cardio flash cards

The ability of cardiac cells to generate electrical impulses sponateously.

The ability of non-pacemaker heart cells to respond to an electrical impulse.

The ability to transmit an electrical stimulus from cell membrane to cell membrane.

The ability of atrial and ventricular muscle cells to shorten fiber length in response to electrical stimulation, generating sufficeint pressure to propel blood foward.

The sinoatrial (SA) node.

AV junction, Provides atrial kick.

AV node

• Sympathetic NS, will increase heart rate.
• Parasympathetic NS will decrease heart rate.
• This is the flight/fight meachanism and the calming effects afterwards.

• It releases neural hormones such as norepinephrine and adrenalin
• Adrenalin increases the strength of the ventricular contractions and therefore the stroke volume
• and norepinephrine aids the spread of impulse thus speeding up the heart rate.

The PNS releases acetylcholine which slows the spread of impulses, slowing down the HR.

It is the P wave

• PR segment
• Atrial kick

• 1. Determine HR by counting R waves in a six second segment then multiplying by 10
• 2. Determine the heart rythm. This can be done by marking the R waves on a clean sheet of paper and "marching" it down the strip to determine the rythm.
• 3. Measure the PR intevals.
• 4. Measure the QRS duration.
• 5. Interpret the rythm.

During atrial depolarization, the main electrical vector is directed from the SA node, towards the AV node, and spreads from the right atrium to the left atrium.

P wave depicts the SA node fired.

PR interval depicts electrical impulse traveling through the atrium.

• Maltam branch
• James branch
• Buckman branch

Without this delay, the atria and ventricles would contract at the same time and blood would not flow effectively from the atria to the ventricles.

The delay forms much of the PR segement on the EKG. The atria is starting to relax, allowing sodium and potassium to go back into place.

Electrical impulses gouing through the Prujenke fibers and myocardium.

ventricular repolarization.It is the last event of the cycle.

Atrial depolarization. If the P wave is absent, abnormally positioned, or negatively deflected, it implies that the impulse originated outside the SA node.

No. However, It is alwasys present if a HX of AMI!!

• Measure from the begining of the P wave to the begining of the QRS complex.
• Represents the time it takes for the original impulse to travel from the SA nodwe through the atrium to the AV node.

Possible hyperkalemia, should check potassium levels.

myocardial ischemia, ventricular enlargement, or hyperkalemia.

Hypokalemia-check labs.

1. Myocardial injury or it may be temporary due to cardioversion

2. Myocardial ischemia or digtalis toxicity.

• 40-59 beats/min.
• regular rythm
• One P wave/QRS complex

• Rate is greater than 100, but usually less than180.
• Rythm is regular
• One P wave/QRS complex

An ectopical beat in the right or left atrium sends out an impulse before it is time for the next impulse from the SA nodeto fire, causing an early depolarization.

• Can occur at any rate.
• Rythm after a PAC- a slight delay before the next normal beatand causes a pause in the cardiac rythm.
• P waves either abnormally shaped compared to the other P waves in the strip or is inverted.
• PR is normal
• QRS is normal

• An ectopic site in one of the atria takes over as pacemaker and sends out atrial impulses at a rate of 250-350 beats/minand the atrial rate may rise to 400 beats/min.
• Will always have regular rythm with a 2:1 ratio of conduction.

Palpitations, SOB, anxiety, syncope,angina, and evidence of heart failure may be present.

Many electrical impulses are formed in the atria and cause erratic quivering of the atria which produces no effective atial contraction, thus loosing the atrial kick, the contractions provide no assistance in filling the ventricles. The impulses reach the AV node but only some of the impulses are conducted to the ventricles and then only fired at irregular intervals.

The Sa node is not working correctly. The ventricle do not empty properly, causing the blood to pool,leading to clot formation.

Rythm will always be irregular!!!

Coumadin and lanoxin.

• Coumadin will thin the blood, making it easier to "push"
• and lanoxin will increase cardiac output.

Alteration in speech.

• An ectopic rythm that begins and ends abruptly, at any rate between 130-250 beats/min.
• Has a rapid onset.
• The cause is unknown, but it occurs above the ventricles.

S/S: SOB and Chest pain.

An irritable focus in the ventricles discharges before the arrival of the next anticipated impulse from the SA node.

Canbe unifocal or multifocal

WILL CAUSE DEATH!

Can lead to Venticle tachycardia

3 PVC= venticle tachycardia!

• An irritable ectopic focus in the ventricles takes over as the pacemakre site.
• Defind as three or more PVC with a rate of 110bpm or greater.
• This rythm may terminate on its own or it may deterriorate into ventricullar fibrillation.

• Rythm is regular
• First resposibility: assess airway, breathing and LOC!!

• Multiple ectopic pacemaker sites in the ventricles take over. This make the heart quiver instead of contracting.
• There is no pulse!! BUT... check patient with own eyes before calling a code.. may not even be in the room.

TX: shock the patient but not in "SYNC" mode.

The absence of any cardiac activity.

• Rate should be slow or normal
• normal rythm
• P wave is normal
• PR interval is prolongs and constant in size. Greater than 0.02 sec.
• QRS normal

• All the sinus impulses are blocked at the AV node, bundle of His, or the bundle branches.
• The atrium and ventricles are not working together.

• Rate 15-60 atrial rate is always faster.
• Rythm is regular

A pacemaker.

Clean the area with soap and water prior to use and NEVER shave the area or apply a tincture (alcohol)! It will cause irritation from the patches.

Report any changes in the heart rate. If the HR drops below pacer rate (usually 70), call MD.

Synchronized countershock that may be used in emergencies for unstable ventricular or supraventricular tachydysrythmias or electively fo stabe tachydysrythmias that are resistant to medical therapies.

Asynchronized countershock depolarizes a critical mass of myocardium simutaneously to stop the re-entry circuit and allow the SA node to regain control of the heart.

This is the TX for V-tach, Must always atand clear of patient bed beforedefibrillization. Early defibrillation increases chance for survival.

Widespread abnormal cellular metabolism that occurs when the human need for oxygenation and tissue perfussion is not met to the level needed to maintain cell function.\

It is a "whole" body response and is a syndrome

Any problem that impairs oxygen delivery to tissues and organs can start the syndrome of shock and lead to a life threating emergency.

• Urine output will decrease. Output must not go below 30ml/hr!
• The kidneys are marjor organs and function decreases during shock and if shock is severe enough,output will derease even if you are pushing fluids!

• Inadequate tissue perfussion
• decreased pumping ability of the heart
• weakended cardiac muscle
• Cogenital cardiac anomoly
• pervious Mi
• cardiac diseases
• surgery
• thromboembolic phenomenon

• NONCARDIAC CAUSES
• cardiomyopathy
• valvular heart abnormalities
• cardiac tampanode
• cardiac dyrsythmias

• After MI,monitor hemodynamic studies to watch for cardiogenic shock.
• Cardiac output is decreased
• Mean arterial pressure is decreased.

The MI causes direct pump failure. Afterload increases after MI and can have pulmonary congestion that causes HR to increase and cold clammy skin

TX: oxygen!!

S/S of cardiac shock: increased HR and clammy skin.

A type of shock that occurs when blood volume is NOT lost from the body but is distributed to the intersttial tissues where it cannot circulate and deliver O2.

• Causes:
• Loss of sympathetic tone, blood vessel dilitation, pooling of blood in venous and cap. beds, and capillary leak.

• Occurs when low circulating blood volume causes a mean arterial decrease: oxygen needs of the body are not met.
• Commonly caused by hemorrhage and dehydration.

• Ringer's Lactate.
• Is isotonic and acts as a plasma expander. In the prsence of acidosis the lactate as as a buffer.

WATCH FOR HYPERKALEMIA!

• Ensure patent airway.
• Start IV with LG. bore needle (16).
• Administer O2.
• Apply direct pressure to bleeding.
• Administer drugs as perscribed.
• Do not leave the patient.

• Vasoconstricting drugs to stimulate venous return.
• Inotropic drugs directly stimulate adreneric receptor sites on the heart muscle and improveheart muscle cell contraction.
• Drugs that enhancemyocardial perfusion.

Caused by problems that impair the ability of the normal heart muscle to pump effectively.