Cardiovascular Disorders

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  • 1. Cardiovascular Disorders
    Chapter 10
  • 2. 18
    The Cardiovascular System: The Heart
    DR Jones
    Part A
  • 3. Heart Anatomy
    Approximately the size of your fist
    Location
    Superior surface of diaphragm
    Left of the midline
    Anterior to the vertebral column, posterior to the sternum
  • 4. Heart Anatomy
    Figure 18.1
  • 5. Coverings of the Heart: Anatomy
    Pericardium – a double-walled sac around the heart composed of:
    A superficial fibrous pericardium
    A deep two-layer serous pericardium
    The parietal layer lines the internal surface of the fibrous pericardium
    The visceral layer or epicardium lines the surface of the heart
    They are separated by the fluid-filled pericardial cavity
  • 6. Coverings of the Heart: Physiology
    The pericardium:
    Protects and anchors the heart
    Allows for the heart to work in a relatively friction-free environment
  • 7. Pericardial Layers of the Heart
    Figure 18.2
  • 8. Heart Wall
    Epicardium – visceral layer of the serous pericardium
    Myocardium – cardiac muscle layer forming the bulk of the heart
    Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue
    Endocardium – endothelial layer of the inner myocardial surface
  • 9. External Heart: Major Vessels of the Heart
    Vessels returning blood to the heart include:
    Superior and inferior venae cavae
    Right and left pulmonary veins
    Vessels conveying blood away from the heart include:
    Pulmonary trunk, which splits into right and left pulmonary arteries
    Ascending aorta (three branches) – brachiocephalic, left common carotid, and subclavian arteries
  • 10. Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries
    Veins – small cardiac, anterior cardiac, and great cardiac veins
    External Heart: Vessels that Supply/Drain the Heart
  • 11. External Heart: Anterior View
    Figure 18.4b
  • 12. External Heart: Major Vessels of the Heart
    Vessels returning blood to the heart include:
    Right and left pulmonary veins
    Superior and inferior venae cavae
    Vessels conveying blood away from the heart include:
    Aorta
    Right and left pulmonary arteries
  • 13. Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove)
    Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein
    External Heart: Vessels that Supply/Drain the Heart
  • 14. External Heart: Posterior View
    Figure 18.4d
  • 15. Gross Anatomy of Heart: Frontal Section
    Figure 18.4e
  • 16. Atria of the Heart
    Atria are the receiving chambers of the heart
    Each atrium has a protruding auricle
    Pectinate muscles mark atrial walls
    Blood enters right atria from superior and inferior venae cavae and coronary sinus
    Blood enters left atria from pulmonary veins
  • 17. Ventricles of the Heart
    Ventricles are the discharging chambers of the heart
    Papillary muscles and trabeculae carneae muscles mark ventricular walls
    Right ventricle pumps blood into the pulmonary trunk
    Left ventricle pumps blood into the aorta
  • 18. Pathway of Blood Through the Heart and Lungs
    Right atrium  tricuspid valve  right ventricle
    Right ventricle  pulmonary semilunar valve  pulmonary arteries  lungs
    Lungs  pulmonary veins  left atrium
    Left atrium  bicuspid valve  left ventricle
    Left ventricle  aortic semilunar valve  aorta
    Aorta  systemic circulation
  • 19. Heart Valves
    Figure 18.8a, b
  • 20. Heart Valves
    Figure 18.8c, d
  • 21. Atrioventricular Valve Function
    Figure 18.9
  • 22. Semilunar Valve Function
    Figure 18.10
  • 23. Heart Valves
    Heart valves ensure unidirectional blood flow through the heart
    Atrioventricular (AV) valves lie between the atria and the ventricles
    AV valves prevent backflow into the atria when ventricles contract
    Chordae tendineae anchor AV valves to papillary muscles
  • 24. Heart Valves
    Aortic semilunar valve lies between the left ventricle and the aorta
    Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk
    Semilunar valves prevent backflow of blood into the ventricles
  • 25. Coronary Circulation
    Coronary circulation is the functional blood supply to the heart muscle itself
    Collateral routes ensure blood delivery to heart even if major vessels are occluded
  • 26. Coronary Circulation: Arterial Supply
    Figure 18.7a
  • 27. Coronary Circulation: Venous Supply
    Figure 18.7b
  • 28.
  • 29. Microscopic Anatomy of Heart Muscle
    Cardiac muscle is striated, short, fat, branched, and interconnected TQ
    The connective tissue endomysium acts as both tendon and insertion
    Intercalated discs anchor cardiac cells together and allow free passage of ions
    Heart muscle behaves as a functional syncytium
    PLAY
    InterActive Physiology®: Cardiovascular System: Anatomy Review: The Heart
  • 30. Microscopic Anatomy of Heart Muscle
    Figure 18.11
  • 31. Cardiac Muscle Contraction
    Heart muscle:
    Is stimulated by nerves and is self-excitable (automaticity)
    Contracts as a unit
    Has a long (250 ms) absolute refractory period
    Cardiac muscle contraction is similar to skeletal muscle contraction
  • 32. Heart Physiology: Intrinsic Conduction System
    Autorhythmic cells:
    Initiate action potentials
    Have unstable resting potentials called pacemaker potentials
    Use calcium influx (rather than sodium) for rising phase of the action potential (prolonging contracture)
  • 33. Pacemaker and Action Potentials of the Heart
    Figure 18.13
  • 34. Calcium Channels….
    In cardiac myocytes L type Ca channels open when the plasma membrane is depolarized by an action potential carried along the muscle cells by the opening of voltage gated sodium channels. This action potenial is terminated and its duration determined by the opening of K channels. Ca influx triggers massive release of Ca from intracellularstores by opening the ryanodine sensitive Ca channels in the sarcoplasmic reticulum resulting in an intracellular Ca transient. Ca influx and released Ca directly initiate contraction. Contraction is terminated by the rapid uptake into the SR by SR Ca ATPases (SERCA)
  • 35. CA++ channel blockers
  • 36. Heart Physiology: Sequence of Excitation
    Figure 18.14a
  • 37. Heart Physiology: Sequence of Excitation
    Sinoatrial (SA) node generates impulses about 75 times/minute
    Atrioventricular (AV) node delays the impulse approximately 0.1 second
    Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)
  • 38. Heart Physiology: Sequence of Excitation
    AV bundle splits into two pathways in the interventricular septum (bundle branches)
    Bundle branches carry the impulse toward the apex of the heart
    Purkinje fibers carry the impulse to the heart apex and ventricular walls
  • 39. Heart Excitation Related to ECG
    Figure 18.17
  • 40. Extrinsic Innervation of the Heart
    Heart is stimulated by the sympathetic cardioacceleratory center
    Heart is inhibited by the parasympathetic cardioinhibitory center
    Figure 18.15
  • 41. Electrocardiography
    Electrical activity is recorded by electrocardiogram (ECG)
    P wave corresponds to Depolarization of the atria!!!!
    QRS complex corresponds to ventricular depolarization
    T wave corresponds to ventricular repolarization
    Atrial repolarization record is masked by the larger QRS complex
    PLAY
    InterActive Physiology®: Cardiovascular System: Intrinsic Conduction System
  • 42. Electrocardiography
    Figure 18.16
  • 43. Link for Dr Dubin’s book…..
    http://www.emergencyekg.com
  • 44.
  • 45.
  • 46.
  • 47.
  • 48. Cardiac Cycle
  • 49. Cardiac Cycle
  • 50. Cardiac Cycle
    Cardiac cycle refers to all events associated with blood flow through the heart
    Systole – contraction of heart muscle
    Diastole – relaxation of heart muscle
  • 51. Phases of the Cardiac Cycle
    Ventricular filling – mid-to-late diastole
    Heart blood pressure is low as blood enters atria and flows into ventricles
    AV valves are open, then atrial systole occurs
  • 52. Phases of the Cardiac Cycle
    Ventricular systole
    Atria relax
    Rising ventricular pressure results in closing of AV valves(1)
    Isovolumetric contraction phase(2)
    Ventricular ejection phase opens semilunar valves(3)
  • 53. Phases of the Cardiac Cycle
    Isovolumetric relaxation – early diastole
    Ventricles relax
    Backflow of blood in aorta and pulmonary trunk closes semilunar valves
    Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves
    InterActive Physiology®: Cardiovascular System: Cardiac Cycle
    PLAY
  • 54. Figure 18.20
  • 55. Cardiac Output (CO) and Reserve
    CO is the amount of blood pumped by each ventricle in one minute
    CO is the product of heart rate (HR) and stroke volume (SV)
    HR is the number of heart beats per minute
    SV is the amount of blood pumped out by a ventricle with each beat (or stroke)
    Cardiac reserve is the difference between resting and maximal CO
  • 56. Stroke Volume
  • 57. Regulation of Stroke Volume
    SV = end diastolic volume (EDV) minus end systolic volume (ESV)
    EDV = amount of blood collected in a ventricle during diastole
    ESV = amount of blood remaining in a ventricle after contraction
  • 58. Factors Affecting Stroke Volume
    Preload – amount ventricles are stretched by contained blood
    Contractility – cardiac cell contractile force due to factors other than EDV
    Afterload – back pressure exerted by blood in the large arteries leaving the heart
  • 59. Frank-Starling Law of the Heart
    Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
    Slow heartbeat and exercise increase venous return to the heart, increasing SV
    Blood loss and extremely rapid heartbeat decrease SV
  • 60. Preload and Afterload
    Figure 18.21
  • 61. Extrinsic Factors Influencing Stroke Volume
    Contractility is the increase in contractile strength, independent of stretch and EDV
    Increase in contractility comes from:
    Increased sympathetic stimuli
    Certain hormones
    Ca2+ and some drugs
  • 62. Extrinsic Factors Influencing Stroke Volume
    Agents/factors that decrease contractility include:
    Acidosis
    Increased extracellular K+
    Calcium channel blockers
  • 63. Contractility and Norepinephrine
    Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
    Figure 18.22
  • 64. Regulation of Heart Rate
    Positive chronotropic factors increase heart rate
    Negative chronotropic factors decrease heart rate
  • 65. Regulation of Heart Rate: Autonomic Nervous System
    Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise
    Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS
    PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
  • 66. Atrial (Bainbridge) Reflex
    Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria
    Causes stimulation of the SA node
    Stimulates baroreceptors in the atria, causing increased SNS stimulation
  • 67. Chemical Regulation of the Heart
    The hormones epinephrine and thyroxine increase heart rate
    Intra- and extracellular ion concentrations must be maintained for normal heart function
    InterActive Physiology®: Cardiovascular System: Cardiac Output
    PLAY
  • 68.
  • 69. Arrhythmias
    Bradycardia
    AV delays and blocks
    Tachyarrhythmias
    Fibrillation
    Flutter
  • 70. Congestive Failure
    Inadequate pump function
    “pump” failure
    R L both and how fast it develops
  • 71. Left Ventricular Failure
    Not pumping to the body…backs up in lungs
    Dyspnea,orthopnea,pnd, hemoptysis,occ chest pain, fatique
    HR up Resp rate Up
    Rales
    Etiology: Table 10-1
  • 72. Pathophysiology of Left Ventricular Failure
    Hemodynamic changes- systolic dyfunction with decreased stroke volume
    Diastolic dysfunction- dilitation of atrium and backup of pressure into lungs
    Neurohumoral changes Renin angiotensin as a result of percieved decreased cardiac output Elevated levels of norepinephrine Vasopressin release (adh) Cytokine release and Tumor Necrosis Factor and Endothelin
  • 73. Left Heart Pphys ,continued….
    Ca uptake is slowed by sarcoplasmic reticulum
    Alpha one receptors upregulate and increase in number
  • 74. Right Ventricular Failure
    SOB pedal edema and abdominal discomfort and pain
    Cause same as LV disfunction plus pulmonary hypertension or L-R shunt with increased pressure on the right ventricle
    Elevated Jugular pressure
  • 75. Signs and symptoms of Rt heart failure
    Anasarca- generalized edema
    Ascites – peritoneal accumulation of fluid
    Pedal edema
    Hepatojugular Reflux-pressure on the liver for 5 seconds gives increased volume to RA and backs up in Jugular vein in neck
    Abd pain- liver distentension
  • 76. Valvular Heart Disease
    Stenosis or Regurgitation
    Rare to be found on the right side
    We will concentrate on Left side valves
    Aortic and Mitral valves
    Murmur what is it
    When and what they sound like tells you what is going on………
  • 77. Aortic Stenosis
  • 78. Aortic Stenosis
    Congenital AS is usually asymptomatic until at least age 10 or 20 yr, when symptoms may begin to develop insidiously.
    exertional syncope, angina, and dyspnea
    Murmur
    IHSS
  • 79. Aortic Regurgitation
  • 80. Aortic Regurgitation
    Acute or Chronic
    Develops into L sided failure
    Acute: SOB, pulmonary edema, hypotension, develop quickly
    Increased volume load on the left ventricle eccentric hypertrophy
    Wide pulse pressures
  • 81. Mitral Stenosis
  • 82. Mitral Stenosis
    Mitral stenosis (MS), causes an obstruction in blood flow from the left atrium to left ventricle. There is therefore an increase in pressure within the left atrium, pulmonary vasculature, and right side of the heart, while the left ventricle is unaffected in pure MS
    major cause of MS is rheumatic fever
    Dyspnea , Fatigue and hemoptysis
  • 83. Mitral Stenosis
    increase in pulmonary venous, capillary and arterial pressures and resistance.
    With mild to moderate mitral stenosis, these abnormalities are often only apparent with exercise or other conditions that increase heart rate; they eventually are seen at rest as the severity of the stenosis increases
    In addition to exercise, the onset of atrial fibrillation can also lead to clinical decompensation.
  • 84. Mitral Regurgitation
    For many years, rheumatic fever was the predominant cause of mitral regurgitation. Now, the major etiologies are mitral valve prolapse and coronary disease
    exercise intolerance, dyspnea, or fatigue
    Compensated and uncompensated
    Pulmonary hypertension along with other changes in the ventricle
    ATRIAL ENLARGEMENT AND FIBRILLATION — Chronic MR is often complicated by the development of left atrial enlargement and atrial fibrillation (AF), both of which may have an impact on patient outcome
    Objective measures of LV size and function — The severity of MR can be assessed semiquantitatively by Doppler echocardiography or angiography
  • 85.
  • 86. Coronary Artery disease
  • 87.
  • 88.
  • 89. Coronary Artery Disease
    Chest Pain, SOB, Shock (cardiogenic), Bradycardia, Nausea and Vomiting, Tachycardia
    EKG CHANGES of Ischemia
    Enzyme changes…released from the myocardial damaged cells
  • 90. Pericardial Diseases
    The pain is usually sharp and stabbing.
    can arise slowly or suddenly and can radiate directly to the back, to the neck or to the arm.
    pain can radiate to the shoulder blade
    pain can be made worse with deep breaths (pleuritic).
    pain is frequently positional and made worse when lying flat and better when leaning forward.
  • 91. Pericarditis
    Friction Rub
    May also have pleural effusion
    Tamponade is to be avoided
    AOB
    Elevated Jugular pressure
    Hypotension
    Paradoxic Pulse and muffled heart sounds
  • 92. Figure 18.25
    Examples of Congenital Heart Defects
  • 93. Developmental Aspects of the Heart
    Fetal heart structures that bypass pulmonary circulation
    Foramen ovale connects the two atria
    Ductus arteriosus connects pulmonary trunk and the aorta