Download Cardiac CheckPoint study notes

Review Tips for Adult Health Cardiac CarePoint
as given by Dr. Cummings
Mayo Clinic Hospital
October 6, 2009
1. Know the signs and symptoms of heart failure
a. Right-sided heart failure: congestion in the body. Peripheral edema
Systemic Congestion
[1] JVD
[2] Enlarged liver and spleen
[3] Anorexia and Nausea (Megase)
[4]Dependent edema (legs and sacrum)
[5] Swollen hands and fingers
[6] Polyuria at night
[7] Weight gain (most reliable indicator of fluid loss/gain)
[8]Increased BP (from excess volume) or decreased BP (from failure)
b. Left-sided heart failure: congestion in the lungs. Dsypnea, orthopnea
Decreased Cardiac Output
[1] Fatigue
[2]Weakness
[3] Oliguria during the day
[4] angina
[5] Confusion/restlessness
[6] Dizziness
[7]Tachycardia
[8] Pallor
[9] Weak peripheral pulses
[10] Cool extremities
Pulmonary Congestion
[1] hacking cough, worse at night
[2] Dyspnea
[3] Crackles/wheezes in lungs
[4] Frothy, pink-tinged sputum
[5] Tachypnea
[6] S3/S4 Gallop
[7] AFIB is common
2. Know about the role of sodium retention in heart failure
decreased blood flow to the kidneys stimulates production of renin. Activating the RAAS
promotes retention of sodium and fluids to raise blood pressure. This causes increased
afterload, which causes ventricular remodeling. Hypertrophied muscle uses more oxygen
and also has decreased contractility. Decreased contractility leads to increased preload
and further decrease in contractility. This decrease in contractility leads to decrease in
cardiac output, which starts the whole cycle over again.
3. Weighing patients – can assess fluid volume changes by changes in weight.
4. Review CAD (Coronary Artery Disease) and atherosclerosis
a. Definitions:
CAD: a narrowing of the arteries that supply the heart with blood due to accumulation of
plaque. Increases risk for an MI. Includes stable angina and acute coronary syndromes.
When blood flow through coronary arteries is blocked, ischemia and/or infarction can
occur.
atherosclerosis: collecting of plaques (cholesterol, lipids, cellular debris) in the inner
layer of the walls of arteries.
b. Causes/risk factors
i. Modifiable risk factors: HTN, hyperlipidemia, diabetes, smoking, obesity,
sedentary lifestyle, stress
ii.
Non-modifiable risk factors: age, gender, race/ethnic background,
heredity
c. Dietary factors and dietary modifications as part of treatment plan
5. Know med classes for blood pressure control (the list below is from Dr. Ancheta’s
PowerPoint presentation):
a. Diuretics: thiazides are first. (most “gentle”)
b. Beta-Blockers: “-olol” - block beta receptors (beta1 is specific to heart.
Nonspecific for beta1 and beta2 can have pulmonary side effects) Beta1 is
adrenergic (stimulatory). Blocking these prevents vasoconstriction → lower BP.
c. Calcium channel Blockers: diltiazem, cardizem – block calcium from entering
smooth muscle, prevents vasoconstriction → lower BP. Also slows heart rate.
d. ACEIs / ARBs: ACEIs (“-pril”) act in lungs; ARBs (“-sartan”) act in kidneys.
Both work by interrupting the RAAS, thus keeping overall volume and BP lower.
e. Vasodilators: actually dilate blood vessels (whereas other HTN meds work by
preventing vasoconstriction, but don't actually cause dilation). Examples include
clonidine (Catapres), doxazosin (Cardura)
6. If you want to decrease blood pressure rapidly (you can’t wait for something like an
ACEI or ARB to take effect), then use one of the following:
a. Calcium channel blocker (e.g. – nicardipine, brand name Cardene)
b. Alpha blocker (e.g. – phentolamine, brand name Regitine)
i. NOTE: I believe Dr. Cummings said “alpha blocker”, but then went on to
give an example, clonidine (brand name Catapres), which is an alpha
agonist, not antagonist. Clonidine is available PO and as a transdermal
patch, with an onset of action of 30 minutes or more. While this is still
faster than the hour or more that it takes for an ACEI to start working, it’s
still pretty slow—maybe clonidine was not what she intended to use as an
example. I did some research, and phentolamine is an alpha blocker,
works immediately to reduce blood pressure when given IV, and is used to
treat hypertensive crisis.
7. A-fib – treat with both:
a. Diltiazem (Cardizem) – a calcium channel blocker
b. Warfarin (Coumadin) – anticoagulant (due to higher risk of clotting from A-fib)
8. Know the importance of the ST segment
a. ST depression = ischemia. A non-STEMI means you are having an ischemic
attack, not an infarction. Not good, but better than a STEMI.
b. ST elevation = MI
i. 80% of MIs are STEMIs (ST Elevation Myocardial Infarctions)
9. Know the labs for an MI (the list below is straight from Dr. Ancheta’s PowerPoints):
a. Troponin T and I- myocardial muscle protein released into the bloodstream with
injury to the myocardial muscle (not found in healthy clients)
b. Creatine kinase - MB (CK-MB) is an enzyme specific to cells of the brain,
myocardium and skeletal muscle. Indicates tissue necrosis or injury, Cardiac
specificity is determined by measuring the isoenzyme activity CK-MB is found in
myocardial muscle CK-MM (skeletal) CK-BB (brain)
c. Myoglobin early marker of MI is a low-molecular-weight heme protein found in
cardiac and skeletal muscle, appears as early as 2 hours after an MI with rapid
decline after 7 hours
d. C-Reactive Protein is a marker of inflammation. Any inflammatory process can
increase CRP in the blood
10. “There may be something on there about the major EKG leads.”
a. No details on this.
Other notes/clarification:
Systolic dysfunction – ejection fraction <40%. EF is decreased because ventricle is so full prior
to contraction (increased preload) that the muscle fibers are so stretched and it doesn't contract
efficiently enough to expel the blood from the chamber.
diastolic dysfunction – ejection fraction is normal or higher than normal. Muscle is becoming
thicker/hypertrophied. Pumps blood out, but less empty space in the ventricle for blood to fill,
and the larger muscle is requiring more oxygen.
*both are types of left-sided HF