Multi-system

1. Asphyxia
2. Distributive shock (e.g., anaphylaxis)
3. Multi-organ dysfunction syndrome (MODS)
4. Multisystem trauma
5. Sepsis/septic shock
6. Systemic inflammatory response syndrome
(SIRS)
7. Toxic ingestions/inhalations (e.g., drug/alcohol
overdose)
8. Toxin/drug exposur

Cardiac Markers

Cardiac markers
Marker	Initial Elevation	Peak Elevation	Return to Baseline
Myoglobin	1-4 h	6-7 h	18-24 h
CK-MB	4-12 h	10-24 h	48-72 h
Cardiac Trop I	3-12 h	10-24 h	3-10 d
Cardiac Trop T	3-12 h	12-48 h	5-14 d

The troponin I is the most sensitive cardiac marker, detectable in serum 3-6 hours after an MI, and its level remains elevated for 14 days.

Anterior Wall MI

Anterior wall infarction results from occlusion of the proximal LAD artery. ST-segment elevation is expected in leads V1 through V4 on the 12-lead ECG, as shown in. If the left main coronary artery is occluded, the ECG manifestations will involve almost all of the precordial leads V1through V6 and leads I and aVL (see above). These specific groups of ECG changes that help to locate the part of the heart that is infarcting are called indicative changes. A large anterior wall MI may be associated with left ventricular pump failure, cardiogenic shock, or death.

LATERAL WALL INFARCT

Left lateral wall infarction occurs as a result of occlusion of the circumflex coronary artery. On a 12-lead ECG, new Q waves and ST-segment T-wave changes are seen in leads I, aVL, V5, and V6.  In reality, very few patients present with only lateral wall ECG changes. Often times some anterior wall leads (V3 and V4) may show evidence of injury or infarction. 

ANSWERS #1-20

1.  A - Nipride

2.  A - PVR
3.  A - Pulmonary Edema
4.  A - RAP
5.  C - Pulmonary HTN
6.  C - Vasoconstriction
7.  A - Increased HR, contractility, conductivity
8.  D - Vasodilation, bronchodilation
9.  B - Dilation of the renal and mesenteric arteries
10. D - Phenylephrine
11. C - Dobutamine
12. A - Isoproternol
13. B - Dopamine at 2 mcg
14. B - V3
15. D - Phenylephrine
16. C - Start large bore IVs, get lab samples and fluid bolus
17. C - Pericardial tamponade
18. D - Perform synchronized cardioversion
19. C - Atrial fib
20. C -Bleeding at the groin site


IF ANYONE NEEDS THE RATIONALE FOR A PARTICULAR ANSWER, EMAIL ME!

CLINICAL TRIAD OF RIGHT VENTRICULAR INFARCT (RVI)

1.  Hypotension

2.  Jugular Vein Distension

3.  Dry Lung Sounds

Inferior Wall MI R/T Right Ventricular Infarct

CLINICAL PEARL: 


If your patient is admitted with an Inferior wall MI always obtain a right sided EKG. 45% of patients that present with Inferior Wall MI will also develop Right Ventricular Infarct (RVI). See image below for placement of electrodes for right sided EKG.


This is important because the treatment is different for RVI.

Inferior Wall Infarction

Inferior wall MI is caused by occlusion of the right coronary artery (RCA). This type of infarction is manifested by ECG changes in leads II, III, and aV_F (See image below).

Conduction abnormalities are expected with an inferior wall MI and are r/t the anatomy of the coronary arterial circulation supply. The RCA perfuses the sinoatrial (SA) node in slightly more than 50% of the population, supplies the proximal bundle of His and atrioventricular (AV) node in more than 90% of individuals, heart block and other conduction disturbances should be anticipated.

Inferior wall infarction has a mortality rate of about 6%. If the right ventricle is involved, the mortality rate rises to 25% to 30%.

The images below show changes seen on a 12-lead ECG with an inferior wall MI. A.   Infarction location on cardiac wall.
B.   ECG leads with expected ST-segment elevation.
C.   A 12-lead ECG from a patient experiencing inferior wall MI.

Correlations Among Ventricular Surfaces, EKG Leads, & Coronary Arteries

Below is a table which list corresponding surface area of the heart with EKG leads and the coronary artery usually involved. The location of infarction is determined by correlating the ECG leads with Q waves and the ST-segment T-wave abnormalities.  Infarction most commonly affects the left ventricle and the interventricular septum; however, the right ventricle can be infracted, and many patients who sustain an inferior MI have some right ventricular damage. The ECG manifestations that are used to diagnose an MI and pinpoint the area of damaged ventricle include inverted T waves, ST-segment elevation, and pathologic Q waves in specific lead groupings as described subsequently.

Surface of Left Ventricle	EKG Leads	Coronary Artery Usually Involved
Inferior	II, III, aVF	Right coronary artery (RCA)
Lateral	V5-V6, I, aVL	Left circumflex (CIRC)
Anterior	V2-V4	Left anterior descending (LAD)
Anterior lateral	V1-V6, I, aVL	Left main coronary artery (L MAIN)
Septal	V1-V2	Left anterior descending (LAD)
Posterior	V1-V2	Left circumflex or right coronary artery (reciprocal changes)
	V7-V9 (direct)

Coronary Circulation

The above image is the coronary circulation. Please print out and review the coronary arteries. It is important to know coronary circulation. If a patient is having an heart attack, the initial treatment is different based on location of infarction.


Stay posted!

CCRN Test Plan

Clinical judgement comprises 80% of the CCRN exam. The other 20% represents professional caring and ethical practice. Listed below is the breakdown of the 80% by system.  This BlogSpot is a guideline to help focus your studying and prepare you will questions. We will start with the cardiovascular system and work our way through the other systems overs the next several months.  Scroll below to find the breakdown of the cardiovascular system by disease specifics.

System Breakdown
A. Cardiovascular (20%)                                      
B. Pulmonary (18%)                                            
C. Endocrine (5%)                                                
D. Hematology/Immunology (2%)
E.  Neurology (12%)                         
F.  Gastrointestinal (6%)
G.  Renal (6%)
H.  Multi-system (8%)
I.  Behavior & Psycho-social 4%

Cardiovascular Breakdown
1. Acute coronary syndromes (including unstable angina)
2. Acute myocardial infarction/ischemia (including papillary muscle rupture)
3. Acute peripheral vascular insufficiency (e.g.,acute arterial occlusion, carotid artery stenosis, endartarectomy, peripheral stents, Fem-Pop bypass)
4. Acute pulmonary edema
5. Cardiac surgery (e.g., valve replacement, CABG)
6. Cardiac trauma
7. Cardiogenic shock
8. Cardiomyopathies (e.g., hypertrophic, dilated, restrictive, idiopathic)
9. Dysrhythmias
10. Heart failure
11. Hypertensive crisis
12. Hypovolemic shock
13. Interventional cardiology (e.g., catheterization)
14. Myocardial conduction system defects
15. Ruptured or dissecting aneurysm (e.g., thoracic, abdominal, thoraco-abdominal)
16. Structural heart defects (acquired and congenital, including valvular disease)

LOOK FOR THE QUESTIONS & ADVANCED PATHO TO START WITHIN THE NEXT WEEK!

You can do it!!! Take 30 minutes everyday to review material and complete at least 10 questions a day and you will be prepared to take the CCRN exam in a few months.