Chapter 20: The Heart

Four functions of the connective tissue fibres of the heart

- 1) Provide physical support for the cardiac muscle fibres, blood vessels, & nerves of the myocardium - 2) Help distribute the forces of contraction - 3) Add strength & prevent over expansion of the heart - 4) Provide elasticity that helps return the heart to its original size & shape after a contraction

Brachycardia

- A condition in which the heart rate is slower than normal - Abnormally slow heart rate (<60 beats per minute) - N.b. definition varies with normal resting heart rate of the individual

Coronary sulcus

- A deep grove that marks the border between the atria & the ventricles

Fibrous pericardium

- A dense network of collegan fibers that forms an outer layer - Stabilises position of heart & associated vessels within mediastinum

Tachycardia

- A father than normal heart rate - Abnormally rapid heartbeat (>100 beats per minute) - N.b. definition varies with normal resting heart rate of the individual

Interatrial septum

- A muscular partition (wall) that separates the atria

Interventricular septum

- A muscular partition (wall) that separates ventricles - Is much thicker than interatrial septum

Cardiac contractile cells action potential step 2 - The Plateau

- A partial repolarization takes place as some potassium ions (K+) leave the cell before most K+ channels close - Voltage-gated calcium ions then open & extracellular calcium ions (Ca2+) enter the cytosol - Slow calcium ion channels remain open for a relatively long period (about 175 msec) - Inflow of positive charges (Ca2+) & reduced outflow of K+ delay repolarization, causing membrane to remain near 0 mV for an extended period (plateau action pot) - Extracellular calcium ions initiate contraction & delay replorization, while triggering release of Ca2+ from sarcoplasmic reticulum - Ends with closure of slow calcium ion channels

Paroxysmal Atrial Tachycardia (PAT)

- A premature atrial contraction triggers flurry of atrial activity - Ventricles are still able to keep pace & the heart rate jumps to about 180 beats per minute - Generates normal QRS

Electrocardiogram (ECG)

- A recording of the electrical events of the conducting system (i.e. can see electrical events of heart) - Used to assess functions of specific pacemaker, conducting, & contractile cells - Provides summation of all electrical potentials - P wave = atrial depolarization - QRS complex = ventricular depolarization (hides atrial repolar) - T wave = ventricular repolarization - Time between R & R = heartbeat

Aortic valve

- A semilunar valve - Blood leaves left ventricle through this & then goes into ascending aorta, then into the aortic arch & finally enters the descending aorta - The arrangement of cusps in aortic valve is the same as in pulmonary valve - Once blood is pumped out of heart & into systemic system then aortic valve prevents backflow into left ventricle - Doesn't need muscular braces like antrioventricular valve

Trabeculae carneae

- A series of muscular ridges on internal surface of right ventricle - Moderator band

Relative refractory period

- A shorter period (50 msec) that follows the absolute refractory period - During this period, the voltage-gated sodium ion channels are closed, but can open - The membrane will respond to a stronger-than-normal stimulus by initiating another action potential

Heartbeat

- A single cardiac contraction - All chambers of the heart contract in a series: first the atria & then the ventricles - Electrical impulses of the conducting system initiate the contraction of the heart chambers

Fossa ovalis

- A small, shallow depression (remnant of foramen ovale) observed in the adult heart

Anterior cardiac veins

- AKA anterior veins of right ventricle - Drains the anterior surface of the right ventricle, empty directly into the right atrium

Sinoatrial (SA) node

- AKA cardiac pacemaker, it is part of conducting system & is the primary driver of the heart rate - Generates impulses at regular intervals - Is embedded in posterior wall of right atrium near entrance of superior vena cava - Generates action potential at faster rate than AV node, so it establishes heart rhythm (sinus rhythm) due to reaching threshold first - Connected to Atrioventricular (AV) node by the internodal pathways in atrial walls

Systole

- AKA contraction & is a phase of cardiac cycle - Chamber contracts & pushes blood into adjacent chamber or into an arterial trunk - Blood pressure within each chamber rises - Followed by diastole

Pacemaker cells

- AKA nodal cells as they are found in the sinoatrial (SA) & atrioventricular (AV) nodes - Are essential for establishing the normal heart rate

Diastole

- AKA relaxation & is a phase of cardiac cycle - Chamber fills with blood & prepares for next cardiac cycle - Blood pressure within each chamber falls

Visceral pericardium layer

- AKA the epicardium - Inner layer - Covers & adheres closely to outer surface of heart

Process of action potential in cardiac contractile cells

- Action potential begins when membrane of ventricular contractile cell reaches threshold of about - 75 mV - Threshold normally reached next to intercalated disc - Typical stimulus is excitation of adjacent contractile cell - Once threshold reached, action potential proceeds in 3 steps which are: 1) Rapid depolarisation, 2) Plateau, & 3) Repolarization

The Role of Calcium Ions in Skeletal Muscle Contractions

- Action potential is relatively brief & ends as the resulting twitch contraction begins - Twitch contraction is short & ends as sarcoplasmic reticulum reclaims the Ca2+ it released - Refractory period ends before peak tension develops, thus twitches can summate & tetanus can occur

Veins

- Afferent vessels, return blood to heart

Impulse conduction through the heart - Step 4:

- After brief delay, impulse travels along interventricular septum within the atrioventricular bundle & bundle branches to pukinje fibers & (through moderator band) to papillary muscles of the right ventricle

Affects of autonomic activity on contractility

- Alters degree of contraction & changes ESV in the following ways - Sympathetic stimulation has +ve intropic effect - Parasympathetic stimulations from vagus nerves has -ve inotropic effect

End Diastolic Volume (EDV)

- Amount / volume of blood that each ventricle will hold at the end of ventricular diastole - Total filling in each ventricle - EDV = ventricular filling time (HR) + venous return - Increase venous return, increase volume volume of blood you can get into the heart - Determined by available filling time & rate of venous return

Stroke volume (SV)

- Amount of blood pumped out of a ventricle during each contraction - Volume of blood ejected from heart per heart beat - Most important factor in an examination of a single cardiac cycle - SV = end diastolic volume (EDV) - end systolic volume (ESV) - Peaks when EDV is highest & ESV is lowest

End Systolic Volume (ESV)

- Amount of blood remaining in ventricle when semilunar closes at end of ventricular systole (after contraction) - Dependent on: 1. Preload (degree of myocardial stretching) 2. Contractility (force of contraction, which is adjusted by hormones & autonomic innervations) 3. Afterload (arterial resistance to blood flow out of heart)

Venous return

- Amount of blood returned to the heart by the veins, which directly affects pacemaker cells - When increases, atria receives more blood so walls stretched thus cardiac pacemaker cells of the SA node are stretched, resulting in rapid depolarisation & increase in heart rate

Contractility

- Amount of force produced during a contraction at a given preload - Under normal circumstances can be altered by autonomic innervation or by circulating hormones - Under special circumstances can be altered by drugs or by abnormal ion concentrations in extracellular fluid - Factors affecting this are either positively or negatively inotropic

Cardiac output (CO)

- Amount of of blood pumped by left ventricle in one minute - Indication of blood flow through peripheral tissues (& without adequate blood flow homeostasis cannot be maintained) - Provides useful indication of ventricular efficiency - Can be adjusted by changes in either heart rate (HR) or stroke volume (SV) (e.g. if these increase then CO increases) - CO = heart rate (HR) X stroke volume (SV) - Cannot increase indefinitely, mainly because the available filling time shortens at HR increases

Afterload

- Amount of tension the contracting ventricle must produce to force open the semilunar valve & eject blood - Increases with increased resistance to blood flow out of ventricles - Increase / greater afterload results in: longer period of isovolumetric contraction, shorter duration of ventricular ejection, increase / larger ESV, & decrease in stroke volume (heart has to work harder to eject same amount of blood) aka systemic blood pressure - Any factor that restricts blood flow through arterial system increases afterload -High arterial blood pressure increases afterload

Rheumatic fever

- An important cause of Carditis (an inflammation of the heart) - Is an inflammatory autoimmune response to an infection to streptococcal bacteria - It most often occurs in children

Conducting system of the heart

- An internal network that coordinates the contractions of cardiac muscle cells - The cells that initiate and distribute the stimulus to contract are part of heart's conducting system - Network of specialized cardiac muscle cells, called pacemaker cells & conducting cells, that initiates & distributes electrical impulses Includes: 1. Sinoatrial (SA) node 2. Atrioventricular (AV) node 3. Conducting cells

Arrhythmia

- An irregularity in the normal rhythm or force of heartbeat - May indicate damage to mayocardium, injuries to pacemakers or conduction pathways, exposure to drugs, or abnormalities in electrolyte composition of extracellular fluids

Foramen ovale

- An oval opening that penetrates interatrial septum & connects the two atria of the fetal heart - Before birth: permits blood to flow from right atrium to left atrium while the lungs are developing - At birth: foramen ovale closes, & the opening is permanently sealed off within three months of delivery to result in the fossa ovalis

The Role of Calcium Ions in Cardiac Contractions

- Appearance of an action potential produces a contraction by causing an increase in the Ca2+ concentration around the myofibrils in 2 steps 1. Ca2+ ions crossing the plasma membrane during plateau phase provide 20% of Ca2+ required for a contraction 2. Arrival of this extracellular Ca2+ triggers release of more Ca2+ from reserves in the sarcoplasmic reticulum - Thus, extracellular calcium ions have both direct & indirect effects on cardiac contractile cell contraction

QRS complex

- Appears as ventricle contractile cells depolarize (SA node has fired) - Relatively strong because ventricular muscle is much more massive than atria - Ventricles begin contracting shortly after the peak of the R wave - Excessively large QRS complex often indicates that the heart has become enlarged

Great vessels

- Are the largest veins & arteries in the body, with these being connected to the heart - Are attached at the base of the heart

Capillaries

- Are thin-walled vessels that interconnect the smallest arteries & the smallest veins - Often called exchange vessels as their thin walls permit exchange of nutrients, dissolved gases, & wastes between blood & surrounding tissue

Coronary artery disease (CAD)

- Areas of partial or complete blockage of coronary circulation - Reduction of blood flow (& thus reduced oxygen & nutrients) to heart muscle produces a corresponding reduction in cardiac performance via coronary ischemia - Most common result: heart attacks

Cardiac contractile cells action potential step 3 - Repolarization

- As plateau continues, slow calcium ion channels begin closing, & slow potassium channels begin opening - As these channels open, potassium ions (K+) rush out of the cell, & the net result is a period of rapid repolarization that restores the resting membrane potential

Cardiac contractile cells action potential step 1 - Rapid depolarization

- At threshold, voltage-gated sodium ion channels open, & membrane suddenly becomes permeable to Na+ - A massive influx of sodium ions rapidly depolarises the sarcolemma - Channels involved are called fast sodium channels as they open quickly & remain open for a few milliseconds

Impulse conduction through the heart - Step 2:

- Atrial activation begins due to conducting cells passing stimulus to contractile cells of both atria, so the action potential then spreads across atrial surfaces by cell-to-cell contact, to reach the AV node - Only atria affected by stimulus as cardiac skeleton isolates atrial myocardium from ventricular myocardium

Electrical impulses leading to heartbeat via contractions

- Begins with action potential (AP) generated by cells (at SA node - pacemaker) of conducting system - Other cells of conducting system then propagates & distributes electrical impulse to stimulate contractile cells to push blood in right direction at proper time - Electrical impulse arrives at cardiac contractile cell's plasma membrane produces AP that triggers contraction of cardiac contractile cell - Atria contract first, which drives blood into ventricles through atrioventricular valves - Ventricles contract second, driving blood out of heart through semilunar valves

Right ventricle

- Blood travels from right atrium into right ventricle through tricuspid valve - Internal surface contains a series of muscular ridges known as the traveculae carneae - Has moderator band - Superior end tapers to conus arteriosus (cone-shaped shaped pouch that ends at pulmonary semilunar valve)

Left and right pulmonary arteries

- Branch repeatedly within lungs before supplying capillaries (where there's gas exchange)

Electrocardiogram (ECG) and blood studies

- Can be used to diagnose a myocardial infarction (MI) AKA heart attack - Elevated enzymes (e.g. cardiac troponin T, cardiac troponin I, & CK-MB) can be measured in diagnostic blood tests

Electrocardiography

- Can monitor electrical events of conducting system from surface of body

Examples of different histological characteristics that distinguish cardiac contractile cells from skeletal muscle fibres

- Cardiac contractile cells: 1) Small in size (smaller than skeletal muscle fibre (SMF)) 2) Have single centrally located nucleus (multiple in SMF) 3) Have branching interconnections between cells (SMF instead have connective tissue fibres) 4) Has presence of intercalated discs (none in SMF)

Myogenic heart (AKA property of autorhythmicity )

- Cardiac muscle tissue contracts on its own without neural or hormonal stimulation (unlike skeletal muscle)

Pulmonary circuit

- Carries oxygen-poor blood from the right ventricle, through the pulmonary arteries, to the lungs (for gas exchange) - Also carries oxygen-rich blood from the lungs, through the pulmonary veins, to the left atrium

Systemic circuit

- Carries oxygen-rich blood from the left ventricle, through the systemic arteries, to the rest of body - Also carries oxygen-poor blood through systemic veins back to the right atrium

Left atrium

- Collects blood from pulmonary circuit & empties it into the left ventricle

Coronary thrombosis

- Condition which involves formation of a clot (thrombus) at a plaque causes blockage in vessels of coronary circulation - Vessel already narrowed by plaque formation may also become blocked by a sudden spasm in smooth muscles of vascular wall

Internodal pathways

- Conducting cells of these are in the atrial wall - Distribute contractile stimulus to atrial muscle cells as this electrical impulse travels from SA node to AV node

Papillary muscles

- Conical muscular projections that arise form inner surface of right ventricle - Contraction of these muscles via moderator band applies tension to chordae tendineae --> braces AV valves (limits their movement) --> this tension prevents backflow

Papillary muscles

- Conical muscular projections that arise from the inner surface of the right ventricle

Chordae tendineae

- Connective tissue fibers attached to each cusp of tricuspid valve - Originate at papillary muscles - Without chordae tendineae to anchor free edges of cusps, they wouldn't prevent blood blackflow (i.e. would be like swinging doors & permit blood flow in both directions)

Parietal layer of serous pericardium

- Consists of an outer dense fibrous layer, & an inner mesothelium

Cardiac skeleton (AKA fibrous skeleton) of the heart

- Consists of four dense bands of tough elastic tissue that encircle the heart valves & the bases of the pulmonary trunk & aorta - These bands stabilise the positions of the heart valves & ventricular muscle cells - The bands also electrically insulate the ventricular cell from the atrial cells

Pulmonary semilunar valve of right ventricle and blood flow

- Consists of three semilunar cusps of thick connective tissue - Prevent backflow as right ventricle relaxes (from pulmonary trunk into right ventricle) - Do not need muscular braces because arterial walls do not contract & relative positions of cusps are stable - Blood flowing from the right ventricle passes through this valve into the pulmonary trunk (start of pulmonary circuit) then into the left & right pulmonary arteries within the lungs to eventually supply the capillaries so gas expanse can occur

Left antrioventricular valve (AKA bicuspid valve or mitral valve)

- Contains 2 cusps - Permits blood to flow from left atrium into left ventricle - Prevents backflow when the left ventricle contracts

Cardioinhibitory center

- Controls parasympathetic neurons that slow heart rate - Found in medulla oblongata - Regulated by reflex pathways

Cardioaccelatory center

- Controls sympathetic neurons that increase heart rate - Found in medulla oblongata - Regulated by reflex pathways

Valves of the heart

- Covered openings that direct the flow of blood between chambers & vessels - Cardiac skeleton stabilises the position of these valves - Two pairs of one-way valves which are the two atrioventricular valves & the two semilunar valves - Prevent backflow of blood as the chambers contract

Endocardium

- Covers inner surfaces of heart including those of the heart valves - Made of simple squamous epithelium & underlying areolar tissue - This simple squamous epithelium is continuous with endothelium of attached great vessels

Visceral layer of the serous pericardium (AKA Epicardium) as part of the heart wall

- Covers the surface of the heart & is the outer layer of the heart wall - This serous membrane consists of an exposed mesothelium & an underlying layer of loose areolar connective tissue that is attached to myocardium

Ventricular tachycardia (VT or V-tach)

- Defined as 4 or more PVCs without intervening normal beats - Multiple PVCs & VT may indicate that serious cardiac problems exist

Preload

- Degree of stretching in ventricular muscle cells during ventricular diastole (or degree of stretching of cardiac muscle cells prior to contraction) - Is directly proportional to EDV e.g. the greater the EDV, the larger the preload - Affects ability of muscle cells to produce tension - As sarcomere length increases past resting length, the amount of force produced during systole increases - Its amount, & thus degree of myocardial stretching, varies with demands on heart - Affected by venous return (& filling time) e.g. when exercise --> venous return increase --> more blood flow to heart --> EDV increases --> myocardium stretches further --> sarcomere reaches optimum length --> more efficient contraction of contractile cells --> more forceful contractions of heart

Serous pericardium

- Delicate two-layered membrane that is composed of an inner visceral layer (epicardium) & outer parietal layer - Lines the pericardial cavity

Right and left coronary arteries

- Delivers blood to the myocardium - Originate at right & left aortic sinuses (at base of ascending aorta)

Comparison of the right and left ventricle

- Demands of both very different so have significant structural differences - Left ventricle is much larger than right ventricle - Both ventricles hold & pump equal amounts of blood - Left ventricle has much thicker muscular walls so can push blood through the body's extensive systemic circuit - Right ventricle only needs to pump blood to & from the lungs - When left ventricle contracts, bulges into right ventricle cavity so makes right ventricle more efficient - Right ventricle normally does not need to work very hard to push blood through pulmonary circuit so muscular wall very thin

Other differences between cardiac contractile cells and skeletal muscle fibres

- Difference in terms of: 1) Nature of action potential 2) Source of Ca2+ 3) Duration of resulting contraction

Filling time

- Duration of ventricular diastole, when blood can flow into the ventricles - Depends entirely on heart rate as the faster the heart rate the shorter the filling time - Venous return variable over this period as varies in response to changes in cardiac output, blood volume, peripheral circulation & skeletal muscle activity

Hormones and drugs affecting heart contractility

- E.g. epinephrine (E), norepinephrine (NE), glucagon, & thyroid hormones are +ve inotropic - Before synthetic inotropic drugs were available, glucagon was used to stimulate cardiac function & is still used in cardiac emergencies & to treat some forms of heart disease - Drugs isoproterenol, dopamine, & dobutamine mimic E & NE by stimulating beta-1 receptors on cardiac contractile muscle cells - Many of the drugs used to treat hypertension are -ve inotropic, while calcium-channel blockers such as nifedipine or verapamil are also -ve inotropic

Arteries

- Efferent vessels, carry blood away from the heart

Hormones effecting heart rate

- Epinephrine (E), norepinephrine (NE), & thyroid hormone (T3) increase heart rate by their effects on SA node - Release of NE (or similarly E) results in pacemaker cells of SA node reaching threshold more quickly, while E also affects cardiac contractile cells

P-R interval

- Extends from start of atrial depolarization to start QRS complex / ventricular depolarization (rather than to R) - Amount of time it takes for signal to travel from SA to AV node

Inotropic factors

- Factors that strengthen (increase) heart contraction are positively intropic, while factors that weaken (decrease) heart contraction are negatively intropic - +ve inotropic agents stimulate Ca2+ entry into cardiac contractile cells, thus increasing force & duration of ventricular contractions - -ve inotropic agents may block Ca2+ movement or depress cardiac muscle metabolism - +ve & -ve factors include ANS activity, hormones, & changes in extracellular ion concentrations

Ventricular diastole & its steps

- For rest of cycle ventricles fill passively, both atria & ventricles are relaxed - Continues through atrial systole in next cycle 1. Isovolumetric relaxation (IR) occurs: - All heart valves closed & ventricular myocardium is relaxing. - As ventricular pressures are still higher than atrial pressures, blood cannot flow into ventricles (IR) 2. Atrioventricular valves open; passive ventricular filling occurs: - When ventricular pressures fall below those of atria, the atrial pressures force AV valves open. - Atria still in diastole which leads to passive filling of ventricles

Cardiac contractile cells

- Form the bulk of the atrial & ventricular walls - Gets stimulus from Purkinje fibers - Account for 99% of muscle cells in heart - Are interconnected by intercalated discs

Tricuspid valve (AKA right atrioventricular (AV) valve)

- Formed of three fibrous flaps (cusps) - Blood travels from right atrium into right ventricle through a broad opening bordered by tricuspid valve - Free edge of each cusp is attached to connective tissue fibers called chordae tendineae - Closes when right ventricle contracts so prevents backflow of blood

Heart sounds

- Four heart sounds (named S1, S2, S3, & S4) - First & second heart sounds can clearly be heard (with stethoscope) & accompany closing of heart valves - First: "lubb" (S1) lasts longer than second: "dupp" (S2) - S1 marks start of ventricular contraction, when atrioventricular valves close & semilunar valves open - S2 occurs at beginning of ventricular filling, when semilunar valves close & atrioventricular valves open - Third & fourth sounds very faint, are associated with blood flowing into ventricles (S3) & atrial contraction (S4)

Circumflex artery

- From left coronary artery - Curves to the left around coronary sulcus - It eventually meets & fuses small branches of right coronary artery

Frank-Starling Principle

- Greater the EDV, the larger the ventricular preload & the larger the stroke volume - General role of "more in = more out" - Ability of heart to change its contractility (contraction force) & thus SV in response to changes in venous return - Increasing venous return, increases EDV --> increase SV - Increase venous return --> increase preload --> increase tension on cardiac muscle --> increase contractility (force of contraction) --> increase SV

Atrial diastole

- Happens after atrial systole - Begins at same time as ventricular systole - Continues until start of next cardiac cycle

The heart

- Has four muscular chambers: right atrium, right ventricle, left atrium, & left ventricle - When heart beats, atria contract first, then ventricles - Ventricles contract at same time & eject equal volumes of blood into pulmonary & systemic circuits - Located directly posterior to sternum - Typical heart: 5 inches from base to apex - Centre of base lies slightly to left of midline

Heart Wall

- Has three distinct layers which are the epicardium, myocardiuim, & endocardium

Pacemaker cell characteristics

- Have excitable membranes that do not have a stable resting potential --> each time it repolarizes, membrane drifts toward threshold - This gradual depolarisation is called pacemaker potential & results from a slow inflow of Na+ without a compensating outflow of K+

Atria of the heart

- Have relatively thin muscular walls & are highly expandable - When not filled with blood, the outer portion of each atrium deflates & becomes wrinkled flap (auricle) - Function is to collect blood that is returning to heart & to convey it to ventricles (check)

Impulse conduction through the heart - Step 5:

- Impulse distributed by pukinje fibers (radiate from apex toward base of heart) is then relayed throughout ventricular myocardium, atrial contraction finishes & ventricular contraction begins - Ventricles contract in a wave that begins at apex & spreads toward base & this contraction pushes blood toward base of heart into aorta & pulmonary trunk

Impulse conduction through the heart - Step 3:

- Impulse slows as it leaves internodal pathways & enters AV node as AV nodes are smaller in diameter than the conducting cells (creates delay), & atrial contraction begins - Delay is important as allows atria to contract before ventricles do

Atrial fibrillation (AF)

- Impulses move over atrial surface at rates of 500 beats per minute - Atrial wall quivers instead of producing an organized contraction -ventricular rate cannot follow atrial rate & may remain normal within limits - Atria are now nonfunctional, but condition can go unnoticed because ventricles fill 75% passively - No P waves

R wave

- In QRS complex - Ventricles begin contracting shortly after peak of R wave

Action potential differences

- In a ventricular contractile cell lasts 250-300 msec - This is about 30 times as long as a typical action potential in a skeletal muscle fibre

Cardiac centers

- In medulla oblongata & includes cardioaccelatory center & cardioinhibitory center - Regulated by reflex pathways - Receive input from parasympathetic & sympathetic centres in the hypothalamus - Monitor baroreceptors & chemoreceptors innervated by glossopharyngeal & vagus nerves - Adjusts heart's activity to maintain adequate circulation to vital organs - Respond to changes in blood pressure (reported by baroreceptors) & changes in arterial concentrations of dissolved oxygen & CO2 (reported by chemoreceptors)

Connective tissues of the heart

- Include large numbers of collagen & elastic fibres - Each cardiac muscle is wrapped in a strong but elastic sheath - Adjacent cells are tied together by fibrous cross-links (AKA struts), while these fibres are interwoven into sheets that separate the superficial & deep muscle layers

Cardiac tamponade

- Increased production of pericardial fluid (due to pericarditis) causes fluid to collect in the pericardial cavity, restricting movement of the heart - Can also result from traumatic injuries (such as stab wounds) that produce bleeding into the pericardial cavity

Bainbridge reflex (AKA atrial reflex)

- Indirect effect of the venous return on heart rate (is an autonomic reflex) - Involves adjustment in heart rate due to increase in venous return - Walls of right atrium are stretched so stretch receptors (in atria) triggers reflexive increase in heart rate by stimulating sympathetic activity - Increase in venous return --> increase heart rate --> increase cardiac output

Pericarditis

- Inflammation of the pericardium due to infections by pathogens - The inflamed pericardial surfaces rub against one another, making a distinctive scratching sound (called a friction rub) - Pericardial inflammation often commonly results in an increased production of pericardial fluid

Absolute refractory period

- Initially membrane of cardiac contractile cells cannot respond at all, because sodium ion channels are either already open or closed & inactivated - In ventricular contractile cell, this period lasts about 200 msec - It includes the plateau & the initial phase of rapid repolarization

Conducting cells

- Interconnect SA & AV nodes - Distribute contractile stimulus throughout myocardium - In atria: found in internodal pathways in atrial walls - In ventricles: found in AV bundles (aka bundle of His), bundle branches, & Purkinje fibers

Arterial anastomoses

- Interconnections between arteries & small tributaries continuous with those of posterior interventricular artery - Provide back-up mechanism as blood supply to cardiac muscle remains relatively constant despite pressure fluctuations in the left & right coronary arteries as the heart beats

Pectinate muscles

- Internal ridges of myocardium in right atrium & both auricles - Prominent muscular ridges along the inner surface of the auricle & across the adjacent anterior atrial wall

Ectopic pacemaker (AKA ectopic foci)

- Is the origin of abnormal signals (faster than those of SA node) - Caused by abnormal conducting cell or ventricular contractile cell generating action potentials at higher rate, so these impulses override those of SA or AV node - Usually created by disease - Activity of ectopic pacemaker partially or completely bypasses conducting system --> disrupting timing of ventricular contraction (can be dangerous)

Great cardiac vein

- It begins on the anterior surface of the ventricles, along the interventricular sulcus - It drains blood from the region supplied by the anterior interventricular artery (a branch of left coronary artery) - This vein reaches the level of the atria & then curves around the left side of the heart within the coronary sulcus

Sympathetic stimulation has +ve intropic effect on contractility

- It causes release of norepinephrine (NE) by postganglionic fibres of the cardiac nerves & the secretion of epinephrine (E) & NE by adrenal medulla - These hormones affect heart rate & also stimulate alpha & beta receptors in cardiac contractile cell plasma membranes - This stimulation increases metabolism of these cells - Thus ventricles contract more forcefully, increasing ejection fraction & decreasing the ESV

Coronary ischemia

- Lack of blood flow to the heart muscle due to partial or complete blockage of coronary arteries - Usual cause is formation of fatty deposit (or atherosclerotic plaque) in wall of coronary vessel - The plaque or associated clot (AKA thrombus) narrows the passageway & reduces blood flow - Spasms in smooth muscles of vessel walls can further decrease or stop blood flow

Purkinje cells

- Large diameter --> fast conduction of action potentials - Receive impulse from atrioventricular bundle & the bundle branches

Atrioventricular (AV) node

- Located at junction between atria & ventricles - Sits within floor of right atrium near opening of coronary sinus - Pacemaker cells of this node send on signals from cells of SA node, & act as backup to SA node pacemaker cells - AV nodes are smaller in diameter than the conducting cells

Symptoms of myocardial infarction (MI) AKA heart attack

- May experience intense pain in the chest that often radiates down the left arm & persists even at rest - Pain does not always accompany a heat attack thus silent heart attack poss more dangerous as may go undiagnosed or treated before it becomes fatal

Faulty heart valves and the three associated malfunctions

- Most common valve to falter is the mitral valve - E.g. due to untreated bacterial or viral infection that infiltrates valve cuspids, so cuspids become inflamed & later scarred - (1) Stenotic valve: can become rigid so that it does not fully open - (2) Regurgitant valve: it fails to close properly - (3) Prolapsed valve: it actually flops backward - Faulty valves can be heard as heart murmurs with a stethoscope

Moderator band

- Muscular ridge that extends horizontally from inferior portion of interventricular septum & connects to anterior papillary muscle - Contains part of conducting system - Delivers stimulus for contraction to papillary muscles so causes these muscles to begin tensing cordae tendineae before rest of ventricle contracts

Energy for cardiac contractions

- Normal heart gets energy as mitochondria break down fatty acids (stored as lipid droplets) & glucose (stored as glycogen) - Oxygen must be readily available to perform these aerobic reactions - In cardiac contractile cells oxygen molecules are bound to heme units of myoglobin molecules - Combination of circulatory supplies plus myoglobin reserves is enough to meet oxygen demands of heart

S-T segment

- Normally flat - Atria relaxed, ventricles contrated - If elevated: recent cardiac injury - If depressed: myocardial ischemia

Heart rate (HR)

- Number of heart beats per minute (bpm) - Can be adjusted by activities of autonomic system or by circulating hormones

Premature Atrial Contractions (PACs)

- Occur in healthy people - Normal atrial rhythm is momentarily interrupted by a "surprise" atrial contraction - Increased incidents seen with stress, caffeine, & various drugs due to increasing permeability of SA pacemakers - Impulse spreads along the conduction pathway & a normal ventricular contraction follows the atrial beat - No normal QRS

Premature ventricular contractions (PVCs)

- Occur when a purkinje cell or ventricular myocardial cell depolarizes to threshold & triggers premature contraction - Single PVCs are common & not dangerous - Cell responsible is called an ectopic pacemaker - PVC frequency can be increased by exposure to epinephrine, to other stimulatory drugs, or to ionic changes that depolarise cardiac muscle plasma membranes

Heart murmer

- Occurs if valve cusps are malformed or problems with papillary muscles or chordae tendineae so heart valves may not close properly - Aatrioventricular valve regurgitation occurs during ventricular systole - The surges, swirls, & eddies that accompany this regurgitation create a rushing, gurgling sound - Minor heart murmurs are common & inconsequential

Angina pectoris (chest pain)

- One of the first symptoms of Coronary artery disease - A temporary ischemia develops when workload of heart increases - Feel comfortable at rest, but exertion or emotional stress can produce a sensation of pressure, chest constriction, & pain

Inferior vena cava

- Opens into posterior & inferior portion of right atrium - Carries blood to right atrium from rest of trunk, viscera, & lower limbs

Superior vena cava

- Opens into posterior & superior portion of right atrium - Delivers blood to right atrium from head, neck, upper limbs, & chest

Coronary arteries

- Originate at base of ascending aorta at aortic sinuses - Highest blood pressure here of all systemic circuit - When left ventricle (LV) contracts it forces blood into aorta so arrival of blood stretches elastic walls of aorta - When LV relaxes the blood no longer flows into aorta so pressure declines & the walls of aorta recoil (AKA elastic rebound) - Elastic rebound pushes blood both forward into systemic circuit & backward through left & right aortic sinuses into respective coronary arteries - Ensures a continuous flow of blood to meet demands of active cardiac muscle tissue

Parietal pericardium layer (check)

- Outer layer - Lines the inner surface of the tough pericardial sac that surrounds the heart

Impulse conduction through the heart - Step 1:

- Pacemaker cells of SA node produce action potential that starts travelling down internodal pathways in atrial walls (connected to Atrioventricular (AV) node)

Autonomic intervention (extrinsic control) of the heart by the autonomic nervous system (ANS)

- Parasympathetic & sympathetic divisions innervate heart via cardiac plexus (a nerve network) - ANS divisions both innervate SA & AV nodes & the atrial muscles - Also both innervate ventricular contractile cells too, but sympathetic fibres outnumbers parasympathetic - Parasympathetic effects dominate in healthy, resting individuals - Without autonomic innervation - pacemaker cells of SA node would establish HR

Influence of Parasympathetic divisions on heart rate

- Parasympathetic stimulation releases acetylcholine Ach - Ach opens chemically gated K+ channels in plasma membrane, so K+ leaves pacemaker cells of SA node - This extends repolarization & decreases rate of spontaneous depolarisation - As a result heart rate declines

Myocardial infarction (MI) AKA heart attack

- Part of coronary circulation becomes blocked, & cardiac muscle cells die from lack of oxygen - Death of affect tissue creates a nonfunctional area known as an infarct - Most commonly result from severe coronary artery disease (CAD) as well as coronary thrombosis - If near start of coronary arteries, damage will be widespread & heart may stop beating

Cardiac cycle

- Period between the start of one heartbeat & the beginning of the next - Includes periods of contraction & relaxation - For any one chamber of the heart can be divided into two phases: systole & diastole - Blood flows from one chamber to another only if pressure in first chamber exceeds that in the second - Include phases which are: atrial systole, atrial diastole, ventricular systole, & ventricular diastole

Angiography

- Plaques may be visible - Effects on coronary blood flow can be detected in digital subtraction angiography (DSA) scans of heart - Looking for artery blockages

Chordae tenineae and papillary muscles

- Play an important role in the normal functioning of the atrioventricular (AV) valves - When ventricles relaxed the chordae tenineae are loose so AV valves offer no resistance as blood flow from atria into ventricles - When ventricles contract the cusps swing together due to blood moving towards atria, while papillary muscles tenses chordae tendineae, so cusps don't swing into atria -when pressure in ventricle exceeds pressure in atrium --> AV valve closes (check)

Left atrium

- Posterior wall of left atrium receives blood from two left & two right pulmonary veins (no valve between these veins & the left atrium) - Has an auricle (like RA) - Mitral valve (AKA left atrioventricular valve or bicuspid valve) guards entrance to left ventricle -Parts: 1. pulmonary veins (2 right, 2 left) 2. antrioventricular valve (AKA bicuspid or mitral)

Antrioventricular valves: Atria to ventricles

- Prevent back flow of blood from ventricles to atria when ventricles contracting - Chordae tendineae & papillary muscles play important roles in normal function of these valves

Parasympathetic stimulations (from vagus nerves) has -ve inotropic effect on contractility

- Primary affect of acetylcholine (ACh) is at cardiac contractile cell membrane surface, where it produces hyperpolarization & inhibition - Thus force of cardiac contractions reduced - Atria show greatest changes in contractile force as ventricles aren't extensively innervated by parasympathetic divisions - However under strong parasympathetic stimulation, ventricles contract less forcefully, the ejection fraction decreases, & ESV becomes larger

Conducting deficits and example

- Problems caused by damage to the conducting pathways which disturbs the normal rhythm of the heart - If SA node or internodal pathways become damaged, heart continues to beat, but at slower rate (now dictated by AV node)

Semilunar valves: Ventricles to great vessels

- Pulmonary & aortic semilunar valves prevent back flow of blood from pulmonary trunk & aorta into right & left ventricles - Don't need muscular braces (unlike antrioventricular valves) as the arterial walls don't contract & relative positions of cusps are stable - When these valves close the 3 symmetrical cusps support one another like legs of a tripod - When aortic valve opens, the aortic sinus prevents the individual cusps from sticking to the wall of the aorta

Semilunar valves

- Pulmonary & aortic valves between the ventricles & their great vessels (pulmonary artery for right ventricle & aorta for left ventricle) - Ensures blood flows into these vessels

Circuits of the heart

- Pulmonary circuit & Systemic circuit - Each circuit begins & ends at the heart, & blood travels through these circuits in a sequence - Thus, blood returning to the heart from the systemic circuit must complete the pulmonary circuit before reentering the systemic circuit

Coronary sinus

- Receives blood from cardiac veins draining myocardium - A large, thin-walled vein that opens into right atrium near the base of the inferior vena cava -Its opening lies near posterior edge of interatrial septum

Left ventricle

- Receives blood from left atrium - Pumps blood into systemic circuit

Right ventricle

- Receives blood from right atrium - Pumps blood into pulmonary circuit

Right atrium

- Receives blood from systemic circuit & passes it to right ventricle

Right atrium

- Receives blood from systemic circuit through two great veins which are the superior vena cava & inferior vena cava - Blood travels from right atrium into right ventricle through right atrioventricular (AV) valve (tricuspid valve) - External parts include superior vena cava, inferior vena cava, coronary sinus, & auricle F - Internal parts include fossa ovalis (foramen ovale in fetal heart) & pectinate muscles

T wave

- Repolarization of ventricular contractile cells - Size & shape of wave affected by any condition that slows ventricular repolarization (starvation, coronary ischemia, or abnormal ion concentrations reduce wave size)

Ventricular fibrillation (VF)

- Responsible for cardiac arrest - Rapidly fatal as ventricles quiver & stop pumping blood

Prepotential (AKA pacemaker potential)

- Resting potential of conducting cells - Conducting cells gradually depolarizes toward threshold - Results from slow inflow of Na without outflow of K - SA node depolarizes first, establishing heart rate

Anterior interventricular sulcus & Posterior interventricular sulcus

- Shallower depressions than coronary sulcus that mark boundary between left & right ventricles - Substantial amounts of fat lie in coronary & interventricular sulci - Contain arteries & veins that carry blood to & from cardiac muscle

Left ventricle

- Similar internal organisation to right ventricle but has no moderator band - Has prominent trabeculae carneae - Pair of large papillary muscles tenses chordae tenineae that anchor cusps of mitral valve & prevent backflow into left atrium -blood leaves left ventricle through aortic valve (aortic semilunar valve) & enters ascending aorta

P wave

- Small wave that accompanies depolarization of atrial contraction cells - Depolarization of these cells causes atrial contraction - Cannot see repolarization because signal hidden within QRS complex - takes place while ventricles are depolarizing

Dicrotic notch

- Small, temporary rise in pressure when semilunar valve closes & pressure rises again as elastic arterial walls recoil - Rebound from aorta

Risk factors for coronary artery disease (CAD) and myocardial infarction (MI) AKA heart attack

- Smoking, high blood pressure, obesity, diabetes, high cholesterol, male over age 70, high circulating low-density lipoproteins, severe emotional distress, genetic disposition, & sedentary lifestyle

Atrioventricular block

- Something blocking signal from SA --> AV node - Message from SA node does not reach ventricles or is impaired

Pulmonary trunk

- Start of pulmonary circuit - Lead onto the left & right pulmonary arteries

Ventricular systole

- Starts at same time as atrial diastole - Ventricles push blood through the systemic and pulmonary circuits toward the atria

Conus arteriosus

- Superior end of right ventricle tapers at this - Cone-shaped pouch that ends at pulmonary (pulmonary semilunar) valve

Left coronary artery

- Supplies blood to the left ventricle, left atrium, & interventricular septum - Gives rise to circumflex artery & anterior descending artery (AKA left anterior descending artery (LAD))

Coronary circulation

- Supplies blood to the muscle tissue of the heart - Includes an extensive network of coronary blood vessels, both arteries & veins

Pericardium (AKA pericardial sac - check)

- Surrounds heart - Consists of outer fibrous pericardium & an inner serous pericardium

Anterior descending artery (AKA left anterior descending artery)

- Swings around pulmonary trunk & runs along surface within anterior interventricular sulcus - LAD supplies small tributaries continuous with those of posterior interventricular artery (arterial anastomoses)

Summary of influence of autonomic nervous system (ANS) on heart rate (HR)

- Sympathetic stimulation increases HR, & parasympathetic decreases it - Under resting conditions, parasympathetic tone dominates, & HR is slightly slower than intrinsic HR - When activity level rises, venous return increases & triggers Bainbridge reflex, to result in an increase in sympathetic tone & increase in HR

Influence of Sympathetic divisions on heart rate

- Sympathetic stimulation releases norepinephrine (NE) that binds to beta 1 receptors - Leads to opening of sodium & calcium ion channels, so have influx of positively charged ions - This increases rate of spontaneous depolarisation & shortens repolarization - Pacemaker cells reach threshold more quickly, & as a result heart rate increases

Valvular Heart Disease (VHD)

- Symptoms of this condition appear when valve function has deteriorated to where heart cannot maintain adequate circulatory flow of blood - Congenital malformation may be responsible, but in many cases the condition develops after carditis which is an inflammation of the heart

Auscultation

- Technique to listening to the heart, which is a simple & effective method of cardiac assessment - Often use stethoscope to listen for normal & abnormal heart sounds - Where stethoscope is placed depends on which valve is under examination

Other cardiac veins of the heart

- Tend to empty into the great cardiac vein or the coronary sinus, includes the following: 1.) Posterior vein of left ventricle, which drains the area served by the circumflex artery 2.) Middle cardiac vein, which drains the area supplied by the posterior interventricular artery 3.) Small cardiac vein, which receives blood from the posterior surfaces of the right atrium & ventricle

Cardiac reserve

- The difference between resting & maximal cardiac output

Pericardial cavity

- The fluid-filled space between the parietal & visceral layers of the serous pericardium - Contains pericardial fluid (secreted by pericardial membranes) that acts as lubricant, reducing friction between the opposing surfaces as the heart beats

Mediastinum

- The heart sits in anterior portion of this region - Is the region between two pleural cavities - Contains the great vessels, as well as the thymus, esophagus, & trachea

Apex

- The inferior pointed tip of the heart

Myocardium as part of the heart wall

- The thickest section/ layer of the heart wall - Made of cardiac muscle tissue that forms the atria & ventricles - This muscular layer contains cardiac muscle cells, connective tissues, blood vessels, & nerves - Atrial myocardium contains muscle bundles that wrap around atria & form figures of eights that encircle the great vessels - Superficial ventricular muscle wrap around both ventricles, & deeper muscle layers spiral around & between the ventricles towards the apex in figure-eight pattern

Refractory period of cardiac contractile cells

- The time during which the membrane of a cardiac contractile cell will not respond normally to a second stimulus after an action potential begins - Includes absolute refractory period that is followed by relative refractory period

Factors effecting heart rate

- Those that increase heart rate are positively chronotropic, while those that decrease heart rate are negatively chronotropic - Altered by autonomic nervous system (ANS)

Intercalated discs of cardiac contractile cells

- Transfer the force of contraction from cell to cell & propagate action potentials - At each disc, the interlocking membranes of adjacent cells are held together by desmosomes & linked by gap junctions - Desmosomes prevent cells from separating during contraction, while gap junctions allows ions to pass & electrically couple adjacent cells - Allows heart muscle to behave as a functional syncytium (a mechanically, chemically, & electrically coupled, multinucleate tissue)

Atrioventricular (AV) valves

- Tricuspid & mitral are the two AV valves - Are folds of fibrous tissue that extend into the openings between atria & ventricles - Permit blood to flow only in one direction from the atria to the ventricles - Prevent backflow of blood from ventricles to artia when ventricles are contracting

Q-T interval (not fini - check)

- Ventricular depolarization & repolarization - How long it takes ventricles to undergo a single cycle of depolarization & repolarization - Long interval: slow heart rates, hypokalemia (hyperpolarization), hypocalcemia, myocardial disease, coronary ischemia ?Short interval: hypercalcemia, hyperthyroidism, hyperkalemia (increased extracellular K --> potentials depolarized)

Ventricles

- When contract the antrioventricular valves closes & semilunar valves open - When relaxed the antrioventricular valves open, semilunar valves closed - Contract in synchrony - at same time - Ventricle fills passively

Auricle

- When not filled with blood the outer portion of each atrium deflates & becomes a lumpy wrinkled flap - This expandable extension of an atrium is named an auricle as it reminded early scientists of the inner ear

atrial reflex (not in book?)

- involves adjustments in HR in response to incrase in venous return - increase in venous return --> increase in HR --> increase in CO

Heartbeat? (check - unreferenced in book)

-Each time heart beats: wave of depolarization spreads through atria --> pauses at AV node --> interventricular septum --> apex --> turns and spreads through ventricular myocardium towards base -Time between R-R (how often ventricular contraction happens

Cardiac muscle (not fini - check???)

-Gap junction -Sarcolemma - membrane of cardiac muscle; AP comes down sarcolemma: goal - get Ca -sarcoplasm - cytoplasm in cardiac muscle; contains Ca storage -myofilaments: actin, myosin, tropomyosin, troponin (binds Ca) -sarcoplasmic reticulum

Right coronary artery

-Inferior to right atrium & follows coronary sulcus around heart - Fills via elastic rebound of aorta - Supplies blood to: (1.) Right atrium, (2.) portions of both ventricles, & (3.) portions of electrical conducting system of heart (SA node and AV node of RA) - Gives rise to the marginal arteries (across surface of right ventricle) & to the posterior interventricular artery (runs toward apex within posterior interventricular sulcus)

intercalated disc (check)

-connect cardiac muscle cells -join membranes of adjacent cells through desmosomes and linked gap junctions -transfer force of contraction form cell to cell and propagate APs

Preload - extension not in book?

-increase preload --> increase ability of heart to perform work -increase stretch --> increase stroke work --> more ventricular filling (more efficient) -resting cardiac cells are usually shorter than their optimal length -increased venous return --> increase preload --> increase tension on cardiac muscle --> increase contractility --> increase SV

cardiac muscle cells (check)

-interconnected by intercalated discs

ventricular filling (check)

-ventricular diastole -AV valves open, semilunar valves closed

ventricular contraction (Check)

-ventricular systole -AV valves closed, semilunar valves open

In both cardiac contractile cells and skeletal muscle cells

1. Action potential leads to appearance of Ca2+ among myofibrils 2. Binding of Ca2+ to troponin on the thin filaments initiates contraction

Steps of ventricular systole

1. Atrioventricular valve close: AV valve pushed closed as pressures in the ventricle rise about those in atria 2. Isovolumetric ventricular contraction occurs: ventricles are contracting but blood flow has yet to occur (ventricular pressures not yet high enough to force open semilunar valve); ventricles contract isometrically as heart valves are closed & ventriclular pressure rises 3. Ventricular ejection occurs: once pressure in ventricles exceeds that in arterial trunks, semilunar valves open & blood flows into pulmonary trunk & aortic trunk; ventricles now contracting isotonically (ejects stroke volume). After reaching a peak, ventricular pressures gradually decline near end of ventricular systole 4. Semilunar valves close: ventricular pressures start declining rapidly, blood in aorta & pulmonary trunk flows back towards ventricles thus closing semilunar valves, when valves close, pressure rises as elastic arterial walls recoil

Cardiac muscle cells in normal heartbeat

1. Specialized autorhythmic cells (Pacemaker & conducting) of the conducting system control & coordinate the heartbeat 2. contractile cells produce the powerful contractions that propel blood

Factors affecting Stroke volume (SV)

1. increase venous return --> increase EDV ---> increase SV 2. increase filling time --> increase EDV --> increase SV 3. Increase contractility --> decrease ESV --> increase SV 4. increase afterload --> increase ESV --> decrease SV

Parts of the left ventricle

1. trabeculae carneae 2. papillary muscles 3. chordae tendineae 4. aortic valve 5. ascending aorta 6. aortic arch 7. descending aorta

Parts of the right ventricle

1. tricuspid 2. chordae tendineae 3. papillary muscles 4. trabeculae carneae 5. moderator band 6. conus arteriosus 7. pulmonary (semilunar) valve 8. pulmonary trunk 9. pulmonary arteries

Atrial systole steps

1.) Atria contraction begins: - At start, ventricles already filled with 70% of normal capacity, due to passive blood flow during end of previous cardiac cycle 2.) Atria contracts, so ejects blood into ventricles: - Due to the rising atrial pressures pushing blood into ventricles through open right & left atrioventricular valves, thus topping off ventricles - Blood cannot flow into atria because atrial pressure exceeds venous pressure - Blood takes path of least resistance - At end, each ventricle contains the maximum amount of blood that it will hold (end-diastolic volume);

Phases of Cardiac cycle

A) Atrial systole begins: atrial contraction forces a small amount of additional blood into relaxed ventricles B) Atrial systole ends, thus atrial diastole begins C) Ventricular systole (1st phase): ventricular contraction exerts enough pressure on blood to close atrioventricular valves but not enough to open semilunar valves D) Ventricular systole (2nd phase): As ventricular pressure rises & exceeds pressure in the arteries, the semilunar valves open & blood is ejected E) Ventricular diastole (early): As ventricles relax, pressure in ventricles drops; blood flows back against cusps of semilunar valves & forces them closed. Blood flows into the relaxed atria. F) Ventricular diastole (late): All chambers are relaxed. Ventricles fill passively.