Cardiovascular system.txt

  1. Was the average size of the heart?
    Size of your fist .5" x 3.5"
  2. What is the PMI or point of maximal impulse?
    • Pulsation arising at the apex of the heart; tip of the left ventricle
    • Apical pulse
    • 5th ICS midclavicular line
  3. What are the four chambers of the heart?
    • Right atrium
    • Right ventricle
    • Left atrium
    • Left ventricle
  4. What are the layers of the heart?
    • Endocardium: inner lining of the heart, chambers and valves
    • Myocardium: actual muscle, conductive system
    • Pericardium: sac surrounds the heart: composed of visceral and parietal layer
    • Epicardium: outer surface of the heart, contains the coronary arteries; visceral layer of the pericardium
    • Pericardial space: small amount of fluid in space acts as a lubricant; there is friction caused by movement of the layers with each contraction, contains about 50 mL of serous fluid
  5. Valves of the heart
    • Prevent backflow of blood; keep blood flowing in one direction
    • Atrioventricular valves: tricuspid valve, mitral valve (first heart sound, S1)
    • Semilunar valves: aortic, pulmonic (second heart sound, S2)
    • Tricuspid and mitral (atrioventricular) prevent backflow of blood into the atria during contraction
    • Pulmonic and aortic (semilunar) prevent regurgitation into the ventricles at end of each ventricular contraction
    • Chordae tendeneae prevent eversion of the valve leaflets during ventricular contraction
  6. Arterial coronary blood flow
    • Coronary arteries branch off just as the aorta leaves the heart
    • Right coronary artery: supplies blood to the right anterior surface of the heart, part of the inferior wall of left ventricle, and conduction system (SA & AV)
    • Left main coronary artery: branches into the left circumflex (supplies the posterior and lateral left atrium and ventricle)
    • Left anterior descending: supplies the anterior wall of left ventricle to apex
    • Left circumflex: supplies lateral wall of left ventricle
  7. What is ischemia?
    • Deficiency of blood due to constriction or obstruction of a blood vessel
    • Results in tissue hypoxia which reduces the mechanical & electrical activity of the heart
    • Indicates there is myocardium that is at risk, but if you intervene may be able to salvage it
  8. Is ischemia reversible?
    May be reversible, depending on length of time ischemia occurs and the extent of muscle involved
  9. What is an infarction?
    • Permanent loss of blood flow to myocardium; not reversible
    • Results in cell death
    • Overall effect depends on the size of area deprived of O2
    • Alternate routes are developed in time to nourish the endangered myocardium (collateral blood supply)
    • Causes: emboli and atherosclerotic plaque buildup in the arterial blood supply
  10. Electrical conduction system
    • Conduction system is composed of specialized nerve tissue responsible for creating and transporting the electrical impulse, or action potential
    • Cardiac cells have the ability to transmit electrical impulses
  11. Depolarization
    • Rapid influx of sodium & calcium ions into the cell & outflux of potassium ions
    • Shift in electrolytes
    • Causes muscle fibers to shorten and contract
    • T wave
    • Electrical activity is synchronous with mechanical activity
    • Cells become positive inside
    • Firing of SA node depolarizes the atria
  12. Repolarization
    • Return to resting phase; electrical recovery
    • Potassium moves back into cell and sodium and calcium return to extracellular space
    • Cell returns to negative state
  13. SA node
    • Intrinsic pacemaker of the heart; right atria near entrance of superior vena cava
    • Creates an electrical impulse
    • Intrinsic rate of 60-100.
  14. AV node
    • Conducts impulse to Bundle Branches
    • Internodal pathways to reach the left atrium
    • Rate of 40-60
  15. Bundle Branches
    • Conduct impulse to Purkinje fibers resulting in ventricular contraction
    • Impulse terminates in the Purkinje fibers which trigger a uniform ventricular contraction
  16. ECG
    Electrical activity of the heart detected on one’s body surface
  17. ECG waves
    • P wave: depolarization of fibers in atria (lasts .06-.12 seconds)
    • PR Interval: conduction through A-V node (.12-.20 seconds); time it takes to get thru AV node (if prolonged, indicates conduction problem in AV node)
    • QRS: ventricular contraction/depolarization (.04-.12 seconds); if wider than normal, there is a conduction blockage below the AV node
    • T wave: ventricular repolarization
    • U wave: delayed ventricular repolarization; may be associated with hypokalemia, Digoxin toxicity
    • Repolarization of atria is buried under the QRS interval
  18. What is the significance of a prolonged PR interval?
    • Delayed AV conduction or at atria
    • AV block
  19. What is the significance of a prolonged QRS interval?
    Delay below AV node or at ventricles
  20. What is the significance of a prolonged QT interval?
    • Rhythm disturbances
    • At risk for serious ventricular arrhythmias (ventricular tachycardia)
    • There are some drugs that can prolong the interval as well as a genetic component
  21. What are the clinical consequences of SA node dysfunction?
    • Lower pacemakers should take over and run the heart, however not as efficient
    • HR may still be bradycardic (rate at AV node is around 40 to 50 bpm, in ventricles is around 20 to 30 bpm)
  22. What is cardiac output?
    • Heart Rate x Stroke Volume (SV determined by preload, contractility and afterload)
    • Total amount of blood pumped by each ventricle in 1 minute
    • Normal adult at rest is 4L to 6L
    • Amount of blood ejected from the ventricle with each heartbeat; approximately 70ml
  23. What is preload?
    • Volume of blood in ventricles at end of diastole before next contraction (end of filling)
    • It determines the amount of stretch placed on myocardial fibers
    • Heavily influenced by fluid volume status
    • Increased in hypervolemia and regurgitation of cardiac valves
    • If preload increases, cardiac output increase (due to Starling's Law; the more the ventricle is filled, the more blood that has to go out)
  24. What is contractility?
    • Ability of the heart to depolarize; the force of contraction
    • Affected by the autonomic nervous system
    • If contractility increases, cardiac output increases
  25. What is afterload?
    • Peripheral resistance which left ventricle must pump against to circulate the blood
    • Affected by size of ventricle, wall tension, and arterial blood pressure
    • Influenced by hypertension, aortic stenosis, peripheral vasoconstriction (the more clamped down the vessels are the more resistence; ex: clamped down water hose)
    • If afterload increases, cardiac output decreases (the harder the heart has to work to get blood out against resistance)
  26. What is Starling’s Law?
    • The more the myocardial fibers are stretched the greater the force of contraction
    • The more the heart is filled, the greater the squeeze of the heart and the larger the cardiac output
    • As the heart is stretched overtime the likelihood that the muscle will lose contractility increases
  27. Autonomic regulation of the cardiovascular system
    • Barorecptors in aortic arch and carotids responsive to stretch
    • Chemoreceptors in aortic arch and carotids responsive to pH, PO2 and PCO2
    • Information conveyed to vasomotor center in brainstem
  28. Baroreceptors
    • Pressure sensitive
    • If pressure decreases, message is sent to brain stem that more cardiac output is needed
    • SNS is activated releasing epi and norepi to increase HR and contractility to increase cardiac output
    • If pressure gets too high, baroreceptors indicate that there is too much pressure and needs to decrease cardiac output
    • PNS is activated via vagus nerve (decreases HR and contractility)
  29. Sympathetic stimulation
    • Release of Epinephrine and Norepinephrine (stimulates β-1 receptors)
    • NE stimulates α-1 receptors in periphery (vasoconstriction causes increase in afterload; increases BP)
    • Increases heart rate, conduction, contractility, and peripheral vasoconstriction
  30. Parasympathetic stimulation
    • Mediated by vagus nerve
    • Slows HR, contractility and conduction
    • No effect on periphery
  31. What are the 3 major types of blood vessels?
    • Arteries
    • Capillaries
    • Veins
  32. Arteries
    • Carries oxygenated blood away from heart, except for pulmonary artery
    • Thick walls and elastic tissue
    • High pressure system, major control of arterial BP
  33. Veins
    • Carries deoxygenated blood toward heart, except for pulmonary veins
    • Returns blood to right atrium
    • Thin walled and large in diameter
    • Low pressure system, high volume
    • Reliant on valves, changes in muscle contraction, and changes in thoracic pressure
  34. Capillaries
    • Endothelial cells
    • No elastic or muscle tissue
    • Thin walled vessels
    • Diffusion of gases; exchange of O2 and CO2 (cellular nutrients and metabolic end products)
  35. Diagnostic studies of the heart
    • Chest x-ray (size of heart, any fluid volume overload)
    • ECG (rhythm disturbances, conduction, heart blocks, ischemia
    • Holter Monitor/Event Monitor
    • Echo (2D or transesophageal)
    • Exercise stress test (patient on treadmill to get HR to increase; looking for EKG changes and areas of ischemia)
    • Stress echo (sonogram of heart; stress heart and look for areas that lack perfusion after exercise)
    • Nuclear stress test (injection of a nuclear isotope and stress the heart; looking for areas that lack perfusion)
    • conduction defects, arrythmias, ischemia
  36. Echocardiogram
    • Looking at size of heart, chambers and valves
    • Any ischemic areas
    • Injection fraction (% of volume that is in ventricle that comes out with each squeeze; normally between 50% to 65%; if less than 20% indicates decreased contractility and weak myocardium)
  37. Holter Monitor
    • Worn by patient when having syncope, palpitations, rhythm disturbances
    • Patient keeps monitor on for 24-48 hours and must keep a log of activities at all times (including any symptoms experienced)
    • Information is stored in monitor and printed out at a later time
  38. Stress test
    • Patient walks on treadmill or rides stationary bicycle
    • Leads are placed on chest
    • BP and O2 level is monitored
    • Stop test if reach peak HR, peak exercise tolerance, chest pain, significant ST segment depression (indicates ischemia)
    • Helps diagnose left ventricular function.
  39. Cardiac enzymes
    • Used to diagnose infarction
    • Indicate damage to myocardial cells
    • CK-MB (5% of total; rise in 3-12 hours; peak in 24 hours; return to baseline in 48-72 hours)
    • Troponin T < 0.1 ng/ml is normal.
    • Troponin I < 0.4 ng/ml is normal.
    • Troponins (elevate within 3 hours; peak in 24-48 hours; return to baseline in 5-14 days)
  40. Cardiac catheterization
    • Invasive exam of heart
    • Looks at valve function, ventricular function and presence of CAD (plaque)
    • Catheter is threaded through femoral artery (left cath) or vein (right cath)
    • Contrast dye is injected (ask about allergies to iodine, shellfish, renal function, look at BUN and Cr labs; need to hydrate patient after contrast to prevent toxicity)
    • Xrays are taken
    • Potential complications: aneurysm, hemorrhage, clots, MI, embolus, arrhythmias, death
    • Assess patients vitals (decreased BP from bleeding), peripheral pulses (perfusion; clot in artery that breaks off would result in decreased peripheral pulses), puncture site (bleeding or development of hematoma)
  41. Cardiac catheterization nursing considerations
    • Informed Consent
    • NPO 6-12 hours prior
    • Assess Allergy History
    • Post-procedure must keep leg straight for 6 hours (can dislodge a clot and can start to bleed)
    • Monitor V/S, peripheral pulses, puncture site
  42. Electrophysiology Study (EPS)
    • Invasive study to diagnose, induce and treat arrhythmias
    • Catheter inserted to right side of heart via femoral vein
    • Electrodes detect site of arrhythmia
    • Can ablate aberrant conduction pathways
    • Requires informed consent, NPO 6-8 hours prior
    • Can put patient into ventricular tachycardia to assess and try to locate site of arrhythmia
  43. Cardiovascular effects of aging
    • High rates of atherosclerosis (increases with age, even though not normal sign of aging)
    • Increased incidence of hypertension
    • Increased rates of valvular calcification
    • Decreased HR response to exercise
    • Decreased baroreceptor function (at risk for orthostatic hypotension)
  44. Modifiable cardiovascular risk factors
    • Hypertension
    • Hyperlipidemia
    • Diabetes
    • Smoking
    • Excessive ETOH
    • Obesity
    • Sedentary Lifestyle
  45. Non-modifiable cardiovascular risk factors
    • Family History
    • Age
    • Race
    • Sex
  46. Cardiovascular assessment
    • Past medical history (heart disease, MI, angina, cardiac testing, arrhythmias, valve disease, rheumatic fever, DM, HTN, Meds)
    • Past surgical history (PTCA, CABG, valve replacement)
    • Family history
    • Social history (smoking, alcohol, drug use, diet, exercise)
    • Review of systems (fatigue, chest pain, syncope, dyspnea, palpitations, claudication, edema, orthopnea)
    • Paroxysmal nocturnal dyspnea (when laying supine all fluid from extremities goes back up to heart; will back up into lungs if heart is not functioning properly)
  47. Cardiovascular physical exam
    • Vital Signs (BP, pulse, resp, O2 sat)
    • Neck (JVD, carotids palpation and auscultation for bruits)
    • Precordium (PMI, heaves, lifts, thrills)
    • Auscultation of heart (S1, S2, rate, rhythm, murmurs, rubs, gallops)
    • Abdominal vessels (Abdominal aortic aneurysm or bruit)
    • Assessment of periphery (peripheral pulses, capillary refill, color, temperature, edema)
Card Set
Cardiovascular system.txt
CV System Med-Surg I Quiz 3