Cardiovascular Physiology Chapter 14 Cardiovascular Physiology

Overview of the Cardiosvascular System Heart and Blood vessels Products transported to sustain all cells Table 14-1: Transport in the Cardiovascular System

Circulation Reviewed Heart – "four chambered" Right atrium & ventricle Pulmonary circuit Left atrium & ventricle Systemic circuit Blood Vessels – "closed circulation" Arteries –from heart Capillaries– cell exchange Veins – to heart

Figure 14-1: Overview of circulatory system anatomy Circulation Reviewed Figure 14-1: Overview of circulatory system anatomy

Blood Flow: Pressure Changes Flows down a pressure gradient Highest at the heart (driving P), decreases over distance Hydrostatic (really hydraulic) pressure in vessels Decreases 90% from aorta to vena cava

Blood Flow: Pressure Changes Figure 14-2 : Pressure gradient in the blood vessels

Some Physic of Fluid Movement: Blood Flow Flow rate: (L/min) Flow velocity = rate/C-S area of vessel Resistance slows flow Vessel diameter Blood viscosity Tube length Figure 14-4 c: Pressure differences of static and flowing fluid

Some Physic of Fluid Movement: Blood Flow Figure 14-6: Flow rate versus velocity of flow

Figure 14-7 g: ANATOMY SUMMARY: The Heart Heart Structure Pericardium Chambers Coronary vessels Valves- (one-way-flow) Myocardium Figure 14-7 g: ANATOMY SUMMARY: The Heart

Figure 14-10: Cardiac muscle Cardiac Muscle Cells: Autorhythmic Myocardial Intercalated discs Desmosomes Gap Junctions Fast signals Cell to cell Many mitochondria Large T tubes Figure 14-10: Cardiac muscle

Mechanism of Cardiac Muscle Excitation, Contraction & Relaxation Figure 14-11: Excitation-contraction coupling and relaxation in cardiac muscle

Modulation of Contraction Graded Contraction: proportional to crossbridges formed More [Ca++]: crossbridges, more force & speed Autonomic n & epinephrine modulation

Modulation of Contraction Figure 14-12: Modulation of cardiac contraction by catecholamines

More Characteristics of Cardiac Muscle Contraction Stretch-length relationship  stretch,  Ca++ entering  contraction force Long action potential Long refractory period No summation No tetanus

More Characteristics of Cardiac Muscle Contraction Figure 14-13: Length-tension relationships in skeletal and cardiac muscle

More Characteristics of Cardiac Muscle Contraction Figure 14-15c: Refractory periods and summation in skeletal and cardiac muscle

Autorhythmic Cells: Initiation of Signals Pacemaker membrane potential I-f channels Na+ influx Ca++ channels – influx, to AP Slow K+ open – repolarization

Autorhythmic Cells: Initiation of Signals Figure 14-16: Action potentials in cardiac autorhythmic cells

Sympathetic and Parasympathetic Sympathetic – speeds heart rate by  Ca++ & I-f channel flow Parasympathetic – slows rate by  K+ efflux &  Ca++ influx Figure 14-17: Modulation of heart rate by the nervous system

Coordinating the Pump: Electrical Signal Flow AP from autorhythmic cells in sinoatrial node (SA) Spreads via gap junctions down internodal pathways and across atrial myocardial cells (atrial contraction starts) Pause – atrioventricular (AV) node delay AV node to bundles of His, branches & Purkinje fibers Right and left ventricular contraction from apex upward

Coordinating the Pump: Electrical Signal Flow Figure 14-18: Electrical conduction in myocardial cells

Coordinating the Pump: Electrical Signal Flow Figure 14-19a: Electrical conduction in the heart

Electrocardiogram (ECG): Electrical Activity of the Heart Einthoven's triangle P-Wave – atria QRS- wave – ventricles T-wave – repolarization Figure 14-20: Einthoven’s triangle

Electrocardiogram (ECG): Electrical Activity of the Heart Figure 14-21: The electrocardiogram

Electrocardiography (ECG) Measures galvanically the electric activity of the heart Well known and traditional, first measurements by Augustus Waller using capillary electrometer (year 1887) Very widely used method in clinical environment Very high diagnostic value 1. Atrial depolarization 2. Ventricular depolarization 3. Ventricular repolarization

12-Lead ECG measurement Most widely used ECG measurement setup in clinical environment Signal is measured non-invasively with 9 electrodes Lots of measurement data and international reference databases Well-known measurement and diagnosis practices This particular method was adopted due to historical reasons, now it is already rather obsolete Einthoven leads: I, II & III Goldberger augmented leads: VR, VL & VF Precordial leads: V1-V6

ECG Information Gained (Non-invasive) Heart Rate Signal conduction Heart tissue Conditions Figure 14-24: Normal and abnormal electrocardiograms

Vectorcardiogram (VCG or EVCG) Instead of displaying the scalar amplitude (ECG curve) the electric activation front is measured and displayed as a vector (dipole model)  It has amplitude and direction Diagnosis is based on the curve that the point of this vector draws in 2 or 3 dimensions The information content of the VCG signal is roughly the same as 12-lead ECG system. The advantage comes from the way how this information is displayed A normal, scalar ECG curve can be formed from this vector representation, although (for practical reasons) transformation can be quite complicated Plenty of different types of VCG systems are in use

Heart Cycle Figure 14-25: Mechanical events of the cardiac cycle

Heart Cycle: Heart Chambers and the Beat Sequence 1. Late diastole: all chambers relax, filling with blood 2. Atrial systole: atria contract, add 20% more blood to ventricles 3. Isovolumic ventricular contraction: closes AV valves ("lub"), builds pressure

Heart Cycle: Finish and Around To the Start 4. Ventricular ejection: pushes open semi lunar valves, blood forced out 5. Ventricular relaxation: aortic back flow slams semi lunar valves shut ("dub") AV valves open refilling starts – back to start of cycle

Summary of Heart Beat: Electrical, Pressure and Chamber Volumes Figure 14-27: The Wiggers diagram

Regulators of the Heart: Reflex Controls of Rate Range: about 50 – near 200 Typical resting: near 70 AP conduction Muscle Contraction Parasympathetic slows Sympathetic speeds

Regulators of the Heart: Reflex Controls of Rate Figure 14-28: Reflex control of heart rate

Definition of Afterload The "afterload" for any contracting muscle is the total force that opposes shortening, minus the stretching force that existed prior to contraction. For cardiac muscle, the afterload is the force against which the myocardial fibers must contact during the ejection phase of systole. Force equals pressure times area, by definition. The total force opposing LV contraction (i.e., the afterload) is the product of the LV pressure and the internal surface area of the LV cavity. In hypertensive subjects, of course, the arterial and LV pressures are abnormally high during systole and, therefore, the LV afterload tends to be high. The internal surface area of the LV varies directly with the volume of blood in the ventricle. If the hypertensive subject also has a dilated LV, the internal area of the LV will be greater than that for a normal subject. Hence, for any given pressure, the afterload tends to increase as the ventricular volume becomes greater. The internal surface area of the ventricular cavity is extremely difficult to measure precisely. Furthermore, both pressure and area change continually throughout ejection. Therefore, it is difficult to assess afterload accurately.

Cardiac Output: Heart Rate X Stroke Volume Around 5L : (72 beats/m  70 ml/beat = 5040 ml) Rate: beats per minute Volume: ml per beat EDV - ESV Residual (about 50%)

Deep Vein Thrombosis

Clot

Leg Swelling from Deep Vein Thrombosis

Pulmonary Embolus

Vena Caval Filter

Cardiac Output: Heart Rate X Stroke Volume Figure 14-26: The Wiggers diagram

Left Ventricular Pressure-Volume Loops Pressure-volume loop plots LV pressure against LV volume through one complete cardiac cycle Factors affecting: Preload Afterload Contractility IHSS Valvular problems

Left Ventricular Pressure-Volume Loops KNOW: When the mitral and aortic valves are open and closed during each phase When systole begins (B) and ends (D) When diastole begins (D) and ends (B) Diastolic filling occurs between points A and B Ejection occurs between points C and D

Left Ventricular Pressure-Volume Loops Acute changes in preload Increased preload: Filling increases SV increases Decreased preload: Filling decreases SV decreases *NOTE: the ventricle empties to the same end-systolic volume after either an increase or decrease in preload

Left Ventricular Pressure-Volume Loops Acute changes in Afterload Increased afterload: Ventricle empties less completely SV decreases Increase in BP (shifts up and right) Decreased afterload: Ventricle empties more completely SV increases Decrease in BP (shifts down and left)

Left Ventricular Pressure-Volume Loops Altered contractility Increased contractility: Ventricle empties more completely SV increases BP increases (shifts up and left) Decreased contractility: Ventricle empties less completely SV decreases BP decreases (shifts down and right)

Left Ventricular Pressure-Volume Loops Summary of concepts: Alterations in preload: end-diastolic volume increases or decreases, but the amount of blood in the chamber at end-systole does not change Stroke volume falls: result of either an increase in afterload or a decrease in contractility, the volume of blood in the LV chamber increases (chamber dilates) Stroke volume increases: result of a decrease in afterload or an increase in contractility, the volume of blood in the LV chamber decreases (chamber shrinks)

Left Ventricular Pressure-Volume Loops A = Normal B = Mitral stenosis C = Aortic stenosis D = mitral regurgitation (chronic) E = aortic regurgitation (chronic)

Regulators of the Heart: Factors Influencing Stroke Volume Starlings Law – stretch Force of contraction Venous return: Skeletal pumping Respiratory pumping

Regulators of the Heart: Factors Influencing Stroke Volume Figure 14-29: Length-force relationships in the intact heart

Regulators of the Heart: Factors Influencing Stroke Volume Figure 14-31: Factors that affect cardiac output