Heart Physiology CH 11 Anatomy and Physiology. Conduction of Impulses Cardiac muscle can contract without nerve stimulation Different cells contract at.

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Presentation transcript:

Heart Physiology CH 11 Anatomy and Physiology

Conduction of Impulses Cardiac muscle can contract without nerve stimulation Different cells contract at different rates –Atria 1/sec –Ventricles 1/5sec –Must be regulated Autonomic nerves control rate Intrinsic Conduction System (pacemaker)

Intrinsic Conduction System Also called the nodal system Composed of a hybrid muscle/nervous tissue Sets the rhythm at around 75 bpm SA node is the pacemaker AV node contracts atria AV bundle carries signal to apex Purkinje fibers contract ventricles

Poor conduction Damage to AV node is called heart block –Ventricles contract on their own Damage to SA node –May need internal pacemaker Major damage due to ischemia may disrupt normal conduction –Ventricles may go into fibrillation Major cause of death in MI patients Can require defibrillation (AED)

Electrocardiogram (ECG) Electrical signals in the heart can be traced externally Electrodes are placed on the skin P wave atria depolarize QRS ventricles depolarize T wave Vent Repolar

Cardiac Cycle One complete heart beat Systole is contraction Diastole is relaxation In cardiac cycle they apply to the ventricles unless otherwise noted Average 75 bpm or 1/0.8 sec

1. heart relaxed and filling, AV valves open, end with atrial contraction 2. AV valves close due to increased pressure, semilunar vales forced open, atria relax and fill 3. ventricles relax, AV valves reopen and ventricles refill

Heart Sounds AV valve closing before ventricular contraction causes “lub” sound –Long and loud Semilunar valves closing after contraction makes “dub” sound –Short and sharp Any abnormal sound is called a murmur –May be normal or pathological

Cardiac Output (CO) Product of stroke volume (SV) and heart rate (HR) CO = SV x HR CO = 70 ml/beat x 75 beats/min = 5250 ml/min entire volume is 6000 ml A change in either results in a change in CO

Changing SV Stroke volume related to stretch on ventricle wall Increase venous return increases volume leading to more stretch –Exercise increases heart rate and muscular pump action

Changing HR ANS control –Sympathetic increases HR in times of demand –Parasympathetic slows the HR when crisis is over (Vagus Nerve) Drugs such as digitalis Hormones Ions

Homeostatic Imbalance of pumping Congestive Heart Failure (CHF) –Progressive condition –Caused by coronary athlerosclerosis –Left side failure leads to lung congestion –Right side failure leads to peripheral swelling –Failure of one side puts stress on the other and will lead to total failure if untreated