2x normal= myocardial damage

Advantages: Low cost

Specific to cardiac muscle

detect reinfacrtion 

6-12 hours 3 samples apart

Disadvantages

false positives 

Normal Ratio CK-MB1 to CKMB2=1:1 CKMB2 increases with myocardial tissue 1:2

Advantages

high sensitivity to early AMI

can detect early extension of MI

Disadvantages

low cardiac specificity with false positives:

UTI Heart failure seizures urosepsis 

Small 02 binding protein 

Advantages: Rises within 1-4 hours after onset of CP

HIgh sensitivity 

elevation in circulation before CK-MB

Disadvantages

Low cardiac specificity

False positives (Trauma, shock, renal failure)

THIS IS ALL MUSCLE FOR BODY

FIRST TO RISE 1-2 Hours after chest pain

Elevations occur with minor myocardial damage

specific to myocardial tissue

Advantages: Sensitive and specific to late AMI

Disadvantages

Low sensitive to early AMI

not useful for reinfarction  

NOrmally LDH 2 is higher than LDH1

Reversed ratio= AMI LDH1 Higher than LDH2

Advantages: Late marker for myocardial tissue damage

Disadvantages: Low sensitiveity and specificity during 1st 24 hours of AMI 

Angiography/Cardiac Cath is the gold standard in diagnosing the CAD

Complications include hemotoma bleeds, allegric to dye, reperfusion dystrimias, infarction

(discomfort, sedation, medications) Best test but very expensive

Antidysrimic drugs 

aspirn anti cogulauant

morphine- pain- 02 use

prepare for transport 

assess them take labs WBC- infection 

Need to be inplemented asap but effective is within 12 hours of ONSET of symptoms chest pain

agents used for thrombolytic thearpy

allegric reactions happen because its human tissue 

TNKase

Eminase

break down the clot 

Active internal bleeding

Cerebrovascular processes (previous stroke, any brain event in the past year, recent spinal surgery, neoplasm in brain)

prolonged CPR

bp 200/120 

pregnancy recent delivery 

Thrombolytic therapy 

Relative contraindications: Use with Caution

endocarditis, pericarditis, homeostatic defects, use of anticogualants, hypertension, pregnancy, trauma, surgery (2-4weeks)

active peptic ulcer

noncompressible vascular punctures 

Resolution of Chest pain-successif subsides with morphine

normalization of incrase ST segments

development of dysrhythmias-reocculsion of coronary artery- free radicals toxic material v-tach, v-fib

allergic reactions 

hemorrhage-bleleding in crazy places

hypotension - open up vascular tree bleeding out

You are activating the TPA clot buster... 

decreases heart having to pump and work with the blood has oxygen

Balancing cardiac output while minimizing cardiac workload

Nursing Management Drugs: 

Dobutamine,dopamine

Postiive inotropic durgs

maintain BP

Vasodilators 

Aceinhibitors- vasodilators- perfuse cells promote L ventricular less work to do 

Dialates arteries and appropriate perfusion to decrease heart workload. 

PAWP pressure is less than 18 than not enough filling pressure, no ejection, no fluid volume pulmonary complications  

Higher than 18=PUlmonary  congestion or cardiac shock 

HypoKalemia

<2.5

HyperKalemia

>6.6

Hypocalcemia 

<7

Hypercalcemia

>12

Low Magnesium 

<0.5

High Magnesium

>3.0

Cycle of Rhythm

Pump Failure

Output Syndrome

Functional status

Stages of Heart Failure

Class I MILD

Tach- doesn't have time to fill

Brady- not pumping enough no ejection

PVC- not complete fill 

AV conduction is slow does reach ventricles 

Causes: Hypkalemia, ischemia, Dig Toxi(SLow heart rate ), Excessive vagal response

NO S&S

NO TREATMENT due to drug thearpy

Atropine (Brady) 

Can live with this condition 

AV BLOCK

Second Degree Type I 

Take longer to reach ventricles AV NODE

Eventually BLOCKED= DROPPED BEAT

more P waves than QRS wave

Cause: drugs, myocarditis, INFERIOR Wall of MI 

AV BLOCK

SEcond Degree TYPE I

Symptoms- Bradycardia

Tx: O2-Atropine, Pacemaker

AV BLOCK

SECOND DEGREE TYPE II

INFRANODAL- Occurs below the bundle of His 

QRS wide, dropped beats 

Cause: anterior wall MI, conduction problems, Rheumatic heart disease, degenerative disease of conduction systems

Bradydyshythmia

TX: Temporary pacing, 02, atropine, isoproterenol (isuprel)

AV BLOCK 

Third Degree

*test question*

Also called complete heart block 

none of the sinus impulses reach the ventricles clocks atrial conduction.  

an idependent pacemaker paces the ventricles 

Regular A & V rhythms but independent

more p waves than QRS complexes

PR INTERVAL not constant 

Pacemaker*** pt cant resolve cardiac output at all times

causes: CAD, MI, Hypoxia, aortic stenosis, drugs, electrolyte imbalance, heart surgery

AV BLOCK

Third Degree

Symptoms

confusion, lightheadedness, syncope, myocardial ischemia, heart failure, hypotensio, cardiac arrest, VT, VF, asystole no conduction

TX: O2, atropine, isoproterenol (Isuprel)

Pacemaker

Heart Block: Bundle Branch Blocks

Below Bundle of His

If the QRS wave is uneven- rabbit ears and widen thats BBB 

Tx: o2 pacemaker 

Pacemakers? 

Temporary pacing...

Synchronous- demand pacing

asynchronous Fixed Rate Pacing

if you see a sharp wave line on atrial P wave... thats atrial shock ventricular conduction shock 

To see the atrial Pacemaker you look at the EKG? 

To see ventricular pacing you look? 

Lead II

SA NODE atrium pacemaker, P wave spike sharp lines

Ventricular you look at V1

requires intervention call the physcian STAT 

Coming from surgery - warm up slowly AVOID SHIVERING 

Pulmonary congestion and respiratroy distress

eventually results in R. HF

S&S dyspnea, on exercisin, orthopnea, cough, crackles, extra heart sound, pulsus alternans, Cheyne stokes, weakness, fatigue, difficulty concentrating, anxiexty restlessness

Congestion of peripheral tissue and viscera

Progressive fatigue, difficulty concentrating, progressive peripheral pitting edema, weight gain, increase abd girth, (hepatomegaly, ascites, jaundice, tenderness) JVD nausae, weakness, anexity