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56 Cards in this Set
- Front
- Back
Clinical Manifestations of Cardiac Dysfunction
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Fatigue
Fluid Retention (right side) SOB (Left Side) Pain ascites (right side) |
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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 |
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PDV
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Peripheral Vascular Disease
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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. |
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CAD
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Coronary Arteries Disease
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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 |
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CK-MB
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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 |
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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 |
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LVEF
Define Normal Danger |
Left Ventricular Ejection Fraction
55-65% Under 40% Dangerous |
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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. |
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Thalium Scan
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Cells Uptake.
Injection of Thallium to check cells uptake (Necrotic cells will not have uptake) Sometimes done with treadmill |
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PVC
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Premature Ventricular Contraction
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P-R interval
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Beg. of P to Beg of QRS
0.12-0.20 If prolonged - Block |
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QRS interval
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Vent Depolarization
From Q to where S is back to baseline. 0.04-0.10 Sec |
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How to measure rythm?
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P-P (tops) for atrial
R-R (tops) for ventricular |
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Atrial Fibrillation
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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) |
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Stenosis
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Narrowing
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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) |
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CHF
Define Causes |
Congestive Heart Failure
Enlargment and streching of ventricles-> Impaired systoli->blood accumulates/Stasis. Alcohol Abuse CAD/MI Autoimmune Postpartum Viral |
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Hypertrophic
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(Hypertrophy=increase in size)
Increase in weight. Esp. in septum. Impaired flow A->V. Genetic Chest pain dysrythmia |
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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 |
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3 major types of Angina
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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. |
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Angina Treatment
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Incr Supply - Dcr Demand
NTR Dialate vessels. Incr perfusion. Drugs: Dcr myocardial contractility (works less demands less) |
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Myocardial infarction.
Define: Causes |
Tissue deprovation of O2. After 6 hours-> necrotic. Slow: (CAD) or sudden (Thrombus)
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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) |
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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 |
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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. |
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Heart Failure
Define |
Inability of the heart to pump sufficient blood to meet demands.
Due to: Incr demand (V overload) Decr supply (poor pump) |
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Left Sided Heart Failure
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Think blood backs up:
SOB Paroxysmal Nocturnal Dyspnia Wet Lung Sounds Cough Tachycardia Think low perfusion: Mental state (hypoxia) Fatigue Oliguria Nocturnia |
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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 |
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CHF and Cardiogenic Shock Treatments
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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 |
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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 |
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Preload
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Myocardial stretch at end of diastole (just before ctx).
LVEDP/V: Left Ventricle End Diastolic Volume (pressure). |
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Afterload
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The Pressure or resistance ventricle needs to overcome to open valves and eject to circulation.
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Starling's Law of the Heart
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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. |
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Stasis
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Stagnation (no movement/kipaon) of the blood or other fluids.
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Angina
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A severe, often constricting pain or sensation of pressure, usually referring to angina pectoris
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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.) |
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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! |
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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 |
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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 |
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Inotropic
Define |
Influencing the contractility of muscular tissue.
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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. |
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O2 Sat normals
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>95 normal
<93 need for O2 therapy |
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BP
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Sys 90-140
Dias 60-90 |
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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. |
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Na+
Normal Blood Normal Urine |
135-145mEq/L
50-130mEq/L |
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Hyponatremia Treatments
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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) |
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When administering/lowering Na--how much?
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IV no more than 12mEq/first day.
lowered no more than 2mEq/hour |
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Hypernatremia treatment
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Hypotonic solutions:
D5W .45% saline |
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SIADH
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Release of ADH when the blood is already diluted
CNS demage. Cancer. |
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hyponatremia Diagnostic Assessment
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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) |
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Exogenous ADH
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Aqueous Vasopressin (pitressin)
Vasopressin Tannate DDAVP- desmopressin acetate Synthetic ADH |
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Vasopressin
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hormone (trade name Pitressin); reduces urine flow by affecting reabsorption of water by kidney tubules
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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 |
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CK-MB
Indicates Necrosis only |
0-6%
Rise 4-6hrs Peak 24Hrs Stays 48hrs |