Summary

This lecture covers the anatomy and physiology of the human heart. It details the structure, function, and circulation of blood through the heart, including the chambers, valves, and coronary circulation. The lecture also discusses the microscopic structure of cardiac muscle and the cardiac cycle.

Full Transcript

Lecture 13: The Heart ===================== **Please read pages 727--757 (excluding 20.7) for this lecture.** **Learning Objectives:** - Describe the anatomical location of the human heart. - Describe the structure of the human heart, including the pericardium, heart wall, surfaces, apex...

Lecture 13: The Heart ===================== **Please read pages 727--757 (excluding 20.7) for this lecture.** **Learning Objectives:** - Describe the anatomical location of the human heart. - Describe the structure of the human heart, including the pericardium, heart wall, surfaces, apex, and base. - Explain how the heart is divided into chambers and describe the structure of these chambers. - Compare and contrast the thickness of each of the chambers of the heart and relate heart wall thickness in each of those chambers to chamber function. - Describe the structure and the function of the heart valves. - Trace the flow of blood into, through, and out of the heart, through pulmonary, and through systemic circulation. - Trace the flow of blood through coronary circulation and describe the function of coronary circulation. - Describe the microscopic structure and function of cardiac muscle tissue. - Explain the basis for autorhythmicity of cardiac muscle tissue. - Describe the structure and function of the cardiac conduction system. - Compare and contrast cardiac action potentials with action potentials in skeletal muscle tissue. - Define refractory period. - Explain how the structure of the heart prevents it from being susceptible to tetanus. - Define electrocardiogram (ECG). - Explain what is occurring in the P, QRS, and T waves of ECGs. - Describe the events that compose the cardiac cycle, especially with respect to blood pressure and volume. - Define heart sounds and explain their physiological basis. - Define cardiac output and describe the factors that regulate stroke volume and heart rate. - Explain how exercise affects heart structure and function. Anatomy of the human heart -------------------------- - **Remember the convention:** The left and right sides of all diagrams are the **left and right sides of that individual's organs** - The cardiovascular system: - Consists of the heart, blood, and blood vessels - The heart is the \_\_\_\_\_\_pump\_\_\_\_\_\_\_\_ that pushes blood throughout the body - Every day, the heart beats 100 000X = \_\_\_35\_\_ \_\_\_\_\_\_\_milllion\_\_\_\_\_\_ times/year = 2.5 billion times/lifetime! - **\_\_\_\_\_\_\_\_cardiology\_\_\_\_\_\_\_\_\_\_\_\_** is the scientific and medical study of the heart, cardiac homeostasis, and homeostatic imbalances - The heart is \~ size of a clenched fist - 250 g in females; 300 g in males - Found in \_\_\_\_\_\_\_\_mediastinum\_\_\_\_\_\_\_\_\_\_ of thoracic cavity Diagram Description automatically generated - The **\_\_\_\_apex\_\_\_\_** (pointed tip) rests on the diaphragm - Formed by the most inferior tip of the **left ventricle** - Points slightly left - The **\_\_\_base\_\_\_\_\_** of the heart (opposite the apex) is angled slightly posteriorly - Formed by the **atria** - The **inferior surface** of the heart rests on the \_\_\_\_\_\_\_diaphragm\_\_\_\_\_\_\_\_\_ - The **right surface** faces the right lung - The **left surface** faces the left lung - The **anterior surface** is deep to and faces the \_\_\_\_\_sternum\_\_\_\_\_\_\_\_ ![A picture containing plastic Description automatically generated](media/image5.tiff) Diagram Description automatically generated **Above left**: Frontal section of the heart. Label the base and apex of the heart. **Above right**: Location of the heart in the thoracic cavity. - The **pericardium** wraps the heart - The **pericardium** comprises two layers: 1. The **fibrous pericardium** - Made of \_\_\_\_\_inelastic\_\_\_\_\_\_ dense irregular CT - Fused with central tendon - Functions: - Protects the heart from \_\_\_\_\_\_\_\_overstretching\_\_\_\_\_\_\_\_\_\_\_ - Anchors the heart in position in the mediastinum 2. The **serous pericardium** - \_\_\_\_\_deep\_\_\_\_\_ to the fibrous pericardium - More fragile - Subdivided into two more layers: I. The **\_\_\_\_\_\_\_\_parietal\_\_\_\_\_\_\_ serous pericardium** - Fused to the fibrous pericardium II. The **\_\_\_\_\_\_visceral\_\_\_\_\_\_\_\_ serous pericardium** i. A.k.a. the **epicardium** - **Pericardial cavity** is the space between the parietal and serous layers - Filled with **pericardial fluid** - Reduces \_\_\_\_\_\_\_\_friction\_\_\_\_\_\_\_ between the heart and its layers during contraction ![Diagram Description automatically generated](media/image12.tiff) - The **heart wall** is deep to the fibrous pericardium - The heart wall consists of three layers: 1. **Epicardium** (or the visceral serous pericardium) - A \_\_\_\_\_\_serous\_\_\_\_\_\_\_\_ membrane: mesothelium + connective tissue - Higher body fat % = more adipose tissue here - Thicker over ventricles, especially left ventricle - Rich with blood vessels and \_\_\_\_\_\_\_\_lymphatics\_\_\_\_\_\_\_\_\_ - Makes the heart slippery Diagram Description automatically generated 2. **\_\_\_\_\_\_\_\_\_\_myocardium\_\_\_\_\_\_\_\_\_\_\_\_\_** - Made of cardiac \_\_\_\_\_\_muscle\_\_\_\_\_ tissue - Bulk (95%) of the heart wall - Like skeletal muscle, wrapped in endomysium and perimysium - Forcefully contracts to pump blood ![Diagram Description automatically generated](media/image13.tiff) 3. **\_\_\_\_\_\_\_\_endocardium\_\_\_\_\_\_\_\_\_\_\_\_\_** - Made of \_\_\_\_\_\_\_\_\_\_\_endothelium\_\_\_\_\_\_\_\_\_ - Lines the chambers and valves of the heart - Continuous with the lining of blood vessels - Reduces friction between blood and the heart ### The chambers of the heart - The heart has four chambers: - The superior two chambers are called **\_\_\_ventricles\_\_\_\_\_** - The **\_\_\_\_\_\_\_\_\_auricles\_\_\_\_\_\_\_\_\_\_\_** are the anterior "wings" of the atria - Increase the volume of blood each atrium can hold - The inferior two chambers are called **ventricles** - **Sulci** are grooves that provide passage for the coronary arteries - May contain fat - The **\_\_\_\_\_\_\_\_coronary\_\_\_\_\_\_\_\_\_\_ \_\_\_sulcus\_\_\_\_\_\_\_\_** runs the boundary between the right atrium and right ventricle - **Interventricular sulcus** runs the boundary between the left and right ventricles - There are two: anterior and posterior Diagram Description automatically generated ![Diagram Description automatically generated](media/image19.tiff)Diagram Description automatically generated Notes: - What do the chambers of the heart do? - The **atria** accept blood that is entering the heart from \_\_veins\_\_\_\_\_\_ - The **ventricles** pump blood into \_\_\_\_\_\_arteries\_\_\_\_\_\_\_ - The right atrium receives blood from systemic circulation - The **right atrium** receives blood from 1. The superior vena cava 2. The inferior vena cava 3. The \_\_\_\_\_coronary\_\_\_\_\_ \_\_\_\_sinus\_\_\_\_ - Pumps blood into the **right ventricle** through the **tricuspid valve** - The blood entering the right atrium **deoxygenated.** - The right ventricle pumps blood into the pulmonary arteries - Pumps blood to the **pulmonary \_\_\_\_trunk\_\_\_\_\_\_** through the **pulmonary (semilunar) valve** - The pulmonary trunk is a large artery with left and right \_\_\_\_\_\_\_branches\_\_\_\_\_ - Blood continues to the lungs to be **oxygenated** - The left atrium receives **blood** from four **pulmonary veins** - The blood entering the left atrium is oxygenated - Pumps blood into the left ventricle through the **bicuspid or mitral valve** - The left ventricle pumps blood into the aorta - Receives blood from the left atrium - Pumps blood into the **\_\_\_\_aorta\_\_\_\_\_\_\_\_** through the **aortic (semilunar) valve** ### Summary of heart chamber function - *Practice on your* own: Trace the passage of blood through the heart. ![Diagram Description automatically generated](media/image21.jpg) - *Practice question*: The blood entering the pulmonary trunk is \_\_\_\_\_\_\_\_deoxygenated\_\_\_\_\_\_\_ and is exiting the \_\_\_\_right ventricle\_\_\_\_\_: A. Oxygenated; right ventricle B. Deoxygenated; right ventricle C. Oxygenated; right atrium D. Deoxygenated; right atrium ### Myocardial thickness and function - The atria are about the same thickness - The ventricles are **thicker** than the atria - The \_\_\_\_left\_\_\_ ventricle is the thickest chamber of the heart. - *Why?* Because it needs to pump blood to the whole body Diagram Description automatically generated ![Diagram Description automatically generated with low confidence](media/image23.tiff) ### The fibrous skeleton of the heart - Heart structure supported by a **fibrous skeleton** - Four rings of dense connective tissue that encircle the **heart \_\_\_\_\_\_\_\_\_valves\_\_\_\_** - Fuse at the interventricular septum - Functions to: - **Prevent overstretching** of the valves - **Providing points of insertion** for cardiac muscles - **Providing electrical \_\_\_\_insulation\_\_\_\_\_\_\_\_\_\_** between the atria and ventricles Diagram Description automatically generated - The valves of the heart - The tricuspid and mitral valves are **\_\_\_\_\_\_\_atrioventricular\_\_\_\_\_\_\_\_\_\_\_\_\_ valves** (AV valves) - Flaps of tissue called **\_\_\_\_cusp\_\_\_\_\_** - Made of dense irregular CT - Lined by the endocardium - Prevent **backflow** of blood from ventricles into atria - How do valves work? - When the atria contract, they **push** blood through the AV valves - Blood moves from an area of \_\_\_\_high\_\_\_ pressure (atria) to \_\_low\_\_\_\_ pressure (ventricles) - The cusps billow *into* the ventricles ![Diagram Description automatically generated](media/image25.tiff) - When the ventricles contract: - The **\_\_\_\_\_\_\_\_papillary\_\_\_\_\_\_\_\_ muscles** contract pull the **chordae tendineae** taut - High pressure of blood pushes against cusps, *closing* the valve - Tension in the chordae tendineae prevents cusp **\_\_\_\_\_eversion\_\_\_\_\_\_\_** - Prevents backflow of blood to the atria A picture containing text Description automatically generated - How do the semilunar valves work? - The pulmonary and \_\_\_\_aortic\_\_\_\_ \_\_\_\_\_valves\_\_\_\_\_\_ are **semilunar valves** - Permit blood to leave the heart and travel into arteries - When open: - Cusps extend into \_\_\_\_\_\_\_arteries\_\_\_\_\_\_\_ - Blood pressure in the ventricles is **greater than** the pressure in the arteries - After ventricular contraction: - Blood pressure in arteries **\_\_\_\_\_exceeds\_\_\_\_\_\_\_\_** that in ventricles - Blood fills cusps of semilunar valves pushes valve *closed* from arterial side - Prevents backflow of blood into ventricles ![Diagram Description automatically generated](media/image27.tiff) A picture containing text Description automatically generated - Review: ![Diagram Description automatically generated](media/image29.tiff) - *Question*: What prevents blood from flowing back into the veins during **atrial contraction?** Atrioventricular valves Coronary circulation -------------------- - Doesn't the heart already contain enough oxygenated blood to meet its own needs? - Yes but \_\_\_\_\_\_\_\_diffusion\_\_\_\_\_\_\_\_\_\_\_ does not happen \_\_\_\_\_\_\_fast\_\_\_\_\_\_\_\_ enough to support robust heart function - Blood vessels that service the heart are called **coronary vessels** - The coronary arteries - Contraction of the heart squeezes the coronary vessels shut - When the heart relaxes: - Blood from the **\_\_\_\_\_\_\_\_\_ascending\_\_\_\_\_\_ aorta** flows into the coronary arteries - Blood moves from high pressure in the coronary arteries to low pressure in the \_\_\_\_\_\_\_\_capillaries\_\_\_\_\_\_\_\_\_\_\_ Diagram Description automatically generated ![Diagram Description automatically generated](media/image30.tiff) - The coronary veins - Deoxygenated blood containing metabolic wastes flows from capillaries into **coronary veins** - Drain into the **coronary \_\_\_\_sinus\_\_\_\_\_\_\_** - Empties into the **right \_\_\_\_\_atrium\_\_\_\_\_\_\_\_**Diagram Description automatically generated Cardiac muscle tissue and the cardiac conduction system ------------------------------------------------------- ![Diagram Description automatically generated](media/image31.tiff) - Recall: the structure of cardiac muscle tissue - Branching, mononucleated, and striated cells - Rich in \_\_\_\_\_\_\_\_mitochondria\_\_\_\_\_\_\_\_ - Intercalated discs containing **desmosomes** and **gap junctions** facilitate coordinated contraction - Exhibit **\_\_\_\_\_\_autorhythmicity\_\_\_\_\_\_\_\_\_\_\_\_\_\_** - Compared to skeletal muscle fibres: - Mitochondria in cardiac muscle fibres both more numerous and \_\_\_\_larger\_\_\_\_\_ - Up to 25% of sarcoplasmic volume! - T-tubules are wider but less numerous - The sarcoplasmic reticulum is less prominent - Cardiac muscle cells can take in calcium from \_\_\_\_\_\_\_\_\_interstitial\_\_\_\_\_ \_\_fluid\_\_\_\_\_ Diagram Description automatically generated - The cardiac conduction system is responsible for autorhythmicity - During embryonic development, \_\_\_1\_\_\_% of cardiac muscle fibres become autorhythmic - Forms the **cardiac conduction system** - Muscle fibres that electrical signals travel through the heart - Reason that heart \_\_\_\_\_\_\_transplants\_\_\_\_\_\_\_\_ work! - How does the cardiac conduction system work? - Signals follow a specific path: 1. The **\_\_\_\_\_\_\_sinoatrial\_\_\_\_\_\_\_\_\_\_ node** (SA node) generates spontaneous action potentials - A.k.a. the \_\_\_\_\_\_\_\_pacemaker\_\_\_\_\_\_\_\_\_ of the heart - Action potentials travel along the sarcolemma of the atrial muscle fibres - Stimulate **synchronous** contraction of both atria 2. Signal reaches the **atrioventricular** (AV) **node** in the **interatrial \_\_\_\_\_\_septum\_\_\_\_\_\_\_** - Travels \_\_\_\_\_\_\_slowly\_\_\_\_\_\_\_\_ to the **atrioventricular (AV) bundle** (a.k.a. the bundle of His) - Why is this signal transmission delayed? 3. Action potential reaches the **AV \_\_\_bundle\_\_\_\_\_\_\_** 4. Signal splits and travels along left and right \_\_\_\_\_branchers\_\_\_\_\_\_\_\_ of AV bundle - Continues toward apex of the heart 5. Signal reaches the **\_\_\_\_\_\_\_\_Purkinje\_\_\_\_\_\_\_\_ fibres** - Extend from apex \_\_\_\_\_\_\_\_superiorly\_\_\_\_\_ along walls of each ventricle - Action potentials stimulate ventricular contraction - Question: sarcolemma - On average, the human heart beats \~75 times per minute - *How many signals does the SA node fire per minute?* \_\_\_\_\_\_\_\_\_\_\_\_\_ - Can you trace the path of signals through the cardiac conduction system on your own? ### Cardiac action potentials - **Action potentials** are electrochemical signals that travel along membranes of electrically-excitable cells - Recall: every membrane has a resting membrane potential - *Is the membrane potential of human cells **positive** or **negative?*** ***negative*** - *What membrane transporter primarily maintains this **resting membrane potential** in cells?* - The Na^+^-K^+^ pump of animal cells maintains the resting membrane potential ![Diagram Description automatically generated](media/image33.tiff) Practice on your own: - **Circle one**: Sodium tends to diffuse into / out of cells. - **Circle one**: Potassium tends to diffuse into / out of cells. - Cardiac action potentials are unique - Broken into three phases: 1. - Electrical signal opens **voltage-gated \_\_\_\_\_\_sodium\_\_\_\_\_\_ (Na^+^) channels** (VGNCs) - When *many* of the VGNCs open, rapidly reverses the membrane potential of cardiomyocytes - Membrane potential is highly \_\_\_\_\_\_\_positive\_\_\_\_\_\_\_ 2. **Plateau** - Unique to cardiac muscle cells - Depolarization also opens **voltage-gated \_\_\_\_\_calcium\_\_\_\_\_\_\_\_ (Ca^2+^) channels (VGCCs)** - *What is the function of Ca^2+^ release?* - In cardiomyocytes, rate of Ca^2+^ entry = rate of K^+^ efflux prolonged depolarization 3. **Repolarization** - Once signal has passed, VGNCs and VGCCs close - VGKCs are \_\_\_\_\_slower\_\_\_\_\_\_ to close - Transport K+ *\_\_\_into\_\_\_\_* of the cell - Restores resting membrane potential Diagram Description automatically generated with medium confidence - What is a **refractory period**? - Length of time that cell cannot respond to another action potential - Consequence of the **\_\_\_\_inactivation\_\_\_\_\_\_\_\_\_\_\_** of VGNCs - At peak depolarization, channel is physically **plugged**, even though the channel is *\_\_\_open\_\_\_\_\_\_* - Refractory periods are \_\_\_\_\_\_\_\_longer\_\_\_\_\_\_\_\_\_\_ than the length of a contraction in cardiac muscle cells - Permits heart enough time to \_\_\_fill\_\_\_\_\_ between contractions - Reason that cardiac muscle is not susceptible to **tetanus** - What is **tetanus**? - Sustained muscle contraction (a.k.a. lockjaw) - Individual \_\_\_\_\_twitch\_\_\_\_\_\_\_ contractions are not distinguishable from one another - Caused by bacterial infection by ***Clostridium tetani*** - Secretes a \_\_\_\_\_\_\_toxin\_\_\_\_\_\_\_ that blocks the release of inhibitory neurotransmitters that promote muscle relaxation into the NMJ ![Tetanus](media/image39.jpeg) - Practice on your own: *Why isn't the heart susceptible to tetanus?* - How do cardiac muscle cells make ATP so that they can contract? - Examine the **structure** of cardiac muscle fibres - *What is the main metabolic pathway used to generate ATP in these cells?* *Aerobic cellular respiration* - *How do you know*? Diagram Description automatically generated - Cardiac muscle cells mainly oxidize molecules - \_\_\_\_\_\_\_\_\_glucose\_\_\_\_\_ (35%) and fatty acids (60%), mostly - Can also oxidize lactic acid - Can directly generate ATP using creatine phosphate - **Creatine kinase** is abundant in cardiomyocytes - When cell death occurs during **myocardial \_\_\_\_\_\_infarctions\_\_\_\_\_\_\_\_\_**, elevated creatine kinase in blood may be a sign The cardiac cycle ----------------- - The cardiac conduction system sends electrical signals - Induce action potentials in cardiac muscle stimulates contraction - When atria or ventricles contract, called **\_\_\_\_\_systole\_\_\_\_\_\_\_** - When relaxed, heart is in **\_\_\_\_diastole\_\_\_\_\_\_\_\_\_\_** - Repeated systole-diastole is called the **cardiac cycle** ![Chart Description automatically generated](media/image40.tiff) - What is an ECG? - An **electrocardiogram** (ECG or EKG) is the recorded changes in \_\_\_\_\_\_\_\_electrical\_\_\_\_\_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_\_currents\_\_\_\_\_\_\_\_\_\_\_ due to action potentials running through all heart muscle - Measured in millivolts (mV) as electrical potential changes - Each **heartbeat** is actually a series of three "waves" on an ECG 1. The P wave triggers **atrial systole** - During the P wave, atrial muscle cells are **\_\_\_\_\_\_depolarized\_\_\_\_\_\_\_\_\_\_\_\_** after receiving a signal from the SA node - \_\_\_\_\_\_stimulates\_\_\_\_\_\_\_\_\_ atrial **systole** - Note: the contraction occurs *after* the P wave! - There is a pause between the P wave and QRS complex - Called the **P--Q interval** - Time for the electrical current to travel from atria AV node conduction fibres in the septum - *What is happening to the heart during this time?* - A longer P--Q interval could be due to heart \_\_\_\_\_\_\_damage\_\_\_\_\_\_\_\_\_\_ - *Explain below:* Diagram, engineering drawing Description automatically generated 2. The QRS complex stimulates ventricular systole - Once the signal has moved from the AV node to the septum, the Q wave starts - The **QRS complex** measures the rapid **\_\_\_\_\_\_\_depolarization\_\_\_\_\_\_\_\_\_** of ventricular muscle fibres - Stimulates \_\_\_\_\_ventricular\_\_\_\_\_\_\_\_\_ systole 3. The T wave leads to cardiac diastole - The **T wave** measures ventricular \_\_\_\_\_\_\_repolarization\_\_\_\_\_\_\_\_\_\_ - Starts at apex and moves toward base - Slower than depolarization (broader, flatter wave than QRS) - Leads to ventricular \_\_\_\_diastole\_\_\_\_\_\_ - Blood pressure in the heart's chambers increases during systole - Cardiac muscle contraction \_\_\_\_\_\_\_\_increases\_\_\_\_\_\_\_\_\_\_\_ **blood pressure** within the heart chambers - Blood pressure (BP) is the \_\_\_\_\_\_\_force\_\_\_\_\_\_\_ of blood on the walls of the cardiovascular system - Blood moves from **high pressure to low pressure** ![Diagram Description automatically generated](media/image42.jpg) Heart sounds ------------ - **\_\_\_\_\_\_\_\_\_auscultation\_\_\_\_\_\_\_\_\_\_\_\_** is the act of listening for heart sounds using a stethoscope - Is a heartbeat the sound of muscle contractions? - NO! - Sound of blood sloshing against vessel walls as heart valves close - **Blood \_\_\_\_\_\_turbulence\_\_\_\_\_\_\_\_\_** Diagram Description automatically generated - There are four major heart sounds: - First sound **S1:** Blood turbulence as \_av\_\_\_ valves close ("lub") - Second sound **S2:** Blood turbulence as \_\_\_\_\_\_semilunar\_\_\_\_\_\_\_\_\_\_\_ valves close ("dupp") - The last two sounds may be too quiet to be heard - **S3:** Blood turbulence during ventricular filling - **S4:** Blood turbulence during atrial filling Review ------ ![Diagram Description automatically generated](media/image44.tiff) Cardiac output -------------- - How is heart function measured? - **Cardiac output (CO)** is the volume of blood pumped out of the ventricles per minute - **Stroke volume (SV)** = volume of blood (L) pumped by the ventricles per contraction - **Heart rate (HR)** = the number of heartbeats per minute - *Write the mathematical formula for CO below:* \ [\$\$\\left( \\frac{\\mathbf{L}}{\\mathbf{\\text{min.}}} \\right) = \\left( L/beat \\right)x\\ (\\frac{\\text{beats}}{\\text{min.}})\$\$]{.math.display}\ - *This means that:* - *In the average male:* - *SV = 70 mL/beat* - *At rest, HR = 75 bpm* - *Calculate the average male cardiac output:* - *Practice on your own: Lance Armstrong at the peak of his career reportedly had a cardiac output of **39 L/min.** Calculate Lance Armstrong's stroke volume, assuming that his heart rate was 50 bpm at the peak of his career.* - ***Cardiac reserve** is the difference between \_\_\_\_\_\_\_\_\_\_maximum\_\_\_\_\_\_\_\_ CO and CO at rest in one person* - *Average person = cardiac reserve of 4--5X resting value* - *Elite athletes = cardiac reserve of \_\_\_\_7-8\_\_\_\_\_\_\_ X resting value* - *If you have little to no cardiac reserve, simple daily tasks (e.g. standing up from sitting) feel exceedingly difficult* - *The regulation of cardiac output* - *Recall: CO is a product of SV and HR* - *Also recall: cardiac muscle tissue is under **involuntary control*** - *Main way to control CO is to change \_\_\_\_\_heart\_\_\_\_\_\_ \_\_\_rate\_\_\_\_\_\_* - ***Autonomic nervous system** (ANS) can increase or decrease HR* - *The cardiac centre regulates responses to changes in blood pressure* - *The heart must respond to a number of signals coming from:* - ***Higher brain centres:** E.g. Emotional stress responses stimulate the \_\_\_\_\_\_\_limbic\_\_\_\_ system sends a signal to cardiac centre* - ***Sensory receptors**, including:* - ***\_\_\_\_\_\_\_\_\_\_\_proprioceptors\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_**: sense body movement (e.g. elevating heart rate during warm up)* - ***Baroreceptors**: sense changes in blood pressure (e.g. changes in elevation)* - ***Chemoreceptors**: sense chemical changes in blood (e.g. elevated CO~2~)* Diagram Description automatically generated - ***Cardiac \_\_\_\_\_\_\_accelerator\_\_\_\_\_\_\_\_\_ nerves** stimulate **\_\_\_\_\_\_\_\_\_\_\_norepinephrine\_\_\_\_\_\_\_\_\_\_\_\_\_** release* - *Hormone that activates "fight or flight" response (sympathetic NS)* - *Stimulates faster SA node firing* - *Opens slow VGCCs increases heart **contractility*** - *Net effect: increased HR, SV, and CO!* - *Vagus nerves act as part of parasympathetic NS and stimulate **\_\_\_\_\_\_\_\_\_\_acetylcholine\_\_\_\_\_\_\_\_\_\_\_** release* - *Neurotransmitter that can **\_\_\_\_\_\_hyperpolarize\_\_\_\_\_\_\_\_\_\_\_\_\_** cardiac muscle cells* - *Decreases HR and, therefore, CO* - *Other things that affect HR (and, therefore, CO!):* - ***\_\_\_\_\_\_\_\_hormones\_\_\_\_\_\_\_\_\_\_**: changes effectiveness of heart contractions (e.g. norepinephrine)* - ***\_\_\_\_\_\_\_cation\_\_\_\_\_\_** availability: K^+^, Na^+^, and Ca^2+^ all required for cardiac muscle contraction* - *Excess K^+^ can block action potentials* - *Excess Na^+^ can outcompete Ca^2+^ for cell entry* - *Excess Ca^2+^ can increase the rate and strength of heart contraction* - *Age* - *Gender* - *Physical fitness* - *Body temperature* - *Your maximal heart rate is determined by a simple formula:* *Maximal hr= 220 bpm -- age(years)* - *Important because CO does NOT increase linearly with HR* - ***Why would there be a maximum heart rate at which cardiac output stops increasing?*** - *How is SV regulated?* - *Through changing three main **properties** of cardiac muscle tissue* 1. ***\_\_\_\_Preload\_\_\_\_\_\_\_\_\_\_*** - *Measure of \_\_\_\_\_\_\_\_stretching\_\_\_\_\_\_\_\_ as the heart fills* - *Like stretching an elastic band: increased stretch more forceful **contraction*** - *Two important factors affecting preload:* I. *Length (in time) of diastole* II. ***Venous return**: volume of blood returning to the right ventricle* 2. ***Contractility** is the strength of myocardial contraction, given a particular preload* - ***Positive inotropic agents** promote Ca^2+^ \_\_\_\_\_influx\_\_\_\_\_\_ during action potentials* - *Increases force of contractions* - ***Negative inotropic agents** increase K^+^ efflux or decrease Ca^2+^ influx during cardiac action potentials* - *Decreases \_\_\_\_force\_\_\_\_\_\_\_ of contraction* 3. ***Afterload** is the pressure of blood required in the ventricles to push the semilunar valves open* - ***\_\_\_\_\_\_\_\_\_\_hypertension\_\_\_\_\_\_\_\_\_\_** or persistently high blood pressure (BP) means BP in the ventricles remain very high* - ***Why?*** *If high in pressure then the ventricles have to generate even higher blood pressure to push the blood to the places it needs to go* *Blood travels high blood pressure to low pressure* - *Hypertension high afterload and decreased SV* - *Blood left in ventricles after systole* - *Summary and review of CO* - *CO is the product of HR and SV* - *Control of HR is the main way the body modulates CO* - *ANS control can increase or decrease HR* - *SV is a product of preload, contractility, and afterload* - *Many factors affect each of the properties of cardiac muscle tissue* Exercise and the heart ---------------------- - Recall that exercise: - Strengthens our bones - Strengthens our muscles and prevents injury - Sustained aerobic exercise **increases \_\_\_\_\_\_\_\_\_maximal\_\_\_\_\_\_\_ cardiac output** (average = 5--7 L/min.) - Increases cardiac reserve - Strong hearts may be enlarged = **cardiac \_\_\_\_\_\_\_\_\_hypertrophy\_\_\_\_\_\_\_\_\_\_** ![A screenshot of a cell phone Description automatically generated](media/image46.tiff) Source: Prior and La Gerche (2011). - Question: Athletes may have enlarged hearts because of their training (e.g. Lance Armstrong at his peak) - Individuals with sedentary lifestyles may also have enlarged hearts - *Why might **inactive** individuals also experience cardiac hypertrophy?* *Because they are hypertensive* *The heart needs to pump the blood to where it needs to go* Summary ------- - The human heart: - Consists of four chambers: two atria and two ventricles, all wrapped in the pericardium - Circulates blood throughout the body (systemic circulation) and oxygenates it (pulmonary circulation) - Makes ATP mainly through aerobic cellular respiration - Contracts in response to unique action potentials initiated by the SA node - Contractions are affected by many factors including hormones, cations, and other physical parameters - Cardiac output is a measure of heart function - Regulated by factors affecting HR and SV - Affects cardiac reserve - Maximized and preserved by regular aerobic exercise

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