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Physiology 1021
Anita Woods

Physiology- Cardiovascular System Homeostasis- maintenance of the internal environment 1. Transports oxygen and nutrients 2. Removes carbon dioxide and waste 3. Regulate pH and body temperature 4. Transports and distributes hormones throughout the body Roles as a transport system: a. Central pump (Heart) b. Closed system of tubes (Blood vessels) c. Fluid (Blood) Two division of cardiovascular system (Pg. CV-5): 1. Pulmonary circulation:  Delivers blood from lungs to heart  Delivers blood for heart to rest of body  Arteries=Take blood away from heart  Veins= take blood to the heart 2. Systemic circulation Blood Volume Distribution: Total Blood Volume (TBV)= 5 liters of blood  Heart and pulmonary circulation= 15%  System arteries/arterioles= 10% (Distribution vessels- distribute blood)  Systemic capillaries= 5% (Exchange vessels)  System veins/ venules= 70% (Capacitance vessels) Myocardial Cells: Two types of myocardial cells: 1. Contractile cells 2. Specialized Nodal/ Conducting cells. Contractile Cells: Contractile cells vs. skeletal muscle cells Similarities Differences  Striated  Shorter and Branched  Contains similar contractile  Extract 80% of the oxygen proteins (actin and myosin) from the blood  1/3 of volume is occupied by  Ca+2 release from SR mitochondria lots of ATP triggers contractions  Joined by intercalated discs that contain Gap junction o Gap junctions: allow movement of ionic currents (APs) between cells CV- pg. 9 Shows Gap junctions allow action potential to travel through from one side to the next. No transmitters or channels needed. Just pass right through Nodal/ Conducting Cells Contains few contractile proteins Self-excitable: Spontaneously generate Action Potentials Rapidly conduct Action Potentials through the heart  Act more like nerve cells 1. Nodal Cells: a. Sinoatrial (SA) node b. Atrioventricular (AV) node 2. Conduction cells: a. Bundle of His b. Purkinje Fibers Sinoatrial Node The origin of self- excitability Known as pacemaker of the heart  Controls heart rate Heart beats at a rate of roughly 72 bpm Impulses (APs) originate at SA node SA node located in the upper posterior wall of the right atrium Site of fastest spontaneous generation of the action potential To generate an AP, cells in SA node must reach threshold To reach threshold, the cells must depolarize (inside becomes more positive) Cells of the SA node can depolarize of their own (spontaneously) creating their own Action Potential  They are self- excitable. Spontaneous depolarization caused by: 1. SA node cells have a greater Na+ and Ca++ permeability o Allows more Na+ and Ca++ to pass through 2. K+ permeability of SA node cells decreases during diastole o Less K+ leaves these cells during relaxation of the heart SA nodal cells do not have a stable resting membrane potential  Pre- potential or pacemaker potentials Membrane potential varies between -60mV to +15mV  Threshold voltage of -40mV i. Slow depolarization caused by a. Increase permeability of cells to Na+ and Ca++ b. Decrease K+ permeability o Pre potential  pacemaker potential ii. Depolarization phase a. At threshold (-40mV), Ca++ voltage gated channels open b. Ca++ flows into SA nodal cells c. Membrane potential reaches +15mV iii. Repolarization a. Ca++ VG channels begin to close b. K+ VG channels begin to open c. K+ leaves the cell d. Membrane potential returns to -60mV e. K+ Channels begin to close and cycle repeats Conduction System of the Heart (Pg. CV- 12) Action potential is travelled by SA node. Travels to Right Atrium Interatrial band transfers the action potential to left atrium Action potential travels through Atrial Muscle using the use of Gap Junction  Remember: action potential travels from muscle cell to muscle cell Atrial Ventricular Ring: Band of fibrous tissue that electrically isolates the ventricular muscle from the atrial muscle.  Therefore action potential cannot freely move into ventricles. The action potential hits the Atrioventricular Node, which slows the action potential down.  Want to make sure atriums finishing contracting before ventricles start Bundle of His  Two sides: Left and Right  Transport action potential down to (bottom?) Action potential hits the Purkinje Fibers, which causes the action potential and contraction to flow through the Ventricular Muscles  Uses Gap Junction Electrocardiogram Body fluids are good conductors of electricity Cardiac impulses pass through the heart  Pass to surrounding tissue and to the surface of the body Electrodes can pick up these impulses ECG is the sum of all the electrical events in the heart  Both depolarizing and repolarizing P-wave: Depolarization of Atrial muscle  After depolarization  contraction QRS complex: Depolarization of ventricular muscle  Bigger because ventricles are bigger T-wave: Repolarization of ventricular muscle Question: Where is the repolarization of the atrial muscle? Answer: It exists but its not shown on ECG What can the ECG tell you about the heart?  Tells the extent and type of disturbances of rhythm or conduction  The extent and location of myocardial damage  Effects of drugs on the heart  It’s a quick easy wait to find heart problems as you just strap on some sensory whether then MRI or CT scan  Tells heart rate The Cardiac Cycle It shows all the mechanical and electrical events during a single contraction on the left side of the heart. At rest monitors:  Pressure changes in aorta, left atrium and left ventricle  Volume changes in left ventricle  Valves opening and closing Cardiac cycle consists of a period of systole (Contraction) and diastole (relaxation)  Each cycle is initiated by the SA-node On diagram watch for: 1. Pressure gradients (high to low)= blood flow (If valves are open) 2. When blood is flowing  Ventricular volumes change Phase 1: Atrial Systole  Atrial Contract  Increase atrial pressure > ventricular pressure (Left AV valves is already open)  Last 30% of Vent filling  end diastolic volume  End diastolic volume: volume at the end of atrial systole Phase 2: Early ventricular systole (Isovolumetric ventricular contraction)  QRS complex  Ventricles begin contracting pressure builds in ventricles  Ventricular Pressure > Atrial Pressure  AV valve closes  No change in ventricle volume because lower ventricle pressure than aortic pressure  Valves are closed Phase 3: Ventricular systole  Ventricles continue to contract  Ventricular pressure > aortic Pressure  Aortic valves open  blood leaves ventricle Isovolumetric-  Ventricular volume decreases not all blood leaves. End systolic Volume No change in volume (ESV) remains  End systolic Volume: Blood left at the end of systole Phase 4: Early ventricular diastole (Isovolumetric ventricular relaxation_  Ventricles relax  ventricular pressure drops  Ventricular Pressure < Aortic pressure  Aortic Valves closed Phase 5: Late ventricular diastole  Ventricles still relaxing  Ventricular pressure < Atrial pressure  AV valve opens  Blood enters ventricles (70% of ventricular filling takes place)  Cycle repeats. Cardiac Output:  The amount of blood pumped by each ventricle in one minute (l/m)  CO= heart rate X stroke volume  Heart Rate (HR) is the number of heart beats per minutes  Stroke Volume (SV) is the amount of blood pumped by each ventricle during one contraction (avg. 70ml at rest)  CO can vary from 5l/min  20 to 40 l/min.  Resting heart rate= 70 bpm  Resting stroke volume= 70-80ml/beat  At rest, CO= 5 liters/minute During exercise, CO can increase to 20-40 l/min  Change CO by changing HR or SV Control of Heart Rate Resting heart rate is roughly 70 bpm normal individual but can be as low as 50 bpm in trained athletes Maximum heart rate depends on age  Roughly MaxHR= 220- Age Heart rate is controlled by the autonomic nervous system  1. Parasympathetic nervous system: Decreases heart rate  2. Sympathetic nervous system: Increase heart rate  Changes heart rate by changing SA node which changes the pacemaker potential Parasympathetic Nervous system PNS innervates the SA and AV nodes wia the vagus nerve  Nerve admits neurotransmitters PNS releases the neurotransmitter  Acetylcholine (Ach) Acetylcholine opens the K+ channels, which allows a little bit more of potassium to leak out. As it leaves, positive charge leaves the cell. This causes the cell to become more negative then normal. Acetylcholine also closes Ca++ channels, which stops as much calcium from entering causing the cell to become more negative. Causes pacemaker potential to have a longer, steeper slope, which results in a slower action potential. Causes Decrease in heart rate. NOTE: heartbeat takes the same duration of time, however the amount of potential needed to reach action potential is changed Sympathetic Nervous System Sympathetic innervates SA and Av nodes and ventricular muscle SNS releases norepinephrine( and hormone epinephrine from adrenal gland) Norepinephrine and Epinephrine opens Sodium channels causing sodium to flow into the cell. Norepinephrine and Epinephrine opens Ca++ channels causing more sodium to flow into the cell-causing cell to become more positive Causes depolarization quicker with a steeper pacemaker potential Heart rate overall control: 1. Parasympathetic nervous system decreases HR 2. Sympathetic nervous system increases HR Heart rate <100bpm  activate PNS  At rest (70bpm) there is always PNS activity: “Vagal Tone” Heart rate= 100 bpm  no PNS, no SNS Remember: CO=HR X SV  Heart’s own intrinsic rate (Set by SA node) Heart rate>100 bpm Activate SNS Stroke Volume The amount of blood pumped by each ventricle in a single contraction At rest= 70ml  max exercise= 110 to 200 ml Factors that control stroke volume 1. Input from ANS 2. Preload (End diastolic volume) Changing stoke volume by ANS PNS (Vagus nerve decreases heart rate)  PNS released neurotransmitter acetylcholine  Ach closes Ca++ channels  If close Ca++ Channels, less Ca++ flowing into cardiac contractile cells.  Decrease force of contraction  Decrease stroke volume (decrease cardiac output) SNS (Increase heart rate)  Neurotransmitter
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