Cardiac Function Understand the structure of the heart and cardiac cycle. Understand the terms Cardiac output, stroke volume, heart rate and the relationship between them Starter: Put together the circulatory system

5 Functions of the Heart Delivery – O2 and nutrients Removal – CO2 and metabolic waste Transport - Hormones Maintenance – Body temp. Bloods buffering capabilities (ph) + fluid levels. Prevention – dehydration and disease

A system of channels (The blood vessels) All systems must have: A pump (The Heart) A system of channels (The blood vessels) A fluid medium (The Blood)

The Heart Made up of: 2 Atria – acting as receiving units 2 Ventricles – acting as sending units. 2 Semilunar valves which are the entrance and exit of blood from the heart. Tricuspid (right) and bicuspid (left) valves. Which link the atrium to the ventricles. Read through the workings of the heart and fill in the sheet using the word bank. The thickness of the 4 channels varies according to their workload. Left ventricle is the thickest due to high pressure when ejecting the blood. Atrium thin why? Myocardia See diagrams

Heart Valves As each chamber of the heart contracts, it pushes a volume of blood into a ventricle or out of the heart. Valves open and close in response to pressure changes as the heart contracts and relaxes. They ensure one-way flow by opening to let blood through (high pressure) and closing to prevent back flow.

Cardiac Conduction System Cardiac muscle has unique ability to generate its own electrical signal called myogenic. Works without neural stimulation. Its our pacemaker. Made up of 4 components. 1. Sinoatrial node (SA) Hearts Pacemaker 2. Atrioventricular node (AVN) 3. Atrioventricular (AV) bundle of His 4. Purkinje fibres

SA node initiates the electrical impulse in the right atrium typically 60=80bpm. The impulse spreads through both atria and signals the atria to contract almost immediately. AV node (AVN) also within this right atrium also receives this signal and conducts this signal into the ventricles via AV bundle of His located in the ventricular septum running down to the apex of the heart from here the signal is passed onto the Purkinje fibers which spread throughout the heart cause the ventricle to contract However, there is a delay in this message going through the AVN into the Purkinje fibers and this is crucial as it allows the Atrium to contract fully and fill the ventricles (see Starlings law and Stroke volume later)

Other effects on speed of heart rate: Autonomic system Parasympathetic nervous system (brakes) Acts on the heart through the vagus nerve. It has a depressant effect on the heart. Slows impulse conduction thus HR + force of contraction. (after exercise) Sympathetic nervous system (accelerator) Opposite effect increases impulse stimulation > HR, > contraction force (for exercise) Through the cardiac nerve. Endocrine system (hormones) Hormones released by adrenal medulla (adrenaline, norepinephrine). Start of exercise triggered by sympathethic system and helps it keep going Acetylcholine slows it down in conjunction with the parasympathetic.

Key Terms Cardiac Cycle – Time taken for the hearts chambers to go through a complete cycle of contraction (systole) followed by a period of relaxation (diastole). Most of the time taken is with the filling of the heart. (atrial systole? Atrial contracts forcing blood into the ventricles, Atrial diastole Atria fill with blood etc get used to the terms) Stroke Volume – amount of blood ejected from the left ventricle during a contraction. Not all of it leaves, the proportion of blood that leaves is called ejection fraction. Cardiac Output – Stroke volume x Heart Rate. Total amount of blood ejected from the heart per mins. Chemoreceptors – detect changes in blood chemistry found mainly in the carotid arteries. Baroreceptors – detect changes in blood pressure.

What happens to Stroke Volume during exercise? Starling’s Law states that the greater the venous return, the greater the strength of contraction. (More filling during Diastole = stretch of the ventricle and more forceful contraction. However, at higher intensities cardiac muscles contracts at greater force. Why? Due to the shortened period of diastole and reduced ventricular filling of the heart. Therefore stronger contraction to ensure blood is expelled from the heart. This combination leads to dramatic increases of Cardiac output as both HR and SV increase.

Increase of Heart Rate Many reasons but most important is the changes of Carbon Dioxide levels in the blood. Exercise causes this and this affects the acidity of the blood (more acidic lower Ph) These changes are detected by chemoreceptors (found in carotid arteries). These messages are picked up by the Cardiac Centre of the Brain and adjusts nerve stimulation to the SAN. Decreased vagal tone and increased sympathetic system = > HR. Reduction of HR caused by > blood pressure and baroreceptors pick this up and then increase vagal tone.

Long Term Effects Stronger heart = > SV and resting HR With training they say a reduction resting HR reduces by 1 beat per week. Highly conditioned can get down to as low as 30bpm. Below 60bpm is known as bradycardia (athletes heart). Training increases SV but has no effect on resting cardiac output. (why?) Also effect on Max HR. Main benefit is surprisingly that due to the heart becoming stronger it demands less oxygen as beats less thus leaving more for the working muscles.

Changes during increased workload How do we meet need for increased cardiac output? Untrained meets the demand with increase in heart rate. Trained can meet it with increased ejection fraction (explain + consequences) Cardiovascular drift = an increase in heart rate that occurs during prolonged exercise that compensates for a decrease in stroke volume in an attempt to maintain cardiac output. Why? A reduction in fluid in the blood (due to sweating) decreases the venous return and thus stroke volume (Starlings law) Also increased need for oxygen to assist the skin in cooling the body.

Review worksheets H/W revise for test on Cardiac Function