Chapter 18 - The Cardiovascular System: The Heart (2)

What 2 circuits move blood through the body?

1. pulmonary circuit (circulation)

2. systemic circuit (circulation)

Pulmonary Circuit (circulation)

any of the blood vessels that carry blood to and from the lungs

• right side responsible to pumping blood to lungs

• pulmonary arteries

• pulmonary veins

Pulmonary Arteries (Trunks)

pump oxygen-poor blood from the right side of the heart to the lungs

• where its oxygenated

Pulmonary Veins

pump oxygenated blood from the lungs to the left side of the heart

Systemic Circuit (circulation)

any of the blood vessels that carry blood to and from the rest of the body tissues

• left side of the heart is responsible for pumping blood to rest of the body

• any part of the body NOT responsible for oxygenating blood

• oxygenated blood leaves the heart through the aorta (and its branches) to the body tissues

• oxygen-poor blood returns to heart via the the superior vena cava (precava) and inferior vena cava (postcava)

Right Side of Heart

pulmonic → relatively low-pressure

• doesn’t need lots of pressure to move blood to the lungs, since they’re close together

• similar volume of blood per minute as left side

Left Side of Heart

systemic → high-pressure

• needs significantly higher pressure to pump blood against gravity (to head), and also to toes (a few feet)

• walls of left side of heart are very thick

• similar volume of blood per minute as right side

Gross Anatomy of the Heart

the heart is tipped in the thoracic cavity

• apex (inferior “tip” of the heart) points to left hip

• enclosed in pericardium

  • fibrous pericardium

  • serous pericardium

Fibrous Pericardium

outermost portion of the heart

• anchors heart in chest cavity and protects heart

Serous Pericardium

internal portion of the heart

• divided into visceral and parietal layers — forms a fluid-filled sac around the heart

What are the 3 layers of the heart wall?

1. epicardium → outermost layer; visceral pericardium

2. myocardium → middle layer; contains cardiac muscle cells

3. endocardium → innermost layer; slick layer that covers all internal surfaces of the heart

Chambers in the Heart

4-chambered

• 2 atria → superior receiving chambers

  • right atrium

  • left atrium

• 2 ventricles → inferior pumping chambers; contraction begins at the bottom of the ventricle (apex) toward the top of the ventricle

  • this pattern is necessary because the blood vessels attached to the heart are at the top of the heart

    • right ventricle

    • left ventricle

Right Atrium

receives oxygen poor blood from systemic circuit

• blood enters via precava, postcava, and coronary veins

Left Atrium

receives oxygenated blood from the lungs

• blood enters via pulmonary veins

What 2 special features are only in atria?

1. pectinate muscle → increases contractile force of atrium

• gives the atria’s their thinness

2. auricles → two “ears” sitting on the external surface of the heart

• allow walls of atria to expand to allow more blood to return to the heart

Right Ventricle

pumps oxygen-poor blood to the lungs

• pulmonary trunk (artery) pumps from the heart to the lungs

Left Ventricle

pumps oxygenated blood to the rest of the body

• aorta pumps from the heart to the body tissues

What 2 special features are only in ventricles?

1. trabeculae carneae → ridges of muscle that assist with proper functioning of heart valves

• ensure that the heart valves function properly

2. papillary muscle → assist in opening/closing of the heart valves

• important for proper valve function too

Heart Valves

prevent the backward flow of blood through the heart

• 2 types:

  • atrioventricular (AV) valves

  • semilunar (SL) valves

Atrioventricular (AV) Valves

prevents backflow of blood from the ventricles into the atria

• tricuspid valve → found on right side of the heart

• mitral (bicuspid) valve) → found on left side of the heart

Chordae Tendineae

ancohors valve to papillary muscle in the ventricle

• only important when valves are closed

• papillary muscle → takes up slack of chordae tendineae

  • prevents AV valves from flipping into atria

Semilunar (SL) Valves

prevents backflow of blood from blood vessels into ventricles

• aortic semilunar valve → sits at base of aorta

• pulmonary semilunar valve → sits at base of pulmonary trunk

Heart Murmur

condition caused by dysfunctional heart valve(s)

• regurgitation of blood (where this occurs depends on which valve does not work)

• congenital or develop later in life

• the heart makes a “lub-whoosh-dup” sound

• usually not dangerous, but can indicate other dangerous heart conditions

  • “innocent” murmurs → congenital

  • “abnormal” murmurs:

    • children → congenital heart disease

    • adults → severe acquired heart valve issues

Stenosis

valves do not allow enough blood through valve

• stiffening of valves → don’t open or close normally

• congenital or develop later in life

Coronary Circulation

blood supply that provides heart tissue with nutrients

• coronary arteries → when blocked → heart tissue doesn’t get what it needs → heart attack

  • left coronary artery → supplies left side of heart

  • right coronary artery → supplies right side of heart

• coronary veins = drain oxygen-poor blood into right atrium

Cardiac Muscle Cells (myocytes)

contract to propel blood through the heart

• cardiac myocytes are connected to one another

  • desmosomes → cellular velcro → causing cardiac myocytes to stick together

  • gap junctions → communication junctions → cardiac myocytes can send information between each other

• LOTS of mitochondria present (25-30% of total volume)

  • responsible for ATP production

  • keeps muscle cells of the heart GOING

Intercalated Discs

plasma membrane connected via these

• contain both desmosomes and gap junctions

Functional Syncytium

muscle cells contract simultaneously

• telling the cardiac myocytes when to contract

• contracts as a coordinated unit

• important or else different parts of the heart would contract at different times → would affect circulation

What are the 2 important types of cardiac muscle cells?

1. pacemaker cells

2. contractile cardiac cells

Pacemaker Cells

noncontractile cells that spontaneously* depolarize

• spontaneously DOES NOT mean random

  • can cut every nerve to the heart and the heart will STILL pump blood because of pacemaker cells

• don’t contribute to blood movement

• set pace for contraction → establish resting heartrate

Contractile Cardiac Cells

contractile cells that depolarize in response to depolarization of pacemaker cells

• produces a force to move blood

• pacemaker cells communicate with contractile cardiac cells to tell them when to contract

Steps of Action Potential Initiation of Pacemaker Cells (3 steps)

1. pacemaker potential → Na+ channels open, K+ channels close

• Na+ enters the cell

• membrane potential becomes more positive

2. depolarization → Ca2+ channels open at threshold potential

• Ca2+ rushes into the cell

• the threshold potential is -40 mV

• membrane potential becomes more positive

• **THIS CREATES THE ACTION POTENTIAL

3. repolarization → Ca2+ channels close

• K+ channels open = K+ leaves cell

• returns to resting membrane potential

• membrane potential becomes more negative

  • once resting membrane potential is established, the cycle begins again

Sinoatrial (SA) Node

the “primary pacemaker” of the heart

• located in upper right atrial wall

• depolarizes at ~75 impulses/min

• depolarization here → spreads through both atria, eventually reaches AV node

• called the “primary pacemaker” because its most responsible for setting the resting heartrate

Atrioventricular (AV) Node

found at bottom of the right atrium in the interatrial wall

• generates at ~50 impulses/min

  • means nothing if the SA nodes is working → AV node takes over if SA node stops working

• impulse from SA node is delayed by 0.1s at the AV node

  • allows atria to completely contract and fill the ventricles before the AV node takes the impulse and spreads it to the next node

Atrioventricular (AV) Bundle

found in the interventricular septum

• impulses coming from AV node travel through AV bundle

• only place where atria and ventricles are electrically connected

Bundle Branches

right and left branches in wall that divides ventricles

• help conduct impulses toward the apex of the heart

Subendocardial Conducting Network (Purkinje Fibers)

found at heart apex and along outer ventricle walls

• depolarizes the contractile cells of both ventricles

• more elaborate on left side than right

  • walls of the heart are thicker on the left side → need more branches to reach all the cells

Autonomic Nervous System

innervation slightly modifies the intrinsic (“built-in”) conduction system created by pacemaker cells

• sympathetic and parasympathetic systems are involved

Cardioacceleratory Center (medulla oblongata)

sympathetic division (fight or flight)

• postganglionic fibers eventually innervate SA and AV nodes, heart muscle, coronary arteries

• depolarizes faster and increased blood flow

Cardioinhibitory Center (medulla oblongata)

parasympathetic division (via vagus nerve)

• postganglionic motor neurons found in the heart wall, innervates SA and AV nodes

Steps of Action Potential Initiation of Contractile Cardiac Cells (3 phases)

1. depolarization → fast voltage-gates Na+ channels open

• extracellular Na+ flows into cell

• membrane potential reversal from -90mV to +30mV

• membrane potential becomes more positive

• NO THRESHOLD VOLTAGE

2. plateau phase → Ca2+ channels in membrane open = Ca2+ enters cell

• some K+ channels are open = K+ leaves the cell

• membrane potential stays ROUGHLY the same

• positively charged Ca2+ enters and positively charges K+ leaves, so there’s practically a “plateau”

  • held in “depolarized state” in plateau phase, so the more tension it will create

3. repolarization → Ca2+ channels close, all K+ channels open

• inside of the cell becomes more negative

Electrocardiography

detection of the electrical impulses generated in and transmitted by the heart

• creates an electrocardiogram (ECG) → doctors can see heart activity

• ECGs produce several “waves” or complexes:

  • P wave

  • QRS complex

  • T wave

P wave

depolarization of atria

• created by movement of depolarization wave from SA node through atria

  • atria contract shortly after P wave begins

• depolarization moves to AV node after depolarization is complete (2)

QRS complex

depolarization of the ventricles

• peak (R) and troughs (Q and S) occur due to changing depolarization waves through ventricles

  • current changes direction

T wave

repolarization of the ventricles

• T wave is wider than the QRS complex

  • this is because it takes longer for the ventricles to repolarize than to depolarize

RR Interval

period of time between subsequent heartbeats

• can tell if someone’s heart is beating too fast or too slow by the distance between beats (RR interval)

Junctional Rhythms

indication = dysfunctional SA node

• affect of ECGs = P wave no longer evident, heart rate slows

• intrinsic conduction doesn’t happen when there’s little to no SA node function

• RR intervals will be farther apart

Ventricular Fibrillation

indication = APs occur in a rapid and highly irregular pattern in the ventricles

• affect of ECGs = grossly irregular ECG deflections are seen

  • no patterns or waves seen

• doesn’t move blood and is very serious

The Cardiac Cycle

all mechanical events associated with blood flow through the heart in one complete heartbeat

• includes systole (period of contraction) and diastole (period of relaxation)

• each cycle occurs ~75 times/min

What are the 4 phases present per cardiac cycle?

1. ventricular filling (mid to late diastole)

2. isovolumetric contraction phase (systole)

3. ventricular ejection (systole)

4. isovolumetric relaxation (early disastole)

Ventricular Filling (mid to late diastole)

pressure in the heart is low

• atrial systole occurs → atria contract → push remaining blood to ventricle

  • AV valves are open

• ventricles have end diastolic volume (EDV)

End Diastolic Volume (EDV)

maximum volume of blood found in the ventricle before it contracts

Isovolumetric Contraction Phase (systole)

ventricles begin to contract → pressure in ventricles rises quickly

• AV valves close, and SL valves are not yet opened

  • all valves are closed → blood goes NOWHERE

• SL valves will open when the pressure in ventricles exceeds the pressure in the blood vessels

  • this is because blood travels from high pressure to low pressure

Ventricular Ejection (systole)

blood flows from ventricles into aorta and pulmonary trunk

Isovolumetric Relaxation (early diastole)

ventricles relax → ventricular pressure drops rapidly

• end systolic volume (ESV) reached

• SL valves close → ventricles are closes off again

End Systolic Volume (ESV)

volume of blood remaining in the ventricles after they have completely contracted and relaxed

Cardiac Output

the total amount of blood pumped by ventricle in a single minute

How do you calculate Cardiac Output?

Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)

Stroke Volume

volume of blood pumped by ventricle with each beat (EDV - ESV)

• stroke volume is directly correlated with force of ventricular contraction

• average for an adult is ~70 mL blood per beat

Heart Rate

beats per minute

• average for an adult is ~75 beats/min

What happens to Cardiac Output when stroke volume increases? Heart rate? Both?

if you increase EITHER stroke volume OR heart rate → you increase Cardiac Output

Maximal Cardiac Output

the maximum amount of blood that can be pumped in a single minute

• total amount is dependent on the level of physical fitness

  • less fit = lower maximal cardiac output (~20-25 L/min)

  • more fit = higher maximal cardiac output (~35 L/min)

Changing End of Diastole (EDV)

increasing “pre-load“

• refers to stretch of muscle cells prior to contraction

  • you stretch the muscle cells by “pre-loading” the heart with blood before contraction

Frank-Starling Relationship

increasing the total volume of blood at the end of diastole (EDV) will increase strength of contraction during systole

How do you change End Systolic Volume? (2 ways)

1. contractility → intrinsic strength of the ventricle independent of loading conditions

• increasing contractility will increase amount of blood ejected

• in order to increase contractility → increase Ca2+ release

• ESV decreases when contractility increases

2. decreasing “after-load”

• refers to any force that opposes blood ejection from the ventricles

• dependent on resistance created by blood vessels leading out of ventricles

• resistance SLOWS DOWN the ability to pump blood

  • less resistance = more blood moved

  • more resistance = less blood moved

• ESV is lower when afterload is low

What are the 2 ways to regulate heart rate?

1. autonomic nervous system input

2. chemical regulation

Sympathetic (fight or flight)

norepinephrine released

• threshold reached faster → SA node fires faster and heart beats faster

• contractility increases

Parasympathetic (rest and digest)

acetylcholine released

• opposes sympathetic division

• vagal tone → heart rate is slower than it would be if the vagus nerve did not innervate

  • cutting vagus nerve would increase heart rate to ~100 beats/min

What effects do epinephrine and norepinephrine have on the heart?

increase heart rate and contractility

Thyroxine

thyroid hormone that increases the metabolic rate of cells

• increases heart rate (often over longer periods of time)

• can act directly on the heart and increase effects of epinephrine and norepinephrine

Hypocalcemia

calcium → generates action potentials by pacemaker cells

• when someone has too little calcium

• will slow down the heart rate

Hypercalcemia

calcium → generates action potentials by pacemaker cells

• excessive blood-calcium levels

• pacemaker cells have lots of access to calcium and will speed up heart rate

Hyperkalemia

potassium → changes resting membrane potential

• alters the electrical activity of the heart → cardiac arrest

• too much potassium

Hypokalemia

potassium → changes resting membrane potential

• weakened/feeble heartbeat

• too little potassium

What 4 other factors influence heart rate?

1. age → HR declines through age

2. biological sex → females have slightly higher HR than males

3. exercise/physical fitness → increased fitness = lower HR

4. body temperature → higher body temperature increases HR

Congestive Heart Failure

inefficiency of blood-pumping by heart to body tissues

• cardiac output and venous return are not balanced

• usually a progressive condition → weakened myocardium over time

What are some causes of Congestive Heart Failure?

1. coronary atherosclerosis

2. hypertension

3. multiple myocardial infarctions (heart attacks)

4. dilated cardiomyopathy

Pulmonary Congestion

left side fails and right side still operates normally

• pulmonary edema occurs → filling of lungs with fluid → nowhere for air to go if too much fluid

  • blood backs up in the lungs because the left side is pumping so slowly

Peripheral Congestion

right side fails and left side operates efficiently

• edema occurs in systemic body tissues

• cells in body tissue are unable to gain nutrients and oxygen necessary, remove metabolic wastes efficiently

Coronary Atherosclerosis

fatty buildup that clogs coronary arteries

Hypertension

persistent high blood pressure

• high pressure in arteries forces the heart to work harder to overcome high pressure and pump same amount of blood

• myocardium weakens with time

Multiple Myocardial Infarctions (heart attacks)

repeated heart attacks kill muscle cells and cause build up of scar tissue in heart walls

Dilated Cardiomyopathy

ventricles stretch out and myocardium deteriorates = ventricular contractility is compromised

• heart basically gets “massive” and chambers lose ability to contract

Congestion

one side of the heart is failing or can fail while the other still properly functions

Edema

build-up of fluid in tissues