Heart Topics Location of the Heart Chambers of the Heart Heart Valves Coronary Circulation Cardiac Muscle Cardiac Conduction System Cardiac Cycle Cardiac Output

Cardiac Conduction System Involuntary Autorhythmic

Cardiac Conduction System

Assigned Reading Review notes on diagram 20.10 – go through this pathway several times. Review your first term notes on: Muscle contraction - Figures 10.6-10.10 Calcium extraction from bones Types of action potentials

Action Potentials in Neurons Depolarization Plateau Repolarization Refractory Period

Action Potentials in SA Node Depolarization Plateau Repolarization Refractory Period

Action Potentials in Skeletal Cells Depolarization Plateau Repolarization Refractory Period

Action Potentials in Cardiac Cells Rapid Depolarization Plateau Repolarization Refractory Period

Cardiac ATP Production High density of mitochondria in Cardiomyocytes = quick ATP production = resistance to fatigue. Relies on aerobic cellular respiration (unlike skeletal muscle = anaerobic) Fatty acid metabolism (60%) Glucose metabolism (35%) Creatine phosphate Lactic acid metabolism - increases during exercise

Myocardial Infarction Creatine kinase catalyzes the transfer of a phosphate group from creatine phosphate to ADP to make ATP. Normally, CK and other enzymes are confined within cells. Injured or dying cardiac or skeletal muscle fibers release CK into the blood.

The ECG Heart beat creates electrical currents on surface of body. Recording of electrical changes of each cardiac cycle. The initiation of each heartbeat and recording of the action of the entire heart.

The ECG P Wave QRS Complex T Wave

ECG Compare the electrical vs. mechanical activity on these diagrams as we can INFER the mechanical activity caused by the electrical activity.

ECG AP in SA node propagates in atrial muscle  AV node  depolarizes atrial fibers = P wave After start of P wave = atrial contraction (systole). AP slows at AV node (anatomical diff) = atria time to contract = increases ventricular volume.

ECG 3. AP propagates fast again in bundle of HIS  bundle branches (septum = Q)  apex purkinje fibers  ventricles  QRS complex 80-120 ms Atrial repolarization hidden here

ECG 4. Shortly after QRS complex = ventricular fiber contraction Continues during S-T segment Contraction moves from apex to base Blood squeezed towards semi-lunar valves

ECG 5. Repolarization of ventricular fibers starts at apex and spreads = T wave (0.4 sec after P wave) 6. Shortly after start of T wave = ventricular relaxation (diastole) Once repolarization complete, fibers completely relax (by 0.6 sec)

Heart Topics Location of the Heart Chambers of the Heart Heart Valves Coronary Circulation Cardiac Muscle Cardiac Conduction System Cardiac Cycle Cardiac Output

The Cardiac Cycle Atrial Systole Ventricular Systole Relaxation Period

Atrial Systole ECG Connection: from P wave to Q wave AV valves: open SL valves: closed

Atrial Systole Both atria contract Ventricles are relaxed Atrial pressure increases AV valves open Blood flows into both ventricles Ventricles are relaxed Ventricular pressure too low to open SL valves End-diastolic volume = EDV ~130 mL Exercise increases EDV

Ventricular Systole Divided into two periods Isovolumetric ventricular contraction Ventricular ejection Atria are relaxed and filling with blood .

Isovolumetric Ventricular Contraction ECG Connection: begins with R wave AV valves: closed SL valves: closed

Isovolumetric Ventricular Contraction Both ventricles begin contracting Increases pressure AV valves close Ventricular pressure too low SL valves remain closed Isovolumetric

Ventricular Ejection ECG Connection: from S wave to T wave AV valves: closed SL valves: open

Ventricular Ejection Both ventricles continue contracting Ventricular pressure continues to increase AV valves remain closed High ventricular pressure opens SL valves Blood is ejected into pulmonary trunk and aorta Max volume of blood ejected = ~70 mL / ventricle 60 mL remains = End-systolic volume (ESV)

Stroke Volume The volume of blood ejected from each ventricle during systole. SV= EDV-ESV SV =130 ml – 60 ml SV = 70 ml

Relaxation Period Divided into two periods: Isovolumetric ventricular relaxation Passive ventricular filling Both atria and ventricles are relaxed and filling with blood

Isovolumetric Ventricular Relaxation ECG Connection: begins at end of T wave AV valves: closed SL valves: closed

Isovolumetric Ventricular Relaxation Both ventricles begin to relax Ventricular pressure begins to decrease Low ventricular pressure closes SL valves Ventricular pressure too high to open AV valves

Passive Ventricular Filling ECG Connection: after T wave to next P wave AV valves: open SL valves: closed

Passive Ventricular Filling Both ventricles continue to relax Ventricular pressure continues to decrease SL valves remain closed Atrial pressure exceeds ventricular pressure AV valves open Blood fills the ventricles

Cardiac Cycle and Heart Rate Metabolic increase = HR increase Durations of atrial and ventricular systole are relatively constant Increased heart rate  decreased relaxation period

The Cardiac Cycle Pressure Heart sounds Ventricular volume Left side vs. right

Types of questions asked This diagram wouldn’t be on a test but all the content is!! What electrical event initiates an action? What is the pressure relationship on either side of a valve? When are valves open or closed? Where / when is blood moving?

Heart Topics Location of the Heart Chambers of the Heart Heart Valves Coronary Circulation Cardiac Muscle Cardiac Conduction System Cardiac Cycle Cardiac Output

Cardiac Output The heart’s ability to discharge oxygen rich blood needs to be variable to meet the work requirements of your cells. CO = A measure of ejected blood from the ventricles every minute.

Cardiac Output Cardiac Output (CO) = SV X HR At rest CO = 70 X 75 At rest CO = 5.25 L/minute CO adjusted by changing SV or HR Cardiac Reserve = 5 X CO

Regulation of Stroke Volume Preload Contractility Afterload

Preload Increased stretch  increased force of contraction Increased filling during diastole  increased force of contraction during systole

Preload Determined by: Duration of ventricular diastole Venous return

Why Preload? The relationship between ventricular filling (EDV) and preload equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both systemic and pulmonary circulations.

Afterload Afterload – the pressure that the ventricles must overcome to open the SL valves. Increased afterload  decreased SV  increases ESV

Afterload Hypertension

Contractility Positive inotropics increase contraction Norepinephrine and epinephrine Negative inotropics decrease contraction Acetylcholine

Regulation of Heart Rate Regulating HR is the body’s principal mechanism of short-term control of CO Three main mechanisms: ANS Endocrine system Other factors

Regulation of Heart Rate - ANS

Regulation of Heart Rate – Endocrine Epinephrine and Norepinephrine Increase HR and contractility Thyroid hormone Increases HR and contractility

Regulation of Heart Rate – other factors Cations also affect heart rate: Na+ and K+ decrease HR and contractility Ca2+ increases HR and contractility

Exercise and the Heart