The Heart Chapter 18 – Day 4 2/13/08

Wrap up Physiology Muscle contraction in cardiac tissue Pacemaker cells (aka cells of the SA node) Rhythmic depolarization and repolarization Triggers depolarization through internodal cells (aka – start of action potential) Cardiac tissue Ca2+ enters muscle cells via “slow calcium channels” This results in plateau (Fig. 18-15) Arrival of extracellular Ca2+ triggers the release of additional Ca2+ from reserves in SR Sarcomeres shorten = muscle contraction Period of active muscle contraction continues until the plateau ends 2/13/08

Heart – Anatomy: Cardiac muscle Fig. 18.5 2/13/08

Order of Rhythm in Heart Fig. 18.13 2/13/08

Fig. 18.15 2/13/08

Journal of Action Potential in Heart Fig. 18.12 2/13/08

Wrap up Physiology Stimulates intercalated discs Moves action potential nearly instantaneously cell-to-cell Action potential simultaneously affects all tissue in the area All muscle cells in ATRIA contract together Action potential is transferred to AV node (100msec delay from SA node = Ventricles contract after atria) All muscle cells in VENTRICLES contract together We’ve covered EKG/ECG, make sure you are comfortable with it for lecture AND lab exam 2/13/08

Heart Fig. 18.11 2/13/08

Fig. 18.14 2/13/08

Cardiac Cycle Cardiac cycle = 1 heart beat Figure 18-16 2 important events Systole = contraction Diastole = relaxation Each chamber has it’s own systole and diastole 2/13/08

Cardiac Cycle ATRIAL SYSTOLE Ventricles build up pressure Pushes blood into relaxed ventricles Ventricles build up pressure VENTRICULAR SYSTOLE Early – there is enough pressure to close AV valves, but not enough to exceed pressure in blood vessels Pressure exceeds that in blood vessels = 2nd phase of v. systole… Ejects blood out of heart into circulation Meanwhile….ATRIAL DIASTOLE is in progress At the beginning of VENTRICULAR DIASTOLE Atria fill up with blood (returning = venous return) In late ventricular diastole all chambers are relaxed 2/13/08

Fig. 18.16 2/13/08

Fig. 18.17 2/13/08

Fig. 18.18 2/13/08

Heart Health Resting heart rate is efficient Cardiac cycle can give information about heart efficiency As the heart rate increases, less time is spent in each phase, thus… …blood is ejected at a different volume Heart efficiency can be measured as CARDIAC OUTPUT Heart sounds (p522) 4 distinct heart sounds (S1-S4) Lubb (S1) = start of ventricular contraction when AV valves close Dupp (S2) = beginning of ventricular filling when semilunar valves close rushing/, gurgling sound = HEART MURMUR (regurgitation of blood through valves during diastole) 2/13/08

Cardiac Output = volume of blood ejected every minute P. 523 and on board Example Cardiac Output = a major factor in determining blood pressure How hard does the heart have to work for proper circulation Cardiac output (CO) = Stroke volume (SV) mL (VOLUME EJECTED AT EACH HEART BEAT – SYSTOLE) X heart rate (bpm) 2/13/08

Cardiac Output Depends on Figure 18-23 Venous return Stretching of heart muscles Heart rate End diastolic volume (EDV) Volume remaining in ventricle after contraction b/c not all blood is ejected out Figure 18-23 Amount of muscle stretching affects the force of contractions (e.g. pulling a rubber band) Starlings Law of the Heart “Stretch” builds up resistance against the blood More blood is pushed out Why is C.O. important? Maintains proper BP levels to provide efficient blood supply Starlings law of the heart: general rule of “more in = more out” Based on principle that ventricular expansion is limited by myocardial connective tissues, the fibrous skeleton and the pericardial sac The relationship between the amt of vent. Stretching and the contractile force means that, within normal physiological limits, increasing the EDV results in a corresponding increase in the stroke volume. 2/13/08

Factors Affecting Stroke Volume Fig. 18.23 2/13/08

Cardiac Output Blood Pressure Pressure of blood within blood vessels Pressure exerted on ARTERY walls How would C.O. relate?? Higher cardiac output More blood = ↑ BP Less blood = ↓ BP Resistance of blood vessel walls Small diameter = ↑ BP Blood flow is proportional to the radius of the “pipe” Polycythemia (↑ in RBCs) Thicker blood viscocity = ↑ BP (↑ RBCs or loss of water) Length of blood vessel – longer length = ↑ BP 2/13/08

Cardiac Output Cardiac output can be influenced by many factors One of these is HEART RATE Heart conduction system Autonomic nervous system Exercise can increase C.O. Heart muscles are working out Skeletal muscle cells need a fast blood supply The heart has to meet that demand – when exercising, it meets increased demands The force of contraction increases Blood moves faster, so venous return is faster More blood volume is pushed out Does not increase indefinitely, the Heart Rate can out-compete C.O. What is cardiac reserve and where does it fit here?? 2/13/08

Factors Affecting Heart Rate Hormones, ions, nervous system… ANS Fibers connect to the SA node and the AV node Sympathetic Control Medulla – remember the cardiovascular center Norepinephrine, epinephrine Affects the SA node, AV node & myocardium Cardiac Nerve Dilates coronary vessels Parasympathetic control Medulla – cardio-inhibitory center Vagus Nerve (at S.A. node & A.V. node) Secretes ACh ACh changes ion distribution = decrease in heart rate Cardiovascular center of the medulla… 2/13/08

Factors Affecting Heart Rate Ions affect heart rate Ca2+ , Na+ - needed for depolarization K+ - needed for repolarization Ion concentration in blood affects the action potential in the heart Increase K+ outside Less K+ will leave the cell Partial repolarization – slower action potential  HR Increase Ca2+ outside cell  force of contraction – can lead to spasms 2/13/08

Factors Affecting Cardiac Output Fig. 18.24 2/13/08

Heart Problems The normal rhythm of the heart can be disrupted in many ways – be ready to discuss on Friday those in book & those in handouts – you’ll also form your groups for the case study… 2/13/08