Cardiac Dysrhythmias

Front 1

NORMAL CARDIAC PARAMETERS
a.PRI
b.QRS

Back 1

-PR Interval (PRI) .12to.20 or 120 to 200
-QRS .06 to .12 or 60 to 120

Front 2

1.SINUS BRADYCARDIA
2.SINUS TACHYCARDIA
A) WHAT ARE THE PARAMETERS FOR EACH?

Back 2

-All parameters are normal, except the SA nodes discharge at <60 times per minute.
-Sinus Tachycardia, all parameters are normal except the SA node fires at >100 times/min.

Front 3

WHEN WOULD YOU TREAT SINUS BRADCARDIA?

Back 3

-Only if the pt have serious S&S
(eg.SOB,Chest pain, dizziness, fainting, low BP)

Front 4

IF THE PT WAS SHOWING SERIOUS S&S WITH (mneumonic) "All Treatment Depends on Epinephrine) BRADYCARDIA HOW WOULD IT BE TREATED
A) NAME THE AGENTS IN ORDER OF HOW THEY WOULD BE GIVE.

Back 4

1.Atropine SO4
2.Transcutaneous Pacing
5.Dopamine HcL
6.Epinepherine

Front 5

COMMON REASONS FOR SINUS TACHYCARDIA

Back 5

-Increase in metabolic demand
*Exercise, fever, pain,Congestive Failure, Shock, PE, Methampetamines (cocaine), caffeine, Nicotine

Front 6

*Ventricular dysrhythmia is more life-threatening then atrial dysrhythmias*

Back 6

*fyi*

Front 7

SINUS TACHYCARDIA
(CLINICAL PRESENTATION)

Back 7

-May be Asx.
-Sx will vary with rate
-Pt. may report palpatations (feel like butterfly or the heart is coming out)
-Dyspnea
-Regular Rapid pulse

Front 8

SINUS ARREST (SA NODE STOPS)

Back 8

-All paramaters may be normal
-Rate will vary. May be bradycardic.
-SA node doesn't discharge and another cardiac cell isn't compensating.

Front 9

WHAT WOULD CAUSE THE SA NODE TO "ARREST"/SLOW DOWN

Back 9

-Digitalis toxicity (can slow the rate too much).
-Increased parasympathetic tone
-decreased perfusion/metabolic demands, like hypoxemia
-Damage to the SA node

Front 10

DIGITALIS
1. THERAUPEUTIC LEVEL
2.WHEN DO YOU HOLD DIG?
3. WHAT LEVELS DO YOU MONITOR WITH DIGITALIS

Back 10

1.therap.levels 0.5-2.0
2. when the HR is <60 and systolic is <100
3.Monitor labs (potassium)

Front 11

WHAT WOULD THE ECG STRIP REVEAL ON A SINUS ARREST?

Back 11

-Flat. Only worried if it prolongs with regularity
-May do a cardiac cath.

Front 12

WHAT ARE THE CLINICAL PRESENTATIONS OF A SINUS ARREST?

Back 12

-Pt. may feel like their heart skipped a beath
-usually asx
-Irreg. pulse
-

Front 13

SINUS DYSRHYTMIAS
*R/T CHANGE IN RESPIRATIONS, INCREASE WITH INSPIRATION AND DECREASES WITH EXHALATION
-NO TX, PT USUALLY ASX.

Back 13

*FYI*

Front 14

ATRIAL FLUTTER
1. WHAT WILL YOU SEE ON THE EKG STRIP
2.CARDIAC PARAMETERS?

Back 14

1. Sawtooth patter "F" waves
2. The P waves look like flutters "sawtooth pattern" out number the QRS waves.
3. Can't recognize the PRI
4. QRS normal 60 to 100

Front 15

PREMATURE ATRIAL COMPLEX
1. WHAT PART OF THE HEART IS USUALLY THE PROBLEM
2. WHAT ARE SOME REASONS FOR PACs.

Back 15

-Abnormal area in the atria
-Often d/t atrial hypertrophy/enlargement
2. Back flow r/t CHF, valve disease, pulmonary HTN, stimulation, nicotine, atrial stimulation

Front 16

PREMATURE ATRIAL COMPLEX
-WHAT DOES THE P WAVE LOOK LIKE?
-HOW DOES IT COMPENSATE?

Back 16

1. P wave may be different, P wave may be close to each other because they're prematurly firing.
2. Next you will see a wider T and P wave because the body is trying to compensate by creating a bigger spand between the next P wave.

Front 17

*fyi*
PREMATURE ATRIAL COMPLEX
*PAY ATTENTION* BECAUSE THIS MAY BE AN EARLY "PREMATURE SIGN OF FUTURE ARTIAL DYSRHTHMYIAS"

Back 17

*fyi*

Front 18

CARDIAC
(HYPOXEMIA)
1. WHAT CARDIAC DYSRHYTMIAS HAVE HYPOXEMIA AS A ETIOLOGY?

Back 18

1. Sinus arrest
2. Premature Artial Complex
3. Atrial Flutter

Front 19

ATRIAL FLUTTER
1.CAUSES
2. WHAT MEDICAL CONDITION CAN ALSO CAUSE A.FLUTTER?
A) WHAT HAPPENS ONCE IT'S TREATED?

Back 19

1. Atrial stimulation (cardiac cath, pacemaker)
2.Valvular disease
3. CHF
4.Hypoxemia
5.Hyperthyroidism
-Graves Disease
a) Once treated (synthroid)the symptoms goes away

Front 20

ATRIAL FLUTTER
S&S

Back 20

-Pt may report palpatations or angina
-Dyspnea (not enough time for the ventrical to fill with blood, so it reduces the circulating blood volume, decreasing O2)
-Increase ventricular rates may result in hypotension (if the ventrical isn't filling there's low pressure).
-CHF

Front 21

*If an atrial rate is aove 300bpm it's usually not conduted through the AV node*

Back 21

*fyi*

Front 22

1. SA NODE RATE
2. AV NODE RATE

Back 22

1. SA NODE 60 TO 100
2. AV NODE 40 TO 60

Front 23

ATRIAL FLUTTER TREATMENT
-In order
"Synchronize, Digits, And,Quit Procrastinating,And,Rushing"

Back 23

-Synchronized cardioversion (60jules,low vault)
-Digitalis (slows down rate)
-Amiodarone
-Quinidine
-Procainamide
-Anticoagulants
-Radiofrequency Ablation

Front 24

HOW IS PP INTERVAL MEASURED
(WHAT DOES IT MEASURE)?

2. HOW IS THE RR INTERVAL MEASURED
A) WHAT DOES IT MEASURE

Back 24

1. PP interval is measured from the beginning P wave to the beginning of the next
a) It used to determine the atrial rhythm and atrial rate
2. The RR interval is measured from the QRS comple to the next QRS complex
a) The RR interval is to determin the ventricular rate and rhythm

Front 25

ON A ECG STRIP HOW COULD YOU DISTINGUISH THE DIFFERENCE BETWEEN AN ATRIAL FLUTTER AND SINUST TACHYCARDIA WHERE BOTH HAVE MERGING P WAVES ?

Back 25

1. Atrial flutter has a normal QRS (ventrical rate)
2. Sinus Tachycardia has a fast QRS (ventrical rate 100 to 150 beats), P wave regular

Front 26

Cardioinversion

Back 26

.

Front 27

WHAT CARDIAC PROCEDURE WOULD YOU HOLD METFORMIN?

Back 27

1.Hold Metformin for cardiac catheterization because if the dye effects the kidneys with Metformin in the system clients will be at risk for lactic acidosis

Front 28

VENTRICULAR TACHYCARDIA

Back 28

-3 or more PVCs in sequence
-P waves not present
-T waves not present
-QRS: uniform, tall and present

Front 29

TREATMENT OF PVCS
-treat with "ocain"

Back 29

-Lidocaine although High Flow O2 may resolve
-Procainamide

Front 30

VENTRICULAR TACHYCARDIA
(TREATMENT)

Back 30

-First check the client, start with IVP, then drip, then bolus
-Lidocaine 1mg/kg.IVP
-Procainamide IV drip
Amiodarone IV bolus ver 10 mins.

Front 31

*Ventricular Tachycardia*
-Strong indicator of cardiovascular diseaese
-not well tolerated can easil go into V. fibrilation
-Alarm goes off- No immediate loss of contiousness

Back 31

*fyi*

Front 32

VENTRICULAR FIBRILLATION
1. WHAT WOULD THE ECG SHOW?
2. HOW IS THE PT'S LOC?
3.WHAT'S THE BEST METHOD TO RESTORE ELECTRICAL ACTIVITY?

Back 32

-Chaotic, no perfusing rhythm
-Lethal dysrhythmia
-No organized wave patern
a)no P,QRS,T
-Patient loss contiousness

Front 33

ASYSTOLE
1.WHAT WOULD THE EKG SHOW?
2.HOW'S THE PROGNOSIS
3.WOULD THE PT. BE DIFFIB?
4.HOW'S ASYSTOLE CONFIRMED?

Back 33

1. Flat line-no ventricular electrical activity.
2.Poor prognosis
3.Can't diffib pt., need electrical current to diffib
4. Asystole confirmed with two EKGs

Front 34

TREATMENT OF ASYSTOLE
"Estimated Time of Asytole"
-HOW ARE DRUGS ADMINISTERED?

Back 34

1. Epinepherine
2. Transcutaneous Pacing
3. Atropine
-EMERGENCY/CODE. Meds are given IVP.

Front 35

AICDS (AUTOMATIC INTERNAL CARDIOVERTER DEFIBRILLATORS)
-WHAT IS IT?
-HOW DOES IT WORK?

Back 35

-Implantable devices for clients with hx of ventricular fibrillation (runs on batteries)
-Similar principles as pacemakers
-has no chip, no magnents
-When device senses V fib and electrical shock is delivered

Front 36

AICDS
-WHAT IS THE PATIENT RESTRICTED FROM DOING AND FOR HOW LONG?

Back 36

-Pt is restricted from driving for 6mnts.

Front 37

ATRIAL FLUTTER
1.WHAT WOULD A EKG SHOW?
2.WHAT IS A CLASSIC SIGN?

Back 37

1. P waves that look like "saw tooth"-"F" flutter
- More P waves then QRS., unable to distinquish the PRI interval
2.CLASSIC SIGN!!! Rhythm of the P waves are irregularly irregular.