The Cardiovascular System

Week 7

Pericardium

Double walled sac that surrounds heart

Fibrous Pericardium

Superficial layer made of strong fibrous connective tissue, attaches pericardium to surrounding tissues

Serous Pericardium

• Inner layer made up of serous membrane

• Parietal Layer: Outer, fused to fibrous pericardium

• Visceral Layer: Inner, epicardium, surface of heart

Pericardial Cavity

Between parietal and visceral layers of serous pericardium

Pericardial Fluid

Thin film of serous fluid used for lubrication, protection of heart and from infection

Epicardium

• Visceral layer of serous pericardium

• Contains blood vessels, lymph vessels and blood supply to the myocardium (coronary arteries)

Myocardium

• Composed of mostly cardiac muscle tissue

• Involuntary and striated

• Myocardial cells generate and conduct electrical impulses

• Thick asf

Endocardium

• Thin layer of endothelium over thin layer of connective tissue

• Smooth inner lining of chambers and valves (reduces friction, improves blood flow

• Continuous with inner lining of blood vessels that leave heart

Chambers of Heart

• 2 atria: superior and receiving chambers

• 2 ventricles: inferior and pumping chambers

Sulci (sulcus)

Grooves in heart that contain coronary blood vessels and create boundaries between chambers of heart

Right Atrium

• Receives deoxygenated blood from vena cavas and coronary sinus (drains myocardial veins)

• Location of sinoatrial node

• During contraction blood flows through tricuspid/right atrioventricular (AV) valve

Interatrial septum

Separates left and right atria

Right Ventricle

• More muscle tissue than right atrium

• During contraction, blood flows through pulmonary semilunar (SL) valve to right and left pulmonary arteries

Interventricular Septum

Separates left and right ventricles

Left Atrium

• Receives oxygenated blood from pulmonary veins

• During contraction blood flows through bicuspid/mitral/left atrioventricular (AV) valve

Left Ventricle

• Thickest, most muscular chamber, forms the apex

• Responsible for contracting and pumping blood systemically

• During contraction blood flows through aortic semilunar (SL) valve into ascending aorta

Ductus Arteriosus

Blood vessel in a fetus that connects pulmonary trunk to aorta (fetal lungs don’t work until birth) that closes shortly after birth

Chordae Tendineae

• Connected to cusps of AV valves and papillary muscles in ventricles

• Prevents cusps of valves from opening backwards

Papillary Muscles

Contract when ventricle contracts which pulls and tightens chordae tendineae

Semilunar Valves

• Cusps open during ventricular contraction

• Shape and structure prevent backflow

Pulmonary Arteries and Veins

• Pulmonary arteries is only time they carry deoxygenated blood

• Pulmonary veins is only time they carry oxygenated blood

• Different when you’re pregnant!

Coronary Arteries

• Supply heart with oxygen and nutrients

• Branch off ascending aorta and encircle heart

• Squeezed shut during systole, heart tissue is perfused during cardiac diastole

Coronary Veins

Return deoxygenated blood to right atrium

Left Coronary Artery

• Branches off ascending aorta

• Divides into left anterior descending and circumflex

Left Anterior Descending/Interventricular (LAD) Artery

Perfuses walls of both ventricles

Circumflex Artery

Perfuses walls of left atrium and left ventricle

Right Coronary Artery

• Branches off ascending aorta

• Provides blood to right atrium

• Divides into posterior interventricular and right marginal

Posterior Interventricular/Descending Artery

Perfuses walls of both ventricles

Right Marginal Artery

Perfuses wall of right ventricle

Collateral Circulation

• Similar to collateral circulation elsewhere in body

• Has network of blood vessels that are normally closed

• When coronary arteries narrow (coronary artery disease) or are obstructed (MI) vessels open

• Allows blood flow around blocked artery and helps maintain myocardial perfusion

The Cardiac Cycle

Rhythmic pumping action of the heart

Atrial Systole

• Approx 0.1 secs

• Atria contracts while ventricles are relaxed and blood is forced into ventricles

Ventricular Systole

• Approx 0.3 secs

• Ventricles contract while atria are relaxed (atrial diastole) and blood is forced into pulmonary and systemic circulation

• Referring to ventricular systole when speaking about systole

Relaxation Period

• Approx 0.4 secs

• Both atria and ventricles are relaxed (diastole)

• Period shorten as heart rate increases (atrial filling is dependant)

Atrial Filling

• Filling occurs during systole and diastole

• Regulated by movement of blood into ventricles, pressure changes in chambers (high to low), intrathoracic pressure changes

Stroke Volume (SV)

• Quantity of blood ejected by each ventricle (~70mL)

• Regulated by preload, contractility and afterload

Preload

• Represents volume of deoxygenated blood entering the heart

• Determined by venous return and stretch of cardiac muscle fibres

• Abnormally high preload can lead to back up of fluid into circulation

Frank-Starling’s Law of the Heart

• Greater the stretch, the greater force of contraction

• Greater venous return causes greater stretch on cardiac muscle fibres

• Limits are not infinite as heart can only beat so fast and forcefully

Contractility

• Heart’s ability to change force of contraction without changing preload

• Strongly influenced by Ca+

• More Ca = more contraction

Inotropic

• Refers to contractility

• Positive inotropic effect increases force of contraction

• Negative inotropic effect decreases force of contraction

Afterload

• Pressure heart must generate to move blood out of ventricles (to open SL valves)

• Increased SVR will increase afterload

Cardiac Output

• Changing HR affects CO

• Regulated by autonomic and chemical

• If HR increases where ventricles can’t fill up CO drops

Autonomic

• Nervous system control over HR (negative feedback)

• Sensory input received by chemoreceptors and baroreceptors

Chemoreceptors

Monitor chemical changes in blood

Baroreceptors

Monitor pressure changes in arteries

Autonomic Nervous System (ANS)

• Sympathetic: fight or flight

• Parasympathetic: rest and digest/low and slow

Chemicals in Cardiac Output

• Depress cardiac activity: hypoxia, acidosis, alkalosis

• Impact HR and cardiac activity: hormones (epinephrine and norepinephrine)

• Ca+, K+, Na+ play major role in cardiac function

Action Potential

• Ability to stimulate electrical activity in body

• Measured in mV (1mV = 1/1000 of a Volt)

• Positively and negatively charged ions inside or outside cell membrane (K+, Na+, Ca+)

• Different way of contracting in heart for muscle cells

• Pacemaker cells and myocytes have different action potential

Electrophysiology

• Cardiac contraction is caused by electrical impulses in the heart

• Cardiac conduction follows specific pathway (even though myocardial cells have conduction and generating properties)

• Electrolytes effect cardiac contraction (dromotropic), contractility (inotropic) and rate (chronotropic)

• 1% of cardiac muscle fibres are autorhythmic (pacemaker cells and conduction system)

Sinoatrial (SA) Node

• Pacemaker (upper right wall of right atrium)

• Impulse originates here with intrinsic rate of 60-100bpm

• P wave on ECG

• Stimulates contraction of atria via Bachmann’s Bundle

• Works on magic, MF is a wizard

Internodal Pathways

• Myocardial cells conduct impulse from SA node to AV node

• If one pathway is blocked, impulse can travel around blockage

Bachmann’s Bundle

Impulse connection between left and right atria

Atrioventricular (AV) Node

• Briefly delays impulse before contraction of ventricles (allows atria to contract)

• Located in right atrium close to septum and tricuspid valve

• Intrinsic rate of 40-60bpm

• Isoelectric line after P wave on ECG

Bundle of His

• Fibres, inferior to AV node that conduct impulses from AV node to purkinje fibres

• Branches into left and right bundle branches

Purkinje Fibres

• Branch off left and right bundle branches and carry impulse to myocardial cells in left and right ventricles

• Stimulates ventricular contraction

Pacemaker Action Potential

1. Rapid influx of Ca2+, depolarization (threshold: -40mV)

2. Outflux of K+, repolarization (-60mV)

3. Slow influx of Na+, prepotential

4. One cycle approx 0.8 secs

Cardiac Myocyte Action Potential: Phase 4: Resting Membrane Potential

• Resting/unexcited state

• Cardiac myocytes have negative resting membrane potential

• K+ leaking out of cell (keeps membrane potential at -90mV

Cardiac Myocyte Action Potential: Phase 0: Depolarization

• Slow channels open by action potential

• Leakage of Na+ and Ca2+ into cell

• Threshold: -70mV, fast Na+ channels open

• K+ still leaving, Ca2+ moves in slowly

• Membrane potential reaches +20mV (fast channels are voltage gated, close at +20mV)

Cardiac Myocyte Action Potential: Phase 1: Early Repolarization

• K+ fast channels open at +20mV

• Slight drop in charge (5mV)

• K+ still leaking out of slow channels

• Na+ channels partially close

Cardiac Myocyte Action Potential: Phase 2: Plateau

• Voltage gated Ca2+ channels open

• Voltage gated K+ channels still open

• Ca2+ entering and K+ exiting causes temporary plateau

Cardiac Myocyte Action Potential: Phase 3: Repolarization

• Ca2+ and Na+ channels close

• K+ fast channels stay open dropping charge to -90mV

• At -90mV K+ channels close

• Na+/K+ pumps exchange 3 Na+ out for 2 K+ in (rebalances membrane)

Cardiac Myocyte Action Potential

Duration around 200ms

Autorhythmic Fibres Action Potential

• SA node fibres stimulate action potential 60-100 per min

• Faster than chambers contractile fibres

• Prevents different stimulus from initiating HR

• Pacemaker action potential stimulates myocyte action potential (regulated by ANS via Ca2+, Na+, K+)

Refractory Periods

• Pumping action of heart alternates from contracting and relaxing

• Several periods of varying conductivity/excitability in action potential

Absolute Refractory Period

• No external stimuli can cause another action potential (cell can’t depolarize again)

• Very short period in skeletal muscles

Relative Refractory Period

• When membrane potential reaches -70mV but not to resting -90mV

• Larger than normal stimulus, can create action potential

Supernormal Excitatory Period

• Weak stimulus can produce action potential

• Where cardiac arrhythmias originate

• Cells wants to be main character and sends electric impulse to another cell that isn’t ready to produce another action potential

Electrocardiogram

• Represents electrical conduction in heart

• Provides insight on problems with pt

P Wave

Atrial depolarization (firing of SA node)

PR Interval

Time from SA node firing until ventricles contract

QRS Complex

Ventricular depolarization and atrial repolarization

ST Segment

Elevated during MI

T Wave

Ventricular repolarization

Aging

• Cardiac diseases develop with aging, lifestyle and environment factors

• Some can be detected during fetal development