Cardiovascular System Notes

19.1 Overview of the Cardiovascular System

The Pulmonary and Systemic Circuits

• Major divisions of the circulatory system

  • Pulmonary circuit: right side of heart

    • Carries blood to lungs for gas exchange and back to the heart

  • Systemic circuit: left side of heart

    • Supplies oxygenated blood to all tissues of the body and returns it to the heart

The Heart

• Approximately fist size

• Location

  • Superior surface of diaphragm

  • Left of the midline

  • Anterior to the vertebral column

  • Posterior to the sternum

The Pericardium

• Fibrous pericardium: dense CT

• Layers of Serous Pericardium:

  • Parietal pericardium: attached to fibrous pericardium

  • Visceral (epicardium) layer: mesothelium and CT and adipose tissue

• Pericardial sac: fibrous and parietal pericardium

• Pericardial cavity: space between visceral and parietal pericardium contains pericardial fluid, prevents friction

The Pericardium

• Functions:

  • Protects and anchors the heart

  • Allows heart to beat without friction

  • Prevents overfilling of the heart with blood

• Pericarditis—painful inflammation of the membranes

19.2 Gross Anatomy of the Heart

• Expected Learning Outcomes

  • Describe the three layers of the heart wall.

  • Identify the four chambers of the heart.

  • Identify the surface features of the heart and correlate them with its internal four-chambered anatomy.

  • Identify the four valves of the heart.

  • Trace the flow of blood through the four chambers and valves of the heart and adjacent blood vessels.

  • Describe the arteries that nourish the myocardium and the veins that drain it.

The Heart Wall

• 3 layers: epicardium, myocardium and endocardium

• Epicardium (visceral pericardium)

  • Serous membrane covering heart

  • Adipose is thick layer in some places

  • Coronary blood vessels travel through this layer

• Endocardium

  • Smooth inner lining of heart and blood vessels

  • Covers the valve surfaces and is continuous with endothelium of blood vessels

The Heart Wall

• Myocardium

  • Layer of cardiac muscle proportional to work-load

  • Which side has more muscle?

  • Muscle spirals around heart (produces wringing motion)

• Fibrous skeleton framework of collagenous and elastic fibers

  • Provides structural support and attachment for muscle and valves

  • Electrical insulation between atria and ventricles (limits spread of action potentials)

External Heart Features

• Coronary sulcus – separates atria and ventricles

• Interventricular sulcus – overlies interventricular septum that divides the right ventricle from the left. Have anterior and posterior interventricular sulci.

• Sulci contain coronary arteries

Atria of Heart

• Top and receiving chambers of heart

• Each atrium has an auricle (seen on surface) to enlarge chamber

• Pectinate muscles: internal ridges of atria and auricles

• Which veins empty into each atria?

Ventricles of Heart

• Lower and discharging chambers of heart

• Trabeculae carneae: internal ridges in both ventricles

• Which arteries do the ventricles empty into?

Myocardial Walls Separate Chambers

• Interatrial septum

  • Wall that separates atria

  • What hole is here in a fetus?

• Interventricular septum

  • Muscular wall that separates ventricles

The Valves

• Valves: ensure one-way flow of blood

• Atrioventricular (AV) valves—control blood flow between atria and ventricles

  • Right AV valve: Tricuspid valve

  • Left AV valve: Mitral valve (formerly ‘bicuspid’)

  • Chordae tendineae: cords connect AV valves to Papillary muscles

    • Prevent AV valves from flipping (eversion) or bulging into atria when ventricles contract

• Semilunar valves

  • Pulmonary semilunar valve: right side

  • Aortic semilunar valve: left side

Blood Flow Through the Chambers

• Blood enters right atrium from superior and inferior venae cavae.

• Blood in right atrium flows through right AV valve into right ventricle.

• Contraction of right ventricle forces pulmonary valve open.

• Blood flows through pulmonary valve into pulmonary trunk.

• Blood is distributed by right and left pulmonary arteries to the lungs, where it unloads CO2 and loads O2.

• Blood returns from lungs via pulmonary veins to left atrium.

• Blood in left atrium flows through left AV valve into left ventricle.

• Contraction of left ventricle (simultaneous with step 3) forces aortic valve open.

• Blood flows through aortic valve into ascending aorta.

• Blood in aorta is distributed to every organ in the body, where it unloads O2 and loads CO2

• Blood returns to right atrium via venae cavae.

Review!!!

• Right atrium à tricuspid valve à right ventricle

• à pulmonary semilunar valve à pulmonary trunk à pulmonary arteries à lungs

• Lungs à pulmonary veins à left atrium

• à mitral valve à left ventricle à

• aortic semilunar valve à aorta à systemic circulation

The Coronary Circulation

• 5% of blood pumped by heart is pumped to the heart muscle

  • Needs abundant O_2 and nutrients

  • Most blood delivered when heart relaxed

• Arterial supply: right & left coronary arteries branch from the ascending aorta

19.3 Cardiac Muscle and the Cardiac Conduction System

• Expected Learning Outcomes

  • Describe the unique structural and metabolic characteristics of cardiac muscle.

  • Explain the nature and functional significance of the intercellular junctions between cardiac muscle cells.

  • Describe the heart’s pacemaker and internal electrical conduction system.

Structure of Cardiac Muscle

• Cardiomyocytes—striated, short, thick, branched cells

• Repair of damage of cardiac muscle is almost entirely by fibrosis (scarring)

• Intercalated discs (cell junction) contain:

  • Interdigitating folds

  • Desmosomes and fascia adherens

  • Gap junctions (electrical junctions)- ions pass through gap junctions

• Smaller sarcoplasmic reticulum: must depend on influx of extracellular Ca^{2+}

• Depends almost exclusively on aerobic respiration to make ATP

  • Rich in myoglobin and glycogen

  • Huge mitochondria

• Adaptable to different organic fuels

  • More vulnerable to oxygen deficiency than lack of a specific fuel

• Fatigue resistant

The Conduction System

• Autorhythmic cells

  • Composed of an internal pacemaker and nerve-like conduction pathways through myocardium

  • Initiate and distribute action potentials through the heart

  • Leads to depolarization and contraction of the rest of myocardium

The Conduction System

• Sinoatrial (SA) node: modified cardiomyocytes

  • Pacemaker (determines heart rate)

• Atrioventricular (AV) node

  • Electrical gateway to the ventricles

• Atrioventricular (AV) bundle (bundle of His)

  • Bundle forks into right and left bundle branches

• Subendothelial conducting networks (Purkinje fibers)

  • Nerve-like processes spread throughout ventricular myocardium

• Cardiomyocytes then pass signal from cell to cell through gap junctions

The Conduction System

• SA node fires.

• Excitation spreads through atrial myocardium.

• AV node fires.

• Excitation spreads down AV bundle.

• Subendocardial conducting network distributes excitation through ventricular myocardium.

19.4 Electrical and Contractile Activity of the Heart

The Cardiac Rhythm

• Sinus rhythm—normal heartbeat triggered by the SA node

  • SA node actually about 100 bpm but vagus nerve slows it to ~75 bpm (vagal tone)

Pacemaker Physiology = Autorhythmic Cells

• SA node does not have a stable resting membrane potential

  • Starts at −60 mV and gradually depolarizes due to slow Na^+ inflow

    • called pacemaker potential

  • When it reaches threshold of −40 mV, voltage-gated fast Ca^{2+} and Na^+ channels open

    • Faster depolarization

  • K^+ channels then open and K^+ leaves the cell

    • Causing repolarization

  • Once K^+ channels close, pacemaker potential starts over

Electrical Behavior of the Cardiomyocytes

• Voltage-gated Na^+ channels open.

• Na^+ inflow depolarizes the membrane and triggers the opening of still more Na^+ channels, creating a positive feedback cycle and a rapidly rising membrane voltage.

• Na^+ channels close when the cell depolarizes, and the voltage peaks at nearly +30 mV.

• Ca^{2+} entering through slow Ca^{2+} channels prolongs depolarization of membrane, creating a plateau. Plateau falls slightly because of some K^+ leakage, but most K^+ channels remain closed until end of plateau.

• Ca^{2+} channels close and Ca^{2+} is transported out of cell. K^+ channels open, and rapid K^+ outflow returns membrane to its resting potential.

Electrical Behavior of the Myocardium

• Has a long absolute refractory period of 250 ms (compared to 1 to 2 ms in skeletal muscle)

  • Prevents wave summation and tetanus which would stop the pumping action of the heart

Electrical Behavior of Muscle Tissue

• Skeletal Muscle

  • Depolarization (Na^+ rushes in) leads to contraction of muscle.

  • Repolarization (K^+ rushes out) “resets” sarcolemma

  • Action potential: 1-2ms

  • Contraction: 15-100ms

• Myocardium

  • Depolarization (Na^+ rushes in) leads to contraction of muscle.

  • Plateau (Ca^+ flows in) allows long refractory and contraction period

  • Repolarization (K^+ rushes out) “resets” sarcolemma

  • Action potential: 200-250ms

  • Contraction: 200ms

Electrical and Contractile Activity of the Heart

• Cycle of events in heart

  • Systole: contraction

  • Diastole: relaxation

• Usually refer to the action of the ventricles

The Electrocardiogram (ECG or EKG)

• Electrocardiogram (ECG or EKG)

  • Composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs, and chest

The Electrocardiogram

• P wave

  • SA node fires, atria depolarize and contract

  • Atrial systole begins 100 ms after SA signal

• QRS complex

  • Ventricular depolarization

  • Complex shape of spike due to different thickness and shape of the two ventricles

• ST segment—ventricular systole

  • Corresponds to plateau in myocardial action potential

• T wave

  • Ventricular repolarization and relaxation

Arrhythmias on ECG

• Coronary artery disease, myocardial infarction, congenital defect,
  hyperthyroidism and valve defects

19.5 Blood Flow, Heart Sounds, and the Cardiac Cycle

• Expected Learning Outcomes

  • Describe how changes in blood pressure operate the heart valves.

  • Explain what causes the sounds of the heartbeat.

  • Describe in detail one complete cycle of heart contraction and relaxation.

  • Relate the events of the cardiac cycle to the volume of blood entering and leaving the heart.

The Cardiac Cycle

• Cardiac cycle—one complete contraction and relaxation of all four chambers of the heart

• Questions to consider: How does pressure affect blood flow? Fluid flows from high-pressure point to low-pressure point

• Heart chamber contractions increase pressure

• Heart chamber relaxations decrease pressure

The Cardiac Cycle

• Cycle of events in heart

  • Systole: contraction

  • Diastole: relaxation

• Usually refer to the action of the ventricles

Phases of the Cardiac Cycle

• Ventricular filling (during diastole)

• Isovolumetric contraction (during systole)

• Ventricular ejection (during systole)

• Isovolumetric relaxation (during diastole)

• The entire cardiac cycle (all four of these phases) is 0.8 sec in a heart beating 75 bpm

Phases of the Cardiac Cycle

• Ventricular filling—takes place in mid-to-late diastole (when heart chambers relax)

• Blood flows passively into atria

• AV valves are open

• 80% of blood passively flows into ventricles while atria relaxed

• Atrial systole occurs, delivering the remaining 20%

• End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole (130 ml)

Phases of the Cardiac Cycle

• Ventricular systole

• Atria relax and ventricles begin to contract

• Rising ventricular pressure results in closing of AV valves causing first heart sound, “lub”

• Isovolumetric contraction phase (all valves are closed; same blood volume and isometric fibers)

• Ejection phase: SL valves open

• End systolic volume (ESV): volume of blood remaining in each ventricle after they have contracted (60 ml)

Phases of the Cardiac Cycle

• Isovolumetric relaxation occurs in early diastole

• Ventricles relax à ventricular pressure drops

• Backflow of blood in aorta and pulmonary trunk closes SL valves (“dup” heart sound) and causes dicrotic notch (brief rise in aortic pressure)

• Ventricles totally closed off again (isovolumetric relaxation)

• Meanwhile, atria fill with blood

• When atrial pressure exceed ventricular pressure, AV valves open à Phase 1: Ventricular filling

Wiggers Diagram

19.6 Cardiac Output

Cardiac Output (CO) and Reserve

• CO is the amount of blood pumped by each ventricle in one minute

• CO is the product of heart rate (HR) and stroke volume (SV)

• HR is the number of heart beats per minute

• SV is the volume of blood pumped out by a ventricle with each beat

  • CO = HR (75 \frac{beats}{min}) \times SV (70 \frac{ml}{min})

  • SV = EDV (130 ml) - ESV (60ml)

• What is tachycardia? Tachycardia is an abnormally rapid heart rate, generally defined as a heart rate exceeding 100 beats per minute in adults. It can be caused by various factors, including stress, exercise, fever, certain medications, and underlying medical conditions such as hyperthyroidism or heart disease. The rapid heart rate may reduce the heart's ability to pump blood effectively, leading to symptoms like dizziness, shortness of breath, chest pain, and palpitations. Severe or prolonged tachycardia can increase the risk of stroke, heart failure, and sudden cardiac arrest. Diagnosis typically involves an electrocardiogram (ECG) to measure the heart's electrical activity. Treatment options

• Bradycardia? Bradycardia: slow heart rate (below 60 bpm in adults), potentially caused by heart conditions, medications, metabolic issues, electrolyte imbalances, or age. Symptoms include fatigue, dizziness, and potential cardiac arrest. Treatment ranges from medication adjustment to pacemaker implantation.

Cardiac Output: Example

• Normal resting values:

  • CO (\frac{ml}{min}) = HR (75 \frac{beats}{min}) \times SV (70 \frac{ml}{beat})

  • CO = 5250 \frac{ml}{min} (5.25 \frac{L}{min})

• Since the average adult’s total blood volume = 5L, this means the entire volume of blood passes through the heart each minute, even when at rest

• Cardiac reserve is the difference between resting and maximal CO

  • Nonathletic: 4-5 times resting CO (20-25 L/min)

  • Athletic: Up to 7 times resting CO (35 L/min)

Heart Rate

• Positive chronotropic agents—factors that raise the heart rate

• Negative chronotropic agents—factors that lower the heart rate

• Increasing heart rate will increase cardiac output to a point. Then CO will decline. Why? When heart rate increases, cardiac output (CO) initially rises because more blood is being pumped per unit of time. However, there's a limit to this increase. Beyond a certain point, further increases in heart rate lead to a decline in cardiac output due to several factors: - Reduced Filling Time: As heart rate increases, diastole (the relaxation phase when the ventricles fill with blood) shortens. This means there is less time for the ventricles to fill completely with blood before the next contraction. Reduced filling leads to a lower end-diastolic volume (EDV), which is the amount of blood in the ventricles at the end of diastole. - Decreased Stroke Volume: Stroke volume (SV) is the amount of blood ejected by the heart with each beat. Because of the reduced filling time and lower EDV at very high heart rates, the stroke volume decreases. According to the Frank-Starling mechanism, the force of contraction is related to the initial stretch of the cardiac muscle fibers. When there is less filling, there is less stretch, and consequently, a weaker contraction and a reduced stroke volume. - Incomplete Ventricular Emptying: At extremely high heart rates, the duration of systole (the contraction phase) may also shorten. This can lead to incomplete ventricular emptying, meaning that not all the blood is ejected from the ventricles during each contraction. This further reduces stroke volume. The combined effect of reduced filling time, decreased stroke volume, and potentially incomplete ventricular emptying results in a decline in cardiac output despite the increased heart rate. Cardiac output is the product of heart rate and stroke volume (CO = HR \\times SV), so if stroke volume decreases significantly, it can offset the increase in heart rate, leading to a lower

Chronotropic Effects of the Autonomic Nervous System

Chronotropic Effects of Chemicals

• Which of the following are positive chronotropic agents and which are negative?

  • Epinephrine- positive

  • Thyroxine (Thyroid hormone)- positive

  • Nicotine- positive

  • Caffeine- positive

  • K+ (Hyperkalemia vs. hypokalemia)- mainly positive

Factors affecting stroke volume

• Preload (End Diastolic Volume)– stretch of ventricles before contraction

• Contractility – cardiac cell contractile force due to factors other than end diastolic volume

• Afterload – force ventricles have to exert against the resistance of vessels leaving the heart

Frank-starling law of the heart: Stroke Volume is proportional to EDV

• Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume (SV)

• Bottomline: the more blood you can get back to the heart, the higher the SV; the more ventricles are stretched, the harder they contract.

• Slow heartbeat and exercise increase venous return to the heart, increasing SV

• Rapid heartbeat decreases SV due to shorter filling time.

Contractility

• Contractility refers to how hard the myocardium contracts for a given preload

• Positive inotropic agents increase contractility

  • Hypercalcemia

  • Catecholamines: These hormones, such as epinephrine and norepinephrine, enhance cardiac contractility and increase heart rate, thereby improving overall cardiac output.

  • Glucagon

  • Digitalis

Contractility

• Negative inotropic agents reduce contractility

  • Hypocalcemia

  • Hyperkalemia

  • Acidosis

  • Drugs such as calcium channel blockers

Afterload

• Afterload—sum of all forces opposing ejection of blood from ventricle

• Afterload mostly is the blood pressure in aorta and pulmonary trunk

  • Opposes the opening of semilunar valves and limits stroke volume

  • Scarring of semilunar valves increases afterload

  • High blood pressure increases afterload and opposes ventricular ejection