I.

Cardiac Muscle, Conduction, and Fiber Types

● Explore Cardiac Muscle and Conduction

○ The heart is composed of three types of cardiac muscle: atrial, ventricular, and specialized
excitatory and conductive fibers.
○ Cardiac muscle is a syncytium, meaning that cells are interconnected and action
potentials spread rapidly from one cell to the next. There are two syncytia, the atrial and the
ventricular, separated by fibrous tissue.
○ Intercalated discs are cell membranes that fuse to form gap junctions, allowing for rapid ion
diffusion and action potential travel.
○ The specialized excitatory and conductive fibers have few contractile fibrils and instead
exhibit automatic rhythmical electrical discharge and conduction of action potentials.
● Differentiate Cardiac and Skeletal Muscle
○ Both cardiac and skeletal muscle are striated and contain actin and myosin filaments that
slide during contraction.
○ Cardiac muscle contraction lasts longer than skeletal muscle contraction.
○ Cardiac muscle action potentials have a plateau phase due to slower opening of L-type
calcium channels.
○ Calcium ions for cardiac muscle contraction come from both the sarcoplasmic reticulum and
extracellularly during the plateau phase.
○ Skeletal muscle action potentials are caused by fast sodium channels only.
● Distinguish Autorhythmic from Contractile Cardiac Fibers
○ Autorhythmic fibers (e.g., in the SA node) can self-excite, generating rhythmical electrical
impulses. They have a lower resting membrane potential due to leaky sodium and calcium
channels.
○ Contractile fibers (atrial and ventricular muscle) contract in response to action potentials
conducted from the autorhythmic fibers.

II. Action Potentials and the Conducting System

● Explain Cardiac Contractile Fiber Action Potentials

○ Phase 0 (Depolarization): Fast sodium channels open, causing rapid sodium influx and
membrane potential reaches about +20 millivolts.
○ Plateau Phase: L-type calcium channels open, maintaining depolarization.
○ Repolarization: Potassium channels open allowing outward diffusion of potassium, returning
the membrane potential to its resting level.
○ Action potential in ventricular muscle fiber averages 105 millivolts.
● Describe the Heart's Conducting System
○ The conducting system includes:
■ Sinoatrial (SA) node: where the normal rhythmical impulses are generated
■ Internodal pathways: conduct impulses from the SA node to the atrioventricular
(AV) node
■ AV node: where impulses from the atria are delayed before passing into the
ventricles
■ AV bundle (Bundle of His): conducts impulses from the atria into the ventricles
■ Left and right bundle branches and Purkinje fibers: conduct cardiac impulses to
all parts of the ventricles.
○ The Purkinje fibers penetrate about one-third of the way into the muscle mass and become
continuous with the cardiac muscle fibers.
● Compare Ion Effects on Cell Membrane Potentials
○ Sodium influx causes depolarization.
○ Calcium influx during the plateau phase sustains depolarization and activates contraction.
 ○ Potassium efflux causes repolarization.
○ The resting membrane potential of the sinus nodal fiber is lower than that of ventricular
muscle fiber due to leaky sodium and calcium channels.

III. Heart Rhythm and the SA Node

● Identify Conduction System Parts and Functions

○ SA node: Pacemaker of the heart, generating rhythmical impulses.
○ Internodal pathways: Facilitate rapid conduction through the atria.
○ AV node: Delays impulse conduction from the atria to the ventricles, allowing for atrial
contraction before ventricular contraction.
○ AV bundle: Transmits impulses from the AV node to the ventricles.
○ Bundle branches and Purkinje fibers: Ensure rapid and synchronized depolarization of
the ventricles.
● Explain Heart Rhythm Origins
○ The heart's rhythm originates from the SA node due to its faster intrinsic firing rate
compared to other areas of the conduction system.
○ Other parts of the heart (AV node and Purkinje fibers) also have intrinsic rhythmicity, but are
normally overridden by the SA node.
○ AV node fibers discharge at a rate of 40 to 60 times per minute, and Purkinje fibers
discharge at a rate of 15 to 40 times per minute, compared to the SA node's 70 to 80 times
per minute.
● Understand the SA Node's Role as the Pacemaker
○ The SA node's faster discharge rate ensures that it initiates each heartbeat before other
areas of the conduction system can self-excite.
○ The SA node impulse is conducted to the AV node and Purkinje fibers, discharging their
excitable membranes.

IV. Cardiac Conduction System and Arrhythmias

● Discover the Role of the Cardiac Conduction System in Arrhythmias

○ Arrhythmias can arise from abnormal rhythmicity of the pacemaker, shifts in the pacemaker
location, blocks in the conduction pathway, abnormal conduction pathways, or spontaneous
spurious impulses.
○ The conduction system can be damaged by heart disease, especially ischemia, leading to
abnormal heart rhythms.
● Conduction System Creation, Development and Disease
○ The sources do not contain detailed information about the creation and development of the
cardiac conduction system.
○ Disease: Damage to the cardiac conduction system, often from ischemia, can cause bizarre
heart rhythms or abnormal sequences of contraction, severely affecting the heart's pumping
effectiveness.
○ Inflammation of the AV node or bundle can cause heart block.
● Cardiac Cycle Blockages
○ AV blocks are defined as a delay of conduction from the atria to the ventricles.
○ First-degree block is an incomplete AV block with a prolonged PR interval.
○ Second-degree block is an incomplete AV block with dropped beats.
○ Third-degree (complete) block is a complete block of impulses from atria to ventricles, with
the ventricles establishing their own rhythm.

V. Depolarization, ECG, and Cardiac Function

● Learn about Depolarization and ECG Deflection Size

○ Depolarization is the reversal of the normal negative potential inside the muscle fiber.
 ○ The P wave represents atrial depolarization, while the QRS complex represents ventricular
depolarization.
○ The T wave represents ventricular repolarization.
○ The size (amplitude) of an ECG deflection is influenced by the amount of muscle mass
undergoing depolarization, direction of the current flow relative to the electrodes, and
proximity of electrodes to the heart.
● Connect ECG Waveforms to Heart Function
○ The P wave corresponds to atrial contraction.
○ The QRS complex corresponds to the beginning of ventricular contraction.
○ The ventricles remain contracted until after the T wave.
○ There is no electrical potential recorded when cardiac muscle is either completely polarized
or completely depolarized.
● Explain Cardiac Contraction/Relaxation
○ Excitation-contraction coupling occurs when an action potential spreads along the T-tubules
and causes the release of calcium ions into the sarcoplasm, leading to muscle contraction.
○ Relaxation occurs as calcium is removed from the sarcoplasm.
○ Duration of cardiac muscle contraction is mainly a function of the duration of the action
potential.
○ Atrial muscle contracts for approximately 0.2 seconds and ventricular muscle contracts for
approximately 0.3 seconds.

VI. ECG Deflection and Lead Setup

● Recognize That a Parallel Depolarization Vector Maximizes ECG Deflection

○ A vector is an arrow that points in the direction of the electrical potential generated by
current flow.
○ The length of the arrow is proportional to the voltage of the potential.
○ When a heart vector has the same axis as the lead axis, the entire voltage will be recorded.
● Predict the Lead Setup for the Largest ECG Amplitude
○ To maximize the ECG amplitude, place the positive electrode to coincide with the direction of
depolarization, and the negative electrode at the opposite side of the heart.
○ For example, the QRS complex is largest in lead II because the main vector during
ventricular depolarization goes from the base to the apex, with the positive end pointing
towards lead II.
● Chest leads record the electrical potential of the cardiac muscle immediately beneath the electrode.

VII. ECGs in Cardiac Disorders

● Explore the Diagnostic Value of ECGs in Cardiac Disorders

○ ECGs are crucial for diagnosing cardiac arrhythmias, muscle damage, and conduction
system issues.
○ Abnormalities in the ECG can indicate ischemia, hypertrophy, infarction, and other
conditions.
● Examine ECG Patterns for Specific Arrhythmias
○ Atrial fibrillation: Characterized by irregular ventricular rhythm, absence of P waves, and a
low-voltage baseline due to rapid and irregular atrial activity.
○ Premature Ventricular Contractions (PVCs): Characterized by a wide and bizarre QRS
complex that occurs early, often followed by a compensatory pause.
○ Ventricular fibrillation: Characterized by rapid, chaotic, and irregular waves, indicating
uncoordinated ventricular activity.
○ Asystole/Ventricular Standstill: Characterized by a flat line, indicating no electrical activity
of the heart.
VIII. Identifying Arrhythmias

● Identify and Differentiate a Range of Arrhythmias from Rhythm Strips

○ Sinus rhythms: Normal rhythm with a rate between 60-100 bpm, with P waves preceding
each QRS complex.
○ Sinus tachycardia: A faster than normal sinus rhythm, with heart rate >100 bpm.
○ Atrial rhythms: Arrhythmias originating in the atria, including atrial fibrillation and atrial
flutter, will have an abnormal P wave morphology or no discernible P wave.
○ Junctional rhythms: Arrhythmias originating in the AV junction, characterized by an absent
or inverted P wave before or after the QRS complex.
○ Ventricular rhythms: Arrhythmias originating in the ventricles, characterized by wide QRS
complexes.
○ AV blocks: Classified into first, second, and third-degree blocks based on the severity of
conduction delay from the atria to ventricles.

IX. Systole

● Describe Systolic Phases

○ Systole includes:
■ Isovolumetric contraction: Ventricles contract, but volume doesn't change, leading
to increased ventricular pressure.
■ Period of ejection: The aortic valve opens, and blood is ejected from the left
ventricle to the aorta.
● Link ECG, Mechanical, Auditory, and Coronary Events
○ The QRS complex on the ECG precedes the mechanical contraction of the ventricles.
○ The first heart sound (“lub”) occurs at the beginning of systole due to the closing of the AV
valves.
○ Coronary blood flow is reduced during systole due to compression of intramuscular blood
vessels.
● Explain Why Ejection Requires Increased Left Ventricular Pressure
○ The left ventricle must generate enough pressure to exceed the pressure in the aorta in
order to eject blood.
○ Maximum systolic pressure for the normal left ventricle is between 250-300 mm Hg.

X. Diastole

● Describe Diastolic Phases

● Diastole includes:
○ Isovolumetric relaxation: Ventricles relax, but volume does not change, leading to
decreased ventricular pressure.
○ Period of filling: AV valves open, and blood flows from the atria into the ventricles.
● Connect ECG, Mechanical, Auditory, and Coronary Events in Left Ventricular Diastole
○ The T wave on the ECG corresponds to ventricular repolarization, which precedes
ventricular relaxation.
○ The second heart sound (“dub”) occurs at the end of systole due to the closing of the
semilunar valves.
○ Coronary blood flow increases during diastole because there is no longer compression of the
blood vessels.
● Discuss Aortic and Left Atrial Pressure Changes During Relaxation
○ Aortic pressure gradually decreases during diastole but remains higher than ventricular
pressure to maintain blood flow.
○ Left atrial pressure increases as blood fills the atrium.
○ The mitral valve opens when the left atrial pressure exceeds left ventricular pressure.
XI. Arteries, Capillaries, and Circulation

● Discuss Arterial Kinds and Architecture

○ The sources do not explicitly describe different kinds of arteries.
○ Arteries have walls that consist of endothelium, smooth muscle, and connective tissue.
● Capillary Adaptations for Material Exchange
○ The sources do not provide specific information about capillary adaptations for material
exchange.
● Pressure
○ Arterial pressure is higher than venous pressure.
○ Mean arterial pressure is determined about 60% by diastolic pressure and 40% by systolic
pressure.
● Blood Storage
○ Veins can store large volumes of blood.
○ Sympathetic stimulation can decrease venous volume and push blood into the heart.
● Anastomoses and Collateral Circulation
○ Anastomoses are connections between blood vessels that create an alternate route for
blood flow.
○ Collateral circulation is the development of new vessels or the widening of existing
anastomoses to compensate for a blockage.

I. Regulation, Pressure, Resistance, and Blood Volume Control

● Circulatory System Overview: The circulatory system is a transport system that circulates blood
throughout the body in a continuous circuit. It delivers nutrients to tissues, removes waste, carries
hormones, and maintains homeostatic conditions in tissue fluids. The circulation has two main
subdivisions: systemic and pulmonary.
● Hemodynamics: Hemodynamics is the study of the interrelationship among blood pressure, flow,
and resistance.
● Blood Flow: Blood flow is directly proportional to the pressure difference between two ends of a
vessel and inversely proportional to the resistance. This relationship is expressed by Ohm’s Law:
Q=P/R.
● Local Tissue Blood Flow: Local tissue blood flow is controlled according to tissue needs.
● Factors Affecting Blood Flow
○ Vascular cross-sectional area: Velocity of blood flow is inversely proportional to vascular
cross-sectional area.
○ Resistance: Blood flow is impeded by vascular resistance. Slight changes in vessel
diameter markedly change its conductance; conductance increases with the fourth power of
the diameter.
○ Pressure Differences: Blood flows from areas of high pressure to low pressure.
○ Blood Viscosity: Increased blood viscosity increases resistance.
● Mean Systemic Filling Pressure: The mean systemic filling pressure measures how tightly the
circulatory system is filled with blood.
● Arterial Pressure: Arterial pressure is independent of local tissue flow and cardiac output. It is
controlled by nervous reflexes and kidneys. Increased by hydrostatic pressure, especially in the
lower extremities.
● Blood Volume Control: The kidneys play a major role in long-term blood pressure control by
secreting pressure-controlling hormones and regulating blood volume. The renal-body fluid
mechanism is a fundamental mechanism for long-term arterial pressure control.

II. Substance Exchange and Fluid Movement

 ● Microcirculation: Microcirculation involves the smallest blood vessels (arterioles, capillaries,
venules). It is crucial for the exchange of nutrients.
● Capillary Exchange: Fluid filters out of capillaries at their arterial ends and is reabsorbed at the
venous ends. This is due to differences in capillary pressure.
● Fluid Movement:
○ Hydrostatic Pressure: The weight of blood affects veins in different parts of the body.
Capillary hydrostatic pressure forces fluid out of capillaries.
○ Osmotic Pressure: Plasma proteins in the blood create an osmotic pressure that tends to
draw fluid back into the capillaries.
● Edema: Edema develops when there is an imbalance between the forces that cause fluid to move
in or out of the capillaries. An increase in capillary pressure or a decrease in plasma osmotic
pressure can cause edema.

III. Lymphatic System

● Components: The lymphatic system includes lymphatic capillaries, collecting lymphatics, and
lymph nodes.
● Vessel Organization: Lymphatic capillaries are small, thin-walled vessels that collect interstitial
fluid. They merge into larger collecting lymphatic vessels with valves.
● Lymph Dynamics: Lymph flow is determined by interstitial fluid pressure and the lymphatic pump.
● Primary and Secondary Lymphatic Structures: The sources mention "lymph nodes", but do not
fully detail primary and secondary structures. (This concept may be outside the scope of these
sources, and you may need to seek additional material to complete your understanding.)

IV. Blood Vessel Structure and Blood Flow

● Arteries: Arteries carry blood away from the heart. Their walls are strong and elastic. Arteries
transport blood under high pressure.
● Arterioles: Arterioles are small branches of the arterial system that control blood flow into
capillaries. They can constrict or dilate to alter blood flow.
● Capillaries: Capillaries are the smallest blood vessels where exchange of substances occurs.
● Venules: Venules collect blood from capillaries.
● Veins: Veins carry blood back to the heart. They act as a reservoir for blood and can constrict or
enlarge to regulate blood flow. They have thinner walls compared to arteries, and blood flow is at a
slower velocity compared to arteries.
● System of Blood Flow: The heart pumps blood into arteries, which branch into arterioles and then
capillaries. Blood flows through venules into veins, returning to the heart.
● Local Tissue-Level Blood Flow Regulation: Local tissue blood flow is regulated by tissue needs.
Microvessels monitor tissue needs, dilate or constrict to control local blood flow as required.

V. Pulse, Heart Rate, and Pressure

● Pulse: The pulse is caused by the pressure wave of blood moving through the arteries. It can be felt
in arteries close to the surface of the body.
● Systolic Pressure: Systolic pressure is the peak pressure in the arteries during ventricular
contraction.
● Diastolic Pressure: Diastolic pressure is the lowest pressure in the arteries during ventricular
relaxation.
● Pulse Pressure: Pulse pressure is the difference between systolic and diastolic pressure. It is
affected by stroke volume and the compliance of the arterial system.
● Pulse Locations: The sources do not specify pulse locations, but this is a concept you may already
know or need to verify with other sources.
● Tachycardia: Tachycardia is a rapid heart rate.
● Bradycardia: Bradycardia is a slow heart rate.
VI. Blood Pressure Regulation

● Cardiovascular Center: The vasomotor center in the medulla regulates blood vessel diameter.
● Autonomic Nervous System: The autonomic nervous system controls the circulation through
sympathetic and parasympathetic nerves.
○ Sympathetic Nervous System: The sympathetic nervous system increases heart rate,
contractility, and vasoconstriction.
○ Parasympathetic Nervous System: The parasympathetic nervous system decreases heart
rate.
● Baroreceptor Reflex: Baroreceptors in arteries detect changes in blood pressure. The
baroreceptor reflex is a negative feedback mechanism that helps to control arterial pressure.
● Chemoreceptors: Chemoreceptors monitor blood oxygen and carbon dioxide levels and can affect
blood pressure and heart rate.
● Autoregulation: Tissues can autoregulate their own blood flow by constricting or dilating blood
vessels in response to metabolic needs.
● Circulatory Responses to Low Oxygen: When oxygen levels are low, chemoreceptors trigger
increased breathing, heart rate, and vasoconstriction.

VII. Blood Pressure Determinants, Measurement, and Control

● Blood Pressure Determinants: Blood pressure is determined by cardiac output and total
peripheral resistance.
● Blood Pressure Measurement: Systolic and diastolic pressures can be measured using a
sphygmomanometer.
● Long-term Blood Pressure Control: Long-term control of arterial pressure is linked to body fluid
volume, which is regulated by the kidneys. The renal-body fluid mechanism regulates blood
pressure through pressure diuresis and natriuresis.
● Renin-Angiotensin-Aldosterone System: The renin-angiotensin system is a critical long-term
blood pressure control mechanism. Renin release leads to the production of angiotensin II, which
causes vasoconstriction and the release of aldosterone. Aldosterone increases sodium and water
reabsorption in the kidneys, increasing blood volume and pressure.

VIII. Hypertension (HTN)

● Definition: Hypertension is defined as abnormally high blood pressure.

● Symptoms and Signs: The sources do not specifically list symptoms and signs of hypertension.
● Reasons for Treatment: Hypertension is treated to prevent damage to blood vessels, heart,
kidneys and other organs.
● Blood Pressure Goals: The sources do not recommend blood pressure goals.

IX. Cardiac Output

● Definition: Cardiac output is the amount of blood pumped by the heart each minute. It represents
the quantity of blood flowing to the peripheral circulation.
● Calculation: Cardiac output is the product of heart rate and stroke volume.
● Frank-Starling Law: The Frank-Starling law states that the heart pumps more forcefully when more
blood fills its chambers. This increase in contraction is due to increased stretch of the heart muscle,
meaning that increased venous return leads to an increased cardiac output.
● Significance of Frank-Starling law: The Frank-Starling mechanism ensures that the heart pumps
out all the blood that enters it, matching cardiac output to venous return.

X. Stroke Volume and Heart Rate Regulation

 ● Stroke Volume Definition: Stroke volume is the amount of blood ejected by the heart with each
beat.
● Regulation Factors: Stroke volume is influenced by:
○ Preload: The degree of stretch of the heart muscle before contraction.
○ Contractility: The force of the heart's contraction.
○ Afterload: The resistance the heart must overcome to eject blood.
● Heart Rate Regulation: Heart rate is regulated by the autonomic nervous system.
○ Sympathetic Influence: The sympathetic nervous system increases heart rate and
contractility.
○ Parasympathetic Influence: The parasympathetic nervous system decreases heart rate.

I. Venous Blood Return

● Mechanisms of Venous Return: Venous return is the flow of blood back to the heart from the
veins. Several mechanisms facilitate venous return:
○ Pressure Differences: Blood flows from high pressure (peripheral veins) to low pressure
(right atrium).
○ Muscle Contraction: Contraction of skeletal muscles compresses veins, pushing blood
toward the heart.
○ Mean Systemic Filling Pressure: This pressure pushes blood toward the heart.
○ Respiratory Activity: Changes in intrathoracic pressure during breathing can assist venous
return.
○ Venous Valves: Valves within the veins prevent backflow of blood.
○ Sympathetic Stimulation: Sympathetic stimulation can constrict veins, increasing venous
return.
○ Frank-Starling Mechanism: Increased venous return stretches the cardiac muscle, causing
it to contract more forcefully and eject more blood.
● Systemic Veins: The sources mention the vena cavae (inferior and superior) as key systemic veins
that return deoxygenated blood to the right atrium.
● Azygos Vein Components: The azygos vein's function is to drain deoxygenated blood into one of
your body's largest veins (superior vena cava). The superior vena cava carries blood to your heart's
right upper chamber (atrium) so it can reoxygenate blood.

II. Cardiovascular Impact of Long-Term Exercise

● Effects on Lactic Acid: Lactic acid is produced during exercise and is a vasodilator.
● Effects on Respiration: During exercise, there is an increase in respiration to meet the increased
oxygen demand.
● Effects on Cardiac Output: Cardiac output increases significantly during exercise due to increased
heart rate and stroke volume. The cardiac output can increase 4-fold in untrained runners and 7-fold
in marathon runners.
● Effects on Stroke Volume: Stroke volume increases due to increased contractility and venous
return.
● Benefits of Regular Exercise: Regular exercise leads to improved cardiovascular function,
increased cardiac output and reduced risk of cardiovascular disease.

III. Cardiac Reserve, Heart Failure, and Treatment

● Cardiac Reserve: Cardiac reserve refers to the heart's ability to increase its output above normal
resting levels.
○ Changes in Training: Regular exercise increases cardiac reserve.
○ Changes in Heart Failure: Heart failure decreases cardiac reserve.
● Heart Failure Treatment Techniques:
 ○ Medications: The sources mention digitalis as a treatment that increases the strength of
heart contraction and cardiac output in heart failure.
○ Other Treatments: The sources also note that rest is an important part of treating a
myocardial infarction.
● Heart Transplant Procedures: The sources do not describe heart transplant procedures. (You may
need to seek additional material to complete your understanding of this topic.)
● Cardiac Assist Devices: The sources outline how circulatory support devices may be used to
assist in cases of cardiogenic shock.

IV. Heart Sounds

● S1 Heart Sound: S1 is the first heart sound, also known as "lub." It is caused by the closing of the
atrioventricular valves (mitral and tricuspid) at the beginning of systole.
● S2 Heart Sound: S2 is the second heart sound, also known as "dub." It is caused by the closing of
the semilunar valves (aortic and pulmonary) at the end of systole.
● Normal Stethoscope Placement: The different heart valve sounds can best be distinguished by
auscultating specific areas of the chest.
○ Aortic Area: The aortic valve sounds are best heard in the aortic area.
● Normal and Abnormal Heart Sounds: The sources indicate that opening of the valves is typically
not audible while closing of valves produces the normal heart sounds. Abnormal heart sounds can
be indicative of heart defects.
● Abnormal Sound Physiology: The sources do not give details on the physiology of specific
abnormal heart sounds (such as murmurs). You may need to verify this information using outside
sources.

V. Circulation Physiology, Clinical Importance, and Modulation

● Circulation Physiology: The circulation is the system responsible for blood flow, gas exchange,
nutrient delivery and waste removal.
○ Blood Flow Regulation: Blood flow is controlled by tissue needs and regulated by local and
central nervous system mechanisms.
○ Venous Return: Venous return is the flow of blood from the veins to the heart and is critical
for maintaining cardiac output.
● Clinical Importance: Circulatory health is fundamental for the proper functioning of all organs,
making it crucial to prevent circulatory diseases.
● Circulation Modulation: The circulation is modulated by:
○ Autonomic Nervous System: Sympathetic and parasympathetic branches regulate heart
rate, contractility, and blood vessel diameter.
○ Baroreceptors Arterial baroreceptors are important for blood pressure regulation.
○ Chemoreceptors: Chemoreceptors affect blood pressure and heart rate.
○ Hormones The renin-angiotensin system affects long-term blood pressure.
● Blood-Brain Barrier: The sources do not discuss the blood-brain barrier. (You may need to seek
additional material to complete your understanding of this topic.)
● Hypoxia-Induced Pulmonary Vasoconstriction: The sources mention that low oxygen levels
cause blood vessels to relax, but the specific details of hypoxia-induced pulmonary vasoconstriction
are not in the sources. (You may need to seek additional material to complete your understanding of
this topic.)
● Skeletal Muscle Pump: The skeletal muscle pump assists venous return by compressing veins
during muscle contraction.

VI. Heart Supply-Demand and Coronary Artery Disease

● Heart Supply-Demand: The heart's oxygen demand is met by coronary blood flow. The heart
needs increased oxygen during increased activity.
 ● Coronary Plaque: The sources mention coronary artery disease and the formation of plaques.
● Unstable Angina: The sources do not explicitly define unstable angina. (You may need to seek
additional material to complete your understanding of this topic.)
● Myocardial Infarction: Myocardial infarction is caused by blockage of coronary arteries, leading to
reduced blood supply to the heart muscle.
○ Symptoms: The sources do not give specific symptoms of myocardial infarction, but note
that pain is often experienced.
○ Causes: Decreased coronary blood flow, damage to the heart valves, and external pressure
around the heart can all contribute to myocardial infarction.
● Risk Factors: The sources do not explicitly list all the risk factors for heart attack, but do mention
hypertension.
● Strokes: The sources do not define strokes and their causes and types. (You may need to seek
additional material to complete your understanding of this topic.)

VII. Shock

● Definition of Shock: Shock is a state of inadequate blood flow to the tissues, resulting in cellular
damage.
● Four Types of Shock: The sources do not specifically delineate four types of shock, but mention
cardiogenic shock, which results from heart failure. The sources also describe shock due to
hemorrhage.
○ Cardiogenic Shock: Caused by the heart's inability to pump blood effectively.
○ Hemorrhagic Shock Caused by a loss of blood volume.
● Regulation of the Body's Response to Shock:
○ Negative Feedback: The body uses negative feedback mechanisms to try to restore blood
flow and pressure during shock.
○ Sympathetic Nervous System: Sympathetic reflexes are initiated to increase heart rate,
contractility, and vasoconstriction. However, in progressive shock, these mechanisms are not
able to adequately compensate for the reduced blood flow.