Cardio Function 2015

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  • Cardiac muscle contractions last roughly 10 X’s longer than those of skeletal muscle fibers
  • K is principal intracellular ion
  • The Frank–Starling law of the heart (also known as Starling's law or the Frank–Starling mechanism or Maestrini heart's law ) states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume ) when all other factors remain constant. The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully (the so-called Frank-Starling mechanisms). The stroke volume may also increase as a result of greater contractility of the cardiac muscle during exercise, independent of the end-diastolic volume. The Frank-Starling mechanism appears to make its greatest contribution to increasing stroke volume at lower work rates, and contractility has its greatest influence at higher work rates.
  • B
  • B- 4 or 5 ICS
  • A, C, E
  • Cardio Function 2015

    1. 1. ASSESSMENT OF CARDIOVASCULAR FUNCTION Nelia B Perez RN, MS PCU - MJCN nhelzki-2014 ncm-103
    2. 2. LECTURE OBJECTIVES 1. Review anatomy & physiology of the cardiovascular system. 2. Discuss relevant aspects of the patient history. 3. Describe physical assessment of cardiovascular status. 4. Review diagnostic procedures, tests and medications relative to the cardiovascular system. nhelzki-2014 ncm-103
    3. 3. Anatomy & Physiology Functions of the heart & CV system • Pumps blood to tissues to supply O2 & nutrients • Remove CO2 & metabolic wastes (What makes it “tick”!) nhelzki-2014 ncm-103
    4. 4. CARDIAC CELLS HAVE UNIQUE PROPERTIES • AUTOMATICITY  CELLS CONTRACT INDEPENDENTLY (THEY INITIATE THEIR OWN IMPULSE) • EXCITABILITY  ION SHIFT • CONDUCTIVITY  TRANSMIT IMPULSE TO ANOTHER CARDIAC CELL • CONTRACTILITY  HOW WELL THE CELL CONTRACTS Anatomy & Physiology nhelzki-2014 ncm-103
    5. 5. PERICARDIUM / PERICARDIAL SAC • Protects heart from trauma • Serous fluid lubricates and prevents friction • Prevents heart from over filling Anatomy & Physiology nhelzki-2014 ncm-103
    6. 6. CORONARY ARTERIES Right & Left arteries encircle the heart and supply blood to the myocardium during ventricular relaxation( diastole) LEFT MAIN CORONARY ARTERY L ANTERIOR DESCENDING (LAD) L CIRCUMFLEX (LCX) RIGHT CORONARY ARTERY POSTERIOR MARGINAL nhelzki-2014 ncm-103
    7. 7. CORONARY ARTERIES (R) ARTERY (L) ARTERY LAD CIRCUMFLEX nhelzki-2014 ncm-103
    8. 8. CONTRACTION OF CARDIAC MUSCLE The heart can’t pump unless an electrical stimulus occurs Action Potential (AP) – electrical change (depolarization = contraction) Brought about by release of calcium (+ charge) into cells- mechanical change Intrinsic Pacemakers – depolarize and generate the AP nhelzki-2014 ncm-103
    9. 9. CONTRACTION OF CARDIAC MUSCLE The pacemaker with the fastest rate of depolarization stimulates the AP • SA node (60-100 bpm)- Upper R atrium- capable of initiating electrical impulse • AV node (40-60 bpm)- Lower R atrium • Other pacemakers ( 40 bpm) -what can affect SA/AV node function ? nhelzki-2014 ncm-103
    10. 10. 1. Cardiac Innervation: ■ Sympathetic NS → ↑ excitability. ■ Parasympathetic NS (vagus) → ↓ excitability. 2. Effect of ions concentration in ECF: ■ ↑ Ca2+ → ↑ excitability. ■ ↑ K+ → ↓ excitability. 3. Physical factors: ■ ↑ temperature → ↑ excitability. ■ ↓ temperature → ↓ excitability. Factors affecting myocardial excitability
    11. 11. 4. Blood flow: ■ Insufficient bl flow to cardiac ms ↓ excitability & myocardial metabolism for 3 reasons: (1) lack of O2, (2) excess accumulation of CO2, & (3) lack of sufficient food nutrients. 5. Chemical factors (drugs): ■ Digitalis → ↑ excitability. Factors affecting myocardial excitability (continued)
    12. 12. 1. Cardiac innervation. 2. Effect of ions concentration in ECF. 3. Physical factors. 4. Blood flow. 5. Chemical factors (drugs). Factors affecting myocardial conductivity:
    13. 13. 1. Cardiac Innervation: ■ Sympathetic NS → ↑ conductivity. ■ Parasympathetic NS (vagus) → ↓ conductivity. 2. Effect of ions concentration in ECF: ■ ↑ Ca2+ → ↑ conductivity. ■ ↑ K+ → ↓ conductivity. 3. Physical factors: ■ ↑ temperature → ↑ conductivity. ■ ↓ temperature → ↓ conductivity. Factors affecting myocardial conductivity (continued)
    14. 14. 4. Blood flow: ■ Insufficient bl flow to cardiac ms ↓ conductivity & myocardial metabolism for 3 reasons: (1) lack of O2, (2) excess accumulation of CO2, & (3) lack of sufficient food nutrients. 5. Chemical factors (drugs): ■ Digitalis → ↑ conductivity. Factors affecting myocardial conductivity (continued)
    15. 15. 1. Cardiac innervation. 2. Oxygen supply. 3. Calcium & potassium ions concentration in ECF. 4. Physical factors. 5. Hormonal & chemical factors (drugs). 6. Mechanical factors. Factors affecting myocardial contractility: (Inotropic effectors)
    16. 16. 1. Cardiac Innervation: ■ Sympathetic NS → ↑ force of contraction. ■ Parasympathetic NS (vagus) → ↓ atrial force of contraction w no significant effect on ventricular ms. Factors affecting myocardial contractility (continued)
    17. 17. 2. Oxygen supply: ■ Hypoxia → ↓ contractility. 3. Calcium & potassium ions concentration in ECF: ■ ↑ Ca2+ → ↑ contractility. ■ ↑ K+ → ↓ contractility. 4. Physical factors: ■ Warming → ↑ contractility. ■ Cooling → ↓ contractility. Factors affecting myocardial contractility (continued)
    18. 18. 5. Hormonal & chemical factors (drugs): ■ +ve inotropics: (Adrenaline, noradrenaline, alkalosis, digitalis, Ca2+ , caffeine,…) ■ -ve inotropics: (Acetylcholine, acidosis, ether, chloroform, some bacterial toxins (e.g. diphtheria toxins), K+ , …) Factors affecting myocardial contractility (continued)
    19. 19. 6. Mechanical factors: a. Cardiac ms. obeys ‘all or none law’: i.e. minimal or threshold stimuli lead to maximal cardiac contraction, because cardiac ms. behaves as a syncytium. Factors affecting myocardial contractility (continued)
    20. 20. b. Cardiac ms. can’t be stimulated while it is contracted, because its excitability during contraction is zero due to long ARP, so it can’t be tetanized. c. Cardiac ms. can perform both isometric & isotonic types of contractions. Factors affecting myocardial contractility (continued)
    21. 21. d. Starling’s law of the heart: ■ “Length-tension relationship” ‘Within limits, the greater the initial length of the fiber, the stronger will be the force of its contraction; However, overstretching the fiber as in heart failure its power of contractility decreases’ i.e. within limits, the power of contraction is directly proportional to the initial length of the ms. ■ Cardiac ms accommodates itself (up to certain limit) to the changes in venous return. Factors affecting myocardial contractility (continued)
    22. 22. e. Cardiac ms shows staircase phenomenon (gradation), if providing all other conditions kept constant. i.e. if an isolated heart is stimulated by successive equal & effective stimuli, the 1st few contractions show a gradual ↑ in the magnitude of contraction. Factors affecting myocardial contractility (continued)
    23. 23. 1. Cardiac innervation. 2. Effect of ions concentration in ECF. 3. Physical factors. 4. Chemical factors (drugs). Factors affecting myocardial rhythmicity (chronotropic effectors):
    24. 24. a. Sympathetic stimuli: → Tachycardia, by ↑ spontaneous depolarization of SA- node. How? ■ ↓ SA- node membrane permeability to K+ → less K+ efflux. ■ ↑ membrane permeability to Ca2+ → more Ca2+ influx. ■ As a result, the slope of depolarization ↑, causing ↑ rate of SA- node firing & ↑ HR. Factors affecting myocardial rhythmicity: 1. Cardiac Innervation:
    25. 25. b. Parasympathetic stimuli (vagus): → Bradycardia, by ↓ spontaneous depolarization of SA- node. How? ■ ↑ SA- node membrane permeability to K+ → more K+ efflux. ■ ↓ membrane permeability to Ca2+ → less Ca2+ influx. ■ As a result, the prepotential slope ↓, causing ↓ rate of SA- node firing & ↓ HR. Factors affecting myocardial rhythmicity: 1. Cardiac Innervation (continued)
    26. 26. a. Warming: → ↑ rhythmicity. b. Cooling: → ↓ rhythmicity. c. Exercise: → ↑ HR as a result of ↑ sympathetic n. stimulation & ↓ vagal inhibition to SA- node. d. Endurance-trained athletes: Resting bradycardia due to high vagal activity. Factors affecting myocardial rhythmicity: 3. Physical factors:
    27. 27. a. Thyroid hormones & catecholamines: → ↑ rhythmicity. b. Ach: → ↓ rhythmicity. c. Hypoxia: → ↓ rhythmicity. Factors affecting myocardial rhythmicity: 4. Chemical factors (drugs):
    28. 28. DISRUPTION IN SERUM ELECTROLYES CAN RESULT IN ALTERATION IN CARDIAC CYCLE • Potassium • Calcium • Sodium • Magnesium nhelzki-2014 ncm-103
    29. 29. MONITORING MOVEMENT OF THE CARDIAC ACTION POTENTIAL (AP) • EKG – monitors the movement of the AP, in other words, the electrical changes. • How are the mechanical changes ( cardiac output ) monitored ? nhelzki-2014 ncm-103
    30. 30. CARDIAC CYCLE CARDIAC CYCLE – all the activities occurring in the heart during one contraction, and subsequent period of relaxation. Graphically represented on an EKG (ECG). nhelzki-2014 ncm-103
    31. 31. CARDIAC CYCLE EKG – A 12 lead EKG is a graphic record of the electrical forces produced by the heart nhelzki-2014 ncm-103
    32. 32. CARDIAC CYCLE Polarized (resting) cell – represented on EKG as baseline or isoelectric line Depolarization – impulse over specialized cardiac cells (not neuromuscular impulse) Repolarized cell – returns to normal. Na moves out of cell, K moves in – requires ATP How will ischemic tissue change the cardiac cycle ? nhelzki-2014 ncm-103
    33. 33. ELECTRODE POSITIONS “LEADS” • Leads measure electrical activity between 2 points • Movement toward ⊕ electrode causes positive deflection • Movement away from ⊕ electrode causes negative deflection nhelzki-2014 ncm-103
    34. 34. ELECTRODE POSITIONS A 12 Lead EKG shows electrical activity from 12 different positions in the heart, concentrating on (L) ventricle A 14 Lead EKG includes (R) ventricle activity nhelzki-2014 ncm-103
    35. 35. Cardiac output • SV- • CO- • Preload- • Afterload- • Ejection fraction • GOAL is to maintain adequate MAP so perfusion of oxygenated blood to vital organs occurs nhelzki-2014 ncm-103
    36. 36. Regulation of cardiac function & BP • Autonomic nervous system • Sympathetic norepinephrine • Parasympathetic – acetylcholine • Stimulation of adrenals by SNS – norepinephrine • Peripheral baro receptors • Stretch receptors • chemorecptors • hormones nhelzki-2014 ncm-103
    37. 37. STROKE VOLUME (SV) & CARDIAC OUTPUT (CO) • SV – amount of blood ejected by 1 ventricle in 1 beat • CO – volume ejected in 1 min Control of SV and HR = SV&HR are continually adjusted by the body, and are affected by the return of blood from the tissues (think of exercise) CO = SVxHR nhelzki-2014 ncm-103
    38. 38. STROKE VOLUME (SV) & CARDIAC OUTPUT (CO) Extrinsic control of HR is a more powerful way of controlling CO than changing SV 11  CVP causes stretching of (R) atrial muscle which stimulates SNS &  HR (to help pump all the blood returned to it) Remember “Starling’s Law” nhelzki-2014 ncm-103
    39. 39. STROKE VOLUME (SV) & CARDIAC OUTPUT (CO) 2. Stretch baroreceptors (aorta & carotid) detect in pressure which stimulates SNS & HR  (to ensure adequate blood supply to heart/ brain) 3. If  pressure detected, then PSNS is stimulated & HR is slowed (vagus nerve) (prevents excess arterial pressure which can damage organs) nhelzki-2014 ncm-103
    40. 40. CARDIAC LOAD Preload = degree of myocardial fiber stretch at the end of diastole and just before contraction Afterload = pressure against which ventricles must eject blood. This pressure is affected by systemic vascular resistance (SVR) nhelzki-2014 ncm-103
    41. 41. nhelzki-2014 ncm-103
    42. 42. Blood Pressure •Reflects the driving pressures produced by the ventricles •Because arterial pressure is pulsatile, a single value is used to represent the overall driving pressure. This is called the mean arterial pressure. MAP = diastolic P + 1/3(systolic P-diastolic P) Why does diastolic pressure account for a greater proportion of the overall value? SVR = systemic vascular resistance CO = cardiac output SV = stroke volume MAP = Q x Rarterioles Explain how these two equations are equivalent
    43. 43. What factors influence blood pressure? •Blood volume •Vascular resistance •Autoregulation •Autonomic influences
    44. 44. Regulation of Blood Pressure • Main coordinating center is in the medulla oblongata of the brain; medullary cardiovascular control center • Reflex control of blood pressure •Baroreceptor reflex
    45. 45. Age related changes • Decreased myocardial contractility • Thickening of endocardium & valves • Coronary arteries rigid & thickened • Decreased elasticity of vessel walls • Decreased internal diameter of vessels nhelzki-2014 ncm-103
    46. 46. CARDIAC ASSESSMENT Cardiac status of all patients should be routinely assessed. Everyone has a 1. Objective 2. Subjective CP Dyspnea Fatigue What else ? nhelzki-2014 ncm-103
    47. 47. IMMEDIATE NURSING INTERVENTIONS FOR ACUTE CARDIAC EVENT MOVIE Acronym M- Monitor for pain O- O2 and pulse ox V- Vital signs I- Intravenous fluids E- EKG monitoring Anything else?? nhelzki-2014 ncm-103
    48. 48. Pain Assessment SLIDA or Precipitating/alleviating factors Quality Radiation Severity Timing nhelzki-2014 ncm-103
    49. 49. OTHER ELEMENTS OF CARDIAC ASSESSMENT • Previous cardiac hx • Other medical conditions that may affect heart function • Chest injury • Previous heart surgery • Past medical hx • Medications: prescribed, OTC, herbals • Activity tolerance • Health habits • Family hx nhelzki-2014 ncm-103
    50. 50. EXAMINATION • Inspection • Palpation • Percussion-? • Auscultation = S1, S2 at PMI Aortic Pulmonic Tricuspid Mitral nhelzki-2014 ncm-103
    51. 51. Heart Rhythm Regular, Irregular, Regular Irregular Abnormal Sounds: Gallops Murmurs Bruits S3 ventricular gallop – heard in early diastole S4 atrial gallop – generally abnormal nhelzki-2014 ncm-103
    52. 52. Assessment of Murmurs Turbulent blood flow in valvular disorders and septal defects Timing of murmurs is a must! Systolic murmurs occur between S1 & S2 Diastolic murmurs occur between S2 & S1 Grade 1 – 6 identifies intensity of murmur nhelzki-2014 ncm-103
    53. 53. nhelzki-2014 ncm-103
    54. 54. Other assessments • Jugular vein pressure – assess JVD which reflects increased filling volume and pressure on (R) side of heart  JVD associated with (R) HF, SVC obstruction (Normal is 3- 10cm H20) • Pulse deficit – the difference between apical HR and peripheral pulse-associated with Afib, and heart blocks • Pulse pressure – the difference between systolic & diastolic pressurenhelzki-2014 ncm-103
    55. 55. Other assessments • Respiratory: Lung sounds = rate, rhythm, quality, sputum • GI-Abdomen • Peripheral Vascular:Lower extremities nhelzki-2014 ncm-103
    56. 56. Diagnostic Procedures 1. EKG 12 Lead continuous cardiac monitoring holter monitor 2. Chest x-ray – detects enlargement of heart & pulmonary congestion nhelzki-2014 ncm-103
    57. 57. Diagnostic procedures 3. Echocardiography – ultrasound that reveals size, shape and motion of cardiac structures Evaluates heart wall thickness, valve structure, differentiates murmurs 4. TEE – transesophageal echocardiography provides a clearer image because less tissue for sound waves to pass through nhelzki-2014 ncm-103
    58. 58. Diagnostic procedures 5. Angiography / cardiac catherization determines coronary lesion size, location, evaluate (L) ventricular function, measures heart pressures 6. Exercise tolerance test 7. Radionuclide Imaging nhelzki-2014 ncm-103
    59. 59. 1. Cardiac enzymes = enzymes are released when cells are damaged (MI). Enzymes are found in many tissues/muscles, and some are specific to cardiac tissue. Serial measurement can aid in dx, and monitor course of MI Cardiac enzymes = CPK – MB (CK-MB),myoglobin, Troponin In general, the greater the rise in the serum level of an enzyme, the greater the degree or extent of damage to the muscle. LDH Lab Studies nhelzki-2014 ncm-103
    60. 60. LAB studies CONT 2. Electrolytes 3. Lipid panel 4. CBC 5. C – Reactive Protein 6. BNP- Human B- Natriuretic Peptide 7. Blood coags-PT/PTT/INR nhelzki-2014 ncm-103
    61. 61. REVALIDATION TIME Mary is attending a sophomore level nursing class on anatomy and physiology. Which statement, if made by Mary, demonstrates a good understanding of the anatomy and physiology of the heart? A."The heart is encapsulated by a protective coating called the endocardium.“ B."The SA node is considered the main regulator of heart rate.“ C."The left atrium receives deoxygenated venous blood from all peripheral tissues.“ D."Stroke volume is the amount of blood ejected by the right ventricle during each diastole nhelzki-2014 ncm-103
    62. 62. Kirsten is completing her graduate clinical rotation in a large urban teaching hospital in a medical coronary care unit (CCU). Which observation demonstrates a good understanding of completing a thorough cardiac examination? • A. In an obese client, an adult cuff size of 12 to 14 cm is preferable. • B.The carotid artery on the neck is auscultated to assess for the presence of a bruit. • C.The apical impulse is auscultated over the fifth intercostal space in the midclavicular line. • D.Palpation is used to determine cardiac size. nhelzki-2014 ncm-103
    63. 63. Edward is a 40-year-old white male. He is an accountant who works on average 11 hours per day. He reports feeling stressed each day, even with mundane things such as a traffic jam. His father had a massive myocardial infarction at the age of 48. His mother has a history of congestive heart failure. He seldom has time to exercise, but does eat balanced meals when possible, although he does not get to eat three meals a day. Select all factors that place Edward at risk for heart disease. • A.Family history • B.Age • C.Coping-stress tolerance • D.Race • E.Occupation nhelzki-2014 ncm-103
    64. 64. Ready for more?

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