reentry supraventricular tachycardia
atrial fibrilation
reentry supraventricular tachycardia
sinus bradycardia
coarse ventricular fibrillation
atrial flutter
second degree AV block type 1 (wenckenbach)
reentry supraventricular tachycardia
sinus bradycardia
monomorphic ventricular tachycardia
second degree AV block mobitz type 2
second degree AV block mobitz type 2
coarse ventricular fibrillation
normal sinus rhythm
third degree AV block
reentry supraventricular tachycardia
polymorphic ventricular tachycardia - aka torsades
sinus tachycardia
reentry supraventricular tachycardia
sinus bradycardia
second degree AV block type 1 (wenckenbach)
reentry supraventricular tachycardia
sinus bradycardia
fine ventricular fibrillation
second degree AV block mobitz type 2
second degree AV block mobitz type 2
normal sinus rhythm
third degree AV block
...
...
anterior leads
V2, V3, V4
left lateral leads
I, aVL, V5, V6
inferior leads
II, III, aVF
right ventricular leads
aVR, V1
Lead I - angle
+0�
left lateral
Lead II - angle
+60�
inferior
Lead III - angle
+120�
inferior
Lead aVF - angle
+90�
inferior
Lead aVR - angle
-150� - "la la land"
right ventricular
Lead aVL - angle
-30�
left lateral
Normal PR segment length
0.12 - 0.2 sec
3 - 5 small boxes
Normal QRS interval
0.06 - 0.1 sec
1 - 3 small boxes
Normal QT interval
40% of cardiac cycle
Normal P amplitude & duration
< 0.12 sec (3 small boxes)
< 2.5 mV (2.5 small boxes)
Positive P waves in?
left lateral (I, aVL, V5, V6) & inferior (II, III, aVF); usually most positive in II
& most negative in aVR
Often biphasic P in?
III, V1
Tall R waves in?
left lateral (I, aVL, V5, V6) & inferior (II, III, aVF)
Q waves in?
in one or several of left lateral leads (I, aVL, V5, V6), sometimes in inferior leads (II, III, aVF)
T wave positive in?
Usually in leads w/ tall R waves; left lateral (I, aVL, V5, V6) & inferior (II, III, aVF)
Waveform & orientation of I?
+0�
predominantly + (L arm +, R arm -)
left lateral
Waveform & orientation of II
+60�
predominantly + (R arm -, L Leg + (think "ll=LL")
inferior
Waveform & orientation of III
+120�
typically biphasic (L arm -, L Leg +)
inferior
Waveform & orientation of aVR
-150� "la la land"
predominantly - (R arm +, all others -); center of heart ? R arm
right ventricular
Waveform & orientation of aVL
-30�
typically biphasic (L arm +, all others -); center of heart ? L arm
left lateral
Waveform & orientation of aVF
+90�
predominantly + (both legs +, both arms +); center of heart ? feet
inferior
Normal axis?
I +
aVF +
Right axis deviation?
I -
aVF +
Left axis deviation?
I +
aVF -
R atrium enlargement?
Leads II (parallel) & V1 (perpendicular; biphasic)
1) P wave > 2.5 mm in II, III, aVF
aka "p pulmonale
Precise axis determination?
Look for most biphasic wave - it will be perpendicular to this.
p pulmonale?
RA enlargement, almost always related to pulmonary system; usually causes backup into the ventricle & atria, causing enlargement of atria
L atrium enlargement?
1) V1 terminal portion, P > 1mm below line
2) Terminal portion of P > 0.04 sec (1 small box)
"p mitrale
p mitrale
LA enlargement due to mitral valve issue
RVH - criteria
1) R > S in V1
2) R progressively smaller from V1-V6
3) S > R in V6
- will cause right axis deviation
(also tall R in III)
LVH - precordial criteria
1. V5: R > 26 mm
2. V6: R > 18 mm
**3. S (V1 or V2) + R (V5 or V6) > 35 mm (most useful)
4. V6 R > V5 R
axis is not a great indicator (L axis shift)
Sensitivity is low, specificity is high
LVH - limb criteria
1. aVL: R > 13 mm
2. aVF: R > 21 mm
3. I: R > 14 mm
4. R (I) + S (III) > 25 mm
2� repolarization in ventricular hypertrophy - criteria?
1. Down-sloping ST segment depression
2. T wave inversion (R +, T -)
Tends to be most evident in leads most affected by size change
RVH = V1, V2
LVH = V5, V6
causes of arrhythmias
HISDEBS: hypoxia, ischemia/irritability, SNS, drugs, electrolytes, bradycardia, stretch (hypertrophy/enlargement)
symptoms of arrhythmias
none, "palpitations," light-headedness, syncope, angina, HF, sudden death
Types of arrhythmias
1. Sinus origin
2. Ectopic
3. Re-entrant (abnormally shaped path)
4. Conduction blocks (blocked signal)
5. Pre-excitation (shortcut in pathway)
Arrhythmias - 4 quick questions
1. Normal P waves?
2. Wide QRS? (> 0.12 sec indicates pacemaker below Bundle of His)
3. One P for every QRS?
4. Normal rate & rhythym?
Sinus bradycardia - criteria
HR < 60 bpm
Sinus tachycardia - criteria
HR > 100 bpm
Sinus arrhythmia
Appearance is ALMOST NORMAL:
Respiratory - Circulatory interaction
Rate INCREASES with INSPIRATION (IN=IN)
Sinus arrest - criteria
Rate: Regular or Bradycardia
P wave: Normal
QRS: Normal
Conduction: Normal
Rhythm: Irregular: length of pause ? multiple of normal rate (random)
Junctional Escape Beat/Rhythym - criteria
Rate: Bradycardia
P wave: Absent or Inverted P; if present, may occur during or after the QRS
QRS: Normal
Conduction: Escape beat: P-R interval < 0.12 seconds (if P present)
Rhythm: Irregular when it occurs (late)
If occurs 3 or more times in a row, is co
Sinus exit block - criteria
Rate: Regular or Bradycardia
P wave: Normal
QRS: Normal
Conduction: Normal
Rhythm:
Irregular: length of pause = multiple of normal rate
(Signal blocked leaving SA node; block is exactly equal to multiple of rate - one or more impulses "missed")
PACs (premature atrial contractions/atrial premature beats) - criteria
Rate: Regular underlying rate
P wave:
Abnormal - they originate from an ectopic pacemaker
QRS: Normal
Conduction:
Normal (except for PACs)
Rhythm:
Irregular when PACs occur (early)
PJCs (Premature Junctional Contractions)
AKA: Junctional Premature Beats
Rate: Regular underlying rate
P wave:
Absent or Inverted (like junctional escape)
QRS: Normal
Conduction:
PJC: P-R interval < 0.12 seconds (if P waves are present)
Rhythm:
Irregular when PJCs occur (early)
PSVT (Paroxysmal Supraventricular Tachycardia) AKA: AV nodal Re-entrant Tachycardia
Rate: Tachycardia (usually 150 - 200)
P wave: Absent or Inverted (like junctional escape)
QRS: Normal (may be wide, pseudo R')
Conduction: P-R interval < 0.12 seconds (if P)
Rhythm: Regular (abrupt onset and termination)
Carotid massage: slows or terminat
vagal stimulation
PNS stimulation - slows conduction through AV node; not if suspected carotid plaques
- valsalva, squatting, etc.
Atrial flutter
Rate:Atrial 250-350
Ventricular: 100 -175
P: Irregular or absent, often "saw tooth"
QRS: Normal
Conduction: AV Block (2:1 > 3:1, 4:1)
Rhythm: Regular (usually)
- Often underlying cardiac disease
Carotid massage: increases block
atrial fibrillation
Rate: Atrial 400-650;
Ventricular usually 120 - 180
P wave: Not present; often wavy baseline
QRS: Normal
Conduction: Variable AV conduction
Rhythm: Irregularly Irregular
- chaotic, unpredictable depolarizations w/i atrium, no atrial kick
- CAD, HTN, COPD,
MAT (Multifocal Atrial Tachycardia):
Rate: Atrial varies, Ventricular 100-200
P wave: ? 3 different 'P' waves
QRS: Normal (narrow)
Conduction: Variable AV conduction, P-R intervals vary
Rhythm: Irregularly irregular
- Various unpredictable atrial pacing sites
- Etiology: Often severe lung di
Wandering Atrial Pacemaker
Rate: Atrial & Ventricular 45 - 100
P wave: ? 3 different 'P' waves
QRS: Normal
Conduction: P-R intervals vary
Rhythm: Irregularly irregular
- slower form of MAT
Carotid massage: no effect
PAT (Paroxysmal (episodic) Atrial Tachycardia)
Rate: 100 - 200; Ventricular response 1:1 (or 2:1, 3:1, 4:1)
P wave: Usually present, abnormal
QRS: Normal
Conduction: P-R interval varies (due to ectopic sites)
Rhythm: Regular (may see warm up &/or cool down); unlike abrupt stop/start of PSVT; may be ha
MC ventricular arrhythmia?
PVCs - common in healthy people
bigeminy?
1:1 ratio of normal:PVC
trigeminy?
2:1 ratio of normal:PVC
PVCs (Premature Ventricular Contractions)
Rate: Regular underlying rate (usually); may happen occasionally in otherwise normal heart
P wave: Absent (or abnormal) in PVC
QRS: PVC: wide > 0.12 seconds; shape is bizarre; T wave inversion
Conduction: Normal before & after PVC
Rhythm: Irregular; may o
Reasons to worry about PVCs?
- Frequency increasing
- Runs of 3 or more consecutively
- Multiple PVC foci
- R-on-T Phenomenon
- PVC in acute MI
Multiple PVC foci
Beats 1 and 4 are sinus in origin. The other three beats are PVCs. The PVCs differ from each other in shape (multiform), and two occur in a row.
PVC - R on T
A PVC falls on the T wave of the second sinus beat, initiating a run of ventricular tachycardia.
Ventricular tachycardia
Rate: 120 - 200 usually
P wave:
Usually absent (unrelated to the QRS)
QRS: Wide & bizarre shape (PVCs)
Conduction: No correlation between 'P' if present and QRS
Rhythm: Regular or Irregular
Cannon A waves may be present
Carotid massage: no effect
Ventricular Fibrillation
Rate: Not attainable
P wave: Obscured by ventricular waves
QRS: No true QRS
Conduction: Chaotic electrical activity
Rhythm: Irregularly Irregular
Accelerated Idioventricular Rhythm
Rate: 50 - 100 usually (usually slow)
P wave: Obscured by ventricular waves (occur during ventricular contraction) - SA node slower than faster ventricular pacing than should be
QRS: Wide QRS
Conduction: Ventricular only
Rhythm: Regular
- benign rhythm th
Torsades de Pointes
Rate: 120 - 200 usually
P wave: Obscured by ventricular waves
QRS: Wide QRS - "Twisting of the Points"
Conduction: Ventricular only
Rhythm: Slightly irregular
1� AV block
Rate: Normal (usually)
P wave: Normal
QRS: Normal
Conduction: P-R interval is > 0.2 seconds (delay) - slowing at the AV
Rhythm: Regular
2� AV Block - Wenckebach or Mobitz Type I
Rate: Normal or Bradycardia
P wave: Normal morphology & constant P-P interval
QRS: Normal
Conduction: P-R interval is progressively longer until P wave is blocked; the cycle begins again 'long, longer, lost'
Rhythm: Irregular
2� AV Block - Mobitz Type II
Rate: Bradycardia
P wave: Normal morphology & constant P-P interval
QRS: Nl or widened (~ assoc with bundle branch block)
Conduction:
P-R interval normal or prolonged (constant); some P waves are not conducted to ventricles (varies)
3� AV Block
Rate: Atrial 60-100; Ventricular 30-45
P wave: Nl with constant P-P interval ("marching through")
QRS: Usually widened (depends on location of escape pacemaker)
Conduction: Atrial & Ventricular activities are unrelated (complete block)
Rhythm: Irregular
Bundle branch blocks - general criteria
Due to changes related to the block, cannot say there is hypertrophy - BBB will make it look like hypertrophy
Rate: Regular or Bradycardia
P wave: Normal usually
QRS: Wide > 0.12 seconds
Conduction: Block occurs in the right or left bundle branches (or bo
Right bundle branch block (RBBB)
Right ventricular depolarization is delayed
Criteria:
- Wide QRS
- RSR' in V1, V2 ("bunny ears") with ST depression and T wave inversion
- Late S waves in I, aVL, V5, V6 (reciprocal changes)
"rabbit ears
Left bundle branch block (LBBB)
LV depolarization is delayed
Criteria:
- Wide QRS > 0.12
- Broad (+/- notched) R waves, ST depression & T-wave inversion in
I, aVL, V5, V6
- Broad S waves in V1, V2
- Left axis deviation may be present
MI evolution: three phases
Acute Onset:
- T-wave Peaking (Hyperacute T)
- T > � R wave
A Few Hours Later:
- T-wave Inversion
- ST Elevation (STEMI), NSTEMI
- "tombstone sign" (similar shape) - often assoc with MI
Last: (days to weeks later)
- Significant Q-wave (true infarct)
Ischemic signs
ST elevation or ST depression:
> 1mm related to baseline (0.08 s (2 boxes) after QRS)
Also
symmetric
T-wave inversion in multiple precordial leads
NSTEMI
no Q wave or ST elevation
- T wave inversion
- ST DEPRESSION
- elevated cardiac enzymes (CPK-MB, troponin)
- high risk for later infarction!
Other causes of T-wave inversion?
LBBB: asymmetrical (with wide, upsloping +/- notched QRS); may mask ischemia & bury Q or P
LVH: asymmetrical
Other causes of ST elevation
J-Point elevation
(often <40)
At rest, returns to baseline if exercising
Flat, very distinct T wave
NO CLINICAL SIGNIFICANCE!
ST-elevation in MI - characteristics
ST segment and T wave merge into each other without a clear demarcation between them.
Prinzmetal's Angina
- ST elevation w/o infarction & ischemia
- Angina that occurs unprovoked at rest (coronary artery spasm) +/- underlying CAD
- Provide nitroglycerin & ST returns to baseline
Significant Q waves?
1) Q wave depth ? 1/3 the height of the R in the same QRS
2) Q wave duration > 0.04 seconds (1mm)
Ignore Q waves in?
aVR - almost always has significant-appearing Q waves!
Insignificant Qs common in?
Small Qs in I, AVL, V5 & V6 , II, III
- Due to depolarization of septum
Posterior infarct - reciprocal changes in?
V1 (poss. V2)
- large R = large Q
- upright T (T inversion)
Inferior infarct - arteries & leads?
RCA or distal LAD
II, III, aVF
- Reciprocal changes in anterior and left lateral leads.
Inferior infarct - with time?
May lose Q-wave significance within 6 months
Lateral infarct - arteries & leads?
LCX or diagonal branch of LAD
I, aVL, V5, V6
- Reciprocal changes in inferior leads.
Anterior infarct - arteries & leads?
LAD
I, V2, V3, V4
- Reciprocal changes in inferior leads.
Posterior infarct - arteries & leads?
- RCA distal branches
- Reciprocal changes in V1 (poss. V2)
ST-segment depression, tall R wave
anterior infarct
inferior infarct
lateral infarct
posterior infarct
RVH v. posterior MI
Both may have tall R waves in V1 & V2, but only RVH will have right axis deviation
Hemiblock
conduction block of 1 of 3 LBB fascicles
aka fascicular block
L anterior hemiblock
L axis deviation (dt impulse wrapping around from behind)
- Normal QRS duration, ST & T-wave
- Left axis deviation (-30� & -90�)
- No other causes of axis deviation (LVH, LBBB)
L posterior hemiblock
R axis deviation dt flow from anterior fascicle (wrapping around behind)
- Normal QRS duration, ST and T-wave
- Right axis deviation (+90� & +180�)
- No other cause of axis deviation (RVH, MI)
bifascicular block
RBBB + either L hemiblock:
RBBB - wide QRS, RSR' V1 & V2
(RBBB by itself, usually no axis deviation)
+
- Anterior - Left axis deviation
- Posterior - Right axis deviation
RBBB - underlying
May be otherwise normal (sometimes in athletes)
LBBB - underlying
Usually underlying cardiac disease
Bundle branches evident?
All the time, or only w/ increased HR
Incomplete BBB
no QRS & lead changes - not quite meeting criteria
Wolff-Parkinson-White Syndrome (WPW)
- By-pass pathway (bundle of Kent) between atria & ventricles
- No pause at AV node - short PR interval
- Delta Wave: Slurred initial upstroke of R
Short PR interval < 0.12 seconds
Wide QRS > 0.1 second with delta wave
WPW risks
- PSVT dt reentrant pathway present;
may be narrow QRS if via AV node & back up Kent, or wide (& hard to distinguish from V tach) if via Kent & back up AV node
- a fib - Kent acts as free conduit for chaotic atrial activity; may lead to V fib
Lown-Ganong-Levine
Intranodal James fibers bypass AV node
- PR interval less than 0.12 seconds
- Normal QRS width
- No delta wave.
Risks of LGL
Not really; mostly reduced CO during stress as no time for atrial kick, impaired filling
Hyperkalemia
Evolution of (1) peaked T waves, (2) PR prolongation and P wave flattening, and (3) QRS widening. Ultimately, the QRS complexes and T waves merge to form a sine wave, and ventricular fibrillation may develop.
Hypokalemia
- ST segment depression
- Flattening (or inversion) of the T wave
- Appearance of a U wave.
Hypercalcemia
shortened QT
Hypocalcemia
Prolonged QT
- risk of R on T leading to Torsades de Points
causes of long QT
- Medications: many antiarrhythmics, tricyclic antidepressants, quinolone antibiotics (z-pack).
- hypocalcemia
- Inherited Disorder: Long QT Syndromes
Digitalis/Digoxin - indications
- Increase contractility
- Slows AV junction conduction
- Used to tx HF
Digitalis effect - therapeutic levels
Asymmetric
ST depression, flat/inverted T-wave
Digitalis toxicity
- enhances automaticity --> tachyarrhythmias
- slowed AV conduction --> AV blocks
- PAT with block MC
pericarditis
DIFFUSE flat or concave ST elevation
- A large effusion can cause low voltage and electrical alternans.
pericardial effusion
1) low voltage - diffuse smaller waves
2) electrical alternans - axis changes w/ each beat; large QRS then small QRS
COPD
- Low voltage,
- Right axis deviation (RVH),
- poor R wave progression
- P pulmonale (right atrial enlargement;
tall P >2.5 in II) & abnormal P in V1) - "barrel chest" - increase AP diameter
Acute pulmonary embolism
RVH, RBBB
- Blood not getting through dt clot
Arrhythmias
S1Q3: large S in lead I, deep Q wave ONLY in lead III (if deep Q in several, then infarct)
- sinus tach & a fib MC arrhythmias
Brugada syndrome
structurally normal hearts
- autosomal dominant, M > W
- Resembles RBBB; ST elevation & RSR' in leads V1, V2, and V3.
- can cause fast polymorphic V tach (looks like torsades de pointes).
- ICD required
Common in athletes
- sinus bradycardia as low as <30 bpm
- ST segment elevation in the precordial leads with T wave flattening or inversion.
- LVH, sometimes RVH criteria
- Incomplete RBBB
- 1� or Wenckebach AV block.
- Arrhythmias (junctional, wandering atrial pacemaker)
Hypothermia
Osborne waves (ST elevation- abrupt ascent at J point & sudden plunge back to baseline) prolonged intervals, sinus bradycardia, slow atrial fibrillation. Beware of muscle tremor artifact.
CNS disease
Diffuse T wave inversion, with T waves typically wide and deep; U waves.
Indications for stress test
- eval CP/ro CAD
- eval >40 w/ risk factors for CAD
- assess pt response to interventions
- ?eval asx adults who want to start vigorous exercise (lots of false +)
criteria for selection of pts for stress test
- sx classic, atypical, or not at all angina-like?
- established CAD?
- functional tolerance to exercise?
stress test - contraindications
- angina at rest
- uncontrolled HF
- acute systemic illness
- severe aortic stenosis
- hypertrophic cardiomyopathy (sudden death)
- ability to walk/exercise
- caution if systolic > 200 or diastolic > 120; risk of hemorrhagic stroke!
normal physiological response to stress test
- incr SNS
- incr CO
- incr skeletal mm perfusion
- incr O2 extraction
- decr PVR
- incr systolic BP
stress test - pt preparation
- DC meds which may interfere (b-blockers, CCBs, digoxin, nitrates)
- no food, smoking, drink 2-4 hrs before
- pretest EKG
- pretest BP
stress test - finished when?
1) pt cannot tolerate dt compliance or sx
2) 90% of max HR reached
3) Significant EKG changes
stress test - positive when?
Horizontal or down-sloping ST depression (> 1mm & > 0.08 sec); earlier occurrence in test, more significant;
or exercise-induced hypotension, severe arrhythmia, or areas of heart w/ reduced blood
ST segment elevation - reasons
- With an evolving infarction
- In Prinzmetal's angina.
ST segment depression
- With typical exertional angina
- In a non-Q wave infarction.
Also:
- positive stress test.
- J point elevation
- Acute pericarditis
- Acute myocarditis
- Hyperkalemia
- Pulmonary embolism (S1Q3)
- Brugada syndrome
- Hypothermia
coronary cath - reasons?
testing & interventions; can be used w/ balloon angioplasty or stenting
echocardiogram
Transesophageal or transthoracic - 2D or 3D, Doppler, basically ultrasound of heart; can see movement of blood, valve regurgitation - can see valves & cardiomyopathies very well
Ashman phenomenon
Aberrant conduction of a supraventricular beat commonly seen in patients with atrial fibrillation; wide SV beat after a QRS complex that is preceded by a long pause.
1. BLS: Basic Life support SURVEY ---> Steps 1, 2, 3, 4 ---->
2. ACLS: Advance cardio life support SURVEY --> "ABCD
1.
- FUNDAMENTAL to every ACLS Algorithm is the BLS survey.
- The BLS Survey is the first 4 steps that you will take when treating ANY emergency situation:
THE 4 steps in the BLS Survey:
(1) Check responsiveness
- By tapping and shouting, "Are you all rig
Outline of the 4 steps in the BLS Survey : " CAB
(1) Circulation:
- Check for a carotid pulse for 5-10 seconds.
- If (-) pulse: start HIGH QUALITY CPR.
- if (+) pulse: start RESCUE BREATHING
(2) Activate the emergency response system and obtain a AED/Defibrillator.
- If (-) pulse: check for a shockable
AFTER "CAB" OF BLS --->
The ABCD's of the ACLS Survey are DONE:
(A) Airway:
- Maintain airway and use advanced airway if needed.
- Ensure confirmation of placement of an advanced airway and
- Secure the advanced airway device.
(B) Breathing:
- Give bag-mask ventilation, provide supplemental oxygen, and avoid excessive
Circulation:
- Check for a carotid pulse for 5-10 seconds.
1. If (-) no pulse: START CPR ---->
2. If (+) pulse: START RESCUE BREATHING --->
1. Start w/ 30 Chest compressions --> 2 breaths
i. On sternum -->
- FAST: 100 compression/min/2 inches deep.
ii. Allow full recoil.
iii. Switch q2min
2. Start rescue breathing --> 1 breath per 5-6 sec --> 10 -12 breaths per min.
- check pulse q2 minutes.
Rescue Breathing:
1. (+) absent or abnormal breathing (+) pulse
2. With BAG-MASK OR ADVANCE AIRWAY DEVICE PROVIDE 1 breath per 5-6 sec --> 10 -12 breaths per min
3. Check pulse q2 minutes.
1. ADVANCE AIRWAY DEVICES used during ACLS include:
2. Once an advanced airway is in place -->
1.
i. Combitube,
ii. LMA (Laryngeal mask airway)
iii. ET tube (endotracheal tube).
2.
- Chest compressions are no longer interrupted for ventilations --> Give 1 breath every 6-8 seconds (8-10 breaths/ minute) as compressions are done.
HIGH QUALITY CPR INCLUDES:
1. Compression Quality
2. Compression Pauses
3. Ventilation
4. CPR Sequence
1. 30 Compressions to 2 breaths:
- adequate depth (at least 2 inches)
- rate (100/MIN),
- allowing complete chest recoil.
2. Minimize the pause between compressions & shock to improve the chances of shock success.
3. Excessive ventilation should be avoide
Respiratory Arrest:
1. In ACLS, respiratory arrest typically means:
2. Tx:
---> ACLS "ABCD"
1. Respirations absent /inadequate for oxygenation
BUT (+) pulse
2. Tx starts w/ BLS-SURVEY: "ABC"
START RESCUE BREATHING ---> With BAG-MASK OR ADVANCE AIRWAY DEVICE -----> PROVIDE 1 breath per 5-6 sec --> 10 -12 breaths per min---> Check
When is artificial airways (OPA/ NPA) used?
unconscious with no cough or gag reflex.
Excessive ventilation should be avoided BC:
1. Hyperventilation lead to ---> increased intrathoracic pressure --> decreased venous return to the heart ---> diminished cardiac output,
and
2. Increased gastric inflation.
Major BLS Changes
-Encourage Hands only (compressions only) CPR for the untrained lay rescuer.
-CPR sequence changed from A-B-C to C-A-B.
TX of Respiratory Arrest includes these interventions:
1. Give oxygen
2. Open the airway
3. Provide basic ventilation
4. Provide respiratory support: Artificial airways (OPA/NPA)
5. Suction to maintain a clear airway
6. Maintain airway with advanced airways
The most common cause of airway obstruction in a patient that is unresponsive is
1. This type of obstruction is prevented with an airway opening technique called_____.
2. If spinal injury is suspected, ______ maneuver can be utilized allowing one to maint
the loss of tone in throat muscles ---> tongue falls back & obstructs the airway.
1. the head tilt-chin lift
2. the jaw thrust w/o head extension
2 ways to Opening the Airway:
1. The head tilt-chin lift:
2. The jaw thrust:
1. used no spinal injury is suspected
2. Used when spinal injury is suspected
ACLS Ventilation
- 5 basic airway skills used to ventilate a patient:
1.) Head tilt-chin lift;
2.) Jaw thrust when spinal injury is suspected.
3.) Mouth-to-Mouth ventilation;
4.) Mouth-to-Barrier device (using a pocket mask);
5.) Bag-mask ventilation.
The most common method of providing positive-pressure ventilation is
Bag-Mask ventilation with the E-C technique.
Ventilation:
1. MC method of providing positive-pressure ventilation:
2. Both the _____ airway & the _____ airway can be used as adjuncts to improve effectiveness of ventilation.
3. The _____ airway is only used on unconscious pts bc it stimulates gagging
1. Bag-Mask ventilation
2. oropharyngeal, nasopharyngeal
3. oropharyngeal
4. nasopharyngeal
1. If the airway is being maintained with the basic airway skills listed above_______ become the primary causes of an obstructed airway in the unconscious patient.
2. _____ should be used to clear the airway if it becomes occluded with these body fluids.
1. blood, secretions, and vomit
2. Suctioning
3.
suctioning,
less than 10 seconds
hypoxemia ---> oropharyngeal suctioning -----> causes vagal stimulation resulting in bradycardia ---> hypoxemia.
____ along with clinical assessment is the most reliable method of confirming and monitoring correct placement of an ET tube.
Continuous waveform capnography
What is Waveform Capnography?
1. The continuous, noninvasive measurement & display of end-tidal carbon dioxide/ETCO2 (also called PetCO2).
2. It is a direct measurement of ventilation in the lungs.
3. Indirectly measures metabolism and circulation.
- Normal ETCO2 in adult patient shou
Combitube
- A blind insertion airway device to provide an airway for mechanical ventilation
- A double lumen airway device designed for emergency ventilation of a patient in respiratory arrest when visualization of the airway and endotracheal intubation are not pos
Laryngeal mask airway
An advanced airway device that is blindly inserted into the mouth to isolate the larynx for direct ventilation; consists of a tube and a mask or cuff that inflates to seal around the laryngeal opening
Endotracheal tube
this tube ensures an open airway to the level of the lungs but is is an advanced life support technique not done by EMTs