Class 8 (03|08|22) Myocardial infarction and life-threatening arrhythmias Flashcards
What is the first thing one should so when a patient monitor is showing no rhythm?
Always assess the patient first: monitor is there to support us, but how the patient is reacting to is more important
What are common assent findings with arrhythmia’s?
Chest, neck shoulder or arm pain Cold, clammy skin Decreased blood pressure Decreases LOC Decreased O2 saturation Diaphoresis Dizziness, syncope Dyspnea Extreme restlessness Felling of impending doom Irregular rate and rhythm, palpitations Nausea & vomiting Numbness, tingling of arm Pallor Weakness & fatigue
What is clinical significant in the first assessment?
- The patient response to the arrhythmia determine the gravity of the situations
- interpret the rhythm & rate
- Hemodynamic response
- Identify the cause
- Initiate priority intervention
What is the first intervention on a patient that is pulseless and unconscious?
CPR
What are the initial interventions for arrhythmias? (7)
- Ensure patent airway
- Administer O2 VIA nasal cannula
- Attach combo pads
- Establish IV access
- Apply cardiac monitoring electrodes
- Identify underlying rhythm
- Identify ectopic beat
What must be considered when administering O2 during arrhythmias?
Depending if patient is breathing, oxygen saturations, WOB
Depends on how much oxygen, and the route of delivery
Not breathing = bag-valve mask ventilation and connect to oxygen
What is being continuously monitored for arrhythmias? (7)
What could be possibly be looking for?
Monitor vital signs, level of consciousness, O2 saturation, and cardiac rhythm
Anticipate need for intubation if respiratory distress is evident
Prepare to initiate CPR or defibrillation or both
ex) V-Tach → can progress too more lethal heart rhythms like V-Fib and asystole
What are possible medical interventions for Cardiac Arrest/Arrhythmias?
- Defibrillation
- E
- Amiodarone
- Lidocaine
- Treat reversible causes
Described defibrillation.
the “shock”; the machine will deliver energy in the form of joules to the patient
→ transmitted through the heart
→ effort to stimulate the heart to start correcting rhythm and beating again in a normal sinus rhythm (or non-lethal cardiac rhythm)
Describe the use of E in arrhythmias and cardiac arrest.
Epinephrine: used int cardiac arrest but increasing heart rate, increasing contractility and increasing peripheral vascular resistance
peripheral vascular resistance: vasoconstriction in an effort to shunt blood to the vital organs
What is peripheral vascular resistance?
peripheral vascular resistance: vasoconstriction in an effort to shunt blood to the vital organs
E can cause it
Describe the use of amiodarone for arrhythmias and cardiac arrest?
Amiodarone: antiarrhythmic medication that is effective in atrial and ventricular arrhythmias and effective at treating ventricular tachycardia or ventricular fibrillation that are refractory to shocks rate
- are not responding to defibrillation
- Very effective medication at converting patient to a more stable cardiac rhythm
Describe the use of Lidocaine in arrhythmias and cardiac arrest.
Lidocaine: antiarrhythmic medication used to help convert abnormal cardiac rhythms and restore them into a perfusing stable cardiac rhythm
What is the most common reason for a child to go into arrest?
Majority of kids that run into trouble is because of a respiratory issue
Either had respiratory arrest, and then they end up in cardiac arrest as a result
What is the differences between Adult Cardia Arrest Algorithm and the Pediatric Cardiac Arrest Algorithm? (2)
The amount of medication that we are giving (lower dose based on weight)
Shocks/joules delivered is based on the patient’s weight
What is ventricular fibrillation?
V-fib: Abnormal, deadly heart rhythm where ventricles (lower chambers of the heart) lose the ability to contract and circular blood to the rest of the body
Why is V-Fib so deadly?
can be cause from severe oxygen deprivation or abnormality in conduction causing a loss in coordinating signalling in verticals and create a rapid random and chaotic signalling
Leads to ventricular wall spasming, which means that blood is not circulating through the body, and all other organs are being deprived of oxygen
What can occur if V-Fib is not reversed quickly?
If V-fib is not reversed immediately through electrical shock, you are going to have permanent brain damage and death (brain and body are not getting enough oxygen)
In a normal heart rate, describe the electrical route and function of the ventricles.
Normal Heart
In a normal heart, the electrical conduction starts at the SA (sinoatrial) node
This signal travels from the SA node
→ AV (atrioventricular) node
From AV node
→ signals to the ventricles to make the ventricular cells and walls contract and blood is pushed to the rest of the body
What are some clinical manifestations for V-Fib?
- not going to be conscious (since there is no blood circulating)
- Pulseless
- right before someone collapses from V-fib, they might complain of - – S/S of a heart attack — ex) chest pain, numb/tingle in left arm (due to oxygen deprivation
- Pale/blue skin (cyanosis)
What does V-Fib look on a EKG?
Why?
Z EKG = course squiggly lines
- Because you lose the smooth signaling from SA → AV node → ventricles
- Ventricles are just spasming
What are some V-Fib risk factors? (3)
- general irritability to the ventricular cells (over-fire; abnormal fire)
- scar tissue formation: Scar tissue does not conduct signals like regular heart tissue. Instead, it sets up for abnormal firing/circuits in the heart
- Electrocution: Outside source of electricity entering the body; disrupts the normal signalling (not common)
What are examples can cause V-Fib by general irritability to the ventricular cells? (2)
Coronary artery disease (blood vessels get clogged = less blood flow/oxygen),
electrolyte abnormalities (high potassium, low calcium, low magnesium)
What happens when scar tissue is formed on the heart?
What are some examples that can cause V-Fib through scar tissue formation? (2)
: Scar tissue does not conduct signals like regular heart tissue. Instead, it sets up for abnormal firing/circuits in the heart
Heart attack- coronary artery gets clogged and no blood can flow dying tissue and scar tissue
cardiomyopathy: disease of the heart and it loses function through infection, genetics, years of CAD
What is ventricular tachycardia?
Rapid heart beat that arises from cells in the lower chambers of the heart (ventricles)
In V-Tach, BPM can be as high as 250
What occurs when the BPM is high in V-Tach?
Fast; has a hard time circulating enough blood to the rest of the body
Decreases the amount of blood circulating in the body
Circulation can get to be so poor that you do not feel a pulse anymore
In a normal heart rate, describe the what happens in the time between heartbeats?
What makes the pulse palatable?
Time between heartbeats = ventricular wall relaxes, ventricles fill with blood
Contraction = push blood through great vessels and out to the rest of the body
This forward movement is what makes you feel the pulse
What are the two types of V-Tach?
Focal V-Tach
Reentrant V-Tach
Describe focal V-Tach.
What can cause this?
Cells in the ventricles that get irritated and over fire → send extra stimuli to the ventricular conduction system → ventricles beat rapidly (V-Tach)
due to hormones; stress hormones, or thyroid hormones, low oxygen levels, stretch in heart tissue
What are the risk factors for V-Tach?
Coronary Artery Disease electrolyte abnormality (high potassium, low calcium, low magnesium)
Describe reentrant V-Tach.
What must the electrical pulse do then?
Scar formation (group of dead cells replaced by protein), which disrupts normal electrical conduction
Electrical current has to go around this patch of dead cells
Everytime it goes around, it is going to send a signal out to all these ventricular conduction cells → spread through the ventricles → ventricles beat rapidly (V-Tach)
What are the risk factors for reentrant V-Tach?
Anything that can cause scare tissue formation
Heart attack (re-entrant V-Tach), hypertrophic cardiomyopathy (re-entrant V-tach) dilated cardiomyopathy
What are the s/s & clinical manifestations of V-Tach?
S/S similar to those of other diseases with rapid heart rates
SOB, chest pain, palpitations, light headed, dizzy, faint, pass out
At some point, the person may have inadequate blood pressure (blood cannot circulate oxygenated blood to the body)
What can V-Tach progress into?
Can turn into V-Fib (walls spasm, no blood circulating)
When it gets to V-Fib, it needs to be corrected in seconds-minutes or else there will be death
How does V-Tach show in an EKG?
Course wide QRS complexes (QRS complex is greater than 3 small boxes)
Heart rate greater than 100 BPM
What are the two types of cardiac arrest?
What is the common clinical manifestation?
Ventricular Asystole
Pulseless Electrical Activity (PEA)
In both, the patient does not have a pulse (blood is not pumping to the rest of the body)
Describe Ventricular Asystole.
How does it show on EKG?
No electrical activity in the heart (ventricle walls are not contracting)
Asystole = no ventricular contractions = no electrical activity = no cardiac output = no pulse
EKG = flatline
Describe a PEA.
How does it show on a EKG?
There is electrical activity seen on a EKG, but it does not result in a pulse
The electrical activity seen on the
EKG could be something that normally produces a pulse (ex. Normal sinus rhythm, heart block, sinus bradycardia etc.)
PEA = electrical activity without a pulse that is not v-fib or pulseless v-tach
What are two possible reason for no pulse in asystole and PEA?
electro-mechanical uncoupling
Cardiac tamponade/something blocking the heart
Describe electro-mechanical uncoupling.
When the heart is under extreme stress (heart is being deprived of oxygen for a long time), the system gets disconnected
Despite the fact that cells can undergo and propagate action potentials, the action potentials do not result in muscle contraction
Describe electro-mechanical coupling (normal).
electro-mechanical coupling: heart’s electrical activity causes the muscles to contract. So you have action potentials that propagate or go through the heart, and they’ll lead to muscle contraction.
Describe how Cardiac tamponade/something blocking the heart can lead to asystole and pulseless electrical activity.
Pericardium can be full of blood, which will press down on the heart and not leave room for the heart to beat
heart is constricted by this fluid filled sac around the heart, and the heart can’t pump
Even though you can have action potentials and electrical activity in the heart, you’re not going to be able to pump, and won’t have a pulse
What rythms should not be shocked?
Why?
Asystole
PEA
Defibrillation only works on very specific abnormal cardiac rhythms that can potentially be reversed with an electric shock (shockable rhythms)
What rythms can be shocked?
V-Fib (ventricular walls are spasming),
pulseless V-Tach (abnormal conduction in the ventricles that cause high ventricular pump rate)
What is the genreal treatment for asystole and PEA?
- Start with CPR
- Treate reverible conditions (H’s & T’s) through Vasoconstrictive medications
Describe what vasoconstrictive medications do for the treatment of asystole and PEA.
Vasoconstrictive medications: Potentially reversible conditions (H’s & T’s) that could be causing or contributing to the cardiac arrest.
Conditions where there is some sort of lack of adequate blood circulating through the body, or adequate oxygen delivery to the body and heart
What are the H’s of asystole and PEA? (6)
Hypovolemia Hypoxia Hydrogen Ions Hypokalemia/Hyperkalemia Hypoglycemia Hypothermia
What are the T’s of asystole and PEA? (6)
Toxins
Tamponade
Tension Pneumothorax
Thrombosis
Describe how Hypovolemia can contribute to asystole and PEA.
(low blood volume)
→ usually from excessive bleeding
- Not enough blood is circulating, so not enough oxygen is getting around
Describe how Hypoxia can contribute to asystole and PEA.
(inadequate oxygen supply)
Describe how Hydrogen Ions can contribute to asystole and PEA.
Acidosis (body pH is too low); usually due to long periods of hypoxia
Describe how Hypokalemia/Hyperkalemia can contribute to asystole and PEA.
Potassium is important in maintaining electrical conduction in the heart
Describe how Hypoglycemia can contribute to asystole and PEA.
Can lead to cardiac arrest, and is easily fixed
Anyone with cardiac arrest is going to have their blood sugar checked
Describe how Hypothermia can contribute to asystole and PEA.
Less than 35 degrees Celsius
As core temperature drops, the heart’s pacemaker cells fire less and less (can lead to the heart stopping)
Describe how Toxins can contribute to asystole and PEA.
Can cause arrythmias``
prescription medications & street drugs)
Might have a reversible agent available
Describe how Tamponades contribute to asystole and PEA.
Blood fills the pericardium → constrict heart → hard for heart to pump blood
Describe how a tension pneumothroax can contribute to asystole and PEA.
Air enters the pleural space (usually due to a trauma to the chest), and the air cannot leave
Air puts pressure on the lungs and heart (heart can stop)
Describe how Thromdosis can contribute to asystole and PEA.
Blood clot
Concerned about a blood clot to the coronary artery that supplies the heart with oxygenated blood, or with a clot in the lungs (PE)
What is a dysrhythmia?
prompt assessment of abnormal cardiac rhythms
What is a normal cardiac electrical impulse?
begins in the senatorial (SA) node in upper right atrium
transmitted over the atrial myocardium via bundle of Bechmann and internodal pathways causing atrial contraction
impulse travels atrioventricular (AV) node through the bundle of His and down the left right bundle branches
ending in the Purkinje fibres which transmit the impulse to ventricles
Describe each interval on a EKG to the contractility of the heart.
R interval
Conduction to the point just before the impulse leaves the Purkinje fibres takes
QRS complex
impulse emerges from the Purkinje fibres, ventricular depolarization occurs, producing mechanical contraction of the ventricles
ST segment
time between ventricular depolarization and repolarization (flat line)
T wave
represents repolarization of the ventricles
QT interval
represents the total time for depolarization and repolarization of the ventricles
Whats is the purpose of the vegas nerve?
stimulation causes a decrease in the rate of the firing fo the SA node, slowing the impulse conduction of the AV node decreasing the force the cardiac muscle are contracting.
What is the purpose of the sympathetic nerve?
stimulation causes an increase in the rate of the firing for the SA node, increasing the impulse conduction of the AV node increasing the force the cardiac muscle are contracting.
Describe the semipermeability and polarity of the cardiac cells.
Inside cardiac cells/intracellular: potassium is high remain high and sodium to remain low
Polaries state
Outside cardiac cells/intercellular: high concentration of sodium and a low concentration of potassium
Describe the mechanism of action of Antidysrhythmia drugs.
effect the various phases of the action potential where there is an ionic shift in the cardiac cells and the action potential mechanism
Describe an action potential in the electrical activity in a heart.
- each of the 5 phases represents a particular electrical event
PHASE 0: upstroke of rapid depolarization that corresponds with ventricular contractions
PHASE 1,2,4: represent repolarization
PASE 4: complete repolarization (polarized state) and corresponds to diastole
Describe the P wave.
What is the normal duration?
What could be a possible source of variation?
P wave
Represents time for the electrical impulse causes atrial depolarization (contraction) to pass through the atrium; should be upright
0.06 - 0.12
Disturbance in contraction within atria
Describe the PR interval.
What is the normal duration?
What could be a possible source of variation?
Measured from beginning of P wave to beginning of QRS complex; represents time taken for implies to spread through the atria, the AV node and bundle of His branches and Purkinje fibres to a point of immediately before ventricular contraction
0.12 - 0.20
Disturbances in conduction usually in AV node, bundle go His or bundle branches but can be in atria as well
Describe the QRS interval.
What is the normal duration?
What could be a possible source of variation?
QRS interval
Measured from beginning to end of QRS complex; represents the time taken for depolarization (contractionO) of bother ventricles (systole)
0.06 - 0.20
Disturbance in conduction in bundle branches or ventricles
Describe the ST segment.
What is the normal duration?
What could be a possible source of variation?
ST segment
Measured from S face of the QRS complex to the beginning of the T wave; represents the time between ventricular depolarization and repolarization (diastole); should be isoelectric (flat)
Normal during is not applicable
Disturbances usually caused by ischemia, injury or infraction
Describe the T wave.
What is the normal duration?
What could be a possible source of variation?
Represents time for ventricular repolarization; should be upright
the normal duration is not applicable
Disturbances usually cause by electrolyte imbalances, ischemia or infraction
Describe the QT interval.
What is the normal duration?
What could be a possible source of variation?
QT interval
Measured from beginning of QRS complex to the end of T wave; represents tine taken for entire electrical depolarization and repolarization of the ventricles
0.34 - 0.43
Disturbances usually affecting repolarization more than depolarization and caused by drugs, electrolyte imbalances and change in HR
