Cardiovascular Physiology

Functioning of Heart Mechanical Events Electrical Events Automatic or involuntary Electrical Events

Mechanical Events Cardiac cycle Four Phases One cycle = One beat Isovolumic Contraction Time (IVCT) Systole Isovolumic Relaxation Time (IVRT) Diastole

IVCT Immediately before systole All four valves closed Volume remains the same in ventricle Atrial volumes change Pressure builds in ventricle

Systole Ventricular Pressure Rises Ejection AV valves closed When pressure in ventricle is greater than the pressure in the great vessels the Semilunar valves open Ejection Begins at apex and goes up AV valves closed Pressure pushes against valves Pressure in Great Vessels Rise When pressure in the great vessels gets higher than pressure in the ventricle the Semilunar valves close The closure of the semi lunar valves is the 2nd Heart Sound

IVRT Immediately before diastole All four valves closed Volume remains the same in ventricle Atrial volumes change Atrial pressure rises Pressure drops in ventricle

Diastole Atrial Pressure Early Diastole When the atrial pressure gets higher than the ventricular pressure the AV valves open Early Diastole LV pressure at lowest Rapid Filling Phase “sucking effect” because of negative pressure 70-75% of filling If heart abnormal may hear 3rd Heart Sound

Diastasis As ventricular walls become stretched, flow slows down Left ventricle and atrium pressure equalize out Atrial Kick Happens at end-diastole 30% of blood Corresponds to “P” wave on EKG 4th Heart Sound in some abnormal hearts

End Diastolic Volume Pressure Increases The amount of blood in the ventricles at this point Largest amount of blood in the heart during entire cardiac cycle (measurements at End Diastole) Pressure Increases Pressure in the ventricles increases Forces the AV Valves to close Closure of the AV Valves is 1st Heart Sound

The Heart Must Have Volume and Pressure

Cardiac Function Supply and Demand Heart’s job to provide us supply of oxygen This is done through Cardiac Function Systolic Function Diastolic Function

Systolic Function Definition - Ability of ventricles to efficiently eject blood out of the heart and into systemic and pulmonary systems Decreased systolic function-indicator of heart disease

Diastolic Function Definition – Ability of the ventricles to relax and fill. (referred to as ventricular relaxation and compliance) Indicates whether the ventricular filling pressure or normal or increased (referred to as ventricular end diastolic pressure Decreased diastolic function (Diastolic Dysfunction) precedes Systolic dysfunction

Diastolic Dysfunction Definition – failure of the ventricles to relax and allow normal filling Indicator of heart disease

Cardiac Function Components Cardiac function dependant on several factors Wall thickening Wall motion Chamber size Ventricular end diastolic pressure

Wall Thickening and Wall Motion Known as Contractility Indicator of adequate coronary blood flow and oxygenation

Terminology Hyperkinetic Hypokinetic Dyskinetic Akinentic Excessive wall motion Hypokinetic Decreased wall motion Dyskinetic Movement away from the center of the cavity. This may indicate myocardial infarction (MI) Akinentic Mo movement or thickening of the myocardium

Facts about Akinesis Akinesis may be indicator of hibernation or MI Hibernation-ischemic segment that is akinetic but not infarcted. Can be reversed with restoration of blood flow Echo can not differentiate between hibernation and MI. But chronic infarct may have thinning walls

Wall Motion Abnormality Normal wall- concentrically thicken and contract approx 30% toward center of chamber during systole If does not thicken or contract properly called wall motion abnormality (WMA) WMA indicator of ischemic heart disease Can be global or localized

Dysfunction When myocardium become ischemic, ventricle will have abnormal relaxation (ability to accept blood and fill) This is called diastolic dysfunction Ischemia will cause decreased systolic function (ability to pump blood effectively) If severe may become akinetic or is can not compensate for increased pressure, may become dyskinetic

Chamber Size Normal-should concentrically decrease in size during systole (contract) During diastole- should concentrically increase in size (filling) Measurements – several methods to quantify

Pressure End diastolic pressures (EDP) corresponds to degree of fiber stretch in ventricles The degree of fiber stretch depends on the quantity of blood in the chamber prior to contraction The greater the amount of blood entering the chamber, the greater the contraction required to expel the blood (Frank-Starling Law) EDP can be determined by examining flow through the valves with doppler

Cardiac Output If you go for run your body’s demand for oxygenated blood increases Your heart must meet the demand for oxygen with supply. Can meet demand by increasing heart rate and/or stroke volume

Heart Rate Stroke Volume (SV) The number of times the heart beats per minute (bpm) Normal resting 60-100 Stroke Volume (SV) Definition - the volume of blood ejected with each heart beat Normal resting 70-100 ml SV depends on Left Ventricular End Diastolic Volume (LVEDV) and Heart Rate (HR) The greater the LVEDV and/or HR; the greater the SV The combination of HR and SV determine Cardiac Output (CO)

Cardiac Output Definition - the volume of blood pumped from the ventricle each minute Calculated as stroke volume X heart rate Normal 4-8 liters per minute ( l/min) CO(l/min)= SV X HR

Cardiac Index Cardiac index is the CO corrected for body surface area (BSA) Normal 3-4 l/min2 BSA is the calculated surface area of the human body Normal 1.73 m2 (but varies with size and age) Mosteller formula (Height [inches] X weight [lbs] / 3131)(1/2)

Review Equations SV =EDV-ESV CO = SV X HR CI = CO / BSA (hint…hint…)

Blood Pressure Reading that corresponds to pressure in arteries Systolic Diastolic Reads as fraction mmHg Normal 100-140 60-90

The heart’s ability to increase the CO dependent on Preload Afterload Inotropic Force Chronotropic Force

Preload Preload-The volume (load) in the heart at the end of diastole LVEDP-The degree of fiber stretch related to the quantity of blood in the chamber prior to contraction

Frank Starling Law Frank Starling Law- (Length–Tension Relationship) The more blood that enters the heart during diastole (preload); the greater the force of contraction (systole) required to eject the blood In other words…Increased myocardial fiber length means increased tension

Interval-Strength Relationship The longer the interval between heartbeats; the stronger the contraction required to eject the blood PVC Increased preload requires stronger contraction to eject blood This is called extrasystolic potentiation

Force-Velocity Relationship The greater the force required to eject the blood; the slower the velocity of muscle fiber shortening

Facts About Preload Preload is increase by any state of fluid overload, such as valvular regurgitation, ventricular septal defect (VSD), atrial septal defect (ASD), or Patent Ductus Arteriosus (PDA)

Valvular Regurgitation Abnormal backwards flow through a “closed” valve that doesn’t close properly

Ventricular Septal Defect A defect in the interventricular septum that allows abnormal flow between the left and right ventricle

Atrial Septal Defect Defect in the interatrial septum that allows abnormal flow between the left and right atrium

Patent Ductus Arteriosus When the Ductus Arteriosus (a connection between the aorta and pulmonary artery during fetal circulation) does not close properly at birth and remains patent (open)

The ductus arteriosus, shown encircled with suture on the specimen on the left, extends from the pulmonary artery ventrally to the aorta dorsally, bypassing the lungs in fetal circulation. After birth the blood oxygen tension increases, causing the ductus to constrict and eventually become the ligamentum arteriosum, shown encircled on the specimen on the right

Increased preload (volume) results in dilation of the heart chambers

Afterload Afterload- The resistance that the heart must pump against The higher the resistance; the greater the contractility of the ventricles The resistance can be anywhere in the circulatory system- not just in heart

Facts About Afterload Afterload is increased by any state of pressure overload such as aortic stenosis, idiopathic hypertrophic subaortic stenosis, pulmonic stenosis, systemic hypertension, of pulmonary hypertension

Ventricular Outflow Tract Obstructions Aortic stenosis, idiopathic subaortic stenosis, pulmonic stenosis are all forms of outflow tract obstructions

Systemic Hypertension Definition-systolic B/P above 140 mmHg and a diastolic B/P above 90 mmHg on three consecutive readings

Pulmonary Hypertension Definition- An increased systolic pulmonary artery pressure above 30

Increased afterload results in hypertrophy (thickening) of the myocardium because the myocardium is required to generate more tension in order to perform its task

Inotropic Force Definition – Force of contraction (contractility of the heart muscle)

Chronotropic Force Definition – Rate of contraction (heart rate)

Autonomic Nervous System Involuntary nervous system Controls tissues that are not under volunatary control Heart Smooth muscles Glands Responds to the metabolic needs of body Sympathetic Parasympathetic

Sympathetic Fight or Flight Increases heart rate to give body extra oxygen it needs for “fight” or “flight” Survival instinct

Parasympathetic Decreases heart rate by the vagus nerve (not Vegas) Rest and digest system, functions with actions that do not require immediate reaction A useful acronym to summarize the functions of the parasympathetic nervous system is SLUDD(salivation,lacrimatation,urination, digestion and defecation).

Maneuvers That Alter Cardiac Physiology Valsalva Most common in echo Bearing Down Releasing Amyl Nitrate Small capsule that is broken and ask pt to inhale fumes Decreased peripheral resistance which increased HR rate, SV and CO

Other Maneuvers Inspiration increases venous return, SV & CO Expiration decreases venous return, SV & CO Squatting increases venous return, SV & CO Standing decreases venous return, SV & CO

The End