A + P 2: Cardiovascular System, Heart

Veins

Carries blood to the heart

Arteries

Carries blood away from the heart towards the lungs

Capillaries

Most numerous, smallest diameter, thinnest walls. Site of gas and nutrient exchange into/out of blood vessels

Heart moves blood through 2 circuits:

Pulmonary and systemic

Pulmonary circuit

Carries blood to/from lungs. Right side of heart

Systemic circuit

Carries blood to/from the (non-lung) tissues of the body

Unoxygenated blood

Body → right side of heart → lungs

Pictured as blue (actually dark red)

Oxygenated blood

Lungs → left side of heart → body

Bright red

Position of the heart

Thoracic cavity, medially between the lungs and the mediastinum. Leans left. About the size of a fist, broad at the top (base), tapers to a point (apex). Rests on its side and is slightly rotated in the body

CPR technique

If heart stops, CPR can maintain the flow of blood. Applying pressure to the sternum will squeeze blood out of the heart and into circulation. Proper positioning of the hands on the sternum is between the lines at T4 and T9

Pericardium

Fluid filled sac that encases the heart. Provides protection and allows movement (beating) by reducing friction. 3 layers

Layers of the heart

Pericardium

Myocardium

Endocardium

Pericardium

Outermost layer. Parietal and visceral layers; w/ fluid filled pericardial cavity

Myocardium

Middle layer of heart casing. Mainly cardiac muscle

Endocardium

Deepest tissue layer of heart casing

Heart development

Develops from 2 blood vessels that fuse, then twist and fold upwards

4 chambers of the heart

Right and left atrium, right and left ventricles

2 important nodes

SA node and atrioventricular node (AV)

Septa

Separate chambers of the heart

(interatrial, interventricular, atrioventricular)

Interatrial septum

Separates right/left atria

Interventricular septum

Separates right/left ventricles

Atrioventricular septum

Separates atria and ventricles (contains valve opening)

4 heart valves

Prevent backflow and ensure blood movement in one direction. Atrioventricular valves (x2) and semilunar valves (x2)

Atrioventricular valves (x2)

Between atrium and ventricle (tricuspid → right side, bicuspid/mitral → left side)

R. atrium → R. vent through tricuspid valve

L. atrium → L. vent through bicuspid valve

Semilunar valves (x2)

Separates the r/l ventricles (pulmonary and aortic valves)

R. vent → pulmonary artery through pulmonary valve

L. vent → aorta through aortic valve

Chordae tendinae and papillary muscles

Prevents backflow of blood, ensures blood flow is only happening in one direction. Ensures that the large tricuspid and bicuspid valves do not invert into the atria

Cardiac skeleton

Provides structural support for the heart valves (fibrous tissue). Also separates the electrical activity of the atria and ventricular muscles

Foramen ovale

Connects right atrium and left atrium (hole between). One of the two shunts that allow blood to bypass the lungs (pulmonary circulation)

Ductus arteriosus

Connects pulmonary trunk → aorta

Patent foramen ovale

Opening in interatrial septum (usually failure of foramen ovale to close)

Patent ductus arteriosus (PDA)

Failure of ductus arteriosus to close. Small holes typically are not that big of a deal

Coronary blood vessels

Supply heart tissues with blood flow. R/L coronary arteries branch from base of aorta. Coronary sinus drains venous blood into the right atrium

Atherosclerotic coronary arteries

Coronary angiogram (x-ray) showing 2 occluded coronary arteries. Decreased blood flow (ischemia) and insufficient O2 (hypoxia) can lead to cardiac muscle death (myocardial infarction)

Caused by blockage. Coronary artery bypass surgery. Avoids block → connects new artery with aorta

Cardiac cycle

Heart ventricles contract (systole) and relax (diastole) in a rhythmic cycle

Ventricles vs. atrium

Muscles of ventricles are thicker (stronger) than atria. Left is thicker than right (left sends blood to whole body, right sends blood only to lungs)

Systole

Ventricles contract, push blood out, time of highest BP in ventricles. Stimulated

Diastole

Resting. Ventricles relax/fill with blood, time of lowest BP in ventricles

Pressure changes in the heart chambers drive the flow of blood

Blood flows direction = higher → lower pressure area

Contraction of ventricle

Becomes smaller. Blood is compressed in the chamber, which increases pressure = blood leaves ventricles (systole)

Relaxation of ventricle

Becomes larger. Blood is not compressed as much, which decreases pressure = blood enters ventricles (diastole)

Auscultation

Act of listening to the heart, lungs, etc. sounds

Heart murmurs

Sounds that occur when blood does not flow properly through the valves

Ex. valve prolapses allow blood to flow in the opposite direction

Muscle cell contraction

Triggered by movement of ions across the cell membrane

1. Resting: slight negative charge

2. Stimulated: membrane channels open and charged ions (Na+, K+) move, cell becomes positively charged

Depolarization event (action potential) triggers muscle cell contraction

Cardiomyocytes

Cardiac muscle cells. They have sarcomeres composed of actin and myosin that generate contractile force, and T tubules transmit electrical impulse (cell membrane depolarization) to the interior of the cell

Unique: intercalated discs, connects muscle cells and contain gap junctions (allows electrical pulse to spread) and desmosomes

Types of myocardial cells

Myocardial contraction cells, myocardial conducting cells

Myocardial contraction cells

About 99% of cardiac cells; produces the contractile force that moves blood

Myocardial conducting cells

About 1% of cardiac cells; modified to act more like neurons - initiate and coordinate the heartbeat

Contractile cells

1. Rapid depolarization

2. Long plateau before repolarization and return to resting state (slow voltage gated Ca2+ channels cause the plateau)

Ensures a delay of about 250 ms before the next contraction

Conducting cells

Cardiac conducting cells - possess ‘autorhythmicity’. Generates an electrical impulse (depolarize) in the absence of hormonal and nervous system input

Causes heart beats

Sinoatrial (SA) node

Primary pacemaker, located in wall of right atrium. Hormones and NS alter heart rate by affecting how quickly the SA node creates an electrical impulse (ex. epinephrine, norepinephrine, thyroid hormones, cortisol)

Electrical events during a heartbeat

1. Atrial contraction. Electrical impulse from SA node spread through atria, causing a wave of muscle contraction moving from top to bottom

2. After a slight delay (about 100 ms, makes sure atria is fully empty), the electrical impulse triggers the AV node to send an electrical impulse through the ventricles (wave of muscle contraction doesn’t spread directly to ventricles because atria and ventricles are electrically separated)

3. Ventricular contraction (systole). Electrical impulse from AV node moves to ventricles via a conducting pathway

   1. Travels down bundle of his (clusters of cells between ventricles)

   2. Travels through purkinje fibers

Purkinje fibers

Contract ventricle muscle cells, initiating a contractile wave that spreads to ventricles (electrical impulse travels to bottom of ventricles before contracting muscle cells. Causes wave of muscle contraction to travel from bottom towards the top, allowing more efficient pushing of blood up and into arteries)

SA node

Causes contraction of the heart. Cells of the SA node reach threshold the quickest → they initiate the wave of depolarization that causes the heart to contract

Spontaneous depolarization rates

SA node = about 100 beats/min (if signal is blocked = bradycardia, slower heart rate). If signal is blocked, heart contraction is initiated by other conducting cells

AV node = about 50 beats/min

Bundle of his = about 30 beats/min

Purkinje fibers = about 20 beats/min

Electrocardiograms (ECGs)

Record electrical events in the heart. Can detect electrical impulses (using electrodes at specific body locations)

Wave patterns represent electrical events that cause muscle contraction or relaxation

Abnormal patterns diagnose damage or disorders

Intervals/segments correspond to specific electrical events and cardiac muscle

P wave

Atria depolarize, atria contract (atrial systole)

QRS complex

Ventricles contract (atria relax), ventricles depolarize, atria repolarize

T wave

Ventricles relax, and repolarize (diastole)

Normal sinus rhythm

Typical/healthy electrical pattern

Second degree (partial) block

P waves are not always followed by QRS complex and T waves

Atrial fibrillation

Electrical pattern abnormal prior to QRS, increased frequency between QRS complexes

Ventricular fibrillation

No normal electrical activity

Defibrillators

Stop the heart (by disrupting the electrical activity) so the SA node can trigger a normal conduction cycle

Pacemakers

Implantable devices that take over for the conduction cells. Monitors cardiac cell depolarization and sends an electrical pulse if it senses slowed, missed, or irregular depolarization patterns

Cardiac output

Measure of how much blood leaves the heart per minute

Heart rate (BPM) x stroke volume (liters per beat) = cardiac output

CO = HR x SV

HR decrease, CO decrease

SV increase, CO increase

Receptors in the body communicate with the brain

Cardiovascular centers in medulla oblongata (brain) receive input from receptors throughout body and adjust heart rate as needed (cardiac reflexes)

Types of receptors

Proprioreceptors, chemoreceptors, baroreceptors

Proprioreceptors

Detect movement of muscle, tendon, etc. More movement = higher heart rate

Chemoreceptors

Detect metabolic byproducts (CO2, lactic acid, H+) in blood. More metabolic byproduct = increased heart rate

Baroreceptors

Detects blood pressure in major blood vessels and heart. Increase in blood pressure = decrease in heart rate

Cardiovascular centers in brain change heart rate via autonomic innervation

Sympathetic cardiac nerves = increased HR

Parasympathetic (vagus nerves) = decreased HR

At rest, heart receives both sympathetic and parasympathetic stimulation (autonomic tone)

Other factors that impact heart rate

Hormones (epinephrine, norepinephrine, thyroid hormones) and blood electrolytes (Ca2+, Na+, K+)

Regulation of stroke volume

Measured as the differences between end diastolic volume and end systolic volume

SV = EDV - ESV

End diastolic volume (EDV)

Volume in ventricles after filling

End systolic volume (ESV)

Volume remaining in ventricles after contraction

What regulates stroke volume?

Preload, contractility, afterload

Preload

Degree of muscle stretch at start of systole (end diastolic volume) (ventricle volume). How does it increase stroke volume: When more blood is in the ventricles (greater end diastolic volume), the muscle cells become more stretched. Stretching creates more optimal overlap between actin-myosin = more force generated

Higher preload (EDV) = higher stroke volume

Can be increased by longer filling time (longer time in diastole), more blood is returned to the heart (venous return), such as when blood vessels are constricted by contracting skeletal muscles

Contractility

How forceful the muscle contracts (independent of preload). Force of ventricular muscle contraction, independent of EDV. For any end diastolic volume (amount of actin-myosin overlap), the ventricles generate more force

Higher contractility = higher stroke volume

Other factors that impact contractility:

Increased contractility = sympathetic NS stimulation, epinephrine, thyroid hormones, etc.

Decreased contractility = parasympathetic NS stimulation, low blood O2, etc.

Afterload

Resistance to blood flow through blood vessels. Resistance that ventricles must overcome to pump blood. Lower afterload = increased stroke volume

Resistance can be higher for many reasons: high pressure in blood vessels, damage to heart valves that makes it harder for them to open, etc.

Way blood moves (2 circuits)

Body → Inferior/superior vena cava → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary arteries → lungs

Lungs → pulmonary veins → left atrium → bicuspid valve → left ventricle → aortic valve → aorta → body