Cardiac Mechanics PDF

CARDIAC MECHANICS Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc. 1 ...

CARDIAC MECHANICS Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc. 1  2 Learning Objectives *Acquired from the Human Anatomy and Physiology Society (HAPS) with personal additions  Describe the cardiac cycle, systole and diastole.  Describe the phases of the cardiac cycle including ventricular filling, isovolumetric contraction, ventricular ejection and isovolumetric relaxation.  Relate the ECG waveforms to the normal mechanical events of the cardiac cycle.  Explain how atrial systole is related to ventricular filling.  Relate the opening and closing of specific heart valves in each phase of the cardiac cycle to pressure changes in the heart chambers.  Relate the heart sounds to the events of the cardiac cycle.  Define systolic and diastolic blood pressure and interpret a graph of aortic pressure versus time during the cardiac cycle.  Given the heart rate, calculate the length of one cardiac cycle.  3 Learning Objectives *Acquired from the Human Anatomy and Physiology Society (HAPS) with personal additions  With respect to cardiac output (CO):  Define cardiac output and state its units of measurement.  Calculate cardiac output, given stroke volume and heart rate.  Predict how changes in heart rate (HR) and/or stroke volume (SV) will affect cardiac output.  Discuss the concept of cardiac reserve.  With respect to stroke volume:  Define end diastolic volume (EDV) and end systolic volume (ESV) and calculate stroke volume (SV) given values for EDV & ESV.  Define venous return, preload and afterload and explain the factors that affect them as well as how each of the affects EDV, ESV and SV.  Explain the significance of the Frank-Starling Law of the heart  Discuss the influence of positive and negative ionotropic agents on SV.  With respect to HR:  Discuss the influence of positive and negative chronotropic agents on HR.  Explain the relationship between changes in HR and changes in filling time and EDV.  4 Quick Review Cardiac Anatomy Heart Sounds Systole vs Diastole Electrical vs Mechanical Intra-atrial vs Intra-ventricular pressure  R Depolarization SA node Repolarization P T 5 Q S 1 Atrial depolarization = P wave. R AV node P T QS 2 impulse is delayed @ AV node. Atrial systole R P T QS 3 Ventricular depolarization = the QRS complex. Atrial repolarization occurs. Begin ventricular systole Figure 18.17, step 3  Depolarization R Repolarization 6 P T QS 4 Ventricular depolarization done. Ventricular systole. 1ST sound R P T QS 5 Ventricular repolarization = T wave. R P T QS 6 Ventricular repolarization complete. 2nd sound Figure 18.17, step 6 7  8 Mechanical Events: The Cardiac Cycle  Remember, the heart is an efficient pump  Simply a series of pressure and therefore volume changes  Mechanical events always follow electrical events  Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat  Systole—contraction  Diastole—relaxation  9 Mechanical Events Ventricular Filling Ventricular Systole Isovolumetric Relaxation (Quiescent Period)  1 0 Phases of the Cardiac Cycle 1. Ventricular filling —takes place in mid-to-late diastole  AV valves are open, SL valves are closed  80% of blood passively flows into ventricles --------------------------------------------------------------------------  Transition into atrial systole which begins just after depolarization (P wave on ECG)  Atrial systole occurs, delivering the remaining 20% blood volume  Ventricles are currently at their end diastole (having received nearly 100% of the total blood volume they can hold, known as EDV)  Electrically, the wave sof depoalrization has spread from the atria into the ventricles (QRS wave on ECG)  End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole  1 1 Phases of the Cardiac Cycle 2. Ventricular systole  Atria are relaxed (diastole)  Ventricles begin to *mechanically* contract (wave of depolarization has just occurred in last phase), further raising the pressure inside the ventricle, closing the AV valves (*First heart sound*)  Isovolumetric contraction phase – for a split millisecond - (all valves are closed)…pressure is building…  Ventricles contract (full systole, end of the QRS wave)  By the ventricles contracting, pressure exceeds the pressure in the large arteries in direct association with the ventricles, forcing the SL valves open (ejection phase)  blood flows into the Pulmonary aa & Aorta  End systolic volume (ESV): volume of blood remaining in each ventricle after contraction …therefore causing ventricular relaxation…  1 2 Phases of the Cardiac Cycle 3. Isovolumetric relaxation occurs in early diastole (just following T wave on ECG)  Ventricles relax…less pressure (majority* of the blood just passed into the Pulmonary aa and Aorta)  Rapid drop in pressure in the ventricles, yet high pressure in the Pulmonary aa and Aorta (Backflow of blood in aorta and pulmonary trunk) closes SL valves  Closure of the SL valves leads to a rapid increase in the Pulmonary aa and aorta, causes blood to violently rebound off of the closed SL valves, causing dicrotic notch (brief rise in aortic pressure)  *This is second heart sound*  Left heart QRS P T P Electrocardiogram Heart sounds 1st 2nd 1 3 Dicrotic notch Ventricular Pressure (mm Hg) Aorta Atrial systole Left ventricle systole (contraction) Atrial systole Left atrium (contraction) EDV volume (ml) Ventricular SV ESV Atrioventricular valves Open Closed Open Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular Atrial Isovolumetric Ventricular Isovolumetric Ventricular filling contraction contraction phase ejection phase relaxation filling 1 2a 2b 3 Ventricular filling Ventricular systole Early diastole (mid-to-late diastole) (atria in diastole)  1 4 Review...  List the phases of the cardiac cycle.  Ventricular filling is associated with what other important events?  Explain the link between the electrical events of the cardiac cycle with the mechanical events.  1 5 USEFUL TERMS  EDV  volume of blood in each ventricle at the end of ventricular diastole  ESV  volume of blood remaining in each ventricle after contraction  SV  volume of blood pumped out by the ventricle with each beat  CO  amount of blood pumped out by each ventricle in 1 minute CO = HR X SV SV = EDV - ESV  1 6 Cardiac Output (CO) Volume of blood pumped by each ventricle in one minute CO = heart rate (HR) x stroke volume (SV) HR = number of beats per minute SV = volume of blood pumped out by one ventricle with each beat  1 7 Regulation of Stroke Volume  SV = EDV – ESV == volume ventricle pumps to body is the total it fills with minus the amount left in heart after it contracts Avg= 70 ml/beat which is around 60% of blood in chambers Three main factors affect SV Preload Contractility Afterload  1 8 Regulation of Stroke Volume Preload: degree of stretch of cardiac muscle cells before they contract length-tension relationship (like in skeletal mm) Blood filling compartments stretches cells INCREASE PRELOAD  INCREASE SV Slow heartbeat and exercise increase venous return…increase EDV, SV and force of contraction Frank-Starling law of heart  Increased blood return stretches ventricles and increases contraction force so more is propelled out.  1 9 Regulation of Stroke Volume According to Starling’s law, the more stretch placed on the cardiac muscle, the greater the stroke volume VENOUS RETURN is the most important factor present that stretches ventricular walls Therefore, anything that increases venous return (volume or speed), increases EDV and therefore SV, contraction and force (& vice versa)  2 0 Regulation of Stroke Volume  Preload (cont.)  Most important factor in preload stretching of cardiac muscle is venous return—amount of blood returning to heart  Slow heartbeat and exercise increase venous return  Increased venous return distends (stretches) ventricles and increases contraction force Venous Return EDV SV CO Frank-Starling Law  2 1 Factors Aiding Venous Return 1. Muscular pump: contraction of skeletal muscles "milks" blood toward heart; valves prevent backflow 2. Respiratory pump: pressure changes during breathing move blood toward heart by squeezing abdominal veins as thoracic veins expand 3. Venoconstriction under sympathetic control pushes blood toward heart 2 2  2 3 Regulation of Stroke Volume Contractility: contractile strength INDEPENDENT of muscle stretch and EDV (intrinsic factors) Increase SV, decrease ESV Increased Ca2+ from sympathetic stimulation (extrinsic factor) Epinephrine and norepinephrine  2 4 Regulation of Stroke Volume Chemicals that increase contractility are called Positive ionotropic factors  Epinephrine (What about caffeine???)  Thyroxine & Glucagon  Digitalis (Rx)  High extracellular Ca++ Other chemicals decrease contractility (Negative ionotropic factors)  Acidosis  Increased extracellular K+  Calcium channel blockers  2 5 Extracellular fluid Norepinephrine Adenylate cyclase Ca 2+ 1-Adrenergic Ca2+ receptor G protein (Gs) channel ATP is converted Cytoplasm to cAMP a Phosphorylates GDP plasma membrane Inactive protein Ca2+ channels, Active kinase A increasing extra- protein cellular Ca2+ entry kinase A Phosphorylates SR Ca2+ channels, Phosphorylates SR Ca2+ increasing intracellular Ca2+ b c pumps, speeding Ca2+ release removal and relaxation Enhanced binds Ca2+ actin-myosin Troponin to Ca2+ interaction Ca2+ uptake pump SR Ca2+ Cardiac muscle channel force and velocity Sarcoplasmic reticulum (SR) Figure 18.21  2 6 Regulation of Stroke Volume Afterload: pressure that must be overcome for ventricles to eject blood Backpressure from blood in aorta and pulmonary vessels on valves Hypertension increases afterload, resulting in increased ESV (blood left over) and reduced SV (blood pumped out to body)  makes it more difficult for the ventricles to eject blood 2 7  2 8 Congestive Heart Failure (CHF)  CO is so low that blood circulation is inadequate to meet tissue needs  The heart attempts to work harder, therefore Ca++ levels in cardiac cells increases…sustained increase in Ca++  increased calcineurin  encodes for cardiac myocytes to literally alter the architecture of the heart in response to different demands  Caused by:  Coronary atherosclerosis (artery clogging)  (different from arteriosclerosis)  Persistent high blood pressure  Dead cardiac cells from heart attacks  Dilated cardiomyopathy (DCM)  2 9 Review...  List the three factors that affect stroke volume.  Analyze the significance of Frank Starling’s Law of Contraction.  Identify the clinical significance preload and afterload has.  What is “contractility?”  3 0 Autonomic Nervous System Regulation Atrial (Bainbridge) reflex: a reflex from increased venous return Stretch of the atrial walls stimulates the SA node Also stimulates atrial stretch receptors activating sympathetic reflexes == increase HR  3 1 Chemical Regulation of Heart Rate 1. Hormones  Epinephrine from adrenal medulla enhances heart rate and contractility  Thyroxine increase in heart rate and enhances the effects of norepinephrine and epinephrine 2. Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function  3 Exercise (by Heart rate Bloodborne Exercise, 2 skeletal muscle and (allows more epinephrine, fright, anxiety respiratory pumps; time for thyroxine, see Chapter 19) ventricular excess Ca2+ filling) Venous Sympathetic Parasympathetic Contractility return activity activity EDV ESV (preload) Stroke Heart volume rate Cardiac output Initial stimulus Physiological response Result Figure 18.22