fire and the AV node takes over.

Junctional Rhythms are characterized by:

  • Rate 40-60 (Accelerated Junctional* is 60-100 bpm)
  • Irregular rhythm
  • P wave is absent or inverted or inverted and after the QRS
  • PRI, if present, will be less than 0.12 seconds
  • Normal QRS of less than 0.11 seconds

Causes: Inferior wall MI, SA node disease, increased vagal tone, post cardiac resuscitation, valvular heart disease etc. If bradycardia persists, follow the bradycardia algorithm.

Junctional Tachycardia* Junctional tachycardia is a junctional rhythm that exceeds 100 beats per minute.
Causes of Junctional Tachycardia include: ACS, digoxin toxicity, heart failure, or theophylline administration. Any rate above 150 is to be considered SVT and treated as such- Cardiac Output will suffer.

Rhythms Originating in the Ventricles* If both the SA node and AV junction (node) fail to initiate an impulse, the ventricles may take over as pacemaker for the heart. When the ventricles are pacing, expect to see wide complex QRS complexes (greater than 0.12 seconds) and an absent P-wave.

Premature Ventricular Complex (PVC)* A PVC is not a dysrhythmia, but is instead, an early ventricular complex that appears within another rhythm.
PVCs are characterized by:

  • Rate dependent on underlying rhythm
  • Irregular rhythm
  • P-wave is absent preceding the PVC
  • No PRI
  • Wide QRS of greater than 0.12 seconds
  • The T-wave is usually opposite in direction than the QRS

Note: PVC’s can be distinguished as Unifocal, or Multifocal.

  • Unifocal PVCs look identical to one another and come from the same focus
  • Multifocal PVCs look different from one another because they come from different foci.

PVCs can also occur as couplets (meaning two consecutive PVCs) which is called a Ventricular Couplet. A “run of V-Tach” is indicated by three or more PVCs in a row. Should PVCs become so common they are present in every other beat (meaning normal-PCV-normal-PVC…) this is called Ventricular Bigeminy. If every third beat is a PVC (meaning normal-normal-PVC) then this is Ventricular Trigeminy

Causes: Can be caused by the same factors as PACs, PJCs, however, they are most often from cardiac ischemia in the ventricular tissue. Note: Multifocal PVCs, bigeminy, trigeminy, and PVC couplets are more worrisome than unifocal PVCs. *look out for an R-on T PVC→ this is when an R wave of a PVC occurs during the T wave of the preceding QRS complex and can lead to VT or VFib.

”Run of VTach” with 8 consecutive PVCs

Ventricular Bigeminy

PVC Couplets

Ventricular Trigeminy

Idioventricular Rhythm (IVR)* The term “idioventricular rhythm” indicates that only the ventricles are involved. This means that both the SA node and AV junction have failed to pace the heart effectively. IVR is characterized by:

  • Rate between 20-40 bpm (less than 20 = agonal rhythm, greater than 40 but less than 100 = accelerated IVR)
  • Regular rhythm
  • P-wave is absent
  • No PRI
  • Wide QRS of greater than 0.12 seconds

Accelerated IVR Causes: MI, digitalis toxicity, electrolyte imbalances, cardiomyopathies or heart disease. Treatment: Follow the bradycardia algorithm. Ventricular Tachycardia (VTach)* VTach is a series of three or more sequential ventricular beats at a rate of 100+bpm. VTach is defined as having:

  • Regular Rhythm
  • Absent P-waves
  • Wide, uniform QRS complexes greater than 0.12 seconds (this is monomorphic)
    • If QRS complexes are of varied height and width, and the QT interval is lengthened, it is Polymorphic (torsades de pointes)

Monomorphic VTach

Polymorphic VTach (Torsades de pointes) Note: due to the rate of contraction, adequate CO is unable to be maintained and can lead to ventricular failure or ventricular fibrillation. Causes: Prolonged QT can be caused by congenital or acquired by medication use. Medications known to prolong the QT interval include: amiodarone, quinidine, procainamide, sotalol, phenothiazines, and tricyclic antidepressants.

Treatment: Follow the ACLS Tachycardia algorithm (if a pulse is present) With a pulse, monomorphic, wide QRS complex, and STABLE:

  • Lidocaine: 1.5 mg/kg IV, repeat 0.75 mg/kg every 5-10 minutes x2. Max total dose of 3mg/kg
  • Lidocaine (Peds): 1 mg/kg IV, repeat 1mg/kg every 5-10 minutes x2. Max total dose of 3mg/kg
  • Amiodarone: 150 mg in 100 mL normal saline over 10 minutes. Repeat as needed if VT recurs. Followed by maintenance infusion of 1 mg/min for the first 6 hours. With a pulse, monomorphic, wide QRS complex, and UNSTABLE:
  • Synchronized Cardioversion: Synchronized, then adjust joules to following
  • Zoll: 100, 120**, 150 200J (**for Torsades Des Pointes, start at 120J unsynchronized)
  • LifePak: 100, 200, 300, 360J

With a pulse, polymorphic, wide QRS complex

  • Defibrillation: LifePak: 360J, Zoll: 120, 150, 200J Unsynchronized
  • Magnesium Sulfate: 2 grams over 2 minutes slow IVP, repeat in 5 minutes

Follow the ACLS Cardiac Arrest algorithm if pulseless.

ACLS Cardiac Arrest Algorithm Ventricular Fibrillation (VFib)* Ventricular Fibrillation is when many different cells within the ventricles depolarize independently, rather than in response to an impulse from the SA node. This causes an ineffective quivering of the ventricles in no discernable pattern.

VFib is defined as having:

  • Chaotic underlying baseline
  • Absent P-waves
  • No QRS complexes
    • Fibrillating waves greater than 3mm in amplitude is defined as “course VFib”
    • Less than 3mm is defined as “fine VFib)

Treatment: Follow the ACLS Cardiac Arrest Algorithm.

Other Rhythms (PEA & Asystole)* Asystole* Asystole is the only true arrhythmia and is when the heart is no longer contracting without any sign of organized electrical activity (also known as cardiac standstill). P-waves can sometimes be seen without a corresponding QRS complex and this is called P-wave asystole, ventricular asystole, or ventricular asystole. This is a non-shockable rhythm (remember that the purpose of defibrillation is to depolarize myocardial cells and thereby enable the SA node to resume pacing the heart when the cells depolarize following the defibrillation.)

Asystole

Ventricular Asystole (P-waves still present)

Treatment: Follow the ACLS Cardiac Arrest Algorithm.

Pulseless Electrical Activity (PEA)* PEA is defined as an organized cardiac rhythm without a corresponding pulse. In PEA there is either no accompanying mechanical ventricular activity to the electrical signal, or the ventricular activity is too weak to produce a palpable pulse. This can be caused by a multitude of reasons including: hypovolemic/hemorrhagic shock (not enough blood in the tank to mechanically move, but the heart is electrically still working as it should), cardiac tamponade (a form of obstructive shock), massive pulmonary embolism, electrolyte imbalance (hypokalemia in the renal patient) and overdose. PEA can be any underlying organized rhythm (besides asystole) where no pulse is present.

Treatment: Use the ACLS Cardiac Arrest Algorithm

12-Lead ECGs

Indications for a 12 lead:

  • Before and after electrical or chemical therapy
  • Chest or upper abdominal discomfort
  • Electrical injury
  • Known or suspected electrolyte imbalance
  • Known or suspected medication overdose
  • RVF and/or LVF
  • Post-syncope
  • Stroke
  • Syncope or near syncope
  • Hemodynamically unstable with unknown etiology

**Obtain a 12-Lead every 5-10 minutes in high-risk patients or those given cardiac treatment

Basic terminology: Let’s review some basic terminology so that we are all talking the same language about the same things:

  • Electrode – the end of the wire that connects the patient to the monitor
  • Cables – the bundle of wires used to connect electrodes from the patient to the monitor
  • Lead – made up of a negative and positive electrode that looks at different aspects of the heart depending on where the electrodes are located relative to each other. This may seem basic but keeping these terms straight will help out as we move along. A 12-lead ECG is made up of a tracing of the electrical activity of the heart from 12 different points of view. The point of view comes from the location of the positive electrode of each lead. The positioning of these electrodes is broken down into 3 categories:
  1. the limb leads (lead I, II & III)
  2. the augmented leads (aVR, aVL & aVF)
  3. the precordial or chest leads (V1, V2, V3, V4, V5 & V6).

For Limb Leads: For the limb leads, this mnemonic is a lot easier, but it only works for ECGs that follow the American Heart Association (AHA) color system:

  • Right-side: Clouds over grass (white lead (RA) above the green lead (RL))
    • Remember that white is on the right!
  • Left-side: Smoke over fire (black lead (LA) above the red lead (LL) For Precordial Leads (V1-V6)
  1. Place V1 and V2 on the RIGHT and LEFT margins of the sternum, respectively. This is the edge of the hard part (the sternum bone) in the middle of the chest. They should be on the same level at the 4th intercostal space (ICS).
  2. Skip V3 for now. Place V4 at the 5th ICS at the left midclavicular line. This is aligned with the middle of the left collarbone.
  3. Place V5 at the 5th ICS at the anterior axillary line. This is defined as the imaginary line down your frontmost armpit fold (anterior axillary fold).
  4. Place V6 at the 5th ICS at the midaxillary line. This is the imaginary line that follows down the middle of your armpit. Note that the ribs move in a curved line, so V5 and V6 will be a bit higher than V4. Just trace the ribs properly and you’ll get the correct area.
  5. Lastly, place V3 in the middle of V2 and V4.

How to Interpret a 12-Lead ECG Follow this order to interpret:

  1. Review the snapshot
    1. Look for anything that immediately stands out (extreme rate, artifact, etc)
  2. Interpret the dysrhythmia (as mentioned earlier)
    1. Identify the P-QRS-T waves
    2. Measure the PRI
    3. Measure the QRS complex
    4. Determine rhythm regularity (regular vs irregular)
    5. Determine rate
  3. Determine the Axis (discussed later)
  4. Identify conduction system disturbances (such as AV blocks and preexcitation, bundle branch blocks, and fascicular or hemiblocks)
  5. Review for zones of ischemia, injury, or MI.

https://oxfordmedicaleducation.com/ecgs/ecg-examples/ Determining the Axis (why it matters, what it is, and how to determine it)

    Cardiac Axis is the average direction of the flow of electricity (direction of depolarization) in the heart. The QRS axis is a single vector that represents the mean (or average) of all vectors created by the ventricles during depolarization. Electricity flows towards the area of the heart with more muscle. I.e the more muscle that is in the right ventricle, the more the axis deviation will rotate to the right and vice versa.

How to:

  1. Look at leads Ⅰ and AVF and determine if they are mainly positive or negative in direction.

Lead Ⅰ Lead AVF Axis Deviation Positive Positive Normal axis Positive Negative Left-axis deviation Negative Positive Right-axis deviation Negative Negative Extreme right axis deviation

Step 1: Look at Leads 1, 11, AVF Step 2: Look at QRS direction If all up, = Normal Axis If up in 1, and down in 11, AVF = Left Axis Deviation If down in 1, and up in 11, AVF = Right Axis Deviation

                   How to find reciprocal leads^^

Identifying Conduction System Disturbances:

Left and Right Bundle Branch Blocks What is a Bundle Branch Block A bundle branch block (BBB) is a block of the right or the left bundle branches that propagate depolarizations from the Sino-Atrial node to and through the ventricles. The signal is conducted first through the healthy branch and then it is distributed to the damaged side. This skewing of one ventricle taking longer than the other widens the QRS-complex abnormally. QRS will be GREATER than .120 seconds (3 small boxes).

How to Recognize a Left versus Right Bundle Branch Block (traditional)

Left Bundle Branch Block: If the QRS looks like W in V1 and M in V6 it is LBBB. (WiLLiam)

Right Bundle Branch Block If the QRS looks like a M in V1 and a W in V6 it is RBBB (MoRRow)

Turn Signal Method

  • When using this method you look at lead V1, if the J point deflection in this lead is "up" then you have a RBBB, if it is "down" then you have a LBBB. Or: Rotate ECG paper so that the demographics portion is to the right. Look at V1 and determine the direction of QRS. QRS deflection to the right = RBBB, QRS deflection to left =LBBB

Heart Failure (pages 1262)

What is Heart Failure?

  • Heart failure is when the heart is unable to pump powerfully enough or fast enough to empty its chambers. This causes blood to back up into the systemic unit (think circulation to the whole body), the pulmonary unit (think deoxygenated blood traveling to lungs for gas exchange), or both. Causes of Heart Failure
  • Coronary Artery Disease
  • Chronic Hypertension
  • Diabetes (chronic high glucose damages the vessels within the heart causing cardiomyopathy)
  • Thyroid Disorders
  • Alcohol/Cocaine/Drug Use
  • Dysrhythmias
  • Chemotherapy/Radiation
  • Infectious Agents that cause inflammation (HIV, ARDS, COVID)

Chronic versus Acute Heart Failure

  • Chronic Heart Failure: Slow, Gradual Onset
  • Acute Heart Failure: Sudden Onset **Chronic Heart Failure can become Acute

Note: Cardiac Output = Stroke Volume x Heart Rate (CO= SV x HR) Preload = Diastolic BP Afterload = Systolic BP

  • Stroke Volume is affected by:
    • Preload: the volume of blood in the ventricles at the end of diastole (diastole= between heart beats) and is a reflection of venous return to the heart)
    • the amount of pressure that the left ventricle needs to exert to eject the blood during ventricular contraction: increasing afterload decreases Cardiac Output (CO).
    • Cardiac Contractility: refers to the heart's ability to contract the cardiac muscles and forcibly expel blood.

Left Ventricular Failure: the left ventricle is unable to pump enough blood into the body causing blood to back-up into the left atrium. Increased pressure in the left atrium results in stretching of the atrial fibers causing potential atrial dysrhythmias. With the left atrium full, the pulmonary veins are unable to empty into the left atrium and blood now backs up into the pulmonary vessels within the lungs (remember, the pulmonary vein carries oxygenated blood from the lungs back to the left atrium of the heart). Increased pressure within the pulmonary vessels causes fluid to cross from the pulmonary capillaries, out of the alveolar walls, and into the capillaries causing edema. This edema creates a wider gap between the alveolar-capillary membrane, thus impaired gas exchange, Generally occurs over several weeks to months with increasing dyspnea. Most common type of heart failure and generally occurs before RVF.

Signs/Symptoms:

  • BP: Hypertension
  • HR: Tachycardic, pulsus alterans (alternating pulse rate)
  • RR: Tachypnic, retractions/accessory muscle use, tripod breathing
  • Lung Sounds: Crackles
  • May have orthopnea- dyspnea that is improved with sitting upright or standing
  • PND: Paroxysmal Nocturnal Dyspnea is caused by LVF and is sudden severe dyspnea occurring 2-4 hours after falling asleep. Causes wheezing, coughing, and sweating.
  • Skin: Sweating Treatment:
  • Nitroglycerine (oral and/or transdermal paste)
    • 0.4 mg SL Q5 minutes (do not administer with SBP <100)
    • 1 inch (1 gram) nitroglycerine paste on chest after first round of SL Nitroglycerine
  • CPAP (7.5-10.0 cm H2O)

Right Ventricular Failure: the right ventricle is too weak to overcome the high pressure within the pulmonary vessels to eject the blood within its walls. When the right ventricle fails, its contractile function fails. Thus, blood backs up behind the right ventricle, into the right atrium, and into the superior and inferior venae cavae. This creates congestion within the venous system and causes organs to be engorged in blood (i.e the hepatic veins in the liver become engorged and cause hepatomegaly). As venous pressure increases, serous fluid is forced out of the capillaries and into the body tissue causing edema. Heavily Preload Dependent

Signs/Symptoms

  • BP: Hypotensive (think the right ventricle is unable to pump blood out to the lungs effectively causing poor return to the left ventricle and into the body)
  • HR: Tachycardic (compensatory)
  • RR: Tachypnic (compensatory)
  • Weight Gain
  • Liver enlargement from splenomegaly (look for enlarged right upper quadrant of abdomen)
  • Spleen Enlargement (LUQ)
  • JVD if both RVF and LVF
  • Pitting Peripheral Edema

Treatment: Fluid Bolus, ABC’s

Differential Diagnosis of Heart Failure Classification Possible Diagnoses

Cardiovascular Causes


* Cardiac tamponade

  • Cardiogenic pulmonary edema

  • Cardiogenic shock

  • High-altitude pulmonary edema

  • Myocardial ischemia

  • Myocardial infarction

    Respiratory Causes • Acute respiratory distress syndrome • Asthma • Chronic bronchitis • Chronic obstructive pulmonary disease • Pneumonia • Pneumothorax • Pulmonary embolism • Respiratory failure Other Causes • Anaphylaxis • Aspiration • Noncardiogenic pulmonary edema • Toxin exposure

Cardiac Tamponade (pages 1269) What is Cardiac Tamponade? Cardiac Tamponade is when the buildup of pericardial fluid compresses the heart, thus impairing its ability to contract and fill with blood. This is caused by pericardial effusion which is an increase in the volume or change in fluid type (i.e blood) of the pericardial fluid that is in the pericardium (a protective sac that surrounds the heart). Limited ventricular filling caused by cardiac tamponade causes decreased stroke volume (SV) and Cardiac Output (CO) causing Obstructive Shock.

Causes of Cardiac Tamponade:

  • Aortic dissection
  • Auto immune disease
  • Blunt trauma to the chest (including CPR)
  • Cardiac rupture after MI
  • Cardiac tumors
  • Chronic kidney failure
  • End-stage lung cancer
  • Heart surgery
  • Hypothyroidism
  • Penetrating trauma to the heart
  • Pericarditis, pericardial effusion
  • Radiation therapy to the chest (cancer treatment)
  • Recent invasive heart procedures (angioplasty, central venous catheter insertion, pacemaker wire insertion) **Suspect any patient with penetrating wound to the upper chest/abdomen

Signs and Symptoms:

  • Beck’s Triad
    • JVD
    • Hypotension
    • Muffled Heart Sounds
  • Signs of poor skin perfusion
  • Tachycardia
  • Weak or Absent Peripheral Pulses
  • Narrowing Pulse Pressure (when the difference between SBP and DBP decreases)
  • Pulsus Paradoxus (exaggerated drop in systemic blood pressure during inspiration)
  • Dyspnea
  • Orthopnea

Treatment:

  • ABC’s
  • Maintain SpO2 95-98%
  • IV access and maintain SBP of 90+
  • Rapid TXP to Trauma Center for Pericardiocentesis

OBSTETRICS/NEONATAL

Physiologic Changes During Pregnancy

  • Blood volume increases by 30-50% (increasing rapidly during the first half), Drop in BP is a LATE sign of shock in pregnant women
  • Cardiac Output increases by 30-50% peaking at 20 weeks and decreasing to 20% at term
  • Heart Rate increases by 15-20 beats per minute
  • During vaginal birth, as much as 500 mL of blood may be lost (1000 mL for C-section)
  • RBC increase 33% which increases the mother’s need for iron
    • Prenatal supplements are important to prevent maternal anemia. Anemia can result in preterm labor and spontaneous abortion
    • Increased oxygen consumption by 20-40%, 30-50% increase in tidal volume
  • After 20 weeks, ensure the patient is not lying supine to prevent compression of the inferior vena cava. Transport in left lateral recumbent
  • Decrease in BP is normal until about 24 weeks gestation where it should then increase until birth
  • Increased risk of DVT

Terms to Know:

  • Primigravida: pregnant for the first time
  • Primipara: only one delivery
  • Multigravida: two or more pregnancies, regardless of outcome
  • Multipara: two or more deliveries
  • Nullipara: never delivered
  • Gravida= Number of Pregnancies (remember, G before P)
  • Para= Number of Viable Births
  • Braxton-Hicks: intermittent contractions that occur every 10-20 minutes during the third trimester. Termed as “false labor” but transport regardless
  • Habitual Abortions: Three or more consecutive miscarriages
  • Preterm Labor: Labor that begins after the 20th week but before the 37th week
  • Post-Term Pregnancy: Fetus has not been born after 42 weeks
    • High risk because: the fetus may be malnourished, increased risk of meconium aspiration. Usually requires C-section
  • Meconium Staining: first stool from the baby
    • odorless , greenish-black, tar-like consistency
    • Usually caused by fetal distress
    • Can cause aspiration pneumonia
      • Management:
        • Prepare intubation equipment should you see meconium
        • Suction mouth THEN the nose
        • Dry, warm, and stimulate
          • Intubate if poor vigor, use meconium aspirator and perform deep tracheal suctioning. Remove the ET tube after meconium is removed. Baby should improve
  • Fetal Macrosomia: baby larger than 4,500 grams, most likely a difficult pregnancy
  • Amniotic Fluid Embolism: amniotic fluid enters the woman’s pulmonary and circulatory system through the placenta
    • Results in an allergic reaction
      • Respiratory distress and hypotension
      • Cyanosis
      • Possible seizures
      • Cardiogenic shock and unresponsiveness
      • Possible cardiac arrest
  • Cephalopelvic Disproportion: Head to large to pass through the pelvis

Breech Presentation: Any part of the fetus but the head leads the way through the birth canal

  • 3 Types
    • Frank: Buttocks present first
      • Position mom with knees to chest, allow delivery, once legs are clear support the body out of the vagina. If the head does not deliver in 3 minutes, the newborn may suffocate.
    • Footling Breech: Do not attempt delivery, have mom pant to prevent pushing, knees to chest
    • Shoulder Dystocia: Difficulty in delivering shoulder
      • perform McRoberts maneuver,
  • Prolapsed Cord
    • Shuts off the oxygenated blood supply from the placenta, leads to fetal asphyxia
    • Keep the woman supine w/ hips elevates, have them pant during each contraction, gently push the newborn off of the cord within the vagina. Cover the exposed cord with a moist, sterile dressing.
  • Uterine Inversion: The placenta fails to detach from the uterus and causes the uterus to turn inside out as a result
    • Highly painful, may rapidly cause shock
    • ABC’s, treat for shock, get ONE attempt at replacing the uterus back into place
    • Consider oxytocin to control hemorrhage (oxytocin causes contraction, 10mg IM)
  • Postpartum Hemorrhage
    • Typical blood loss is 150 mL
    • Postpartum Hemorrhage: 500+ mL during the first 24 hours after birth
    • Treat w/ uterine massage, encourage breastfeeding, oxytocin administration, treat for shock
  • Pulmonary Embolism S/S
  • Sudden SOB
  • Tachycardia
  • A-Fib
  • Hypotension
  • Shart, sudden chest or abdominal pain
  • Syncope

Preeclampsia: Presents after the 20th week of gestation (second trimester) is defined as:

  • New Onset SBP >140 mmHg
  • New Onset DBP>90 mmHg

Eclampsia: Same BP effects, however, seizure activity is now present Risk Factors:

  • First Pregnancy before age 20
  • Age 35+
  • Hx multiple pregnancies
  • Diabetes
  • Hypertension
  • Renal Disease

Treatment for both Preeclampsia and Eclampsia consists of:

  • Magnesium Sulfate 2gm in 100 mL NS over 5 minutes x2 (DRUG OF CHOICE)
  • Active Seizing: Midazolam 10mg IM/IN or 2mg IV/IO (give AFTER Magnesium)
  • Labetalol or Hydralazine (antihypertensive medications)

Complications (Preeclampsia) :

  • Liver or renal failure
  • Cerebral hemorrhage
  • Abruptio placenta
  • HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) Complications (Eclampsia)
  • Abruptio placenta
  • Hemorrhage
  • Disseminated intravascular coagulation (DIC)
  • Death

Cholestasis Cholestasis is the slowing or stalling of bile flow from the liver into the gallbladder. If the bile cannot flow normally, it builds up in the liver and begins to seep into the bloodstream.

S/S

  • Profuse, painful itching
  • RUQ pain
  • Jaundice Risk Factors
  • Twins, triplets etc.
  • Familial history of cholestasis
  • Previous liver damage

TORCH Syndrome Refers to infections that can pass through the placenta and into the fetus

  • Toxoplasmosis
  • Other agents
  • Rubella
  • Cytomegalovirus
  • Herpes Simplex

Abortion (Spontaneous Miscarriage)

  • Spontaneous abortion occurs before the 20th week of gestation (usually occurs in first trimester)
    S/S
  • Vaginal Bleeding with abdominal pain or menstrual cramps
  • Severe Abdominal Pain
  • Cervical Dilation

Treatment

  • ABC’s (IV with NS, 100% O2, ECG, Emotional support, watch for signs of shock)

Third Trimester Bleeding (Greatest danger of hemorrhage)

Ectopic Pregnancy (Primary Concern) Implantation of the embryo anywhere but within the uterus

  • Usually presents with severe abdominal pain, hypovolemic shock
  • Occurs between the 6th and 12th weeks of gestation
  • **HIGH INDEX OF SUSPICION for any and all females with ACUTE onset, severe lower abdominal pain. Occurs early in pregnancy before 20 weeks

Abruptio Placenta

  • Is the premature separation of the placenta from the uterine wall
  • Most often occurs during the third trimester of pregnancy S/S
  • Sudden onset, severe abdominal pain that radiates into the back
  • Decreased fetal movement
  • May have vaginal bleeding (not always though as the blood may not exit the cervix)
  • Signs of shock
  • Abdomen will be tender and the uterus tender to palpation Abruption Previa Is when the placenta is implanted low in the uterus and grows to partially or fully block the entrance of the cervix
  • Occurs during the second and third trimester S/S
  • Causes PAINLESS vaginal bleeding, with BRIGHT RED blood near end of term due to dilation of the cervix in preparation for birth
  • Abdomen will be soft upon gentle palpation

Treatment for Vaginal Bleeding

  • Keep patient in left lateral recumbent position
  • Administer 100% O2 via NRB
  • Provide rapid TXP
  • Initiate IV NS and begin with an initial 250 mL bolus. Reevaluate and administer further boluses until a max of 20 ml/Kg to get a SBP of >90 mmHg
  • Use loosely placed trauma pads to stop the flow of blood

Uterine Rupture Occurs during labor and is the actual tearing of the uterus itself S/S

  • Weakness, dizziness, thirst
  • Initial strong contractions that have lessened, replaced by sharp, tearing pain
  • Signs of shock Risk Factors:
  • Prior C-section

Stages of Labor

First Stage

  • Begins with onset of labor pains (contractions)
  • Amniotic sac will rupture near the end of the stage
  • Completes when the cervix is fully dilated Second Stage
  • Begins as the head descends into the birth canal
  • Fetus will undergo several position changes
  • Contractions are more intense and frequent
  • The cervix becomes fully dilated
  • Concludes when the newborn is delivered Third Stage
  • The placenta is expelled
  • Uterine contractions squeeze shut the exposed blood vessels

Birth

  • Gently guide the head DOWNWARD so that the upper shoulder can deliver
  • Gently guide the head upward to allow delivery of the lower shoulder (the trunk and legs will follow rapidly)
  • Once delivered, keep the newborn baby at the name level as the vagina.
  • Dry, warm, stimulate the newborn
    • Dry the entire body
    • Wrap in blanket
  • APGAR at 1 minute and 5 minutes after delivery
  • Clamp 4 inches from newborn, and another two inches after the initial clamp.
    • Cut between the two clamps
  • The placenta delivers within 30 minutes of the baby
    • Instruct the patient to bear down Y

RESPIRATORY PATHOLOGY

Terms to Know

  • Hypoventilation: When the pulmonary system fails to properly function, the body cannot efficiently dispose of carbon dioxide which causes carbon dioxide to accumulate in the blood and mix with water to create the highly acidic carbonic acid. THis is what ultimately causes respiratory acidosis.
  • Hypoxia: inadequate oxygen in the cells and tissue
  • Hypoxemia: Low oxygen in the blood
  • Normal Resting Minute Volume: 6 L/Minute
  • “Pleuritic Chest Pain” = chest upon inspiration
  • Atelectasis: collapse of the alveoli due to smoke/toxin
  • Carpopedal spasms: contracture of the hands and feet as a result of alkalosis (hyperventilation)
  • Pulsus Paradoxus: peripheral pulses are weak or absent during inspiration due to extreme pressure changes in the thorax. Caused by obstructive shock. Pericardial tamponade, tension pneumo, asthma. Drop in SBP of 10 mmHg
  • Adventitious = Abnormal lung sounds
  • Cyanosis = hypoxia
  • Pallor= blood flow reduction to small vessels = poor perfusion (shock, frostbite, lack of sun, anemia, catecholamine release)
  • Orthostatic vital signs ( from seated to standing = BP drop of >10, HR increase >20 = dehydration)
  • JVD: caused by cardiac tamponade, pneumothorax, RVF heart failure, and COPD
    • Hepatomegaly - apply pressure to liver RUQ will cause JVD
  • Diaphragmatic herniation
    • Abdominal contents are pushed through the diaphragm. Stomach will look concave and will hear bowel sounds in the chest. Intubate, NG tube, elevate head
  • Distal Clubbing: sign of chronic hypoxia (COPD etc)

Anytime you hear “gurgling” suction immediately

Pneumothorax:

  • Sharp pain after coughing
  • Increasing shortness of breath in subsequent minutes or hours
  • Treat with O2, monitor for signs of Tension Pneumo (and chest decompression)
  • People at risk:
    • Asthmatics
    • Tall and thin males
    • Smokers Pulmonary Embolism
  • Normal breath sounds, good peripheral aeration
  • Sudden SOB, and cyanosis
  • Sharp chest pain especially with inspiration
  • Cyanosis does not improve with O2 therapy
  • Usually sedentary patients, hx of recent surgery, broken bones
  • S1Q3T3
    • S1= prominent S wave in Lead 1
    • Prominent Q wave in Lead 3
    • Inverted T wave in Lead 3

Hyperventilation

  • Calming measures (breathing w/ patients, distraction techniques), sedation

Asthma: Bronchial asthma is characterized by hyperactivity of the trachea and bronchi to a variety of stimuli. Results in widespread, reversible narrowing of the airways, or bronchospasm. Asthma is an obstructive disease, meaning it makes it difficult for exhalation. This is due to trapping of air in the distal (deep) portions of the lung, so that air cannot enter the alveoli. **Status asthmaticus is a severe, prolonged asthma attack that cannot be stopped with conventional treatment. It is a true medical emergency. 1:4 I:E ratio, difficulty getting air out

Assessment for Asthmatic Patient

  • Frothy pink sputum = LVF
  • Purulent = Infection (white color) Pneumonia, sepsis etc
  • Yellow, green, or brown is an older secretion
  • Clear or White = bronchitis

Abnormal Breathing Patterns

  • Normal Inspiratory to Expiratory ratio is 1:2

  • Most respiratory centers are in the brainstem

    • Apneustic breathing: long inspiratory and short expiratory phase

  • Biot- ICP, Stroke “V-fib of respirations” no pattern (known as ataxic)

  • Cheyne-Stoke- ICP, Stroke, fast to slow to apneic then repeats

  • a type of hyperventilation that's characterized by deep, rapid, and labored breathing at a consistent pace- DKA

Bronchodilators

  • Most stimulate beta-2 specific receptors in the lungs
  • Ipratropium bromide (atrovent)
    • Anticholinergic (acetylcholine causes bronchoconstriction), dries secretions in lungs and stops acetylcholine from reaching lungs, makes bronchodilators work more effectively (similar to how benadryl stops the allergic reaction and epi opens bronchioles)
      • Albuterol-bronchodilation
  • **Nebulizer set to 6-8lpm
  • IV Magnesium for severe asthma attacks (can cause hypotension)
    • Use this if epi 1:1000 IM, then duoneb, then IV Mag (2 grams over 20 minutes, causes smooth muscle relaxation) then solumedrol
  • Solumedrol (methylprednisolone)
    • 2 mg/kg max dose of 125 mg
    • Reduces bronchial edema
    • Must be discontinued slowly
    • Takes a long time to kick in (up to four hours)
    • Good for acute COPD, Asthma

Bronchodilators are ineffective in cases of:

  • Pneumonia
  • Pulmonary edema
  • Heart disease

Pneumonia:

  • One sided adventitious lung sounds (rhonchi), sedentary, fever, bases of lungs
    • Do not give fluids, can make pneumonia worse

Infection of Upper Airway

  • Can lead to laryngotracheobronchitis (croup)
    • Common in children under age of 6
    • S/S: Stridor, hoarseness, barking cough
    • Viral
    • Treatment : 5 mL epi 1:1000 racemic epinephrine (nebulized)
  • Epiglottitis
    • Severe, rapid infection of the epiglottis caused by bacteria.
    • S/S: sore throat, drooling, fever, purposeful hyperextension of the neck, hoarseness
    • Transport, keep calm, and do NOT manipulate airway

Airway Management

  • Avoid intubation at all costs
  • Have partner press on chest to look for bubble stream
  • If you must, intubate with ET tube at least two sizes smaller than typical
  • Cricothyrotomy may be necessary

Obstructive Lower Airway Diseases

S/S: pursed lip breathing, increased I:E ratio (1:4 instead of 1:2), abdominal muscle use, JVD

  • COPD
    • Emphysema
    • Chronic Bronchitis
  • Asthma (reactive airway disease)
    • Bronchial constriction, prevents exhalation (air can come in but difficult to get out)
    • Risk from infection
    • Status asthmaticus
      • Patient has asthma, given an inhaler, and does not improve. Asthma treatment:
  • Edema: Solumedrol 2mg/kg
  • Mucous Production: 0.5 mg nebulizedIpratropium Bromide
  • Bronchospasm: albuterol 2.5-5.0 mg, Epi 1:1000 0.3mg IM
  • **Use IV Magnesium 2 grams/20 minutes if all three do not work

COPD

  • Emphysema damages or destroys terminal bronchiole structures
  • Restrictive lung disease, makes air difficult to move in or out of lungs
  • Alveoli become large blebs (essentially overinflated, stretched out alveolar sac) Chronic Bronchitis
  • Sputum production for most days of the month, for 3+ months over two years
  • Excessive mucus production in bronchial tree
  • Chronic cough, bluish complexion, overweight, smoker, productive cough Emphysema
  • Barrel chest from chronic hyperinflation
  • Tachypnea
  • Use muscle mass for energy to breathe

Cor Pulmonale COPD with right sided heart failure

  • Due to chronic hypoxia, blood hemoglobin levels increase and viscosity increases. This causes pulmonary hypertension forcing the RV to have to contract harder. Causes failure. Look for:
  • Peripheral edema
  • JVD with hepatojugular reflux
  • End inspiratory crackles
  • Progressive SOB
  • Greater than usual fluid intake
  • Improper use of diuretics

Lung Sounds

Diffuse Wheezing

  • Left sided heart failure (cardiac asthma)
  • Smoke inhalation
  • Chronic Bronchitis
  • Acute pulmonary Embolism Localized Wheezing
  • Foreign body or tumor

Stimulus for Breathing:

  • Normal patients: increase in CO2 blood levels
  • COPD: “Hypoxic Drive”- decrease in PaO2 levels

ETCO₂ and Waveform Capnography

ETCO₂ is the maximal amount of carbon dioxide that leaves the body at the end of exhalation.

Numeric Reading
Capnography 
Causes 
Normal 
35-45 mm Hg
Figure 1
N/A
Low ETCO₂ (Alkalytic)
<35 mm Hg
Figure 2 
-Hyperventilation

-Tachypnea

High ETCO₂
>45 mm Hg
Figure 3
-Hypoventilation

-Metabolic acidosis -Pulmonary Embolism -Head Injury

Phase Ⅰ (Point A → B): is the “respiratory baseline” and is the initial stage of exhalation. This contains dead space gas which is free of CO₂.

Phase Ⅱ (Point B → C): is the “expiratory upslope.” At Point B, alveolar gasses mix with dead space glasses, thus resulting in a sharp increase in detected CO₂.

Phase Ⅲ (Point C → D): is the “alveolar plateau” and the gas sampled is entirely alveolar in origin. Point D represents the maximal EtCO₂ level and is the best reflection of the alveolar carbon dioxide level. Note: the height of Point D correlates with the indicated EtCO₂ level shown on the monitor.

Phase Ⅳ (Point D → E): is the “inspiratory downstroke” and is when fresh gas is introduced into the lungs which displaces CO₂. This displacement of CO₂ causes a sharp dip in the waveform to return back to baseline.

Abdominal and G.I Emergencies

Terms to Know:

  • Fistula: Opening between 2 portions of body or between a body part and outside of the body
  • TEF: Connection between the esophagus and trachea
    • Higher risk of pneumonia and sepsis
  • Esophageal Stricture/Stenosis: abnormal narrowing of esophagus
    • Can cause dysphagia, difficulty breathing, and inability to speak
    • Consider glucagon for esophageal obstruction

Peritonitis

  • Caused by infection that occurs due to:
    • Rupture of a hollow internal organ
    • Movement of bacteria out of the intestines
    • Can cause sepsis
      • S/S: Hard abdomen
        • Fever
        • Anorexia
        • Dehydration
          • Treat for shock. Fluid boluses, antiemetics, administer norepinephrine for sepsis

Cholecystitis

  • 5 F’s of Cholecystitis

    • Fair (Caucasian)
    • Fat
    • Female
    • Fertile
    • Forty to Fifty

  • After eating a fatty meal

    • Severe RUQ abdominal pain develops
    • Pain begins as food is emptied from the stomach

  • Positive “Murphy” sign (apply pressure to RUQ during inhalation, will cause pain)

  • Nausea

  • Vomiting

  • Fever

  • Jaundice

  • Epigastric pain

  • Tachycardia

  • Chaarcot triad

Management:

  • Ensure pt. Comfort, pain management, medication for nausea, IV fluids

Appendicitis

  • Fecal and other matter builds up in appendix, can cause rupture
  • Can cause peritonitis, sepsis, and death
  • 3 Stages of Appendicitis
    • Early: periumbilical pain, nausea, vomiting, loss of appetite, low fever
    • Ripe: Pain in lower right quadrant (McBurney Point)
    • Rupture: decrease in pain (due to a decrease in pressure), generalized pain, rebound tenderness
  • Evaluate for signs of peritonitis
    • Dunphy sign: Severe pain in the right lower quadrant when coughing
    • Rovsing: Pain in the right lower abdomen; quadrant upon palpation of the left lower abdominal quadrant Diverticulitis
  • Abdominal pain in LLQ
  • Classic infection signs
  • Constipation or diarrhea

Pancreatitis

  • Sharp pain in epigastric area
  • Pain radiating to back
  • Nausea and vomiting
  • Fever
  • Muscle spasms
  • Cullen sign (bruising around belly button)
  • Grey-Turner sign (bruising on lower back) Liver Disease
  • First stage
    • itching , bruising, nausea, anorexia, joint aches, weakness, poor detoxification
  • Second Stage
    • Jaundice, dark urine, icteric conjuctiva, Ascites, enlarged liver, alcoholic stool (pale)

GI Bleeding

  • Upper GI Bleeds
    • Esophagogastric varices
      • Caused by Hep C, and alcoholism
      • S/S of liver disease (fatigue, weight loss, jaundice, pruritus (itching), edematous abdomen. Varices cause a sudden onset of difficulty dysphagia, vomiting of bright red blood, signs of shock
      • More minor signs include hemataemesis and melena (dark tarry stool from upper GI bleed) are likely
      • ABC’s, treat for shock
    • Mallory-Weiss Syndrome
      • Junction between the esophagus and stomach tears
      • Forceful vomiting that results in a tear in the esophagus near the stomach that does not go completely through the esophageal wall
      • Occurs more often in men
    • Boerhaave Syndrome
      • Occurs during vomiting
      • Esophagus tears longitudinally and completely through the esophagus. Food and liquids escape into the mediastinum.
      • Typically presents after a large meal and alcohol
      • Occurs more often in men
      • Vomiting that is accompanied by severe chest pain, pain with swallowing, little to no visible bleeding (most goes into the mediastinum)
    • Peptic Ulcer Disease and Gastritis
      • S/S: pain in epigastrium that diminishes immediately after eating and returns in 2-3 hours, with pain described as burning or gnawing. Nausea, vomiting, hematemesis, melena.
      • Perforated will result in a sudden increase in the severity and quality of pain. Look for signs of peritonitis
    • GERD
      • Heart burn, patients will prefer sitting upright, may have a cough and difficulty swallowing
  • Lower GI Bleeds
    • Hemmorhoids
      • Present with bright red blood during defecation (called Frank bleeding)
    • Anal Fissures
      • Painful defecation, a small amount of bright red blood may be noted with toilet paper

Operations

Radio Comminications

  • Hold microphone 5-7 centimeters from mouth
  • EMS uses UHF and VHF frequencies
    • The higher the frequency = less interference but shorter transmission range
  • Simplex: Only one person can talk at a time
  • Duplex: you can talk and listen at the same time (like a cellphone)
  • Multiplex: radio + another medium (i.e send an EKG while talking)

Trauma/Neuro

Midazolam (Versed) Class: Benzodiazepine, Schedule IV Mechanism of Action: Inhibits GABA receptors in the CNS which reduces neuron excitability thereby causing sedative, anxiolytic, amnesic, and hypnotic effects Indications: Excited delirium, uncontrolled shivering associated with hyperthermia/heat exposure, active seizures, chemical restraint, poisoning /overdose care. Contraindications: Documented hypersensitivity, EtOH intoxication, neurologic/respiratory depression, acute narrow-angle glaucoma, sleep apnea, shock, barbiturate use, depressed vital signs, CNS depressants (opioids, alcohol, etc) Adverse Reactions/Side Effects: Headache, somnolence (desire to sleep), respiratory depression/arrest, hypotension, cardiac arrest, nausea, vomiting, pain at the injection site Drug Interactions: Use with other CNS depressants may cause respiratory depression, hypotension, profound sedation, and death. Use of Motherwort (herb) may potentiate the sedative effects and cause coma. Mango & grapefruit juice may potentiate its effects. Green tea and St. John’s Wort may reduce effectiveness. Duration of action:

  • Onset: IV/IN = Immediate, IM = 15 minutes
  • Peak effect: IV/IN = 3 to 5 minutes, IM = 30 to 60 minutes
  • Duration: IV/IN = Less than 2 hours, IM = 1 to 6 hours Special Considerations:
  • Pregnancy Safe Class D→ High fetal risk, use only if maternal benefit outweighs fetal risk
  • ½ dose for adults 60+

Dosage and Administration Route Adult Shivering Associated w/ Hyperthermia:

  • IV/IN/IO 2.5 mg → May repeat in 5 minutes
  • IM 5 mg→ may repeat in 10 minutes

Seizures:

  • IV/IO .1mg/kg slowly over 2 minutes (max single dose 4 mg)
  • IM/IN .2 mg/kg (max single dose 10 mg)

Chemical Restraint:

  • IV/IM/IN 5mg

Procedural Sedation:

  • IV .1 to .3 mg/kg (max single dose 10 mg)

Poisoning/Overdose Care

  • IV Give .1mg/kg in 2mg increments over 1-2 minutes via slow IV push. Pediatric Shivering Associated w/ Hyperthermia:
  • IV/IO .1 mg/kg (max single dose 1 mg)
  • IN/IM: .2 mg/kg (max single dose 1 mg) *Note: 5 mg/mL concentration recommended for IN/IM

Seizures:

  • IV/IO .1 mg/kg slowly over 2 minutes (max single dose of 4 mg)
  • IM/IN .2 mg/kg (max dose of 10 mg)

Chemical Restraint:

  • IV .05 to .1 mg/kg (max dose 5 mg)
  • IM .1 to .15 mg/kg (max dose 5 mg)
  • IN .3 mg/kg (max dose 5mg)

Poisoning/Overdose Care:

  • IV .1 mg/kg in 2-mg increments slow push over 1 to 2 minutes (maximum single dose of 5 mg)
  • IN .2 mg/kg (max single dose 4 mg)

Fentanyl (Sublimaze) Class: Opioid Analgesic, Schedule 2 Mechanism of Action: Binds to opioid receptors, producing analgesia, euphoria, respiratory depression, and sedation. Indications: Pain management, anesthesia adjunct, (also used in palliative care) Contraindications: Documented hypersensitivity, patients who have taken an MAOI in the last 14 days (used for anxiety and include selegiline, isocarboxazid, phenelzine, and tranylcypromine), administer with caution for patients with a GCS <15, hypotension, hypoxia after supplemental oxygen therapy, or signs of hypoventilation. Adverse Reactions/Side Effects: Confusion, paradoxical excitation (opposite of expected), delirium , drowsiness, CNS depression, sedation, respiratory depression, apnea (temporary cessation of breathing), dyspnea (difficulty breathing), dysrhythmias, hypotension, syncope, nausea, vomiting, abdominal pain, dehydration, fatigue. Drug Interactions: Increased respiratory depression when given with other CNS depressants. Duration of action:

  • Onset: Immediate
  • Peak effect: 3 to 5 minutes
  • Duration: 30-60 minutes Special Considerations:
  • Pregnancy Safe Class C→ No documented risks to fetus but can not be ruled out
  • Document pain on a scale of 1-10 prior to and after administration
  • Check with BH Physician if significant injury to CHest, Head, or Abdomen

Dosage and Administration Route (Same for both Adults & Pediatrics) Adult Moderate Pain:

  • IM/IN 1 mcg/kg (maximum initial dose 100 mcg, max total 200 mcg) Severe Pain:
  • IV/IO 1 mcg/kg (maximum initial dose 100 mcg, max total 200 mcg) Pediatric Moderate Pain:
  • IM/IN 1 mcg/kg (maximum initial dose 100 mcg, max total 200 mcg) Severe Pain:
  • IV/IO 1 mcg/kg (maximum initial dose 100 mcg, max total 200 mcg)

Ketamine (Ketalar) Class: Dissociative Analgesic, Schedule 3 Mechanism of Action: Blocks pain receptors and minimizes spinal cord activity, affecting the brain’s association pathways between the thalamus and the limbic system. Indications: Procedural sedation, management of agitated or violent behavior, pain control. Contraindications: Known hypersensitivity, infants younger than 3 months of age, pregnancy, angina, heart failure, symptomatic hyperthyroidism, known or suspected schizophrenia, conditions where hypertension may cause harm to patient’s health. Use with caution in any patient with the potential for ICP, intracranial breathing, hydrocephalus, head trauma, or intracranial mass lesions (brain tumors). Adverse Reactions/Side Effects: Hypertension, hallucinations, nausea/vomiting, nystagmus (shaking of the eyes), bronchodilation, tachycardia, increased secretions, hypersalivation, laryngospasm, respiratory depression, mild to moderate increases in blood pressure and heart rate. Drug Interactions: Ketamine may increase the CNS depressant effects of alcohol, opioids, barbiturates (often end in -al), and non depolarizing neuromuscular blockers (such as rocuronium, pancuronium, vecuronium). Note: St. John’s Wort can reduce Ketamine’s effectiveness. Duration of action:

  • Onset: 30 seconds
  • Peak effect: 30 seconds to 5 minutes
  • Duration: 10 to 15 minutes Special Considerations:
  • Pregnancy Safe Class N→ Not classified, contraindicated for pregnant or breastfeeding women.
  • Be ready for the patient to experience an “emergence state” for several hours following the duration of the drug characterized by hallucinations, delirium, confusion, excitement etc…

Dosage and Administration Route Adult Procedural Sedation:

  • IV 1 to 2 mg/kg via IV push over 1 to 2 minutes Pain Control:
  • Moderate Pain: IN .5 mg/kg (Maximum initial dose 55 mg, Maximum total dose 100 mg)
  • Severe to Extreme Pain: IV/IO/IM .25 mg/kg (Maximum initial dose 25 mg, Maximum total dose 100 mg) Chemical Restraint:
  • IV 2 mg/kg
  • IM 4 mg/kg Pediatric Procedural Sedation:
  • IV/IO 1 to 2 mg/kg via push over 1 to 2 minutes

Chemical Restraint:

  • IV 1 mg/kg
  • IM 3 mg/kg

TXA (Tranexamic Acid) Class: Hemostatic agent, antifibrinolytic agent, plasminogen inhibitor Mechanism of Action: Inhibits the activation of plasminogen, which then reduces the conversion of plasminogen to plasmin (plasmin breaks down fibrin clots, fibrinogen, and other plasma proteins). By halting the fibrin’s breakdown, clotting factors and circulating platelet plugs can form a fibrin clot (seal) and reduce hemorrhage. Indications: Patient presents within 3 hours of the onset of bleeding, with hemodynamic compromise. Contraindications: Known hypersensitivity, MOI greater than 3 hours prior to arrival of EMS, subarachnoid hemorrhage, history of PE, DVT, Stroke or other thromboembolic disorder. Hanging or drowning victims, neurogenic shock (spinal injury with hypotension). Reduce the dose in patients with known renal insufficiency. Adverse Reactions/Side Effects: Fatigue, headache, nausea, dizziness, abdominal and back pain, joint pain, musculoskeletal pain, anemia. Rapid infusion may cause hypotension. May increase the risk of thromboembolic disorders. Drug Interactions: Hormonal contraceptives and clotting factor complexes may increase the risk of thromboembolic disorders. Duration of action:

  • Onset: IV/IN = Immediate, IM = 15 minutes
  • Peak effect: IV/IN = 3 to 5 minutes, IM = 30 to 60 minutes
  • Duration: IV/IN = Less than 2 hours, IM = 1 to 6 hours Special Considerations:
  • Pregnancy Safe Class B → Use in pregnant or breastfeeding women should be clearly indicated.

Dosage and Administration Route Adult Hemorrhage: 1 g IV/IO infusion over 10 minutes (100 mL bag of saline)

Pediatric

Not Recommended

Activated Charcoal (Insta-Char, Actidose-Aqua, Liqui-Char) Class: Adsorbent, Antidote Mechanism of Action: Adsorbs ingested toxic substances from the GI tract, thereby preventing systemic absorption. Indications: Most oral poisonings and medication overdoses in the alert patient, can be used after evacuation of poisons. Contraindications: Known hypersensitivity, unprotected airway (beware of aspiration), absence of a gag reflex, ileus intestinal blockage, do not use after ingestion of petroleum distillates (mineral oil, benzene, gasolene-like odor), hydrocarbons (gasoline, diesel etc…), heavy metals, acids, alkalides (corrosives), alcohols, lithium, solvents. Exercise caution in use if a patient reports abdominal pain with unknown origin or a known bowel obstruction. Adverse Reactions/Side Effects: Emesis (vomiting), constipation, black stools, diarrhea, bowel obstruction. Drug Interactions: Bonds with and general inactivates whatever it is mixed with; moderate interactions with acetylcysteine (used to treat acetaminophen overdose), citalopram (an SSRI medication), digoxin (used to lower heart rate), dyphylline (bronchodilator), methotrexate (chemotherapy medication), theophylline (bronchodilator).
Duration of action:

  • Onset: Immediate
  • Peak effect: Dependent on GI movement
  • Duration: Will act until excreted Special Considerations:
  • Pregnancy Safe Class C→ No documented risks to fetus but can not be ruled out
  • Do not administer in a patient with an AMS (altered mental status)
  • Shake vigorously before administering

Dosage and Administration Route Adult + Pediatric >1 Year

  • PO/NG Tube 25 to 100 grams
    Pediatric <1 Year
  • PO/NG Tube 1g/kg

Adenosine (Adenocard) Class: Antidysrhythmic Mechanism of Action: Short acting drug that slows conduction through the AV node; can restore sinus rhythm in patients with SVT and terminate regular tachycardias caused by reentrant AV nodal pathways. Indications: First-line drug for most forms of stable, regular, narrow-complex SVT, including those involving AV nodal reentry. May be considered for unstable narrow-complex reentry tachycardia while preparing for cardioversion. Can be used diagnostically for stable, regular, monomorphic wide-complex tachycardia. Contraindications: Known hypersensitivity. Second- or third-degree AV block or sick sinus syndrome or other sinus node disease unless a functioning artificial pacemaker is present; poison- or drug induced tachycardia. Use with caution in patients with a history of a seizure disorder. May induce bronchospasm in a patient with bronchoconstrictive or bronchospastic lung disease (asthma, COPD). Adverse Reactions/Side Effects: Generally transient and of short duration due to adenosine’s short half-life; flushing with asthma. A brief period of most any dysrhythmia, including asystole, may occur during pharmacologic conversion. Drug Interactions: Additive effects may occur if used in combination with beta-blockers. Methylxanthines (caffeine and theophylline-like drugs) block the actions of adenosine. Dipyridamole (Persantine) potentiates (increases the power of) the effects of adenosine. Carbamazepine (Tegretol- anticonvulsant) may potentiate the AV node blocking effect of adenosine. Nicotine can enhance the adenosine's cardiovascular effects→ may present as an increase in angina-like chest discomfort or increased heart rate or decreased blood pressure. Duration of action:

  • Onset: Seconds
  • Peak effect: Seconds
  • Duration: 10 Seconds Special Considerations:
  • Pregnancy Safe Class C → Use in pregnant women only if clearly indicated.
  • Ensure to continuously monitor the ECG and record a rhythm strip during administration.
  • Adenosine will not convert AF (atrial fibrillation), atrial flutter, or VT.
  • Should not be administered for hemodynamically unstable, irregularly irregular, or polymorphic wide-complex tachycardias. Dosage and Administration Route Adult
  • 6 mg rapid IV/IO bolus over 1-3 seconds injected into the IV port as close to the heart as possible, followed by a 10 mL saline flush.
  • If no conversion occurs after 1 to 2 minutes, administer a 12 mg rapid IV/IO bolus over 1-3 seconds. May repeat the 12 mg dose once if no conversion occurs after 1 to 2 minutes. (Maximum total dosage is 30 mg).
  • ½ the dose for patients taking dipyridamole, carbamazepine, with a transplanted heart, or if given via central IV line. Pediatric
  • Initial dose .1 mg/kg (max initial dose is 6 mg) rapid IV/IO push over 1-3 seconds followed by a 5 to 10 mL saline flush.
  • Second dose .2 mg/kg rapid IV/IO push (maximum second dose is 12 mg) followed by a 5 to 10 mL saline flush.

Albuterol (Proventil, Ventolin, Proair, Accuneb) Class: Sympathomimetic, bronchodilator, short-acting beta-2 adrenergic agonist Mechanism of Action: Selective beta-2 adrenergic agonist that causes bronchial smooth muscle relaxation and inhibits mediator release from mast cells (inflammatory response). Indications: Treatment and prevention of bronchospasm in patients with reversible obstructive airway disease, treatment of inhaled airway/respiratory irritant agents, and hyperkalemia treatment (decreases serum potassium concentration). Contraindications: Known hypersensitivity; dysrhythmias,, especially those caused by digitalis. Synergistic with other sympathomimetics (drugs that stimulate the sympathetic nervous system). Adverse Reactions/Side Effects: Often dose-related; includes tremors, headaches, nervousness, dizziness, dysrhythmias, chest discomfort, palpitations, nausea/vomiting, dry mouth. Drug Interactions: Additive effects with TCAs (used to treat major depressive disorder), MAOIs (most common: selegiline, isocarboxazid, phenelzine, and tranylcypromine), other sympathomimetics. Beta blockers (ex. Metoprolol) may inhibit pulmonary effects, thereby decreasing effectiveness. May potentiate hypokalemia caused by diuretics. Duration of action:

  • Onset: 5 to 10 minutes
  • Peak effect: 30 minutes to 2 hours
  • Duration: 3 to 6 hours Special Considerations:
  • Pregnancy Safe Class C→ Use in pregnant women only if clearly indicated.
  • May worsen angina and dysrhythmias
  • Not to be used for bronchiolitis Dosage and Administration Route Adult

Respiratory Distress:

  • Nebulizer: 2.5 to 5 mg
  • MDI: 1 to 2 puffs (90 to 180 mcg)

Respiratory Distress with Bronchospasm:

  • Nebulizer: 5 mg
  • MDI: 6 puffs (repeat as needed for continuing distress) Hyperkalemia:
  • Nebulizer: 5 mg Pediatric

Mild to Moderate Asthma, or anaphylaxis, or hyperkalemia:

  • Nebulizer (child <20 kg): 2.5 mg/dose
  • Nebulizer (child >20 kg): 5 mg/dose every 20 minutes.
  • MDI w/ spacer: 4-8 puffs every 20 minutes PRN. Respiratory Distress with Bronchospasm:
  • Nebulizer: 5 mg
  • MDI: 6 puffs
    • Repeat at this dose as needed for ongoing distress.

**SBCo. Utilizes Albuterol for Anaphylaxis/Allergic Reactions, Crush Injury/Syndrome, and Shortness of Breath.

SBCo. Shortness of Breath Protocols

Aspirin (acetylsalicylic acid) Class: Platelet inhibitor, NSAID, anti-inflammatory agent Mechanism of Action: Prevents thromboxane A₂ formation (thromboxane A₂ causes platelets to clump together and form plugs that cause obstruction or constriction), has antipyretic (anti-fever) and analgesic properties.
Indications: New-onset chest discomfort suggestive of ACS (Acute Coronary Syndrome) Contraindications: Hypersensitivity to ASA or NSAIDs, bleeding conditions including ulcers (such as ulcerative colitis, hemophilia, hemorrhagic diathesis, hemorrhoids, thrombocytopenia), lactating mothers, hemolytic anemia, G6PD deficiency. Adverse Reactions/Side Effects: Anaphylaxis, bronchospasm/wheezing in allergic patients, GI bleeding, epigastric (upper abdomen) distress, nausea, vomiting, heartburn, Reye syndrome (brain swelling and liver damage) Drug Interactions: Increased risk of bleeding with anticoagulants and other NSAIDs, diminished effects of ACE inhibitors and loop diuretics. Antacids reduce aspirin’s absorption. Increased risk of hypoglycemia occurs with the admin of hypoglycemic medications; effects are decreased by corticosteroids. Herbs such as dong quai, feverfew, garlic, ginseng, ginkgo, and saw palmetto can all increase bleeding due to their antiplatelet properties. Duration of action:

  • Onset: 15 to 30 minutes

  • Peak effect: 1 to 2 hours

  • Duration: 4 to 6 hours Special Considerations:

  • Pregnancy Safe Class D → Do NOT use for women who are > 20 weeks pregnant Dosage and Administration Route Adult

  • 162-325 mg orally

    • Chewing is preferable to swallowing if the ASA is not enteric coated

    Pediatric Not Recommended

Sample (Sample) Class: Mechanism of Action: Indications: Contraindications: Adverse Reactions/Side Effects: Drug Interactions: Duration of action:

  • Onset:

  • Peak effect:

  • Duration: Special Considerations:

  • Pregnancy Safe Class → Dosage and Administration Route Adult

    Pediatric

Glascow Coma Scale

Eye (4) Alert = 4 Verbal=3 Pain=2 Unresponsive=1

Verbal (5) 1 - Makes no sounds (VOICELESS) 2 - Incomprehensible sounds (OOOH) 3 - Utters inappropriate words (INAPPROPRIATE WORDS) 4 - Confused, disoriented (CONFUSED) 5 - Oriented, converses normally (ELEGANT SPEECH)

Motor The mnemonic for motor response is OLD BEN. 1 - Makes no movements (NONE) 2 - Extension to painful stimuli (decerebrate response) (EXTENDS) 3 - Abnormal flexion to painful stimuli (decorticate response) (BENDS) 4 - Flexion / Withdrawal to painful stimuli (DRAWS FROM PAIN) 5 - Localizes painful stimuli (LOCALIZES) 6 - Obeys commands (OBEYS)