The Cardiac Cycle

RUTGERS

The State University of New Jersey

Systems Physiology

Module 2
Lecture 11
The Cardiac Cycle
Cardiac Output
Chapter 12, Sections (12.4)

Important Topics

  • Events of the Cardiac Cycle

  • Systole vs. Diastole

  • Cardiac output = Stroke volume x Heart rate

Events of the Cardiac Cycle

  • Definition: The orderly process of depolarization triggers a recurring cardiac cycle consisting of atrial and ventricular contractions and relaxations.

  • Phases:

    • The cycle is divided into two major phases:

    • Systole: The period of ventricular contraction and blood ejection.

    • Diastole: The alternating period of ventricular relaxation and blood filling.

  • Typical Heart Rate: At a typical heart rate of 72 beats/minute,

    • Systole: period of heart contraction.

    • Diastole: period of heart relaxation.

    • Cardiac cycle: blood flow through the heart during one complete heartbeat.

    • Atrial systole and diastole precede ventricular systole and diastole.

    • The cycle represents a series of pressure and blood volume changes.

    • Mechanical events follow electrical events seen on an ECG.

  • Phases of the Cardiac Cycle:

    • The cycle consists of three main phases, starting with total relaxation.

Periods During Systole of the Cardiac Cycle

  • Isovolumetric Ventricular Contraction:

    • First part of systole; the ventricles contract, but blood cannot exit as all valves are closed.

  • Ventricular Ejection:

    • Blood is expelled from ventricles into the aorta and pulmonary trunk.

    • Aortic and pulmonary valves open due to rising pressure in the ventricles.

    • Stroke Volume (SV): Volume of blood ejected from each ventricle during systole.

    • Ventricular Filling: Occurs mid-to-late diastole.

    • Pressure is low; approximately 80% of blood passively flows from atria through open AV valves into ventricles while SL valves remain closed.

    • Atrial depolarization triggers atrial systole (P wave), allowing the atria to contract and push the remaining 20% of blood into the ventricles.

    • End Diastolic Volume (EDV): Volume of blood in each ventricle at the end of ventricular diastole.

  • Sequential Events:

    1. Depolarization spreads to ventricles (QRS wave).

    2. Atria finish contracting and return to diastole as ventricles begin systole.

Isovolumetric contraction

  • Atria relax, and ventricles begin to contract.

  • Rising pressure in the ventricles causes the closing of AV valves.

  • The isovolumetric contraction phase is a brief moment where the ventricles are completely sealed, maintaining constant volume while continuing to contract.

  • When ventricular pressure exceeds pressure in the large arteries, the SL valves are forced open, with pressure in the aorta reaching about 120 mm Hg.

  • Isovolumetric Relaxation:

    • Occurs in early diastole.

    • Following ventricular repolarization (T wave), the ventricles relax.

    • End Systolic Volume (ESV): Volume of blood remaining in each ventricle after systole.

    • Ventricular pressure declines, causing backflow from the aorta and pulmonary trunk, leading to the closure of SL valves.

    • This phase is noted as an isovolumetric relaxation period where all valves are closed, and volumes remain unchanged.

Isovolumetric Ventricular Relaxation

  • The first part of diastole; ventricles relax, the aortic and pulmonary valves close, and no blood enters or exits the ventricles.

  • Both AV valves remain closed, leading to no changes in ventricular volume.

  • Ventricular Filling:

    • The AV valves open, allowing blood to flow from the atria into the ventricles.

    • Atrioventricular contraction occurs at the end of diastole, but 80% of ventricular filling happens passively before the atrial contraction.

Understanding the Cardiac Cycle

  • The cardiac cycle comprises the events during one heartbeat.

  • By following pressure changes in an atrium, a ventricle, and a major artery, one can determine when cardiac valves open and close, allowing blood flow.

  • Pressure Dynamics:

    • Blood flows from high to low pressure, contingent on open valves.

    • When pressure graphs intersect, valves open or close:

    • AV valves close when ventricular pressure exceeds atrial pressure.

    • SL valves open when ventricular pressure exceeds aortic pressure.

    • SL valves close when ventricular pressure drops below aortic pressure, with backpressure causing a brief rise in pressure (dicrotic notch).

    • AV valves open when ventricular pressure drops below atrial pressure.

  • Key Heart Sounds:

    • The first heart sound occurs with AV valve closure.

    • The second heart sound accompanies SL valve closure.

    • Diastole (ventricular relaxation) occurs between heart sounds, while systole (ventricular contraction) occurs between the sounds.

  • Isovolumetric Phases:

    • Two periods exist where all valves are closed, and volumes cannot change, termed isovolumetric phases.

Heart Sounds

  • Two primary heart sounds (often termed "lub-dup"), correlated with valve closures:

    • The first sound ("lub") correlates with AV valve closure at the onset of ventricular systole.

    • The second sound ("dup") corresponds to SL valve closure at the initiation of ventricular diastole.

    • The pause between these sounds indicates heart relaxation.

  • Abnormal Sounds:

    • Heart murmurs can signal underlying heart disease, commonly indicative of valve dysfunction.

    • Incompetent Valve:

    • Fails to close entirely, resulting in blood backflow that creates a swishing sound as blood regurgitates backward from the ventricle into the atria.

    • Stenotic Valve:

    • Fails to open fully, constraining blood flow which leads to a high-pitched sound or clicking when blood is forced through a narrowed valve.

Regulation of Pumping

  • Cardiac Output (CO):

    • Defined as the amount of blood pumped out by each ventricle in one minute, measured in Liters/minute.

    • CO is calculated by the formula: CO = HR imes SV where:

    • Heart Rate (HR): The number of heartbeats per minute.

    • Stroke Volume (SV): The volume of blood expelled by one ventricle with each contraction.

    • CO correlates directly with the force of contraction.

    • At rest, maximal CO can range from 4–5 times resting CO in nonathletic individuals (20–25 L/min) and may reach up to 35 L/min in trained athletes.

    • Changes in CO (either increases or decreases) occur if SV or HR varies.

Factors Influencing Cardiac Output

  1. Exercise:

    • Influenced by sympathetic activity, including skeletal muscle and respiratory pumps (see Chapter 19).

  2. Ventricular Filling Time:

    • Affects depend on heart rate.

  3. Hormones:

    • Bloodborne epinephrine, thyroxine, excess Ca2+.

  4. CNS Output:

    • Responses during exercise, anxiety, or variations in blood pressure.

  5. Venous Return:

    • The flow of blood returning to the heart after systemic circulation.

  6. Contractility:

    • Strength of the ventricular contraction.

  7. Sympathetic and Parasympathetic Activity:

    • Primarily influence the heart rate.

  8. EDV (Preload):

    • Volume of blood in ventricles before contraction.

  9. ESV:

    • Volume of blood remaining in ventricles after contraction.

Regulation of Stroke Volume

  • Formula: SV = EDV - ESV

  • EDV:

    • Dependent on the length of ventricular diastole and venous pressure (approximately 120 ml/beat).

  • ESV:

    • Dependent on arterial blood pressure and force of ventricular contraction (approximately 50 ml/beat).

  • Normal Stroke Volume (SV):

    • Calculated as: SV = 120 ml - 50 ml = 70 ml/beat

  • Three Main Factors Affecting SV:

    1. Preload:

    • Changes in end-diastolic volume, or the volume of blood in ventricles just prior to contraction.

    1. Contractility:

    • Changes in sympathetic nervous system stimulation to the ventricles.

    1. Afterload:

    • Changes in afterload, the arterial pressures that the ventricles must overcome to pump blood.

The Frank-Starling Mechanism

  • Principle:

    • The ventricle contracts with greater strength during systole when it is filled more extensively during diastole.

    • Stroke volume increases as end-diastolic volume increases.

  • Mechanism:

    • At specific heart rates, an influx of venous return (the flow of blood returning to the heart) compels an increase in cardiac output via rises in end-diastolic volume and consequently stroke volume.

Additional Factors in Stroke Volume Regulation

  • Preload Definition:

    • The extent to which heart muscle cells are stretched just prior to contraction.

    • Changes in preload impact stroke volume and affect end-diastolic volume.

  • Cardiac Muscle Characteristics:

    • Exhibits a length-tension relationship, optimally responding to stretch.

    • Typically, at rest, cardiac muscle cells are slightly shorter than optimal length, leading to a significant increase in contractile force due to stretching of muscle fibers.

  • Key Influencer:

    • Venous return is vital for determining preload.

    • Slow heart rates or exercise can increase venous return, leading to heart muscules distending, thereby amplifying the contraction force.

Contractility Factors

  • Definition:

    • The strength of contraction at a specified muscle length, independent of muscle stretch and end-diastolic volume.

  • Increased Contractility Features:

    • Reduces end-systolic volume and results from:

    • Sympathetic epinephrine release, which promotes increased Ca2+ influx and cross-bridge formations.

  • Afterload Definition:

    • The pressure that ventricles must surpass to evacuate blood.

    • Notable backpressure from arterial blood pushing on semilunar valves is a significant contributor.

  • Pressure Values:

    • Typical aortic pressure is around 80 mmHg, and pulmonary trunk pressure is around 10 mmHg.

    • Hypertension increases afterload, resulting in augmented ESV and diminished SV.

Clinical—Homeostatic Imbalance

  • Hypocalcemia Effects:

    • Increases heart rate and contractility, shortening action potential duration and QT interval.

    • Results in quicker repolarization and shorter contractions.

  • Hypercalcemia Consequences:

    • Depresses heart function, causing arrhythmias via prolonged plateau phases and extended QT intervals.

  • Hyperkalemia Impacts:

    • Alters electrical activity, potentially leading to heart block and cardiac arrest.

  • Hypokalemia Results:

    • Produces weak heart contractions, arrhythmias, and prolonged action potential durations.

  • Tachycardia:

    • Defined as an abnormally elevated heart rate (>100 beats/min).

    • Can lead to persistent conditions such as fibrillation.

  • Bradycardia:

    • Defined as a heart rate below 60 beats/min, potentially resulting in inadequate blood circulation, especially in nonathletic individuals.

    • This may be an intended outcome of endurance training.

Homeostatic Imbalance of Cardiac Output

  • Congestive Heart Failure (CHF):

    • A progressive condition where CO is insufficient to meet tissue needs.

    • Often reflects myocardial weakening caused by:

    • Coronary Atherosclerosis:

      • Clogged arteries impede oxygen delivery to cardiac cells, leading to hypoxic conditions and inefficient contractions.

    • Persistent High Blood Pressure:

      • Aortic pressure exceeding 90 mmHg increases the myocardial force, pushing ESV higher and causing myocardial hypertrophy and weakening.

    • Myocardial Infarcts:

      • Leads to deterioration of heart function as contractile cells are replaced with scar tissue, weakening overall function.

    • Dilated Cardiomyopathy (DCM):

      • Causes ventricles to stretch and become flabby, leading to further myocardial deterioration.

      • Drug toxicity or chronic inflammation may exacerbate these conditions.

  • CHF Effects:

    • Can affect either side of the heart; left-sided failure leads to pulmonary congestion, while right-sided failure results in peripheral congestion.

    • Blood can pool in body organs, causing edema.

    • Ultimately, the failure of one side can weaken the other, leading to decompensated heart conditions, drastically reducing heart efficacy.

  • Treatment Approaches:

    • Fluid removal and medications to lower afterload and enhance contractility are crucial.

Questions for Review

  • Blood flows neither into nor out of the ventricles during which periods?

    • a. the period of isovolumetric contraction

    • b. the period of isovolumetric relaxation

    • c. diastole

    • d. systole

    • e. both a and b

Additional Question Related to Cardiac Cycle

  • During the period of ejection in the cardiac cycle, the AV valves are and the semilunar valves are .

    • a. closed, closed

    • b. closed, open

    • c. open, closed

    • d. open, open