Cardiovascular Physiology Flashcards

Measurement of Arterial Blood Pressure

• Arterial blood pressure is expressed as systolic/diastolic.

• Normal blood pressure is 120/80 mmHg.

  • Systolic pressure: Pressure generated during ventricular contraction.

  • Diastolic pressure: Pressure in the arteries during cardiac relaxation.

• Procedure:

  • Place the cuff just above the elbow, with the arrow pointing towards the artery.

  • Ensure the cuff is the proper size. The inflatable tube inside should cover about 40% of the arm circumference. The cuff itself should cover 80% of the area between the shoulder and elbow.

  • Secure the cuff tightly and inflate to about 160 mmHg if at rest.

  • Place the stethoscope on the antecubital space.

  • Slowly release the air from the cuff.

  • Watch the readings and mark the pressure when you first hear a noise (Korotkoff sounds).

  • Continue deflating until all sounds disappear and mark the pressure.

Hypertension

• Hypertension is defined as blood pressure above 130/80 mmHg.

  • Primary (essential) hypertension:

    • Cause is unknown (multifactorial).

    • Accounts for 90% of hypertension cases.

  • Secondary hypertension:

    • Results from some other disease process.

• Risk factors for hypertension include:

  • Left ventricular hypertrophy

  • Atherosclerosis and heart attack

  • Kidney damage

  • Stroke

  • Vascular damage

Arterial Blood Pressure Calculations

• Pulse pressure: The difference between systolic and diastolic pressure.

• Mean arterial pressure (MAP):

  • Average pressure in the arteries.

  • Minimum of 60 mmHg is needed to provide organs with oxygenated blood.

  • Healthy range is 70 to 100 mm Hg.

  • Formula: MAP = DBP + 0.33 (SBP - DBP)

• Pulse Pressure:

  • A pulse pressure of 40 is generally considered normal.

  • Lower pulse pressure may indicate insufficient blood being pumped.

  • Higher pulse pressure indicates a greater risk for heart attack, stroke, or renal and eye problems.

• MAP Importance:

  • MAP is a better measure of perfusion to tissues than systolic pressure.

Blood Pressure Response During Exercise

• Terminate exercise test if:

  • Systolic pressure reaches greater than 250 mmHg.

  • Diastolic pressure reaches greater than 115 mmHg.

  • An acute drop in diastolic blood pressure of 10 mmHg or more with an increase in workload.

• Normal responses to exercise:

  • Gradual increase in systolic and diastolic blood pressure with an increase in workload.

  • Systolic pressure should increase much more than diastolic pressure.

  • Heart rate should also climb with an increase in workload, leveling off at each submaximal work rate.

Factors Influencing Arterial Blood Pressure

• Factors that increase blood pressure:

  • Blood volume increases

  • Heart rate increases

  • Stroke volume increases

  • Blood viscosity increases

  • Peripheral resistance increases

• Determinants of mean arterial pressure (MAP):

  • Cardiac output

  • Total vascular resistance

  • MAP = Cardiac Output \times Total Vascular Resistance

• Short-term regulation:

  • Sympathetic nervous system (SNS)

  • Baroreceptors in the aorta and carotid arteries

    • Increase in BP = decreased SNS activity

    • Decrease in BP = increased SNS activity

• Blood flow equation: Blood flow = \frac{change \ in \ pressure}{resistance \ to \ flow}

• Resistance and Blood Vessel Diameter

  • Resistance to flow increases when the diameter of the blood vessel is reduced.

  • During exercise, blood vessels delivering blood to the muscles dilate to decrease resistance and increase blood flow.

  • As cardiac output (CO) increases, blood vessels must dilate to maintain or increase blood flow.

  • Changing the radius of a vessel by one-half reduces blood flow by 16 times.

Heart Physiology - Cardiac Output

• Cardiac output (CO) is the amount of blood ejected by each ventricle of the heart per minute.

• CO is dependent on heart rate (HR) and stroke volume (SV).

• CO = HR \times SV

• Cardiac reserve: The difference between resting cardiac output and maximum cardiac output. *Example Values (from Table 9.2):

  • Untrained male at rest: HR = 72 beats/min, SV = 70 ml/beat, CO = 5.00 L/min

  • Untrained female at rest: HR = 75 beats/min, SV = 60 ml/beat, CO = 4.50 L/min

  • Trained male at rest: HR = 50 beats/min, SV = 100 ml/beat, CO = 5.00 L/min

  • Trained female at rest: HR = 55 beats/min, SV = 80 ml/beat, CO = 4.40 L/min

  • Untrained male at max exercise: HR = 200 beats/min, SV = 110 ml/beat, CO = 22.0 L/min

  • Untrained female at max exercise: HR = 200 beats/min, SV = 90 ml/beat, CO = 18.0 L/min

  • Trained male at max exercise: HR = 190 beats/min, SV = 180 ml/beat, CO = 34.2 L/min

  • Trained female at max exercise: HR = 190 beats/min, SV = 125 ml/beat, CO = 23.8 L/min

Regulation of Stroke Volume

• To increase CO, either HR or SV (or both) must increase.

• Strategies to increase SV:

  • Increase blood return to the heart (venous return).

  • Increase blood pressure in veins.

  • Decrease blood pressure in arteries.

  • Increase stretch of myocardium by increasing blood volume after diastole.

• Increase contractility of cardiac tissue.

• Venous return increased by:

  • Venoconstriction: Via SNS.

  • Skeletal muscle pump: Rhythmic skeletal muscle contractions force blood in the extremities toward the heart. One-way valves in veins prevent backflow of blood.

  • Respiratory pump: Changes in thoracic pressure pull blood toward heart.

• Vasoconstriction

  • Exercise causes sympathetic stimulation of smooth muscles in veins, constricting them.

  • This reduces their compliance and stiffens them.

  • More blood is diverted back to the heart, increasing preload.

• Respiratory Pump

  • Inhalation: Thoracic cavity expands, increasing volume and decreasing pressure. Blood pressure in the veins decreases, allowing blood to flow more freely back to the heart.

  • Exhalation: Diaphragm pushes up, decreasing thoracic cavity volume and increasing pressure. Veins in the abdominal cavity are under higher pressure, so blood flows up towards the heart to the area of lower pressure.

• End-diastolic volume (EDV): Volume of blood in the ventricles at the end of diastole (“preload”).

• Average aortic blood pressure: Pressure the heart must pump against to eject blood (“afterload”). Equivalent to mean arterial pressure.

• Strength of the ventricular contraction (contractility):

  • Enhanced by circulating epinephrine and norepinephrine and direct sympathetic stimulation of the heart.

• Frank-Starling mechanism:

  • Greater EDV results in a more forceful contraction due to the stretch of ventricles.

  • Dependent on venous return.
    *Stroke volume is dependent on preload, contractility, and afterload.

  • Preload: Amount of stretch of the myocardium. Follows the Frank-Starling law of the heart.

  • Contractility: Responsiveness of cardiac muscle to contract (calcium).

  • Afterload: Blood pressure pushing back off the semilunar valves.

Ejection Fraction

• Ejection fraction in the ventricles is: \frac{End \ diastolic \ volume}{End \ systolic \ volume}

• At rest, this should be about 60%.

• Increasing this improves cardiac output.

• Decreases in EF impair performance and are indicative of either high blood pressure or changes in the ventricle walls.

Changes to CO after Exercise

• After a cardiovascular training program, several major changes occur:

  • Resting heart rate decreases

  • Resting stroke volume increases

  • Decreased cardiac afterload

  • Increased cardiac preload

  • Increased plasma blood volume

  • Left ventricular compliance increased

  • Increased LV ejection fraction

  • Decreased arterial resistance

Electricity and Muscle Cells

*Skeletal muscle
* Action potential time ~1-2 msec
* No resting potential plateu
*Cardiac muscle
* Action potential time ~200-400 msec
* Resting potential plateu

Pacemaker Potential

• Phase 4: Potassium channels shut, sodium leaks into cell through funny channels. Transient Calcium channels open, further depolarizing cell.

• Phase 0: L type calcium channels open.

• Phase 3: Calcium and Sodium channels shut. Potassium channels open.

Regulation of Heart Rate

• Parasympathetic nervous system:

  • Via vagus nerve.

  • Slows HR by inhibiting SA and AV node.

• Sympathetic nervous system:

  • Via cardiac accelerator nerves.

  • Increases HR by stimulating SA and AV node.

• Cardiac Accelerator Center:

  • Medulla Oblongata

  • Sympathetic neurons

  • Interacts with the SA and AV nodes.

  • Driven by changes in activity level, blood pressure, and the chemical environment.

• Cardiac Inhibitory Center:

  • Medulla oblongata

  • Vagal nerve

  • Parasympathetic neurons

  • Keeps heart rate lower between 60-80 beats per minute.

  • If damaged, heart rate sets to 100 beats per minute.

Beta-Blockade and Heart Rate

• Beta-adrenergic blocking drugs (beta-blockers):

  • Compete with epinephrine and norepinephrine for beta adrenergic receptors in the heart.

  • Reduce heart rate and contractility.

  • Lower the myocardial oxygen demand.

  • Prescribed for patients with coronary artery disease and hypertension.

  • Will lower heart rate during submaximal and maximal exercise.

  • Important for exercise prescription.

Heart Rate Variability

• The time between heartbeats.

  • Standard deviation of the R–R interval.

• Balance between SNS and PNS (Sympathovagal balance).

• Wide variation in HRV is considered “healthy”.

• Low HRV is a predictor of cardiovascular morbidity and mortality in patients with existing cardiovascular disease.

Cardiac Muscle Action Potential Phases

• Phase 0: Rapid Na+ influx through open fast Na+ channels.

• Phase 1: Transient K+ channels open and K+ efflux returns TMP to 0mV.

• Phase 2: Influx of Ca2+ through L-type Ca2+ channels is electrically balanced by K+ efflux through delayed rectifier K+ channels (plateau phase).

• Phase 3: Ca2+ channels close but delayed rectifier K+ channels remain open and return TMP to -90mV.

• Phase 4: Na+, Ca2+ channels closed, open K+ rectifier channels keep TMP stable at -90mV.

Conduction System Anatomy Overview

• Sinoatrial node (SA node):

  • Pacemaker, initiates depolarization.

• Atrioventricular node (AV node):

  • Passes depolarization to ventricles.

  • Brief delay to allow for ventricular filling.

• Bundle Branches:

  • Connect atria to left and right ventricle.

• Purkinje fibers:

  • Spread wave of depolarization throughout ventricles.

Electrocardiogram (ECG)

• Records the heart’s electrical activity.

• P wave: Atrial depolarization.

• QRS complex: Ventricular depolarization and atrial repolarization.

• T wave: Ventricular repolarization.

• ECG abnormalities may indicate coronary heart disease.

  • ST-segment depression can indicate myocardial ischemia.

The ECG Tracing

*ECG Intervals and Segments:
* P wave = Atrial depolarization
* QRS complex = Ventricular depolarization
* T wave = Ventricular repolarization
* P-R interval = Time from start of atrial depolarization to start of ventricular depolarization
* Q-T interval = Time from start of ventricular depolarization to end of ventricular repolarization
* S-T segment = Time between ventricular depolarization and repolarization

Cardiac Cycle and Arrhythmia

• Arrhythmia is an abnormal heart rhythm.

• Any disruption to the electrical conduits in the heart can cause this.

• Disruptions to the electrolyte balances in the body as well.