What are the phases for Membrane Potential and Electrolytes? (0-4)

Electrical impulse is from -90mV to +10 mV

0-Influx of Na+

1-Na+ closes K+ exits

2-Influx of Ca+

3-Influx of K+, Na+ and Ca+ exits

4-Resting State

1-Where does the origin of normal electrical impulse begin in the heart?

2-Where is this node located?

3-What is the inherent rate?

1-The SA node

2-at the top of the right atrium

3-60-100 is the rate

Where does the SA node carry to?

What is the AV nodes rate?

Where does the AV node lead to?

Where does it go afterwards?

AV node rate-40-60bpm

AV node leads to bundle of HIS which branches into the right bundle branch and the left bundle branch

The end of the bundle branches terminates in Purkinje fibers which conduct the impullses throughout the rest of the myocardium and ventricles

If the SA node can not impulse can the AV node take over?

If the SA and the AV node do not work what happens, can the heart still contract?

Yes, the AV node will continue to send impulses to the ventricular muscles so the contractions can continue.

If both the SA and the AV fail then the ventricular muscle has the ability to still contract, but at a rate less than 40 and this is usually not sufficient for adequate CO.

-Electrolyte imbalances

K+, Ca+, Mg++

-Altered tissue perfusion

-Hypovolemia

What is the term that is used to decribe the ability of a tissue to initiate impulses spontaniously?

Why do arrythmias happen?

Automaticity

In the myocardium, when tissue automaticity overrrides the normal electrical conduction pathway the result is an arrythmia, sometimes call dysrhythmia.

Cardiovascular disease causes arhythmias how?

Hypovolemia causes arhythmias how?

What are the two arrythmias that indicate and area of irritability in the myocardial muscle?

altered tissue perfusion to the heart-so decrease in oxygen or (hypoxia)

loss of oxygen to the myocardial muscle

PAC's (premature atrial contraction) and PVC's (premature ventricular contractions).  can be benign but can cause further arrythmias that would be more severe

1-Why is Ventricular tachycardia called the degenerating rhythm?

2-Is V-fib a degerating rhythm

3-what is happening to CO in these 2 rhythms?

1-because if it's not treated appropriately it will degenerate to fibrillation and asystole.

2- Yes, it can degerate into asystole.

3-will not have adequate if any CO and therefore will not be able to maintain muscle function.

-P, QRS, and T are identified and within normal limits

-Waveform occurs prior to a normal interval

-you cannot see the P wave of the premature atrial contraction because it has been buried in the T wave of the previous beat, (There also a delay because PAC offsets the normal rythm)

What causes PAC in the heart?

(Pathophysiology)

-P wave is absent

-QRS complex is early and abnormal shape

-QRS complex is wider than normal limits

If the patient becomes symptomatic and may complaing of palpitations or lightheadedness or other problem if  the PACs are occuring frequently or if they are altering myocardial function in any way.

(In these cases medication would be given and the patient usually responds very well)

Yes,

*If the pt is having more that 5 PVCs per minute

(multifocal)

*If there is a R on T phenomenon-occurs when the QRS complex and the PVC falls directly in the T wave of the preceding beat. (this means the heart is vulnerable to developing V-tach or V-fib)

What does it mean if all PVCs are the same?

What does it mean when they are all different?

All the Same-indicates there's one irritable area on the mocardium

Different-(multifocal PVCs)-indicates several areas of irritability and increases the risk that the individual might develop V-tach or V-fib.

-P wave absent

-QRS complex is wider than normal limits

-Ventricular rate is >100

What are the 2 reasons why V-tach rythm will degenerate if not treated?

(Both factors decrease the amount of CO available)

1-The contraction in myocardial muscle is often asynchronous

2-diastolic filling time is reduced

Typically Cardioversion

(because there are identifiable R waves in V-tach a defibrillator can be set to sychronize to the R wave)

What does cardioversion do for the heart?

What is called a run of V-Tach?

Cardioversion produces a transient asytole which hopefull will allw the myocardium to return to the normal conduction pathway.

Anytime an individual has more than five PVCs in a row.

-P wave is absent

-QRS complex is not identifiable

-Erratic electrical impulse

What is the heart doing when a person goes into V-Fib?

How do we treat V-Fib?

The heart muscle isn't really contracting at all,

it's more like quivering.

It's a pattern of erratic electrical impulses.

 Early Defibrillation

1-What's the difference between Cardioversion and Defibrillation?

2-What does Cardioversion and Defibrillation cause to hopefully get the heart back in sync?

1-Defibrillation is the same as cardioversion except, because the wave forms are not recognizable it cannot be sychronized so in defibrillation the shock can be applied at anytime.

2-They both provide a period of transient asystole.

What is the characteristics of Asystole?

How do we treat this patient in Asystole?

-No identifiable waveforms

-No identifiable electrical impule

Most of the time medication will need to be given prior to the attemp to defibrillate in order to stimulate cardiac muscle.

(Recovery from asystole is relatively rare)

1st Degree-Delay of sinus impulse through the AV node

2nd Degree-Inconsistent transmission of sinus impulse through AV node

3rd Degree-Failed transmission of sinus impulse through AV node

What is the measurment of the PR interval of First Degree Block?

What happens in the heart?

PR interval > .20

The SA node fires appropriatly but there is a delay between the SA and the AV node, once the impulse reaches the AV node, it's conducted through the bundle and Purkinje system normally.

What are the characteristics of a 2nd Degree Block-

Mobitz 1?

What happens in the heart?

-P to P intervals are regular

-PR intervals lengthen till QRS is dropped

Delay of transmission through the AV node

What are the characteristics of 2nd Degree Block-

Mobitz 2?

What happens to the heart?

P to P intervals are regular

PR intervals do not lengthen before QRS is dropped

The SA node is firing in a regular rate and rhythm, however, the PR intervals are not being transmitted through the AV node appropriately and therefore, the PR intervals occur regularly, but a QRS is dropped.

What is the Characteristics of a 3rd degree Block?

What happens in the heart?

P to P is regular with atrial rate of 60-100

R to R is regular with ventricular rate <60

No correlation of P wave to QRS complex

The atria and the ventricles are operating independently,

Constant P waves are not bing conductied through the AV node, the ventricle is firing on its own and is not correleated with the P wave at all.  R to R waves will be regular however they will have a rate less than 60 which indicates the beats are coming form the AV node.

What ar ethe Uni-polar Limb Leads?

What are the Bi-polar Limb Leads?

What are the Precordial Leads?

UNIPOLAR LIMB- AVR, AVL, AVF

BIPOLAR LIMB-Lead 1, Lead 2, Lead 3

PRECORDIAL (all unipoloar)

V1-6

12-lead EKG

(although this could not be diagnosed from a single rhythm strip)

1-What is the difference of the Limb leads?

a-Bi-polar

b-Uni-polar

2-What does the AV mean in the Limb leads and R,L,F

1a-Uni-polar are Positive electrodes

1b-Bi-Polar you have both a positive and negative electrode and the electrical graphic is reading between those two poles.

2-Augmented Ventricle

Right Left and Foot

What kind of leads are used at the bedside?

Where are the precordial leads(pre-cordial leads placed on the body)?

Bi-polar leads (Lead 1,2, and 3)

Placed directly on the chest wall starting on the right dide of the sternum and moving around to the left axillary areas.

Limb Leads (part of the heart view)

What is the AVR for?

Lead 1 and AVL?

Lead 2,3, and AVF?

AVR-Always negative, Atrial view

Lead 1 and AVL- Anterior View

Lead 2,3, and AVF- Inferior View

What are the Precordial Leads for (part of heart?

V1 and V2 ?

V3 and V4 ?

V5 and V6 ?

"SAL"

V1 and V2-Septum

V3 and V4-Anterior

V5 and V6-Lateral

-Chest Pain

-EKG changes

-Elevated enzymes

What part of the Heart does a Transmural-STEMI/Q wave affect?

What is the % rate of occurance as oppose to the other MI?

-Entire thickness of muscle wall

-occurs 66% of the time

What part of the Heart is affected with a Subendocardial-NSTEM/Non Q wave?

How often (%) does this occur compared to the Transmural STEMI/Q wave?

-Inner aspect of  muscle wall

-33% of the time

Damage occurs in a bullseye on the Myocardial tissue.

Core or center becomes to get ischemic and if perfusion is not restored those cells will become injured, ischemia will move to the 2nd ring of core area, if there is still  lack of O2 to the muscle tissue, it will infarct and die, at this point, the injured tissue is directly around the core of infarcted tissue and ischemia spreads out to new tissue.

-Ischemia areas and injured areas can potentially recover 

-Infarcted muscle is dead tissue and will not recover except to form a scar.

What is the EKG of  Ischemia?

How long is ischemia tolerated before injury occurs?

-ST segment depression

(smile face)

-Tolerated about 20 minutes

What is the EKG for Injury?

ST segment elevation

(frowny face)

-Second "zone" of injury

-Progresses to infarct if not reversed

What is the EKG for an Infarct?

What is the extension of re-infarct greatest?

When does scar development happen?

When is the maxium softening?

Pathological Q wave develops

(May only show permanent T-wave inversion if subendocoardial)

-6-14 days extension

-4-6 weeks scar development

-7-10 days maximal softening

When does the heart go through the typical process of inflammation and scar development and is at the greatest risk of resorption and formation of the scar tissue?

When does the pt wan to be especially careful of their activity, and making sure to pay attention to heart rate, and any indication of chest discomfort or chest pain.

4-6 weeks

7-10 days

What must the nurse do when a person has symptoms of a heart attack?

name the steps

A-Airway (device needed?)

B-Breathing (Oxygen, ventilation)

C-Circulation

Rhythm-attach monitor

BP-if palpaple pulse

IV-access

Medications (rhythm, pain)

D-determine diagnosis

Morphine-M

Oxygen-O

Nitrates-N

Aspirin-A

How many leads do you need to see ST changes, Q waves to be considered diagnostic for a MI on a 12-lead EKG?

2ndly if you see patterns of both ST elevation in some of the leads and ST depression in other leads, then?

You have to have at least 2 leasts to be diagnostic

The ST elevation or pattern of injury always wins

What are the 3 cardiac enzymes that must be followed if an MI is present?

Why are these enzymes present with an MI?

Troponin, CPK, or Myoglobin

because these enzymes break apart and are released in the blood with tissue damage or tissue injury.

There are 2 Troponins, which is present in an MI?

When will this Troponin rise in the body?

What enzyme rises between 4-8 hours following injury?

Troponin 1

4-6 hours

CK-MB

What enzyme can show up in just an hour of a MI?

When enzymes are ordered, they are ordered as serial enzymes, what does this mean?

Why do you have serial enzyme tests?

Myoglobin MB1 and MB2

serial=blood draw once every 8 hrs x 3

-Following serial enzymes gives you a chance to see when the levels peak and when they begin to return to normal.

What is C-reactive protein (CRP) used to determine in the body?

Is it diagnostic of a coronary syndrome or MI?

-CRP is used to look at vascular inflammation

-No, not diagnostic but may be used in some cases for predicting the risk for someone to devlop myocardial disease.

Streptokinase (Streptase)

APSAC

Reteplase (Retavase)

t-PA (Tissue Plasminogen Activator)

TNK-ase (Tenecteplase)

Alteplase (Actvase)

Eptifbatide (Integrilin)

Tirofiban (Aggrastat)

Abcimab (Reopro)

What are Thrombolytics?

What is the criteria to be eligible for Thrombolytics?

"clot busters"

-pt cannot have pain for longer than a prescribed period of time because of the risk of reperfusion injury

-pt canno have other certain meds or bleeding disorders.

What is the difference between

Non-selective,

Selective,

or Antiplatelet,

thrombolytic drugs?

Non-selective works at various multiple points along the clotting cascade and the fibrinolytic cascade as far as breaking down the clot.

Selective-very specific points alon the fibrinolytic system to break down clot (less likely to cause generalized bleeding)

Antiplatelet-breaks the platelet plug or stops platelet aggregation and prevents clot formation.

What do Anti-arrhythmics do to the heart?

What are anti-arrhythmics broken into to?

used to alter myocardial automaticity so that you can control the rate and rhythm of the contractions.

Atrial and Ventrical Meds

What are the Anti-arrhythmics

(Atrial)?

control firing or the conduction of impulses through the

Atria and through the AV node

Adenosine

Digoxin

Calcium Channel Blockers

Beta Blockers

Mexiletine

Tocainide

Propafenone

Amidodarone

Bretylium

Sotalol

Lidocaine

Ventricular Arrhythmias such as PVCs

can be used for both emergency as well long term for patients with chronic ventricular arrhythmias.

What does adrenergic Alpha Meds mean?

What does adrenergic Beta 1 Meds mean?

Alpha=Inotropic (+) and Chronotropic (-)

Beta= Intotropic (+) and Chronotropic (+)

Inotropic means squeeze

Chronotropic means time or rate

Alpha Meds are what:(5)

What do they do to the heart knowing they are

Inotropic (+) and chronotropic (-)?

Digoxin, Amrinone, Dopamine, Levophed, and Epinephrine

Increase vascular contractility and muscle contractility but decrease myocardial rate

Beta 1 adrenergic drugs are 2 common:

What do they do if they are

Inotropic (+) and Chronotropic (+)

Dobutamine and Isoproternal

also Beta Blockers (olol) do the opposite so decrease contractility and rate

increase vascular contractility and increase rate as well

 atrial arrhythmias as well as BP

decrease vascular contractions, decrease HR, and myocardial contractility

Inotropic (constrict)

Dopamin, Dobutamin, Epinephrine, Phenylephrine, Vassopressin

potent vasoconstriction which will increase pressure, increase constriction of the vessels, increase the pressure and increase therefore myocardial oxygen consumption

Nitropresside, Nitroglycerine, Papaverine, Milrinone

Decreases vasoconstricton and to increase vascular flow

What are the 3 neuromuscular blockade meds used for skeletal muscle relaxant or used to induce a medical paralysis (long term)?

What is the med to use for intubation "very short acting"?

When given with a sedative such as Versed (Midazolam) what usu. happens to the pt?

Pancuronium (Pavulon)

Vecronium (Norcuron)

Cistacurium (Numbex)

Succinylcholine

The paralysis is frequently not remembered by the pt.

What is the antidote for Benzodiazapines?

Cardioversion is synchronized to what?

Defibrillation is sychronized to what?

Flumazenil

Synchronized to ventricular depolarization (QRS/R wave)

Asynchronous electrical discharge to produce transient asystole

What type of patients have cardioversion?

What type of patients have defibrillation?

Cardioversion-reserved for rhythms such as atrial fibrillation or superventricular tachycardial

Defibrillation-used for rhythms such as ventricular tachycardia, ventricular fibrillation or rhythms where there is not a recognizable wave form.

Tachycardia

Bradycardia

AICD (Automatic Internal Cardiac Defibrillator)-chronic runs of V-tach or chronic V-fib

What are Non-surgical procedures for coronary Reperfusion? (4)

Whart are Surgical procedures for Reperfusion? (3)

Non-surgical-Balloon angioplasty, coronary stents, rotational ablation, laser angioplasty

Surgical-CABG, TMR (Transmyocardial Revascularization), Cardiomyoplasty