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56 Cards in this Set

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Clinical Manifestations of Cardiac Dysfunction
Fatigue
Fluid Retention (right side)
SOB (Left Side)
Pain
ascites (right side)
BP
3 key affecting factors + what effects each?
CO (capacity), Volume (how much has to work with, Resistance (what works against)

1. CO (SV x HR)

2. Preipheral resistance (diameter, length, viscosity)

3. Blood Volume
PDV
Peripheral Vascular Disease
Angiography
Pre test
Post test
Perfusion of coronaries w/Dye

Injection of dye to Coronary Arteries

Pre - NPO, allergy to shellfish, periph pulses (for baseline)

Post - Vitals, puncture site, Periph pulses (watch sites below artery), flat bed rest, Fluids to flush dye.
CAD
Coronary Arteries Disease
Troponin
1. define
2. How long stays in blood?
3. Normals
Protein released from dead/injured heart cells.

Gold Standard

Rises 4 hrs after - Peaks 10-12 hrs - Stays elevated 10-14 days(!)

Normals: 0.5ng/ml
0.5-0.8 Injured
0.8+ accute injury infarction
CK-MB
Enzyme. elevates when injury/necrosis

Rises within 4-6 hrs
Peaks within 24 hrs
RETURN TO NORMAL after 48 hrs

Drawn Q8hrs for 24hrs

<160u/ml - 130u/ml (M and F)
0-6%
>6% indicative of MI
Cardiac Cath
What for?
Complications
Blokage+ Heart shape&function w/Catheter

1. Location of blokage in coronary
2. Size+muscle function of heart
Complication: MI, CVA (stroke), hemorrhage, emboli, death
LVEF
Define
Normal
Danger
Left Ventricular Ejection Fraction

55-65%
Under 40% Dangerous
Muga Scan
What does it measure?
ECG + Computer

computer analyses cardiac cycle, abd calculates ejection fraction.

Can be done to assess muscle improvement after surgury.
Thalium Scan
Cells Uptake.

Injection of Thallium to check cells uptake (Necrotic cells will not have uptake)
Sometimes done with treadmill
PVC
Premature Ventricular Contraction
P-R interval
Beg. of P to Beg of QRS
0.12-0.20
If prolonged - Block
QRS interval
Vent Depolarization
From Q to where S is back to baseline.
0.04-0.10 Sec
How to measure rythm?
P-P (tops) for atrial
R-R (tops) for ventricular
Atrial Fibrillation
No Pwaves. Atrial rythm cannot be counted.
R-R - irregular.
"Saw tooth"
Loss of (30%) arterial kick.
Vent cannot be filled - Hypotens, SOB, dizzy
Clotting Risk (b/c fibrillation)
Stenosis
Narrowing
Cardyomayopathy
Define
Subdivisions
Treatments
Cardio-Myo-pathy (disease)

Chronic cardiac muscle disorder.

Dilated->Congestive Heart Failure
Hypertrophic
Restrictive
Dilated-Restrictive: Same as CHF
Hypertrophic: Same as MI
Implanted Ventricular Assist Device (VAD)
CHF
Define
Causes
Congestive Heart Failure

Enlargment and streching of ventricles-> Impaired systoli->blood accumulates/Stasis.

Alcohol Abuse
CAD/MI
Autoimmune
Postpartum
Viral
Hypertrophic
(Hypertrophy=increase in size)

Increase in weight. Esp. in septum. Impaired flow A->V.

Genetic

Chest pain dysrythmia
Atherosclerosis
Angina
Myocardial infarction

Define, Relationship
Atherosclerosis:
Cumulative build up is the leading cause of coronary artery disease.

Angina
Ischemia of a limited duration. May cause dysrythmia

Myocardial infarction
muscle death (necrosis).
Muscle deprived of oxygen for at least six hours
3 major types of Angina
1. Stable/Exertional - absent at rest

2. Unstable/Crescendo: At rest or minimal exertion

3. Variant/Prinzmetal: Coronary artery spasm (no CAD). High risk of MI.
Angina Treatment
Incr Supply - Dcr Demand

NTR Dialate vessels. Incr perfusion.
Drugs: Dcr myocardial contractility (works less demands less)
Myocardial infarction.
Define:
Causes
Tissue deprovation of O2. After 6 hours-> necrotic. Slow: (CAD) or sudden (Thrombus)
Myocardial failure
Clinical manifestations
1. pathophysiological changes:
Hypoxia - Vasodialte
Acidocis
Stress - Catecholamines - Incr HR and Force of Ctx
Incr O2 demand
Necrosis

2. Pt Reports/Exhibit:
Pain unrelieved by Rest, NTR
Lasting Pain
SOB
Nausia/Vomit/"Indigestion"
Sweat
Confusion (hypoxia)
Palpitation
Faigue.

3.Physical exam Findings:
S3 S4
Cold sweat
wheezes
Preph weak/absent
Temp up
"U wave" Inverted T
ST elevation
Diagnostic markers: Triponin I, CK-MB, Thallium (necrotic area), MUGA (left Vent Function), Card Cath (bloke)
MI
Treatment
Incr supply (incr circulation)
Decr demand

O2 DEMAND:
NTR - Vasodial: dcr Afterload (opens aorta: heart has less to push against). Dcr Preload pulls blood to periph reduced workload.
Beta/Calcium blockers dcr contractility, HR
Morphine fpr Pain +dialation
O2 2-4L

SUPPLY:
Anticoagulants
NTR (dial)
PTCA Percutaneous Transluminal Coronary Angioplasty-"Balloon". Comdition: Discrete non-calcified lesions.
CABG: Bypass Graph
Thrombolytics: Streptokinase,
t-PA
Heart Failure:

Pathophysiological Changes
1. HR incr (back fire: Tachy-> filling time gets longer)
2. SV incr - Increased return. Strech of myocardium produces stronger ctx. To a point + Incr afterload requires energy and strong heart...
3. Aldosterone - Venous Return Incr
4. Myocardial Hypertophy - to incr ctx force. But if circ cannot mainain - O2 deprived.
Heart Failure
Define
Inability of the heart to pump sufficient blood to meet demands.
Due to: Incr demand (V overload)
Decr supply (poor pump)
Left Sided Heart Failure
Think blood backs up:
SOB
Paroxysmal Nocturnal Dyspnia
Wet Lung Sounds
Cough
Tachycardia

Think low perfusion:
Mental state (hypoxia)
Fatigue
Oliguria Nocturnia
Right Sided Heart Failure
Symptoms
Right Vent cannot empty completely -> Venous congestion, Edema:

1. Edema, Weight Gain
2. Liver engogement: GI problems, tenderness
3.polyuria
4. JVD
5. Ascites
CHF and Cardiogenic Shock Treatments
1. Rdc Preload: Reduce overstrech of muscle fibers, and volume: Limit Sodium, Limit fluid intake, Diuretics, NTR

2. Rdc Afterload: Reverse vasoconstriction of arteries. ACE inhibitors. Monitor BP!

3. Improve Contractility: Digitalis/Digoxin. Dcr HR and Incr Ctx.

4. patient Education:
a. report sharp weight gain
b. Dcr excersize tolerance
c. Angina/Dyspnea at rest
d. long "cold"
e. Nocturia
Cardiogenic Shock
Main Cause
What is the physical process
Severe Heart Failure.
End Stage Left Vent Failure.40% Necrotic.

Usually secondary to MI.

Left Vent Fails -> Incr residual volume and pressure -> backs up to lungs vasculature -> Incr residual vasc volume and pressure -> Pulmonary edma, impaired perfusion -> shock
Preload
Myocardial stretch at end of diastole (just before ctx).
LVEDP/V:
Left Ventricle End Diastolic Volume (pressure).
Afterload
The Pressure or resistance ventricle needs to overcome to open valves and eject to circulation.
Starling's Law of the Heart
The more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).

When the diastolic filling of the heart is increased or decreased with a given volume, the volume of blood which is then ejected from the heart increases or decreases by the same amount. More blood in: more blood out.
Stasis
Stagnation (no movement/kipaon) of the blood or other fluids.
Angina
A severe, often constricting pain or sensation of pressure, usually referring to angina pectoris
Heart Failure
Compensatory Mechanism Following
1.Increased HR (too much: tire)
2.Improve SV. SNS improve venous return->greater Ctx force (Starling's). (too much: Cardiomyopathy)
3. Arterial Preiph Constriction. (too much: Incr afterload against which heart must pump)
4. Renin-Aniotensin-Aldosterone-> Incr preload
5. Myocardial Hyperthrophy -more muscle mass for incr ctx. (Too much O2 deprived.)
Digoxin
What does it do?
Consideration for Absorption, Toxicity. Blood Normal. HR
Dcr HR Incr Contractility
Considerations:
Antacids interfere w/ Absorption
Normal-Low K+ potentiate toxicity
Blood Normal: 0.5-2ng/ml
ALWAYS Apical HR - <60 Danger!
Four Classes of Heart Failure
+ Treatments
I Absent Crackles and S3 - Diuretics. Dcr pre-afterload

II Cracles lower lung. S3 possible. III Crackles, Pulmonary edema. NTR (monitor B/P), PAWP,Inotropics.

IV Cardiogenic Shock more than 40% necrotic
Four Classes of Heart Failure
+ Treatments
I Absent Crackles and S3 - Diuretics. Dcr pre-afterload

II Cracles lower lung. S3 possible. III Crackles, Pulmonary edema. NTR (monitor B/P), PAWP,Inotropics.

IV Cardiogenic Shock more than 40% necrotic
Inotropic
Define
Influencing the contractility of muscular tissue.
Cardiogenic Shock
Signs and Symptoms
1. Tachycardia - rapid and weak pulse; Tachypnea
2. Decrease BP by 30 mm Hg from baseline or a systolic less than 90mm Hg.
3. Urinary output less than 30 cc/hr.
4. Cold, clammy skin
5. Poor Peripheral pulses
6. Agitation, restlessness, confusion - due to cerebral hypoxia
7. Pulmonary congestion - crackles
8. Continuing Chest Discomfort, metabolic acidosis.
O2 Sat normals
>95 normal
<93 need for O2 therapy
BP
Sys 90-140
Dias 60-90
BP
Regulated by... (what Organs/Systems)
1. SNS - Vasoconstrict
2. Heart - Baroreceptors. Beta1 - Incr CO, Alpha1- Vasoconstrict
3. Vessels - Tone length, and state. Periph Resist.
4. Blood Volume.
5. Kidneys - Renin-Angiotensin Vasoconstricr. Aldosterone Incr Volume.
Na+
Normal Blood
Normal Urine
135-145mEq/L

50-130mEq/L
Hyponatremia Treatments
If actual Na lost:
Add PO

If water axcess:
Restrict intake (1000cc/day)
Administer Hypertonic solution. No with CHF/ARF. (+lasix).
If SIADH: Lithium (blocks renal sensitivity to ADH)
When administering/lowering Na--how much?
IV no more than 12mEq/first day.

lowered no more than 2mEq/hour
Hypernatremia treatment
Hypotonic solutions:
D5W
.45% saline
SIADH
Release of ADH when the blood is already diluted
CNS demage. Cancer.
hyponatremia Diagnostic Assessment
Urine Na <20. Sp gravity <1.010. (kidneys reabsorb Na-> dilute urine)

SIADH: Urine Na >20 sp Gravity >1.012. Kidneys excrete Na and retain water (Noted by CVP>6)
Exogenous ADH
Aqueous Vasopressin (pitressin)
Vasopressin Tannate
DDAVP- desmopressin acetate
Synthetic ADH
Vasopressin
hormone (trade name Pitressin); reduces urine flow by affecting reabsorption of water by kidney tubules
Troponin I Levels

Indicates Necrosis AND Injury
Stays Up Longer
0.5ng
0.5-0.8 Injury
>0.8 MI

Rise 4hrs
Peak 10-24Hrs
Tays Up 10-14 DAYS
CK-MB
Indicates Necrosis only
0-6%
Rise 4-6hrs
Peak 24Hrs
Stays 48hrs