Cardio #3 Flashcards
What is an electrocardiogram
A recording of the electrical activity of the heart from various views
Quick, fast, painless test that shows cardiac electrical activity in a moment of time
electrocardiogram
Most common leads for electrocardiogram
12-lead EKG
18-lead-EKG and 15 leads-
dependent where work
An __ is usually performed as soon as the patient presents to the emergency department or complains of chest pain
EKG
Can also be performed if the patient has acute cardiac complaints or arrhythmia noted on the cardiac monitor
EKG
Place electrodes on the chest & extremities
EKG
Connect wires to electrodes
EKG
Electrical impulses will be transmitted to the ___ machine
EKG
Instruct patient to uncross arms & legs, lay as still as possible
EKG
The EKG machine will pick up “artifact” if there is movement
EKG
Once an appropriate image is noted on the EKG screen, press “capture”
EKG
Electrical impulses appear as waves on the graph paper
EKG
Remove wires and electrodes from chest
EKG
Similar to telemonitor. Legs on ankles and arms
EKG
EKG placement
White on the right. Snow on grass
Dirt in the middle
Fire over smoke
EKG V1
4th intercoastal space to the right of the sternum
EKG V2
4th intercoastal space to the left of the sternum
EKG V3
Directly between leads V2 and V4
EKG V4
5th intercoastal space at the midclavicular line
EKG V5
Level with V4 at left anterior axillary line
EKG V6
Level with V5 at left midaxillary line (directly under the midpoint of the armpit)
Leg leads on ankle not hips
EKG
12 or 18 lead print
EKG
Different views on the heart, most normal lead is 2. Look at lead 2!
EKG
Every rhythm on the test will be lead 2.
6 second strips,
multiple choice and fill in the blank
Can use abbreviations,
A-fib, V-fib
Electrical impulses generates heartbeat
Cardiac Conduction System
Electrical impulses are affected by electrolytes:
Sodium, potassium, magnesium, calcium
SA node –
60-100 bpm
Interatrial bundles
Internodal bundles
AV node –
40-60 bpm
Bundle of His (right and left) –
20-40bpm, if it has to take over it wont be effective
Purkinje
fibers
If the SA node fails the
AV node takes over
If AV nodes fails-
Bundle of his takes over
The period from the beginning of one heartbeat to the beginning of the next
Cardiac Cycle
Depolarization
(Systole)= Contraction
Repolarization
(Diastole)= Rest
EKG: Each 1 mm (small) horizontal box corresponds to __ second,
0.04
EKG: with heavier lines forming larger boxes that include five small boxes and hence represent ___ sec intervals.
0.20
The ____ is straight line on paper where no positive or negative deflections
isoelectric line
Wave forms Printed on grid like paper- can maximize on computer
EKG
base line of the electrical activity, expect all wave forms to go back down
Isoelectric line-
P-waves and QRS
positively deflective
Negative deflection=
problem
Within normal cardiac cycle, there is a
P wave, QRS complex, and a T wave
not common unless potassium is off, we do not look for ___
U waves
Indicative of the SA node firing
P-wave
Indicates atrial depolarization
Should be rounded
P-wave
Are they present?
P-wave
Do they occur regularly?- is there a ____ for every QRS rhythm
P-wave
Do they look alike? Are they rounded and upright? Should be roundish and similar
P-wave
First positive deflection
Atria are depolarizing (contracting)
P-wave
Time it takes for impulse to travel from SA to AV node
PR-Interval
Identifies electrical delay
PR-Interval
Should be 0.12 – 0.20 seconds (3-5 horizontal squares)
PR-Interval
For “R” think “Respirations” (normal 12-20, put decimal before each number)
PR-Interval
Measured from beginning of increase of P to beginning of QRS complex
PR-Interval
If prolonged= taking longer for the SA node to go to the AV
PR-Interval
First degree AV block- PR interval is longer
PR-Interval
___ come after the P wave
QRS
Represents ventricular depolarization and atrial repolarization
QRS
Tall and skinny
QRS
It they are fat we have a problem
QRS
Minorly deflect, go up and then go down
QRS
Represents time it takes for electrical impulse to travel from AV node rapidly through ventricles
QRS
should measure 0.06-0.10 (1.5-2.5 little boxes)
QRS Interval
Measure from the beginning of Q to the end of S wave
QRS Interval
Count number of squares from end of PR interval to end of S wave
QRS Interval
The wider it is the ventricles aren’t contracting as forcefully as they should be
QRS Interval
If bigger than 2.5 boxes= concern
QRS Interval
If wider= ventricles are having problems, over excited and firing to early
QRS Interval
Time from completion of contraction to recovery
ST Segment
Starts at the end of QRS complex, ends at beginning of T wave
ST Segment
Checked for patients with chest pain
ST Segment
Don’t measure segment
ST
Make sure it goes back to isoelectric line to determine MI, current or past Ischemia indication
ST segment
Stemi-
ST elevated myocardial infarction
Check troponin to check MI
ST segment
When the ST is elevated =
MI happening right now
ST depression or depression or T wave inversion-
MI/ischemia
The ___ follows the QRS complex
T wave
Represents repolarization (resting state) of the ventricles and atria
T wave
Rounded, medium-sized, upward deflection
T wave
Don’t worry about the __ wave
U
Should be positive
Don’t have to measure ___
T wave
Steps to analyze EKG
Regularity of the rhythm
HR
P-waves
PR-interval
QRS-interval
Is the rhythm regular or irregular?
Regularity of the rhythm
Marching out? (Equal distance)
Regularity of the rhythm
Regularly irregular or irregularly irregular?
Regularity of the rhythm
What is the rate? 60-100
HR
Is there a P wave for every QRS?
P Waves
Are the P waves upright and rounded?
P Waves
Do they look the same?
P Waves
Is PR interval normal and constant? 0.12-0.20 seconds?
PR Interval
Is there a QRS complex for each P wave?
QRS Interval
Is the QRS interval 0.06-0.1 seconds?
QRS Interval
Left to right
EKG
How to quick count heart rate
In between the black lines at the top is 15 boxes which equals 3 seconds.
A sheet is 6 seconds
Heart rate second method
6 seconds = 30 big boxes
Count number of complexes in 6 sec strip x =10
Calculating HR
300 divided by the of big boxes between the R waves (QRS) or 1500 divided by the number of small boxes between the R waves
Sinus rhythm? Regularity of the rhythm
Regular (March out)
Sinus rhythm? Heart rate
60-100 bpm (means SA node firing)
Sinus rhythm? P Waves
P wave present, rounded and upright
P wave for every QRS complex
Sinus rhythm? PR Interval
0.12-0.20 seconds (3-5 boxes)
Sinus rhythm? QRS Interval
QRS interval less than or equal to 0.1 seconds.
Also called dysrhythmia
Arrhythmias
An abnormal rhythm of the heart
Arrhythmias
Arrhythmias can result in increased or decreased
HR, early or late beats, or atrial or ventricular fibrillation
Rhythms arising from SA node referred to as
sinus rhythms
Normal Sinus Rhythm, can abbreviate
Sinus tachycardia
Sinus bradycardia
Sinus Bradycardia Regularity of the rhythm
Regular
Sinus Bradycardia Heart rate
< 60 bpm
Sinus Bradycardia P Waves
P wave present, rounded and upright
P wave for every QRS complex
Sinus Bradycardia PR Interval
0.12-0.20 seconds
Sinus Bradycardia QRS Interval
QRS interval less than or equal to 0.1 seconds.
Sinus Bradycardia only abnormality
<60 HR
Sinus Bradycardia: Causes
Medications, Electrolyte imbalances, MI, Hypothyroidism, Hypothermia, Sleep apnea, SA node problems
SB Causes: Medications
Beta Blockers, Ca Channel Blockers, Digoxin
SB Causes: Electrolyte imbalances
Potassium, Magnesium, Sodium and calcium
SB Causes: MI, Hypothyroidism,
Hypothermia, Sleep apnea
SB Causes: Problems with SA node
sick sinus syndrome- put pacemaker in to fix
Past MI can stay in a bradycardia,
ischemia=myocardial infarction
Sinus Bradycardia: Symptoms
Hypotension, Diminished pulses, Fatigue, Syncope (fainting)
Athletes and older people can have
Sinus Bradycardia
Sinus Bradycardia: Treatment Asymptomatic
no treatment
Sinus Bradycardia: Treatment Symptomatic
Atropine IV, Dopamine IV, Transcutaneous pacing and Pacemaker
Atropine IV
Anticholinergic/Antispasmodic
Dopamine IV
Inotropic
Transcutaneous pacing
Temporary pacing
Deliver pulses of electric current through patient’s chest
Pacemaker
generates electrical pulses delivered by electrodes to one or more of the chambers of the heart, the upper atria or lower ventricles.
Sinus Tachycardia Regularity of the rhythm
Regular
Sinus Tachycardia Heart rate
> 100 bpm
Sinus Tachycardia P Waves
P wave present, rounded and upright
P wave for every QRS complex
Sinus Tachycardia PR Interval
0.12-0.20 seconds
Sinus Tachycardia QRS Interval
QRS interval less than or equal to 0.1 seconds.
Sinus Tachycardia only abnormality
HR >100
Sinus Tachycardia: Causes
Physical activity, Hemorrhage, Shock, Medications, Dehydration, Infection, Anxiety, Electrolyte imbalances
Sinus Tachycardia Cause Physical
activity
Sinus Tachycardia Cause Hemorrhage
Initial response as compensation
Sinus Tachycardia Cause Shock
Compensation mechanism
Sinus Tachycardia Cause Medications
Inhaled corticosteroids, SABAs, LABAs, pseudoephedrine, phenylephrine, levothyroxine (Inhalers)
Sinus Tachycardia Cause Dehydration
Compensation
Sinus Tachycardia Cause Infection and
Anxiety
Sinus Tachycardia Cause Electrolyte imbalances
Potassium, magnesium, sodium, calcium
Common Sinus Tachycardia: Symptoms
Angina, Dyspnea, Syncope, Dizziness, Anxiety, Palpations
Could be asymptomatic but symptoms are more common in
Sinus Tachycardia
Sometimes- sweating, diaphoresis
Sinus Tachycardia
Sinus Tachycardia: treatment
Correct the cause and Medications
Sinus Tachycardia: treatment Medications
Beta Blockers
Calcium Channel Blockers
Adenosine
Decrease SNS response
Beta Blockers
___ bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors
Beta Blockers
When these bind blood vessels constrict, HR, BP, CO, and force of contraction increase
Epinephrine and Norepinephrine
Heart has both β1and β2adrenoceptors, although the predominant receptor type is ___
β1
Β1 adrenoreceptors found in the heart and also found in the
kidneys
β2adrenoceptors are found in the smooth muscle like the
lungs and blood vessels
In the kidneys, activation of adrenoreceptors causes release of
renin into the blood
Blocks epinephrine and norepinephrine
Beta Blockers
We want cardiac selective beta blockers if
lung problems are present
Reduce cardiac output thus decrease blood pressure
Beta Blockers
Cause decrease in HR and contractility
Beta Blockers
Decrease myocardial oxygen requirements
Beta Blockers
Have many uses such as hypertension, angina, myocardial infarction, arrhythmias and heart failure
Beta Blockers
Cardio-selective beta blockers
bind specifically to beta-1 receptors (heart kidneys)
Cardio-selective beta blockers: MANBABE
M etoprolol (lopressor) or Metoprolol ER (Toprol XL)
A tenolol (Tenormin)
N ebivolol
B isoprolol
A cebutotol
B etaxolol
E smolol
Non-cardio selective beta blockers (do not specifically target beta-1 receptors):
Propranolol
Nadolol
Labetalol- combo alp/beta
Carvedilol- combo alp/beta
Sotalol
Beta Blockers Nsg Considerations
Check HR and BP prior to administration
Monitor for bronchospasm/SOB
Education- rise slowly (can cause orthostatic hypotension), do not stop abruptly
African Americans not as sensitive to BB
Beta Blockers HR and BP
Less than 60 hold
Systolic is less than 100
African Americans not as sensitive to BB
Increase Dosages
Calcium channel blockerswork toblock the L-type calcium channelsin the: Vascular smooth muscle cells:
coronary arteries and peripheral arteries
Calcium channel blockerswork toblock the L-type calcium channelsin the: Cardiac myocytes:
cells that control the strength of the heart’s contractions
Calcium channel blockerswork toblock the L-type calcium channelsin the: Cardiac nodal tissue:
cells that are responsible for theelectrical conduction of the heart
Causes vasodilation (decreased BP) and decreased HR
CCBs
Have anti-anginal effects
Can be used for arrhythmias
CCBs
Causes vasodilation
CCBs
Can be used with tachycardia with angina = vasodilation causes less angina
CCBs
Calcium Channel Blockers Medications
Diltiazem (Cardizem)
Verapamil (Calan SR)
Amlodipine (Norvasc)
Clevidipine (Cleviprex)
Nifedipine (Procardia)
Hydralazine (Apresoline)
Calcium Channel Blockers Nsg considerations: Check
HR and BP
Calcium Channel Blockers Nsg considerations: Assess for
angina
Calcium Channel Blockers Nsg considerations: Monitor digoxin levels and signs of toxicity
Vision changes, N/V, diarrhea, confusion, arrhythmias, loss of appetite (anorexia)
Calcium Channel Blockers Nsg considerations: Side effects can include
headaches and flushing
Calcium Channel Blockers Nsg considerations: Edema is common side effect with
Amlodipine
Any BP medication can cause
Orthostatic (Postural) Hypotension
Antiarrhythmic
Adenosine
Restores NSR by interrupting re-entrant pathways in the AV node
Adenosine
Slows conduction time through the AV node
Adenosine
Produces coronary artery vasodilation
Adenosine
Need telemonitor
Adenosine
Use cautiously in patients with asthma
May cause bronchospasms
Adenosine
Adenosine Monitor
HR
EKG
BP
Respiratory status
Adenosine Educate
Change positions slowly for at least 24 hrs
Emergent drug- IV
Adenosine
Atria initiate impulses faster than SA node
P wave looks different
Atrial Arrhythmias
Usually faster than 100bpm
Atrial Arrhythmias
Atrial Arrhythmias types
Premature Atrial Contractions (PAC)
Atrial Flutter (A-flutter)
Atrial Fibrillation (A-fib)
Not from SA node but from interatrial bundle
More p waves than QRS
Atrial Arrhythmias
Most common arrhythmia
Premature Atrial Contraction (PAC)
Premature electrical impulse in atrium- think “early” beat
Premature Atrial Contraction (PAC)
First determine underlying rhythm
Premature Atrial Contraction (PAC)
P wave morphology is different than other P waves
Premature Atrial Contraction (PAC)
Look at distance between R waves
Premature Atrial Contraction (PAC)
Atria contracting too soon, most common, early beat
Premature Atrial Contraction (PAC)
Know if it is a PAC
Premature Atrial Contraction (PAC)
Picture does not march out(even)
Premature Atrial Contraction (PAC)
Premature Atrial Contraction (PAC) only abnormal is
P-wave
Premature Atrial Contraction (PAC): Causes
Hypoxia, Cigarette Smoking, HF, Electrolyte imbalances, Caffeine, Alcohol, Meds, Fatigue, Anxiety, Stress
Premature Atrial Contraction (PAC): Causes, Electrolyte imbalances
Sodium, Calcium, Potassium, Magnesium
Premature Atrial Contraction (PAC): Causes, Caffeine
Coffee, soda, energy drinks
Premature Atrial Contraction (PAC): Causes, Meds
Asthma medications
Premature Atrial Contraction (PAC): Symptoms
Palpitations
Dizziness, lightheadedness, syncope more severe
Premature Atrial Contraction (PAC): Tx
Asymptomatic- No treatment
Symptomatic- Beta blockers, CCBs
Figure out cause
SA node firing to quick
Premature Atrial Contraction (PAC) abnormaility
Early P wave- Does not march out
P waves look abnormal
Electrical impulses initiated randomly from ectopic sites= atria quiver
Atrial Fibrillation
Stroke risk is increased due to stasis of blood
Atrial Fibrillation
Can be persistent or paroxysmal(sudden and uncontrolled)
Atrial Fibrillation
Afib Rapid Ventricular Rate (unstable Afib)
HR greater than 100
Still have p waves
Atrial Fibrillation
Multi-atrial firings with interatrial bundle, does not actually contract
Atrial Fibrillation
Stasis, clotting, aspirin=81mg chewable
Atrial Fibrillation
Stroke risk elevated
Atrial Fibrillation
HR could be normal
Atrial Fibrillation
A-fib(stuttering) with rapid ventricular rate=
ventricles are beating raiding, HR greater than 100-150 = ICU
Atrial Fibrillation Regularity of the rhythm
Irregularly Irregular
Atrial Fibrillation Heart rate
Atrial rate of 350-600
Ventricular rate much slower
A-fib with RVR = ventricular rate >100
Atrial Fibrillation P Waves
No P waves
Wavy pattern on EKG
Atrial Fibrillation PR Interval
Unable to determine
Atrial Fibrillation QRS Interval
QRS interval less than or equal to 0.1 seconds.
Atrial Fibrillation (A-Fib) abnormality
Does not march out
Atrial HR- 350-600 or 100-200
Multiple P-waves
Cannot determine PR-interval
Atrial Fibrillation: Causes
Age, Heart Disease, Hyperthyroidism, Sleep apnea, Cardiac surgery, Medications, Unknown
Atrial Fibrillation: Causes, Age
Risk increases after age 65
Atrial Fibrillation: Causes, Heart disease
HF, HTN, MI, valvular disease
Atrial Fibrillation: Causes, Medications
Cardiac stimulants: digoxin, increase SNS activity
Atrial Fibrillation: Causes, Electrolytes
Potassium, Calcium, Magnesium, Sodium
Atrial Fibrillation: S/sx
Hypotension, dizziness, pulse deficit (Hard to palpate), Chest pain (NO O2), palpations, fatigue
Radial pluse can be different than atrial= notify physican
Atrial Fibrillation
Atrial Fibrillation: Treatments
Anticoagulants, Rate and rhythm control, Cardioversion, Cardiac ablasion, Surgery
Atrial Fibrillation: Treatments, Anticoagulants
Warfarin
Eliquis
Xarelto
Lovenox and heparin (Hospital)
Plavix and Asprin (Home)
Warfarin Antidote
Vitamin K
Therapeutic range for INR (Warfarin)
2-3
Lovenox and Heparin Antidote
Protamine sulfate
Plavix antidote
NONE
Aspirin Antidote
Sodium bicarbonate
Eliquis (Apixaban) and Xarelo Antidote
Andexanet alfa (Andexxa)
Atrial Fibrillation: Treatments, Rate and rhythm control= slow and control the heart
Beta Blockers
Ca Channel Blockers
Digoxin
Atrial Fibrillation: Treatments, Cardioversion-
shock the pt. 150 volts, could put in worse rhythm, not an option for a pt that already has a clot
Anticoagulation prior
Atrial Fibrillation: Treatments, Cardiac ablation-
cauterizing, chemically or physically. procedure requiring informed consent, cutting off electrical impulse from the area
Atrial Fibrillation: Treatments, Surgery
Maze procedure- reroute the electrical activity, rare, serious a-fib and rvr, last resort
Aflutter is less likely to turn into __
A-fib
Digoxin: increase CO
Strengthens ventricular contraction
Digoxin: Slows ventricular rate
Decreases conduction through the SA and AV node
Digoxin: Therapeutic range
0.5 – 2 ng/mL
Digoxin: S/SX
vision changes, N/V, diarrhea, confusion, arrhythmias, decreased appetite
Digoxin: Monitor Potassium levels
Hypokalemia increases toxicity risk
Digoxin: Monitor Calcium levels
Hypercalcemia increases toxicity risk
Digoxin: Monitor Magnesium levels
Hypomagnesemia increases toxicity risk
Digoxin: Nsg implications
Monitor apical pulse for 1 full min before administration
Hold if HR < 60 bpm
Monitor ECG during IV administration and 6hr after each dose
Coordinated electrical activity in the atria
Atrial Flutter
Not every impulse goes to ventricles
Atrial Flutter
Fire forms the interatrial bundle, fire consistently
Atrial Flutter
Can see 3-5 p waves
Atrial Flutter
Atria contracting each time and then ventricles contract, can worry about preload in ventricle
Atrial Flutter
HF, cannot pump effectively
Atrial Flutter
Atrial Flutter: Regularity of the rhythm
Atrial rhythm regular,
ventricular rhythm regular or irregular depending on AV conduction impulses
Atrial Flutter: Heart rate
Atrial rate 250-350 bpm
Ventricular rate depends on underlying rhythm
Atrial Flutter: P Waves
Rapid coordinated P waves
Sawtooth pattern
Atrial Flutter: PR Interval
Unable to determine= too many
Atrial Flutter:
QRS interval less than or equal to 0.1 seconds.
Atrial Flutter abnormality
Regularity of the rhythm
HR
P-waves
PR interval
Atrial Flutter: Causes
CHF, MI, Valve disorders, HTN, Rheumatic or ischemic heart disease, PE, COPD, Post-CABG
Atrial Flutter: Causes
Chronic=asymptomatic
Paroxysmal=palpitations
Angina=decrease in O2
Dyspnea
Atrial Flutter Tx
Same as Atrial Fibrillation
Abnormal beats originating in ventricles
Ventricular Arrhythmias
Often cause heart to beat too fast
Ventricular Arrhythmias
Types of Ventricular Arrhythmias
Premature Ventricular Contractions (PVCs)
Ventricular tachycardia(V-Tec)
Ventricular fibrillation(V-fib)
Very common
Premature Ventricular Contractions (PVCs)
Extra abnormal heartbeat of the ventricle
Premature Ventricular Contractions (PVCs)
Ventricles fire prematurely before the SA node causing wide QRS
Premature Ventricular Contractions (PVCs)
2nd most common dysrhythmias
Premature Ventricular Contractions (PVCs)
Ventricular fire prematurely before atria
Premature Ventricular Contractions (PVCs)
Wide QRS problem in the ventricles
Premature Ventricular Contractions (PVCs)
Bundle of his or purkinje fibers, fire too early
Premature Ventricular Contractions (PVCs)
Can have every other beat or every 3rd beat
Premature Ventricular Contractions (PVCs)
Premature Ventricular Contractions (PVCs) risk factors
Caffeine, Tobacco, Alcohol, Exercise, Hypertension, Anxiety, Stimulant use, Underlying heart disease
Premature Ventricular Contractions (PVCs) risk factors, Stimulant use
- speed, methamphetamines
Premature Ventricular Contractions (PVCs) risk factors, Underlying heart disease
congenital heart disease, coronary artery disease, heart attack, heart failure and a weakened heart muscle (cardiomyopathy)
Premature Ventricular Contractions (PVCs) S/Sx
“Flip-Flops”- skipped beats
Skipped beats
Missed beat
Cyanosis, headache, anemia
If 1 PVC may not notice
Premature Ventricular Contractions (PVCs) Tx
Lifestyle changes- energy drinks, Tobacco, Alcohol, Stimulant
Beta Blockers
Calcium Channel Blockers
Amiodarone- common drug for PVC
Cardiac Ablation
Premature Ventricular Contractions (PVCs) types
Unifocal, Multifocal, Bigeminy, Trigeminy, Couplet, Run/V-Tach
Premature Ventricular Contractions (PVCs) Unifocal
Come from the same irritable ventricular area
look the same
Premature Ventricular Contractions (PVCs) Multifocal
Originate from several different irritable areas in the ventricle
do not look the same
Premature Ventricular Contractions (PVCs) Bigeminy- normal, PVC
Every other beat is a PVC
Premature Ventricular Contractions (PVCs) Trigeminy- normal, normal, PVC
Every third beat is a PVC
Premature Ventricular Contractions (PVCs) Quadgeminy- normal, normal, normal, PVC
Every fourth beat is PVC
Premature Ventricular Contractions (PVCs) Couplet- some normals
2 PVCs back to back in a row, likely to get 3 or 4
Premature Ventricular Contractions (PVCs) Run/Vtach
3 or more PVCs in a row (FATAL)
When naming the rhythm when PVC and not saying specific type =
list if its a PVC
Originates in the ventricles
Ventricular Tachycardia (VTACH)
3 or more Premature Ventricular Contractions (PVCs)
Ventricular Tachycardia (VTACH)
Ventricles become the pacemaker instead of SA node
Ventricular Tachycardia (VTACH)
Ventricular Tachycardia (VTACH) Regularity of the rhythm
Regular
Ventricular Tachycardia (VTACH) Heart rate
150-250 bpm
Ventricular Tachycardia (VTACH) P Waves
Absent
Ventricular Tachycardia (VTACH) PR Interval
Unable to determine
Ventricular Tachycardia (VTACH) QRS interval
> 0.1 seconds
Bizarre appearance
wide
PVC fatal if they turn into
V-tech
Lethal rhythms, shockable –
V-tech, V-fib
Tombstone rhythm
Ventricular Tachycardia (VTACH)
Vtach: common causes
Mi, Cardiomyopathy, Hypokalemia, Respiratory acidosis, Myocardial irritability, Drugs, Medications
Vtach: s/sx
Dyspnea, Lightheaded, Angina, Feeling of fast HR, Pulselessness
T-tach, awake and talking, may turn unconscious
Vtach: treatment with pulse
Meds, Synchronized cardioversion, ICD(not best practice), Ablation
Vtach: treatment with pulse, Meds
Lidocaine
Adenosine-stop electrical activity to restart rhythm
Beta Blockers- slow hrt down, lobatolol IV
Amiodarone- antidysrhythmic
Diltiazem- CCB- blood flow to the heart
treatment with no pulse
CPR (call for help)
Defibrillation
Meds
AED- synchronize, follows the beat where the P wave should be
ACLS protocol- meds-not pulse
Vtach: treatment with no pulse, Meds
Epinephrine
Lidocaine
Amiodarone
Tombstone-
V-tach
Cardio aversion-
low shock
Defibrillation-
high shock
Vagal down- act like bowel movement until meds into the room
Wide QRS
V-tach leads to V-fib untreated
Deterioration of the heart, V-fib
Vtach
Mrs. Parker,age 76, is admitted to the long-term care unit where you are working. She has been transferred from the hospital after treatment for a recent myocardial infarction and several episodes of ventricular tachycardia (VT). At 1600 hours, you find her unresponsive, with no palpable pulses and shallow respirations. Vital signs are blood pressure 80/40 mm Hg, apical pulse 150 bpm, and respiratory rate 6 breaths per minute.
Is this patient hemodynamically stable?
No
Why are there no palpable pulses?
Blood is being rerouted to vital organs
What is happening to the heart when VT is occurring?
Ventricles constantly contraction
What action should you take?
Call 911, bring crash cart, cpr when losing pulse completely
Ventricular activity is chaotic, ventricles quiver
Ventricular Fibrillation (V-Fib)
No discernible waves
Ventricular Fibrillation (V-Fib)
No Pulse, will not be responsive
Ventricular Fibrillation (V-Fib)
ACT FAST
Ventricular Fibrillation (V-Fib)
If you see VFIB=DFIB
Always defibrillate these patients
Ventricular Fibrillation (V-Fib)
Start with CPR, epinephrine, and Amiodarone or Lidocaine may be given
Ventricular Fibrillation (V-Fib)
Ventricular Fibrillation (V-Fib) Causes
V-tach, Hyperkalemia, hypomagnesemia, CAD, MI, electrocution
ACLS protocol meds
Ventricular Fibrillation (V-Fib)
Ventricular Fibrillation (V-Fib) Regularity of the rhythm
Irregularly irregular
Ventricular Fibrillation (V-Fib) Heart rate
Unmeasurable
Ventricular Fibrillation (V-Fib) P Waves
Absent
Ventricular Fibrillation (V-Fib) PR Interval
Unable to determine
Ventricular Fibrillation (V-Fib) QRS Interval
None
QRS are small
V-Fib= death
Cannot shock systole
Ventricular Fibrillation
Absence of electrical activity
Asystole
VF usually precedes asystole= sudden cardiac death
Asystole
Unconscious and unresponsive
Hard to bring back
Asystole
Start CPR immediately
Asystole
Asystole causes
Hyperkalemia
V-fib
Massive MI
Shock
hardening of wall and loss of elasticity
Arteriosclerosis
Arteriosclerosis Patho
thickening, loss of elasticity, and calcification of arterial walls
Part of aging process
Plaque
Arteriosclerosis
Atherosclerosis Patho
formation of plaque within arterial wall
Injury to endothelial cells
Lipids, platelets, and clotting factors accumulate
Scar tissue
Atherosclerosis: Growth of smooth muscle cells which secrete:
Collagen and fibrous proteins
Formation of atheroma’s (plaques of lipid material)
Athersclerosis
Thickening of the inner wall and the central wall of the artery
Arteriosclerosis
A fatty streak forms on the lining of the artery- known as plaque
Atherosclerosis
Plaque has jagged edges that allow blood cells and other materials to adhere to wall
Atherosclerosis
Fibrous cap forms- Can tear or rupture and a blood clot forms which can block artery
Atherosclerosis
Vessel can also become narrowed from plaque buildup
Atherosclerosis
Injury to endothelial wall
Clotting and obstruction risk
Perfusion risk
Atherosclerosis
Development of Plaque
Atherosclerosis
Atherosclerosis: Non-modifiable Risk Factors
Age-Men after 50, women after menopause
Gender- Men
Ethnicity- African Americans
Genetics- Family hx. of hyperlipidemia
Atherosclerosis: Modifiable Risk Factors
Physical Inactivity
Obesity
Diabetes Mellitus type 2
Alcohol use
Sedentary lifestyle
Stress
Elevated cholesterol
Hypertension
Nicotine Use
Atherosclerosis: Diagnosis:
Lipid profile, C-reactive protein, Blood glucose levels, Stress Test, Cardiac Catheterization
Atherosclerosis: Diagnosis: Labs- Lipid Profile
Total Cholesterol, Triglycerides, LDL, HDL
Range: <200mg/dL
>200 associated with CAD
Measurement of HDL, LDL, and VLDL
Total Cholesterol
Range: <150mg/dL
Critical value > 400mg/dL
>150 mg/dL at risk
Triglycerides
Range: <130mg/dL
contains both cholesterol and trigs and may deposit cholesterol directly onto walls of arteries
LDL
Range: >45mg/dL-men; >55mg/dL-women
Carry LDL to liver to be broken down and excreted
HDL
Atherosclerosis: Diagnosis: Labs- C-Reactive protein
1.0-3.0mg/L
>3.0 mg/L Indicates low-grade inflammation
Atherosclerosis: Diagnosis: Labs- Blood Glucose levels
elevated levels can increase the risk for atherosclerosis
Shows how heart works during physical activity
Atherosclerosis: Diagnosis: Stress Test
Can be on a treadmill/bike
Atherosclerosis: Diagnosis: Stress Test
If patient unable to exercise adenosine or another vasodilator used to open up vessels
Atherosclerosis: Diagnosis: Stress Test
Nuclear stress test- not common
Atherosclerosis: Diagnosis: Stress Test
Small amounts of radioisotopes given IV
Atherosclerosis: Diagnosis: Stress Test
Photos taken and compared
Atherosclerosis: Diagnosis: Stress Test
Handles increase activity and O2 demand
Atherosclerosis: Diagnosis: Stress Test
Procedure done to visualize anatomy of heart
Atherosclerosis: Diagnosis: Cardiac Catheterization
Thin catheter inserted
Atherosclerosis: Diagnosis: Cardiac Catheterization
Fluoroscopy used to produce real-time images
Atherosclerosis: Diagnosis: Cardiac Catheterization
Contrast dye can be injected
Atherosclerosis: Diagnosis: Cardiac Catheterization
Cardiac Catheterization Nsg implications
Assess for allergies prior
Obtain consent
When patient returns from cath check labs
Keep on bedrest
assess vitals
entry site- bleeding, dressing
6 Ps
Activity restriction, cannot climb more than 2 flights of stairs for minimum for 3 weeks, unable to engage in sexual activity
24-48 hours minimum= 48-72 hrs before cardiac cath- metformin, nephrotoxic
Groin or wrist
insert stent to inflate balloon
Cardiac Catheterization
Atherosclerosis: Therapeutic Measures
Diet- Heart-healthy diet. DASH diet
Smoking Cessation
Exercise
Low-dose aspirin 81 mg chewable
Medications
Assess vitals, continuous q15 blood pressure on monitor
Atherosclerosis: Therapeutic Measures, Diet- Heart-healthy diet. DASH diet
Fruits and veggies, avoid trans fats, reduce saturated fats, reducing sugar and sodium (nothing fried, coconut oil)
Atherosclerosis: Therapeutic Measures, Exercise
Increases HDL and can lower insulin resistance, can lead to development of collateral circulation.
30 mins a day most days can be intervals
Atherosclerosis: Therapeutic Measures, Medications
Often needed to reduce lipid levels, can take up to 4-6 weeks.
Atherosclerosis: Drug Therapy
Statins, Fibrates, Bile Acid Sequestrants, Cholesterol Absorption Inhibitor, Niacin
Reduce cholesterol synthesis (4-6 weeks), rhabdomyolysis. #1 medication for atherosclerosis
Statins
Atorvastatin (Lipitor)
Pravastatin (Pravachol)
Simvastatin (Zocor)
Rosuvastatin (Crestor)
Statins
Reduce triglycerides
Fibrates
Fenofibrate (TriCor)
Gemfibrozil (Lopid)
Fibrates
Increase conversion of cholesterol to bile acids, if statins aren’t fully working
Bile Acid Sequestrants
Cholestyramine (Questran)
Colesevelam (WelChol)
Colestipol (Colestid)
Bile Acid Sequestrants
Inhibits Cholesterol Absorption
Cholesterol Absorption Inhibitor
Ezetimibe (Zetia)
Cholesterol Absorption Inhibitor
Prevents conversion of fats into VLDLs
Niacin:
Caused by atherosclerosis
Coronary Artery Disease (CAD)
Plaque buildup in the walls of coronary arteries causing blockage
Coronary Artery Disease (CAD)
Progressive disease
Coronary Artery Disease (CAD)
Coronary Artery Disease (CAD) risk factors
Same as atherosclerosis
Coronary Artery Disease (CAD) can cause
Age- Men over 50
Woman after menopause
Angina- ischemia or decreased O2 supply
MI
Death
Angina is chest pain due to ischemia
CAD: S/SX: Angina
Narrowed blood vessels unable to dilate
CAD: S/SX: Angina
Carry less blood/oxygen for heart muscle
CAD: S/SX: Angina
Types of angina
Stable, Unstable, Variant or Vasospastic (Prinzmetal) and Microvascular
Occurs in pattern familiar to patient, only lasts a few minutes. Goes away with rest/Nitro. Pattern familiar. Less than 10 mins.
Stable Angina
Increases unpredictably in frequency, occurs at rest, during sleep. Not relieved by meds or rest
Should be treated as emergency, can lead to MI
Can last longer than 10 mins
Unstable Angina
Caused by coronary artery spasms. Pattern is cyclical, lasts longer than stable. In cycles, can treat with nitro
Variant or Vasospastic angina (Prinzmetal angina)
Spasms in walls of tiniest arteries. Pain may be more severe. Brings to knees right away, very painful
Microvascular angina
Tight pressure, crushing=
angina
Discomfort, burning, fullness, pressure, squeezing
CAD: S/SX: Angina
Pain may radiate down arms, to neck and scapula
CAD: S/SX: Angina
Heaviness in arms
CAD: S/SX: Angina
Women may have atypical symptoms: SOB, fatigue, nausea
CAD: S/SX: Angina
Lasts 5-15 minutes
CAD: S/SX: Angina
Nitroglycerin- direct vasodilator Tx
Angina
Nitroglycerin
CAD: S/SX: Angina: Treatment
Dilates arteries thereby reducing workload of heart
Nitroglycerin
Sublingual
Acts in 1-2 minutes
Last 30-40 min.
Nitroglycerin
1 dose Q5min x 3
Nitroglycerin
Nitroglycerin Side effects:
Hypotension, headache (rush of blood to heart and brain)
Assess pain and BP because it dilates
Nitroglycerin
Educate pts to assess bp and keep nitro on them or close
Nitroglycerin
Kept in cool, dry, dark, area because of photosensitivity keep in pockets
Nitroglycerin
Under 100 systolic and 40 diastolic
Nitroglycerin
IV or Patch
Remove patch to give sublingual
Nitroglycerin
12 hrs is cut off-
Nitroglycerin
CAD: Angina: Medications/treatment
CCBs, Anti-ischemic agents, Nitrates
Amlodipine- most common
Felodipine
Calcium channel blockers- vasodilates, check BP and HR
Ranexa
Anti-ischemic agent
Isosorbide mononitrate
Nitro
Avoid erectile dysfunction meds- causes vasodilation ask if Viagra (tidalifil) or Sialis
Nitrates
Includes unstable angina and MI
Acute Coronary Syndrome (ACS)
Caused by sequence of inflammatory processes
Acute Coronary Syndrome (ACS)
80% caused by Thrombus or clot formation leading to reduced blood flow (Unstable angina)
Acute Coronary Syndrome (ACS)
Partial or complete occlusion of coronary artery (MI)
Acute Coronary Syndrome (ACS)
NSTEMI (not ST elevation still myocardial infarction) or STEMI (ST elevated myocardial infarction)
Acute Coronary Syndrome (ACS)
Caused by CAD or atherosclerosis
Acute Coronary Syndrome (ACS)
12 lead EKGs- which coronary artery is effected, fireman’s hat,
nitro, get physician
Chest pain-
New
Worse
Sudden
Occurs at rest, while asleep, with little exertion
Lasts longer than stable angina (over 10 mins)
Not relieved by medicine
Unstable Angina
Usually caused by atherosclerosis, which can rupture leading to blood clot
Unstable Angina
Should be treated as an emergency, can lead to MI
Should be coming to ED
Unstable Angina
Results in death of heart muscle
Myocardial Infarction
80-90% of time caused by thrombus formation
Myocardial Infarction
Ischemic injury happens over hours before complete necrosis takes place
Myocardial Infarction
Area of heart affected depends on coronary artery affected
Myocardial Infarction
STEMI- Most serious, affects full thickness of heart
Myocardial Infarction
NSTEMI- Less serious, blockage is usually partial
Myocardial Infarction
Time is muscle!!!=act quickly. 4 hours time frame from start of symptoms
Myocardial Infarction
Scar tissue may form in the damaged area
Myocardial Infarction
Can give TPA for stroke and MI also (not common)
To break up thrombus
CTA- to see type of stroke
Myocardial Infarction
Typical Myocardial infarction S/Sx:
Heaviness, pressure, tightness, burning, constriction, or crushing pain- “elephant sitting on my chest”
Substernal or retrosternal, may radiate
Fatigue
Weakness
SOB
Anxiety
SNS is activated
Low BP
Elevated HR
Diaphoresis caused by anxiety
Cool, Clammy, gray skin
Nausea/vomiting
Myocardial Infarction/Heart attack symptoms in men
N/V, Jaw, neck, and back pain, Squeezing chest pressure or pain, SOB
Myocardial Infarction/Heart attack symptoms in women
N/V, Jaw, neck, and back pain, chest pain but not always, pain or pressure in the lower chest or upper abdomen, SOB, fainting, indigestion, extreme fatigue
Low Bp
Elevated HR
N/V typical in women
Myocardial Infarction
Denial common
Wait to seek care (no tPA)
Myocardial Infarction: Treatment
“Time is muscle”
Call 911
Do not drive self or ride with others
Reperfusion time critical
Myocardial Infarction: Treatment
Chew one uncoated adult aspirin (324mg= adult aspirin)
If in LTC chew enteric coated
Myocardial Infarction: Treatment
STEMI TX
Educate on nitro and angina
May have atherosclerosis or CAD and not know they had a MI
Myocardial Infarction: Treatment
Diagnostic Tests for MI
Troponin, Myoglobin and creatine kinase, EKG, Magnesium and Potassium
Troponin
The more damage the higher number will be
Myoglobin and creatine kinase
(CK)-MB- not as sensitive as troponin
EKG-
Look at ST segment
Magnesium and Potassium
NOT AS CRITICAL
ST elevation
MI
ST depression
Ischemia
STEMI (HAPPENING NOW) AND
NSTEMI (COULD HAVE HAPPENED) = ISCHEMIA
Myocardial Infarction: emergency Drug Therapy
IV nitro, Antiplatelet Therapy, Systemic anticoagulation, pain management, thrombolytic
Reduces pain
vasodilates which improves blood flow
IV nitro-
Reduce platelets from forming clots
Antiplatelet therapy-
IV Heparin (PROTAMINE SULFATE=ANT)
Systemic anticoagulation-
Usually IV Morphine
Decreases preload and afterload
Decreases BP and HR
Pain management-
Used to dissolve blood clot
STEMI
O2 if O2 is less than 92%
Thrombolytic-
MI- MONA TASS
M orphine
O xygen
N itroglycerin
A spirin
T hrombolytics
A nticoagulants
S tool softeners
S edatives
Myocardial Infarction: Treatment Cardiac catheterization
Balloon angioplasty
Percutaneous coronary intervention (PCI)- can pull out clot
Coronary Artery Bypass Graft (CABG)
Myocardial Infarction: Treatment
Post operative concerns-
perfusion, clots, HR, BP, sites for bleeding, below sites for 6 P’s
Myocardial Infarction: Post Medications
Beta Blockers, ACE inhibitors, (2nd line), Statins, Antiplatelet, Vasodialators
If MI for the rest of their life. Decrease HR, BP, prevent release of renin, reduce preload and afterload. Decrease O2 demand
Beta Blockers
Metoprolol (heart specific)
Carvedilol, or propranolol asthma or COPD should not be on it
Beta Blockers
Lowers BP, reduces workload on heart (hypotension, cough)
ACE inhibitor (2nd line)-
Lisinopril, Ramipril
ACE inhibitor (2nd line)-
Lowers cholesterol
Statin-
Crestor, Lipitor
Statin-
Reduce preload and afterload, reduce oxyIsosorbide mononitrate
en consumption of myocardium
Vasodilators-
Isosorbide mononitrate
Vasodilators-
MI is also called
acute coronary syndrome
Narrowing of arteries that leads to occlusion or obstruction
Peripheral Arterial Disease (PAD)
Strongly related to other CVD (likely to have PAD)
Peripheral Arterial Disease (PAD)
Usually in lower extremities
Peripheral Arterial Disease (PAD)
Reduces blood supply
Leads to ischemia distal to obstruction
Peripheral Arterial Disease (PAD)
Can have one or multiple occlusions
Peripheral Arterial Disease (PAD)
PAD: Risk factors
Smoking, Hyperlipidemia, Hypertension, Diabetes Mellitis, Elevated BMI, Family history of athersclerosis, Age, Ethnicity-African americans
PAD: S/SX
Intermittent Claudication- Pain in calves with activity (causes PT to seek TX)
Paresthesia
Thin, shiny, and taut skin (Rubor)
Loss of hair on the lower legs
Diminished (is okay if they have PAD) or absent pedal, popliteal, or femoral pulses
Pallor of extremity when elevated, reddish-purple when dependent
Cool skin
Thickened toenails
Dry, flaky, scaly skin
Decreased sensation
Pain at rest (Severe PAD)
Atrophy of the skin and underlying muscles (blood and O2 supply inadequate= weak)
PAD: Complications
Delayed healing (blood supply)
PAD: Complications
Wound infection (gangrene, can lead to amputations’)
PAD: Complications
Tissue necrosis (caused by gangrene or no blood supply, occlusion, leads to amputations)
PAD: Complications
Arterial ulcers (difficult to heal, different than PVD ulcers)
PAD: Complications
Amputation
PAD: Complications
Jagged edge not perfect shape, hard to heal bc of
blood supply
On ankles but can be anywhere in lower extremities-
PAD
PAD: Diagnostic Studies
Ankle-brachial index (ABI), Arterial ultrasound, CT or MRI, Angiography
Ankle-brachial index (ABI)
trying to find pulse
Done using a hand-held Doppler
Take systolic of leg and divide by systolic of arm
Angiography-
important, scan of the vessels, uses. Push fluids, allergies, metformin
PVI
No compression socks for
PAD
= balloon-like bulge in vessel
Aneurysm
Aortic aneurysms may involve the
aortic arch,
thoracic aorta
abdominal aorta. (AAA)
Aorta >3cm is considered
aneurysm
Outpouching of the wall of the artery
aneurysm
Aortic Aneurysms: Risk Factors
Age, Male, Smoking, HTN, Atherosclerosis, Family history, High cholesterol, Elevated BMI
Can lead to rupture- HTN control
aortic aneurysm
Types of Aneurysms
Saccular, Fusiform, and Dissecting
Bulges on one side of arterial wall
Saccular
dilation of entire circumference
Fusiform
Cavity is formed from tear in artery wall
Dissecting- not a true aneurism *
Aortic Aneurysm: S/Sx, Thoracic aortic aneurysms
Often asx, SOB, CP, pain that radiates to back
SOB, Chest pain if its bigger, radiates
Aortic Aneurysm: S/Sx, Abdominal Aorta Aneurysm (AAA)
Often asx, Pulsatile mass-no touching, Bruit (bowel sounds- swishing sounds), Back or flank pain, Abdominal pain, feeling of fullness
Hoarseness pushing against the vocal area
dysphagia
Aortic Aneurysm: S/Sx
Aneurysms: Diagnostic Tests
Abdominal Ultrasound
CT
MRI
Aortography
Aortogram or Arteriogram
Definitive test for aneurisms – golden standard
Aneurysms: Treatment Lifestyle changes-
stop smoking, dash diet, increase cardiac activity (little)
Aneurysms: Treatment Surgery- super asymptomatic or large enough
Dilated aorta section is removed, graft sutured in place
Aneurysms: Treatment Endovascular aneurysm repair (EVAR)
Minimally invasive
Catheter threaded through femoral artery, stent and graft placed to support aneurysm
Bigger than 3 cm but they wait about 5 cm to intervene
Aneurysms
Monitor 6 P’s (bilaterally), BP. Every 30 mins to an hour every 4 hours to assess
Aneurysms
Notify physical and anesthesiologist if no pulse
Aneurysms
Aortic dissection- tear of the inner lining of the wall and blood flowing in between
Aortic Aneurysm: Complications
Rupture—serious complication
Aortic Aneurysm: Complications
into retroperitoneal space: if it ruptures
into retroperitoneal space: if it ruptures
into thoracic or abdominal cavity:
Massive hemorrhage
Usually don’t make it to the hospital
Medical emergency
Do not palpate if seeing a pulsating mass
Aneurysm
Monitor for indications of rupture
Cool, Clammy skin. Diaphoresis
Pallor
Weakness
Tachycardia
Hypotension
Abdominal, back, groin, or periumbilical pain
Changes in level of consciousness
Pulsating abdominal mass
Sudden severe pain, sharp
Weakened or absent pulse
Decrease of LOC depend son how much it dissects
Aortic Dissection
Geriatric- more likely to present with hypotension and vague symptoms
Aortic Dissection
Thoracic- tamponade (hypotension, muffled heart sounds
Aortic Dissection
Aortic Dissection: Patho
Tear occurs
Blood “tracks” between inner and middle layer
Inner and middle layers separate (dissect)
Systolic pulsation ↑ pressure on damaged area
Further ↑ dissection
May occlude major branches of aorta
Aortic Dissection: S/Sx
Pain, Cardiovascular, Neurologic, Respiratory, Geriatric presentation
sudden, severe
Something is sharp or tearing in chest
Pain
weakened or absent pulses
Cardiovascular
decreased LOC
dizziness
syncope
Neurologic
dyspnea
Respiratory
More likely to present with hypotension and vague symptoms.
Geriatric presentation
Aortic Dissection: Complications
Cardiac tamponade, Rupture of Aorta, Occlusion of arterial supply to organs
Life-threatening
Blood escapes from dissection into pericardial sac
Hypotension, muffled heart sounds , narrowed pulse pressure
Cardiac tamponade
Hemorrhage, can lead to death
Can hemorrhage into mediastinal, pleural, or abdominal cavity, retroperitoneal space
Rupture of Aorta
(spinal cord, renal, abdominal)
Occlusion of arterial supply to organs
Systolic should be <160 when having an ___
Heart feels like it had to compensate- control hypertension
aneurysm
