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Heart Heart Presentation Transcript

  • 18 The Cardiovascular System: The Heart P A R T A
  • 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
  • Heart Anatomy Figure 18.1
  • Coverings of the Heart: Physiology
    • The pericardium:
      • Protects and anchors the heart
      • Prevents overfilling of the heart with blood
      • Allows for the heart to work in a relatively friction-free environment
  • Pericardial Layers of the Heart Figure 18.2
  • Cardiac Muscle Bundles Figure 18.3
  • External Heart: Vessels that Supply/Drain the Heart (Posterior View)
    • 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
  • Figure 18.4e (e) Superior vena cava Right pulmonary artery Pulmonary trunk Right atrium Right pulmonary veins Fossa ovalis Pectinate muscles Tricuspid valve Right ventricle Chordae tendineae Trabeculae carneae Inferior vena cava Aorta Left pulmonary artery Left atrium Left pulmonary veins Pulmonary valve Aortic valve Mitral (bicuspid) valve Left ventricle Papillary muscle Interventricular septum Myocardium Visceral pericardium Endocardium
  • Right and Left Ventricles Figure 18.6
  • Figure 18.5
  • 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
  • Coronary Circulation: Arterial Supply Figure 18.7a
  • Coronary Circulation: Venous Supply Figure 18.7b
  • Heart Valves Figure 18.8a, b
  • Heart Valves Figure 18.8c, d
  • Atrioventricular Valve Function Figure 18.9
  • Semilunar Valve Function Figure 18.10
  • Microscopic Anatomy of Heart Muscle
    • Cardiac muscle is striated, short, fat, branched, and interconnected
    • 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
    InterActive Physiology ®: Anatomy Review: The Heart, pages 3–7
  • Microscopic Anatomy of Cardiac Muscle Figure 18.11
  • 18 The Cardiovascular System: The Heart P A R T B
  • 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
  • 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
  • Pacemaker and Action Potentials of the Heart Figure 18.13
  • Cardiac Membrane Potential Figure 18.12
  • Cardiac Intrinsic Conduction Figure 18.14a
  • 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)
  • 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
  • Cardiac Intrinsic Conduction Figure 18.14a
  • Cardiac Membrane Potential Figure 18.12
  • Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins Impulse delayed at AV node Impulse passes to heart apex; ventricular excitation begins Ventricular excitation complete SA node AV node Purkinje fibers Bundle branches Figure 18.17
  • Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins SA node Figure 18.17
  • Heart Excitation Related to ECG Impulse delayed at AV node AV node Figure 18.17
  • Heart Excitation Related to ECG Impulse passes to heart apex; ventricular excitation begins Bundle branches Figure 18.17
  • Heart Excitation Related to ECG Ventricular excitation complete Purkinje fibers Figure 18.17
  • Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins Impulse delayed at AV node Impulse passes to heart apex; ventricular excitation begins Ventricular excitation complete SA node AV node Purkinje fibers Bundle branches Figure 18.17
  • Electrocardiography Figure 18.16
  • Electrocardiography
    • Electrical activity is recorded by electrocardiogram (ECG)
    • P wave corresponds to depolarization of SA node
    • 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 ®: Intrinsic Conduction System, pages 3–6
    • Abnormal heart sounds produced by abnormal patterns of blood flow in the heart.
    • Defective heart valves:
      • Valves become damaged by antibodies made in response to an infection, or congenital defects.
    • Mitral stenosis:
      • Mitral valve becomes thickened and calcified.
        • Impairs blood flow from left atrium to left ventricle.
        • Accumulation of blood in left ventricle may cause pulmonary HTN.
    • Incompetent valves:
      • Damage to papillary muscles.
        • Valves do not close properly.
          • Murmurs produced as blood regurgitates through valve flaps.
    Heart Murmurs
  • Heart Murmurs
    • Septal defects:
      • Usually congenital.
        • Holes in septum between the left and right sides of the heart.
        • May occur either in interatrial or interventricular septum.
      • Blood passes from left to right.
  • Electrocardiogram (ECG/EKG)
    • The body is a good conductor of electricity.
      • Tissue fluids have a high [ions] that move in response to potential differences.
    • Electrocardiogram:
      • Measure of the electrical activity of the heart per unit time.
        • Potential differences generated by heart are conducted to body surface where they can be recorded on electrodes on the skin.
    • Does NOT measure the flow of blood through the heart.
  • Ischemic Heart Disease
    • Ischemia:
      • Oxygen supply to tissue is deficient.
        • Most common cause is atherosclerosis of coronary arteries.
      • Increased [lactic acid] produced by anaerobic respiration.
    • Angina pectoris:
      • Substernal pain.
    • Myocardial infarction (MI):
      • Changes in T segment of ECG.
      • Increased CPK and LDH.
  • Arrhythmias Detected on ECG
    • Arrhythmias:
      • Abnormal heart rhythms.
    • Flutter:
      • Extremely rapid rates of excitation and contraction of atria or ventricles.
        • Atrial flutter degenerates into atrial fibrillation.
    • Fibrillation:
      • Contractions of different groups of myocardial cells at different times.
        • Coordination of pumping impossible.
          • Ventricular fibrillation is life-threatening.
  • Arrhythmias Detected on ECG (continued)
    • Bradycardia:
      • HR slower < 60 beats/min.
    • Tachycardia:
      • HR > 100 beats/min.
    • First–degree AV nodal block:
      • Rate of impulse conduction through AV node exceeds 0.2 sec.
        • P-R interval.
    • Second-degree AV nodal block:
      • AV node is damaged so that only 1 out of 2-4 atrial APs can pass to the ventricles.
        • P wave without QRS.
  • Arrhythmias Detected on ECG (continued)
    • Third-degree (complete) AV nodal block:
      • None of the atrial waves can pass through the AV node.
      • Ventricles paced by ectopic pacemaker.
  • ECG Tracings Figure 18.18
  • Extrinsic Innervation of the Heart
    • Heart is stimulated by the sympathetic cardioacceleratory center
    • Heart is inhibited by the parasympathetic cardioinhibitory center
    Figure 18.15
  • Heart Sounds Figure 18.19
  • Heart Sounds
    • Heart sounds (lub-dup) are associated with closing of heart valves
      • First sound occurs as AV valves close and signifies beginning of systole
      • Second sound occurs when SL valves close at the beginning of ventricular diastole
  • 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
  • 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
  • Phases of the Cardiac Cycle
    • Ventricular systole
      • Atria relax
      • Rising ventricular pressure results in closing of AV valves
      • Isovolumetric contraction phase
      • Ventricular ejection phase opens semilunar valves
  • 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
    PLAY InterActive Physiology ®: Cardiac Cycle, pages 3–18
  • Cardiac Cycle
    • Refers to the repeating pattern of contraction and relaxation of the heart.
      • Systole:
        • Phase of contraction.
      • Diastole:
        • Phase of relaxation.
      • End-diastolic volume (EDV):
        • Total volume of blood in the ventricles at the end of diastole.
      • Stroke volume (SV):
        • Amount of blood ejected from ventricles during systole.
      • End-systolic volume (ESV):
        • Amount of blood left in the ventricles at the end of systole.
  • Figure 18.20
  • Cardiac Cycle (continued)
    • Step 1: Isovolumetric contraction:
      • QRS just occurred.
      • Contraction of the ventricle causes ventricular pressure to rise above atrial pressure.
        • AV valves close.
      • Ventricular pressure is less than aortic pressure.
        • Semilunar valves are closed.
          • Volume of blood in ventricle is EDV.
    • Step 2: Ejection:
      • Contraction of the ventricle causes ventricular pressure to rise above aortic pressure.
        • Semilunar valves open.
      • Ventricular pressure is greater than atrial pressure.
        • AV valves are closed.
          • Volume of blood ejected: SV.
  • Cardiac Cycle (continued)
    • Step 3: T wave occurs:
      • Ventricular pressure drops below aortic pressure.
    • Step 4: Isovolumetric relaxation:
      • Back pressure causes semilunar valves to close.
        • AV valves are still closed.
          • Volume of blood in the ventricle: ESV.
    • Step 5: Rapid filling of ventricles:
      • Ventricular pressure decreases below atrial pressure.
        • AV valves open.
          • Rapid ventricular filling occurs.
  • Cardiac Cycle (continued)
    • Step 6: Atrial systole:
      • P wave occurs.
      • Atrial contraction.
        • Push 10-30% more blood into the ventricle.
  • Cardiac Cycle (continued)
  • Correlation of ECG with Heart Sounds
    • First heart sound:
      • Produced immediately after QRS wave.
      • Rise of intraventricular pressure causes AV valves to close.
    • Second heart sound:
      • Produced after T wave begins.
      • Fall in intraventricular pressure causes semilunar valves to close.
  • Figure 18.20
  • 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
    • Cardiac reserve is the difference between resting and maximal CO
  • Cardiac Output: Example
    • CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
    • CO = 5250 ml/min (5.25 L/min)
  • 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
  • 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
    • Volume of blood pumped/min. by each ventricle.
      • Pumping ability of the heart is a function of the beats/ min. and the volume of blood ejected per beat.
    • CO = SV x HR
      • Total blood volume averages about 5.5 liters.
    • Each ventricle pumps the equivalent of the total blood volume each min. (resting conditions).
    Cardiac Output (CO)
  • 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
  • Preload and Afterload Figure 18.21
  • 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
      • Ca 2+ and some drugs
  • Extrinsic Factors Influencing Stroke Volume
    • Agents/factors that decrease contractility include:
      • Acidosis
      • Increased extracellular K +
      • Calcium channel blockers
  • Heart Contractility and Norepinephrine GTP GDP Inactive protein kinase A Active protein kinase A ATP cAMP GTP SR Ca 2+ channel Ca 2+ Ca 2+ binds to Troponin Enhanced actin-myosin interaction Extracellular fluid Cytoplasm Adenylate cyclase Ca 2+ channel Ca 2+  1 -Adrenergic receptor Norepinephrine Ca 2+ uptake pump Sarcoplasmic reticulum (SR) Cardiac muscle force and velocity 1 3 2
    • Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
    Figure 18.22
  • Regulation of Heart Rate
    • Positive chronotropic factors increase heart rate
    • Negative chronotropic factors decrease heart rate
  • Circulatory Changes During Exercise (continued)
    • 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
    Regulation of Heart Rate: Autonomic Nervous System
  • 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
  • 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 ®: Cardiac Output, pages 3–9
  • Figure 18.23
  • Congestive Heart Failure (CHF)
    • Congestive heart failure (CHF) is caused by:
      • Coronary atherosclerosis
      • Persistent high blood pressure
      • Multiple myocardial infarcts
      • Dilated cardiomyopathy (DCM)
  • Baroreceptor Reflex (continued)
  • Renin-Angiotension-Aldosterone System (continued)
  • Regulation by ADH
    • Released by posterior pituitary when osmoreceptors detect an increase in plasma osmolality.
    • Dehydration or excess salt intake:
      • Produces sensation of thirst.
      • Stimulates H 2 0 reabsorption from urine.