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Anatomy and Physiology for the Heart!

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Anatomy and Physiology for the Heart! Powered By Docstoc
					Cardiac Anatomy and Physiology


Geraldine Innes
Development Co-ordinator for Phase III in the Community
Have a Heart Paisley
                            Please Note:


The information contained in this presentation is accurate as of production
   in May 2006. Subsequent changes to clinical or other guidelines since
    this date should be incorporated into any adaptation of this material.
                   Topics
•   Cardio-Respiratory Fitness
•   Disease Process
•   Cardiac Physiology
•   Pharmalogical Therapy
      Cardiorespiratory Fitness
• VO2 Max (Maximum amount of oxygen used, litres consumed per minute)
    = Heart Rate x Stroke Volume x a-Vo2 diff
•    Oxygen Uptake: Normal Resting 3.5ml 02/kg/min = 1 Met
•    Healthy Un-conditioned maximum = 10 METS (Metabolic
     Equivalents)
•    WHAT IS THIS INFLEUNCED BY?
      – Age, Gender, Exercise Training, De-training, Medication, Illness,
        Different Environments
•    Effects of Training
      – Can increase 10-30% with the greatest improvements occurring in
        the most de-conditioned.
CARDIAC PERFORMANCE
           Maximum Oxygen Consumption
                With Coronary Heart Disease


• People with CHD have below average age and
  gender predicted Cardiorespiratory fitness levels
• In Coronary Heart Disease peak VO2 is reduced
  due to reduced cardiac output
• Benefits of exercise training?
   – Improved stamina
   – An ability of tolerate routine - Active Daily
     Living
   – Less fatigue
   – Decrease in angina symptoms
  Myocardial Blood Flow and Metabolism

• Normal contraction requires adequate supply of
  Adenosine Tri Phosphate(ATP) in aerobic
  oxidation
• Myocardium extracts nearly all available oxygen
  from the capillary blood flow (unlike skeletal
  muscle)
• Blood flow is determined by Blood Pressure and
  Vascular Resistance
• A significant decrease in flow can be caused by
  Arteriosclerosis
          Disease Process

•   Arteriosclerosis
•   Endothelial injury and Dysfunction
•   Artery Occlusion – Plaques
•   Progression of Plaques
Arteriosclerosis
Disease Progression
            Injury to the Artery
• Tobacco smoke and other chemical irritants from tobacco
• Low Density Lipoprotein (LDL)
• Hypertension
• Glycated substances resulting from hyperglycaemia and
  Diabetes Mellitus
• Infectious agents (Herpes, Chlamydia)
             Ischaemia
• What is it?
  – When myocardial blood flow is inadequate to provide the
    required amount of oxygen for ATP regeneration


• Ischaemic Cascade
  –   Diastolic Dysfunction
  –   Systolic Dysfunction
  –   Electrocardiogram (ECG) Abnormalities
  –   Symptoms of Angina
        Cardiac Physiology
– Heart Rate
– Stroke Volume
– Cardiac output
– Rate Pressure Product
– Blood pressure = Cardiac Output (CO) x Total
  Peripheral Resistance (TPR)
– Arteriovenous Oxygen (a-v02) Difference
                       Heart Rate
• Normal acute heart rate response to
  exercise
• Abnormal Response
• Chronotropic Incompetence
   – Failure of the heart rate to achieve
     predicted maximum in absence of a beta
     blocker
• Chronic Exercise heart rate response
   – Heart Rate at rest and at any given
     submax workload is less.
                  Stroke Volume
• Stroke Volume is a function of:
   – Preload, Afterload and Myocardial Contractility
• Normal resting 60-100ml/beat, Maximum 100-200ml/ beat
• Ejection Fraction is 57-73%
• Acute Response to Exercise
   – Increases curvilinear up to 50% of maximum aerobic
     capacity
• Chronic Response to Exercise
   – Increased Force of Contraction (FOC) and increased Ejection
     Fraction (EF)
   – Increased Central blood volume which increases End Diastolic
     Volume (EDV)and Stroke Volume (SV)
Cardiac Output (CO)
    • = Heart Rate x Stroke Volume
    • Normal 5 litres per minute
    • Acute Exercise
        – approx max 20 litres . Linear increase from
          both HR and SV up to 50% of oxygen
          capacity
    • In untrained individual heart rate plays
      a bigger role than stroke volume
    • Chronic Exercise: CO remains
      unchanged
    • In CHD clients CO may be reduced
      due to chronotropic incompetence or
      Left Ventricular Dysfunction.
          Rate Pressure Product
• RPP= Systolic Blood Pressure x Heart Rate

• Normal Resting 5400-14000

• Normal Exercise Response >25000

• Chronic Exercise adaptations
   – Reduced myocardial workload due to decrease in Heart Rate and
     Blood Pressure and any given submax workload
                      Blood Pressure
•   BP= CO x TPR
     – Normal >140/90. Max <220/115
•   Acute Exercise
     – Systolic Linear increase with Cardiac
       Output. Diastolic remains the same
     – 10mm Hg / MET
•   Abnormal Response
     – A drop in systolic BP or failure to increase
       with increasing workloads
     – Client with significant CHD may exhibit
       exercise hypotension
•   Chronic Training response
     – Reduction of BP at rest and during exercise
           AVo2 Difference
• Greater exchange of gases
• Increased mitochondria
     • More ATP
• Improved blood flow
         Pharmacological Therapy
– Beta Blockers                      – Nitrates
   • Used for angina, hypertension      • Vasodilate the Coronary
     and arrhythmia                       Arteries which increases flow to
                                          heart muscle
   • Blocks the action of
     norepinephrine                     • Reduces preload and afterload
   • Reduces Heart Rate and Blood       • Possibility of Postural
     pressure                             Hypotension
   • Slows metabolism                   • Increase in exercise tolerance by
                                          preventing angina and
   • Risk of Postural Hypotension
                                          increasing the ischaemic
                                          threshold
                     DRUGS
– Ace Inhibitors                     – Statins
– Used for hypertension, heart       – Inhibits an enzyme that
  failure and post Myocardial          catalyses a step in the
  Infarction (MI)                      synthesis of cholesterol in
– Stops angiotension I converting      the liver
  to angiotension II which lowers
                                     – Reduces LDL, Triglycerides
  blood pressure and reduces fluid
                                       and increases High Density
  retention
                                       Lipoprotein (HDL)
– Reduces afterload enabling the
                                     – No effect on exercise but
  Left Ventricular to pump more
                                       side effect is muscle pains
  easily
– Possible increase in exercise
  capacity for Heart Failure
  patients
                            Drugs
• Anti-Platelet                   • Anti-Arrhythmic
• Aspirin/Clopidogrel             •   Digoxin and Amiodarone
   – Works by decreasing              – Controls heart rate and enhances
                                        contractility
     platelet aggregation
                                      – Lengthens the refractory period,
   – Used for Secondary                 prolonging the period of re-excitation
     Prevention of                      and therefore suppressing arrhythmia’s
     Cardiovascular and               – Possible slower heart-rate response to
     Cerebrovascular thrombosis         exercise
   – Possible risk of bleeding,       – Reduced exercise capacity due to
     safe advise when using             depressant effect on the myocardium
     Gym Equipment
          Selected References
• Clinical Exercise Physiology: Ehrman et al
  (2003)
• Exercise Physiology: McArdle, Katch and Katch
  (1996) Fourth Edition
• American College of Sports Medicine (ACSM)
  Guidelines for Exercise Testing and prescription.
  Seventh Edition 2006

				
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