Dysrhythmias Flashcards
No P wave equals
No SA node firing off
Increase in BP releases what
Baroreceptors which affect vasomotor center and decrease BP
Decrease blood flow to kidneys cause
sodium and water retention resulting in increase BP activation of renin-angiotesion aldosterone mechanism…Resulting in vasoconstriction and sodium retention.
Maintain perfusion- MAP must be at
at least 60 mmhg or between 60 to 70 mmHg to perfuse to the brain and kidneys
Treatment for AFib
decrease ventricular response to less than 100 bpm (controlled by calcium channel blocker, beta blocker), prevent embolic events, convert to SR
Electrical cardoversion for AFib
must have anticoagulation therapy Warfarin for 6 weeks before because it may dislodge clots if present
Synchronized Cardioversion
choice of therapy for hemodynamically unstable ventricular or SVT
delivers a countershock on the R wave of QRS complex
synchronizer switch must be turned on
always check airway first with all patients
Treatment for Tachycardia
clinically stable, vagal maneuvers
give IV Beta Blocker- Metoprolol to reduce HR and decrease myocardial O2 consumption
Coronary Artery blood flow occurs during
diastole (aortic valve is closed)
Adenocard helps with which rhythm
SVT patient will get a pause
Increase Cardiac output
increase HR up to 150 bpm
presence of atrial kick
increase preload
decrease afterload
Average Stroke volume
healthy adult 50-80 mL
Cardiac Ischemia will
decrease contractility
decrease energy production
cause dysrhythmias
increase intracellular activity
Blood returns to R atrium because
pressure in the vessesl systems
Gerontologic Consideration
- age alters the cardiovascular response to physical and emotional stress
- heart valves become thick and stiff
- Frequent need for pacemakers
- Less sensitive to beta-adrenergic agonist drugs
- Increase in SBP, decrease or no change in DBP
Total Cholesterol
Less than 200
Triglyceride
Less than 150
HDL
Greater than 40
LDL
Less than 70 for cardiovascular patients
What influences preload
dehydration and overhydration
P wave equals
depolarization of atrium
PR interval
0.12-0.20 seconds and constant
QRS duration
0.04-0.10 seconds and constant
Pulseless Electrical Activity
electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the patient had no pulse
found in hypothermia
treatment: try IV bolus, CPR, and epinephrine
Normally poor outcome and is not a shockable rhythms
Myocardial oxygen demand reduced from slower rate which can be benefical
Coronary perfusion time may be adequate because of a prolonged diastole, which is desirable
Coronary perfusion my decrease if HR too slow to provide adequate cardiac output and BP-SERIOUS
Bradydysrhythmias HR less than 60 bpm
Major concern in adults patients with CAD
Coronary artery blood flow occurs mostly during diastole when the aortic valve is closed and is determined by diastolic time and blood pressure in the root of the aorta
Can be serious because shorten the diastolic time and coronary perfusion time
Initially CO and BP increases but a continued rise in HR decreases the ventricular filling time because of a shortened diastole, decreasing stroke volume–CO and BP will begin to decrease reducing aortic pressure and coronary perfusion
Increases work of heart and increased oxygen demand
Tachydysrhythmias HR greater than 100 bpm
Palpations, chest pressure or pain, restlessness and anxiety, pale, cool skin, syncope which may lead to CHF
tachydysrhythmias
dyspnea, lung crackles, distended neck veins, fatigue, and weakness
Symptoms of Heart Failure
What do we do for patients with Sinus Brady?
Treat it only if the patient is symptomatic with IV atropine, or use pacemaker therapy
What do we do for patients with Sinus Tachy?
If patient is symptomatic and are clinically stable, vagel maneuvers can be attempted. We may also give IV beta-blocker such as Metoprolol to reduce HR and decrease myocardial oxygen consumption
P-R interval is greater than
0.20 seconds
What is the most significant lab Cardiac Maker in a patient who has had an MI?
Presence of troponin T and I
Cardiac troponin T< 0.20 ng/ml (elevation indication of myocardial injury or infarction
Cardiac troponin I<0.03 ng/ml
Which lab tests are used to predict a patient’s risk for Coronary Artery Disease?
Cholesterol level 122-200 older 144-280
Triglycerides level Female 35-135 Male 40-160
Older 55-260
LDL levels 60-180 older 92-221
decrease in the free hydrogen ion level of the blood and is reflected by arterial blood pH.
Alkalosis
Treatment: Oxygen, Atropine, pacemaker
normal asymptomatic unless ventricular rate is too slow= decrease CO
Second-degree heart block
peripheral component of afterload is the pressure that the heart must overcome to open the aortic valve
Impedance
Less than 200 mg/dl
Evaluating for atherosclerosis
Triglycerides
Variant of NSR
HR increases slightly during inspiration and decrease slightly during exhalation
Irregular rhythm frequently observed in healthy children and adults
Sinus Arrhythmia
When sympathetic nervous system fibers are stimulated, the heart responds by
Increasing HR and increasing contractility
0.04 to 0.10 seconds and constant
QRS duration
Reports of chest pain…. which test is done to determine the location and extent of CAD?
Cardiac catheterization
Which test is performed to determine valve disease of the mitral valve, left atrium, or aortic arch?
Transesophageal Echocardiogram
What are the purpose of an angiogram
Identify an arterial obstruction
Identify an arterial narrowing
Identify an aneurysm
too little circulating blood volume causes a MAP to decrease, resulting in inadequate total body oxygenation
hemorrhage and dehydration
Hypovolemic Shock
Closure of mitral and tricuspid valves
Occurs during beginning of ventricular systole
the first heart sound S1
Aortic and pulmonary valves are closed
Tricuspid and mitral valves are open
During diastole
amount of pressure/force against the arterial walls during the relaxation phase of the heart
Diastolic BP
amount of pressure/force generated by the left ventricles to distribute blood into the aorta with each contraction of the heart
Measure of how effectively the heart pumps and indicator of vascular tone
Systolic BP
Delayed electrical conduction -ranges from bradycardia to heart block -tall T waves -widened QRS complex -prolonged PR interval Hypotension and thready peripheral pulses
Acidosis
Cardiovascular Manifestation
increase of bases (base excess) or a decreae of acids (acid deficit)
caused by loss of gastric juices, overuse of antacids, potassium wasting diuretics (increasing of H+), prolong vomiting
Metabolic Alkalosis
degree of myocardial fiber stretch at the end of diastole and just before contraction
Preload
pressure or resistance that the ventricles must overcome to eject blood through the semilunar valves and into the peripheral blood vessels
afterload
amount of blood ejected by the left ventricle during each contraction
variables include HR, preload, afterload, contractility
stroke volume
Atrial tissue becomes irritable
Impulse before the next sinus impulse is due
Premature P wave may not always be clearly visible because it can be hidden in the preceding T wave
Followed by a pause
Premature Atrial Complex (PAC)
Ventricular tachycardia without pulse or ventricular fibrillation
Medication Amiodaron, lidocaine, epinephrine
Electrical Management: defibrillation
Atrial fibrillation, SVT, or ventricular tachycardia with pulse
Medication: amiodarone, adenosine, and verapamil
Electrical mangement: synchronized cardioversion
The origin of the coronary arteries is
aortic valve
When parasympathetic nervous system fibers are stimulated, the heart responds by
decreasing HR and decreasing contractility
ST elevation/depression indicates which condition
myocardial injury or ischemia
Fluid and electrolyte imbalance
T waves are tall and peaked
obtain an order for which serum level test
Potassium
No pulse and the cardiac monitor shows ventricular fibrillation. Which drugs does the nurse prepare to administer during the resuscitation
lidocaine
epinephrine
amiodarone hydrochloride (Cordarone)
magnesium sulfate
Medication taken for ventricular fibrillation or pulseless ventricular tachycardia receive
epinephrine (adrenalin Chloride)
closing aortic and pulmonary valves
occurs during end of systole
the second heart sounds, S2
Excessive vagal (parasympathetic) stimulation to the heart causes decreasing rate of sinus node discharge
Sinus Bradycardia
most commonly affect the AV junction, which the impulse is either slowed at the AV junction or stopped at the AV junction
ventricular depolarization and QRS compleses are either delayed or blocked
Differentiated by PR intervals
Tendency to pass out and found in boys
Atrioventricular blocks
swishing sounds that may occur from turbulent blood flow in narrowed or atherosclerotic arteries
place the bell of stethoscope on the neck over the carotid artery while patient holds his/her breath
Bruits
Rapid stimulation of atrial tissue at a rate of 100 to 280 bpm
P waves may not be visible
P waves are embedded in the preceding T wave
Supraventricular Tachycardia (SVT)
excessive loss of CO2 through hyperventilation
caused by anxiety fear improper settings on mechanical ventilation fever hypoxia pregnancy high altitudes initial stage of pulmonary emboli
Respiratory Alkalosis
Overproduction of H+ ions can occur with excessive breakdown of fatty acids, anaerobic glucose breakdown (lactic acidosis), and excessive intake of acids
causes diabetic ketoacidosis, ASA OD, shock sepsis, severe diarrhea renal failure
Metabolic Acidosis
atria is depolarized in a disorganized manner
no Pwave no arterial contraction
loss of atrial kick
irregular ventricular response and distance between the QRS complexes
high risk for embolic events- CVE PE causing an uncoordinated effort and confusion
Atrial Fibrillation
each complex is complete and each interval is normal, but the rate is below 60 bpm
myocardial O2 demand decreases
confusion fatigue take apical pulse
normal response to decrease activity athletes excessive vagal stimulation heart disease drugs
Sinus Bradycardia
Myocardial muscle protein released into the blood stream with injury to myocardial muscle
wide diagnostic time frame (several hours after the onset of chest pain)
T< 0.20
I< 0.03
Troponin
< 90
elevation indicates myocardial infarction
earliest marker detected 2hrs after MI with rapid decline after 7 hrs
Myoglobin
produce during rapid passive filling phase of ventricular diastole when blood flows from the atrium to a noncomplaint ventricle
ventricular gallop
Third heart sound (s3)
occurs as blood enters the ventricles during active filling phase at the end of ventricular diastole
atrial gallop
heard in patients with hypertension anemia ventricular hypertrophy MI pulmonary emboli
Fourth Heart sound (S40
produce when blood enters a noncomplaint chamber during rapid ventricular filling
Diastolic filling sounds (S3 and S4)
Females 30-135 males 55-170
valves higher after exercise
elevation indicate possible brain, myocardial, and skeletal muscle necrosis or injury
most specific for MI and shows a predictable rise and fall during 3 days
peaks in about 24 hrs after onset of chest pain
Creatine Kinase (CK-MB)
Excessive vagal stimulation to the heart causes the rate to from the sinus node discharge carotid sinus massage suctioning valsalva moneuver clinical findings- syncope diaphoresis
decrease
Nonsurgical intervention that provides a timed electrical stimulus to the heart when either the impulses initation or the conduction system of the heart is defective
temporary Pacing
inability of cardiac cells to respond to a stimulus until they have recovered from the previous stimulus
Refractoriness
Bradycardia (rhythm less than bpm)
treat is patient is symptomatic
medication: atropine and isoproterenol
electrical management: pacemaker
involves special indwelling catheter which provides information about blood volume and perfusion fluid status and how well the heart is pumping
Hemodynamic Monitoring
beating of many weak ectopic foci in the ventricles resulting in an uncoordinated undulation instead of a coordinated contraction
rhythm cant circulate blood and is not compatible with life
resemble a squirming worm
fetal if not treated within 3-5 min
loss of consciousness, pulseless, apenic, no BP acidosis(no O2) death
ventricular fibrillation
early rhythm complexes
occurs when a cardiac cell/cell group other than SA node becomes irritable and fires an impulse before the next sinus impulse is produced
patient may feel palpitation
ventricular may lead to decrease CO
Premature Complexes
occurs when there is a fast strong stimulus from an ectopic focus that is above the ventricles
150-200 bpm
inadequate refilling time which results in low bp
heart cant sustain this rhythm for long b/c the muscle itself gets tired
Supraventricular Tachycardia
one strong ventricular ectopic focus the heart cant sustain this rhythm very long
can be stable with a pulse
unstable meaning hemodynamically compromised or pulseless
cause heart disease electrolyte imbalance drug toxicity
commonly the initial rhythm before ventricular fibrillation
ventricular tachycardia
many weak ectopic foci in the atria beat in an uncoordinated pattern, resulting in an uneven baseline on many tiny P waves known as fibrillatory waves in the atria
Elderly and shockable rhythm
beats 350-600 bpm
cause systemic hypertension older adults heart disease
atrial fibrillation
single strong ectopic focus in the atrium starts to beat fast 240-360 bpm
AV node acts as a gatekeeper in this rhythm allowing only some impulses through to ventricles
cause heart disease thyrotoxicosis, alcoholism, cardiac surgery, cardiac cath (angiogram)
Shockable rhythm
Atrial Flutter
An increase in venous return will
increase preload
Volume and diameter of vessels are factors of
increasing afterload
each complex is complete and each interval is normal but the rate is above 100 bpm
cause fright fever pain normal response to activity stress disease drugs
enhances CO and BP
sustained = decrease coronary perfusion time/ pressure
increases O2 demand
Sinus Tachycardia
Care of the patient with Dysrhythmias
assess vital signs at least every 4 hours PRN
monitor patient for cardiac dysrhythmias
evaluate and document the patient’s response to dysrhythmias
encourage the patient to notify the nurse when chest pain occurs
assess chest pain
assess peripheral circulation (palpate for presence of peripheral pulses, edema, capillary refill color temperature of extremity
provide antidysrhythmic therapy
Monitor and document patients response to antidysrhythmic medications
monitor appropriate lab values
monitor patient activity level
observe for respiratory difficulty
promote stress reduction
offer spiritual support to patient and family
What would be included in a teaching plan for a patient with a pacemaker?
ROM exercises, follow-up appointment with the physician, teach how to take pulse, what signs and symptoms to report, medications, pacemaker battery follow-up, medical alert bracelet, indications of battery failure, diet, physical activity, do not operate electrical appliances directly over
the pacemaker, inform the dentist regarding pacemaker. Teaching includes information that the use of microwave ovens is safe, avoid MRI scanners,and travel without restrictions.
impulses shift away from sinus node to atrial tissue
atrial depolarization
P wave shape different than normal P wave
-Premature Atrial Complexes (PAC)
-Supraventricular Tachycardia (SVT)
-Atrial Flutter
-Atrial Fibrillation
Atrial Dysrhythmias
