Cardiovascular System Physiology PDF

The Cardiovascular System Part V: Principles of Physiology Anatomy & Physiology II BIOL2220 1 Version 04 The Cardiovascular System ECG Physiology P= Atrial Activation. PR Interval = Onset of Atrial Activation to...

The Cardiovascular System Part V: Principles of Physiology Anatomy & Physiology II BIOL2220 1 Version 04 The Cardiovascular System ECG Physiology P= Atrial Activation. PR Interval = Onset of Atrial Activation to onset of Ventricular Activation. QRS Complex = Ventricular Activation. QRS Duration = Duration Of Ventricular Activation. ST-T Wave = Ventricular Re-Polarization. QT Interval = Duration Of Ventricular Activation And Recovery. U Wave = After-DePolarizations In The Ventricles. 2 The Cardiovascular System ECG Physiology R T P Q S Electrical: Atrial Depolarization Electrical: Ventricular Repolarization Mechanical: Atrial Contraction Mechanical: Ventricular Relaxation Electrical: Ventricular Depolarization Mechanical: Ventricular Contraction 3 The Cardiovascular System ECG Physiology ECG Standard Leads ECG Augmented Limb Leads There are three of these leads which are usually The same three leads that form the standard designated as I, II and III. leads also form the three unipolar leads known as They are all bipolar (i.e., they detect a change in electric the Augmented Leads. These three leads are potential between two points) and detect an electrical referred to as aVR (right arm), aVL (left arm) and potential change in the frontal plane. aVF (left leg) and also record a change in electric Lead I is between the right arm and left arm electrodes, potential in the frontal plane. the left arm being positive. These leads are unipolar in that they measure the Lead II is between the right arm and left leg electrodes, electric potential at one point with respect to a the left leg being positive. null point (one which doesn't register any Lead III is between the left arm and left leg electrodes, significant variation in electric potential during the left leg again being positive. contraction of the heart). A diagrammatic representation of these three leads is This null point is obtained for each lead by adding termed Einthoven's Triangle (shown in blue), after the the potential from the other two leads. For Dutch doctor who first described the relationship. The example, in lead aVR, the electric potential of the central source of electrical potential in the triangle is the right arm is compared to a null point which is heart. obtained by adding together the potential of lead aVL and lead aVF. ECG Precordial Leads These six unipolar leads, each in a different position on the chest, record the electric potential changes in the heart in a cross sectional plane. Each lead records the electrical variations that occur directly under the electrode. 4 The Cardiovascular System ECG Physiology Aorta & To R Systemic R Circulation T T P P U U Q S Q S Isovolumetric Contraction AV Valves Close Isovolumetric Relaxation Atrial ASLV/PSLV Opens Systole Ventricular Ejection ASLV/PSLV Closes Rapid Inflow & AV Valves Open Diastole Pulmonary Vein Influx To Atrium 5 The Cardiovascular System Phases of the Nodal Action Potential Physiology Phase 4 is the unstable rest Phase 0 is the “rapid depolarization” phase. or pacemaker potential (it is a This is caused by a large influx of Ca++ ions ( the “spontaneous calcium is specific to pacemaker cells). depolarization”). It is caused by an influx of sodium (Na+) through voltage-dependent channels, but also an influx of Ca++ and a slow efflux of K+. Phase 3 is the "rapid These Na+ channels, in repolarization" phase, and pacemaker cells, have a it is caused by the closing of particular behavior: contrary Ca++ channels, while the K+ to what usually happens in channels are still open other cells, they open when (allowing efflux of the K+). the voltage is more negative, immediately after the end of a previous action potential. For this reason they are called "funny channels” *T=Transient *L=Long lasting The Nodal Cycle Phase 4 Threshold Phase 0 Phase 3 Influx via open Rapid influx via open Closing of Ca++ VGCs Na+ (f) & Ca++ (T) VGCs. Ca++ (L) VGCs Efflux via open K+ VGCs 6 Although pacemaker activity is spontaneously generated by SA nodal cells, the rate of this activity can be modified significantly by external factors such as by autonomic nerves, hormones, drugs, ions, and ischemia/hypoxia. The Cardiovascular System Phases of the Nodal Action Potential Physiology The Nodal Cycle Phase 4 Threshold Phase 0 Phase 3 Influx via open Rapid influx via open Closing of Ca++ VGCs Na+ (f) & Ca++ (T) VGCs. Ca++ (L) VGCs Efflux via open K+ VGCs 7 Although pacemaker activity is spontaneously generated by SA nodal cells, the rate of this activity can be modified significantly by external factors such as by autonomic nerves, hormones, drugs, ions, and ischemia/hypoxia. The Cardiovascular System Physiology Phases of the Cardiac Myocyte Action Potential Phase 1 is caused by the closure of the “fast” Na+ channels, and Phase 2 is the"plateau" phase of the cardiac the small influx of Cl- along with a small efflux of K+. action potential, and it is caused by the influx of Ca++ and the efflux of K+. Phase 0 is the “rapid depolarization” phase. This is caused by a large influx of Na+ ions Phase 3 is the "rapid via “fast” channels repolarization" phase, and it is caused by the closing of Ca++ channels, while the K+ channels are still open (allowing efflux of the K+). Phase 4 is the unstable resting phase. It is caused by an influx of sodium (Na+) through voltage-dependent channels (f), but also an influx of Ca++ and a slow efflux of K+. The Cardiac Myocyte Cycle Phase 0 Phase 1 Phase 2 Phase 4 Phase 3 Rapid influx Closing of Na+ VGCs Influx of Ca++ Influx via Closing of Ca++ VGCs via Na+ Small influx of Cl- Efflux of K+ open Na+ Efflux via open K+ VGCs VGCs Small efflux of K+ (f) & Ca++ (T) VGCs. 8 The Cardiovascular System Physiology Phases of the Cardiac Myocyte Action Potential The Cardiac Myocyte Cycle Phase 0 Phase 1 Phase 2 Phase 4 Phase 3 Rapid influx Closing of Na+ VGCs Influx of Ca++ Influx via Closing of Ca++ VGCs via Na+ Small influx of Cl- Efflux of K+ open Na+ Efflux via open K+ VGCs VGCs Small efflux of K+ (f) & Ca++ (T) VGCs. 9 The Cardiovascular System Cardiac Output & Other Dynamics Physiology Cardiac Output Starling’s Law Contractile Force CO = HR x SV As The Heart Muscle Stretches, Contractile Force Increases - But CO = Cardiac Output ((l or ml)/Minute) Only To A Point. HR = Heart Rate (Beats/Minute) SV = Stroke Volume ((l or ml)/Beat) Stretch Cardiac Index (Comparative) Afterload CI = CO/m2 (Resistance) Preload CI = Cardiac Index 10 The Cardiovascular System Cardiac Output & Other Dynamics Physiology Preload & Afterload INTRINSIC FACTORS Note that these are Extrinsic Vascular Variables Conduction System Auto-Regulation Functional Syncytium (Starling Mechanism) CO = Heart Rate X Stroke Volume Contractility Parasympathetic Sympathetic Nervous System Nervous System EXTRINSIC FACTORS 11 The Cardiovascular System Physiology Cardiovascular Control Systems Key Variable Abbreviations The Key Equations, and Their ImportanceThis measures the pumping ability of the heart. Remember 1. BP Blood Pressure 1. CO = HR x SV that HR and SV can be modified 2. BV Blood Volume by both intrinsic and extrinsic 3. CI Cardiac Index variables. 4. CO Cardiac Output 5. HR Heart Rate This allows for a CO to be compared based on body size 6. KE Kinetic Energy (Velocity) 1. CI = CO/m2 7. P Pressure This is Poiseuille’s Equation. 8. PE Pressure Energy(BP) There are three primary factors that determine the 9. Q Flow (vol/time) resistance to blood flow within a single vessel: 10. R Resistance vessel diameter (or radius), vessel length, and 11. SV Stroke Volume 1. Q = ∆P/R viscosity of the blood. 12. TE Total Energy (Total Pressure) Of these three factors, the most important 13. TPR Total Peripheral Resistance quantitatively and physiologically is vessel diameter 14. VC Vasoconstriction (VC or VD). 15. VD Vasodilation 1. TE=PE + KE Very small changes in vessel diameter lead to large 16. ∆ “Change in” changes in resistance, which in turn changes flow. Important Assumptions of Bernoulli’s Principle: Kinetic energy and pressure energy can be interconverted so that total energy remains unchanged. This means that the total pressure is constant along a streamline. This would also mean that low pressure in one segment would increase pressure in another connected segment. KE is like “velocity of blood flow”, and PE is “blood pressure”. The two are related reciprocally. Therefore, if one increases, the other must decrease…and vise versa. Although pressure is normally considered as the driving force for blood flow, in reality it is the TE that drives flow between two points 12 Bernoulli does not account for factors such as viscosity, turbulence, or gravity  The Cardiovascular System Vasoconstriction, Blood Flow, and Blood Pressure Physiology Arterioles of the body are collectively known as the total peripheral resistance (TPR) beds. The TPR designation is because they vasoconstrict and vasodilate. In the drawing below, the arteriole is vasoconstricted, and blood of a consistent viscosity is flowing in a laminar (non-turbulant) manner. According to Poiseuille and Bernoulli, what will happen to resistance (R), flow (Q), and pressure (PE) in the drawing? Remember, Bernoulli said that the total pressure (TE) along the streamline should be constant. Therefore, if it drops in one segment, it must rise in another. “Upstream” Artery: This is where we Measure BP “Downstream” Arteriole (TPR) PE-Arteriole VC @ TPR’s R-Arteriole Q-Arteriole KE-Arteriole This is a compensation for the drop in PE at the arteriole. PE-”Upstream” Artery PE-Arteriole VD @ TPR’s R-Arteriole Q-Arteriole KE-Arteriole This is a compensation for the rise in PE at the arteriole. PE-”Upstream” Artery The Cardiovascular System Evaluating Blood Pressure Physiology 1. A cuff that inflates is wrapped around your upper arm and kept in place with Velcro. A tube leads out of the cuff to a rubber bulb. 2. Another tube leads from the cuff to a reservoir of mercury at the bottom of a vertical glass column. Whatever pressure is in the cuff is shown on the mercury column. The mercury is held within a sealed system – only air travels in the rubber tubing and the cuff. 3. Air is then blown into the cuff and increasing pressure and tightening is felt on the upper arm. This cuts of blood flow through the brachial artery. 4. You place a stethoscope in the cubital fossa and listen to the pulse while the air is slowly let out again. 5. The Systolic Pressure is measured when you first hear the Blood pressure is a measurement of the force applied to pulse (return of blood flow). the walls of the arteries (PE) as the heart pumps blood through the body. The pressure is determined by the force 6. This sound will slowly become more distant and finally and amount of blood pumped, and the size and flexibility disappear. (elastic recoil) of the arteries. Blood pressure is continually changing depending on 7. The Diastolic Pressure is measured from the moment you are activity, temperature, diet, emotional state, posture, unable to hear the sound of the pulse. It is created by the physical state, and medication use. elastic recoil of the Aorta. 8. The blood pressure is measured in terms of millimetres of 120mmHg / 80mmHg mercury (mmHg) because it was first examined using a mercury column. Systolic Diastolic 14 Average BP The Cardiovascular System Factors Affecting Arteriolar Diameter Physiology HORMONES: Angiotensin II (Ag II) and Arginine-vasopressin (ADH/AVP), are powerful vasoconstrictors (VC). Norepinephrine and Epinephrine can cause vasoconstriction (VC) in some blood vessels because of alpha receptors. However in the case of Epinephrine, it can cause vasodilation (VD) because of beta-2 receptors. Since epinephrine preferentially activates beta-2 receptors, and those are well distributed in skeletal muscle arterioles, the vasodilation is an important effect in skeletal muscles during exercise. LOCAL CHEMICAL FACTORS: Typically these are added to the interstitial fluid around the body tissues. As such, they cause vasodilation (VD) to help match the local blood flow to the local metabolic requirements. These include CO2, Lactate, and others. GENERAL AUTONOMIC NERVES: Some autonomic nerves can release nitric oxide (NO), which is a vasodilator (VD). Also, nitric Note: Following injury, many inflammatory oxide can be released in many places from the endothelial cells. mediators can also cause VD Important Autonomic Receptors: Alpha 1: VC @ TPR Beds Alpha 2: Inhibits NE release Beta 1: Increased Heart Rate and Contractility 15 Beta 2: VD @ TPR Beds  The Cardiovascular System Key Biochemical Players in Cardiovascular Control Physiology Player Source Effect Stimulus Acetylcholine (ACH) PNS/CNX - Vagus ▼ HR Parasympathetic Activation Aldosterone (ALD) Adrenal Cortex ▲ Na+ Absorption @ Kidney ▼ BP ▲ BV ▬▶ ▲ BP Presence of Ag II Angiotensin II (AGII) Kidney/Liver/ ▲ VC ▬▶ ▲ BP ▼ BP Lungs ▲ Aldosterone & ADH/AVP ▼ Renal Perfusion Atrial Naturetic Heart ▲ Na+ Loss @ Kidney ▲ BP/BV Peptide (ANP) ▼ BV ▬▶ ▼ BP ▲ Atrial Stretch Anti-Diuretic Hormone Hypothalamus/Posterior ▲ H2O Absorption @ Kidney ▼ BP (ADH/AVP) Pituitary ▲ VC In TPR Beds Presence of Ag II ▲ BP Epinephrine (EP) SNS/Adrenal Medulla ▲ VC In TPR Beds: !-1 Sympathetic Activation ▲ VD In TPR Beds: "-2 ▲HR & SV (Contractility) ▲ BP Renin Kidney (JG Cells) ▲ Conversion of Angiotensinogen ▼ BP ▼ Renal Perfusion Nitric Oxide (NO) Vascular ▲ VD ▬▶ ▲ Tissue Perfusion Various Stresses Endothelium/Peripheral Nerves 16 The Cardiovascular System Cardiovascular Control Physiology Systems Factors That Influence Basic Heart Operation: Variable Affected Intrinsic (From Within): SA Node (Pacemaker) HR Contractility (Starling’s Law) SV Intercalated Disks (Functional Syncytium) HR + SV Extrinsic (From Without): PNS – CN X, Vagus HR SNS – Adrenal Medulla HR + SV Preload (Capacitance) SV Afterload (Resistance) SV 17 The Cardiovascular System Cardiovascular Control Physiology Systems Factors That Influence Basic Vascular Operation: Intrinsic (From Within): Endothelial Cells (Paracrine – NO) Metabolic By-Products (CO2, Lactate) Myogenic Auto-Regulation (Stretch, “Precapillary Sphincters”) Elasticity Of Great Arteries (Recoil) Extrinsic (From Without): Neural SNS – VC Mainly, Some Beta-2 VD NO Hormonal Please see Biochemical Players Chart In general, all factors have some influence over resistance, flow, and pressure. 18