chapter 20 · Cardiac Muscle Cells! Contraction mechanism is similar to skeletal muscle because:! • Contraction involves Action Potential, Ca2+, troponin, tropomyosin, myosin, actin!

Chapter 20, The Heart!

1!

Chapter 20!The Heart!

2

SECTION 20-1!The heart is a four-chambered organ, supplied by the coronary circulation, that pumps oxygen-poor blood to the lungs and oxygen-rich blood to the rest of the body!


2!

3

Overview Figure 20-1!

4

The Heart is a Double Pump!

Right heart:!•  Powers pulmonary circulation (circuit)!•  Pumps blood to and from lungs!•  Receives blood from systemic circuit!

Left heart:!•  Powers systemic circulation (circuit)!•  Pumps blood to and from rest of body!•  Receives blood from pulmonary circuit!


3!

5

Blood Vessel Overview!Vessel definitions:!

•  All arteries carry blood away from the heart!•  All veins carry blood towards the heart!

Note that neither of these definitions mentions the word oxygenated or deoxygenated.!

The amount of oxygen carried by blood within a vessel has nothing to do the terms artery and vein! It’s all about the direction of blood flow.!Capillaries: Exchange of nutrients, wastes and gases between blood and ECF occurs here.!

6

Pericardium - 1 - Serous Pericardium!

A.  Serous pericardium = serous membrane!Two layers and an enclosed, fluid-filled space!1. Visceral pericardium (a.k.a. epicardium)!

•  Adheres to outer surface of heart!Pericardial cavity (potential space)!

•  Contains pericardial fluid!•  Secreted by serous membrane!•  Acts as a lubricant between layers!

2. Parietal pericardium!•  Adheres to fibrous pericardium (next slide)!


4!

7

Pericardium - 2 - Fibrous Pericardium!

B.  Fibrous pericardium!•  Dense irregular CT!•  Stabilizes heart and major vessels in

mediastinum!

Figure 20-2c!

8

Heart Wall!

Three layers:!1. Epicardium = visceral pericardium = visceral

layer of serous pericardium!•  Mesothelium + loose CT!

2. Myocardium = heart muscle!•  Cardiac muscle tissue!

3. Endocardium!•  Simple squamous endothelium overlying

areolar CT!•  Continuous with endothelial lining of blood

vessels!


5!

9

The Heart Wall Figure 20-4!

10

Cardiac Muscle Tissue!

Adjacent cells connected by intercalated discs!Desmosomes hold cells to one another!Gap junctions electrically connect cells!

One atrial syncytium!•  If one atrial cell depolarizes, all do!

One ventricular syncytium!•  If one ventricular cell depolarizes, all

do!What is a syncytium?


6!

11

Cardiac Muscle Cells Figure 20-5!

Intercalated discs!

12

Sectional Anatomy of the Heart Figure 20-6a!

Know the path of blood through the heart!!See my schematic heart diagram on our website.!!The pathway constitutes almost 10% of the blood tracing assignment.!!It’s easy. Really.!


7!

13

Path of Blood Through the Heart!

14

Internal Cardiac Anatomy - Right Atrium!

Right atrium!Blood enters from:!•  Superior vena cava (SVC)!•  Inferior vena cava (IVC)!•  Coronary sinus (from coronary circulation)!

Pectinate muscle = muscular ridges!Foramen ovale (fetal) becomes fossa ovalis!•  F. ovale allows flow from R. to L. atrium!•  Valvular flap closes at birth!•  Becomes fossa ovalis at about 3 months!


8!

15

Internal Cardiac Anatomy - Right Ventricle - 1!

Right atrioventricular (AV) valve!•  a.k.a. tricuspid valve (three flaps)!

Chordae tendineae!•  Attach to AV valve and papillary muscle!

Papillary muscle!•  Cones of cardiac muscle!•  Attach to chordae tendineae!

Chordae and papillary muscle prevent eversion of AV valves - do not open or close valves!

16

Internal Cardiac Anatomy - Right Ventricle - 2!

Trabeculae carnae!Muscular ridges!

e.g. moderator band!•  Carries contractile stimulus to

papillary muscles!Conus arteriosus!

Superior end of ventricle!Leads to pulmonary semilunar valve →

pulmonary trunk → R. and L. pulmonary arteries → “ACV” of lungs!


9!

17

Internal Cardiac Anatomy - Left Atrium!

Receives oxygenated blood from two left and two right pulmonary veins!

Left AV valve separates it from left ventricle!a.k.a. bicuspid (two flaps) or mitral valve (looks

like a bishop’s cap)!

18

Internal Cardiac Anatomy - Left Ventricle!

Much thicker wall than right ventricle!•  Pumps blood to entire systemic circuit!

Aortic semilunar valve → ascending aorta!Ascending aorta contains:!

Aortic sinuses!•  Within aorta, just past valve!•  Contain openings for R. and L. coronary

arteries (first branches of aorta)!


10!

19

Aortic Arch!Attached to pulmonary

trunk by ligamentum arteriosum!

Ligamentum arteriosum!In fetus:!•  Is ductus arteriosus!•  Links pulmonary

and systemic circuits!ü  I.e., blood can

bypass lungs!•  Closes at birth!

Anterior view

R. Brachiocephalic A.! L. Common Carotid A.!

Aortic Arch! Ligamentum arteriosum!

Superior vena cava!

Pulmonary trunk!

L. Subclavian A.!

20

THE VENTRICLES PUMP THE SAME VOLUME OF BLOOD EACH MINUTE.!

!!Right ventricle pumps blood to and from lungs!Ventricular wall is thinner!

•  Lungs are nearby!•  Pulmonary vessels short and wide!

Little resistance to blood flow!Pumps like a bellows against left ventricle!

Right vs. Left Ventricle - 1!


11!

21

Right vs. Left Ventricle - 2!

Left ventricle pumps blood through systemic circuit!Requires 6–7X more force!Contraction mechanism not like a bellows:!

1.  Chamber height decreases!2.  Chamber diameter decreases!3.  Bulges into R. ventricle (assists RV

pumping)!

22

Connective Tissues/Fibrous Skeleton - 1!

A.  Connective tissues!Both collagen and elastin (i.e., it’s both tough

and elastic)!1.  Provide support for cells, vessels, nerves!2.  Distribute forces during contraction!3.  Prevent overexpansion of chambers!4.  Allow return to original shape after

contraction!


12!

23

Connective Tissues/Fibrous Skeleton - 2!

B.  Fibrous skeleton!Four bands of elastic tissue around valves!

1.  Stabilize valves!2.  Stabilize ventricles!3.  Physically and electrically isolate atria

from ventricles!•  Two electrical syncytia exist:!

Atrial and ventricular syncytia!Electrically connected at AV node!

24

Connective Tissues/Fibrous Skeleton Figure 20-8!


13!

25

Coronary Circulation Figure 20-9!

Know names at the level of detail

covered in lab.!

26

SECTION 20-2!The conducting system distributes electrical impulses through the heart, and an electrocardiogram records the associated electrical events!


14!

27

Cardiac Conducting System!

a.k.a. nodal system!A system of specialized cardiac muscle cells!

•  Most are smaller than normal cardiac cells!•  Contain few myofibrils!•  Contraction of heart follows spontaneous

depolarization of sinoatrial (SA) node!Autorhythmicity or automaticity!

Neural or hormonal input not required!

28

Conduction System Figure 20-11a!

Insulation by

fibrous skeleton!


15!

29

1. Sinoatrial Node (SA Node)!

Found in R. atrium near superior vena cava opening!•  Fastest rate of spontaneous depolarization!•  Called “cardiac pacemaker”!•  Intrinsic rate = 80–100 depolarizations/min!

Resting heart rate normally slower!Parasympathetic input (Vagus)!

https://www.khanacademy.org/science/health-and-medicine/circulatory-system/!

30

SA Node - 2 Figure 20-11b!

Cells leaky to Na+!•  Leakage leads to prepotential → action potential!•  A.P. spreads via gap junctions:!

To atrial muscle cells!Along internodal fibers to AV node!

(significance of internodal fibers unclear)!


16!

31

SA Node - Slow Response Action Potential!

Slow Response •  autorhythmicity

(Morhman & Heller !2006)!

SA Node!

*Action potential!

*Permeability changes!

32

2. Atrioventricular (AV) Node!

Found in R. atrium near opening of coronary sinus!Delays conduction of A.P. to ventricles!

A. Nodal cells small !•  (How does axon diameter affect

conduction velocity in neurons?)!B. Gap junctions fewer, less efficient!

Allows for coordinated heart beat!•  Atria contract together first, then ventricles!•  This is obviously important!!


17!

33

3. Conducting Cells Transmit the A.P. - 1!

A.  Internodal pathways!•  SA node → AV node!

B.  AV bundle (of His)!•  AV node → bundle branches!

C.  Bundle branches (Right and Left)!•  Bundle branches → Purkinje fibers and

moderator band!•  Travel within interventricular septum!

Left side larger → larger left ventricle!•  High conduction speed!

34

3. Conducting Cells Transmit the A.P. - 2!

D.  Purkinje fibers!•  Innervate ventricular myocardium!•  Fastest conduction speed!•  Cause ventricles to contract from apex to

base!E.  Moderator band!

•  AV bundle → papillary muscles!•  Papillary muscles contract before ventricles!

Pull on chordae tendineae!Tension on AV valves prevents eversion of

valves and backflow of blood into atria!


18!

35

Conduction System Summary Figure 20-11!

Insulation by fibrous skeleton!

36

Impulse Conduction Figure 20-12!


19!

37

Electrocardiogram (ECG or EKG)!

Records electrical activity in body fluids caused by electrical activity in the heart!

Is not a record of muscle contractionECG waves!Record electrical changes from baseline (0 mV)!

•  P wave = atrial depolarization!•  QRS complex = ventricular depolarization!

(Atrial repolarization is hidden)!•  T wave = ventricular repolarization!

38

An Electrocardiogram Figure 20-13!


20!

39

Impulse Conduction Animation!

https://www.youtube.com/watch?v=v3b-YhZmQu8&app=desktop!

40

Cardiac Muscle Cells!

Contraction mechanism is similar to skeletal muscle because:!•  Contraction involves Action Potential, Ca2+,

troponin, tropomyosin, myosin, actin!Mechanism is different from skeletal because:!

•  Action potential time course is longer!•  Refractory periods are longer!•  Contraction lasts longer!•  Source of Ca2+ is both intra- and extracellular!


21!

41

AP in Skeletal and Cardiac Muscle Figure 20-15!

42

1.  Rapid depolarization phase!Resting membrane potential about -90mV!•  Cells innervated and depolarized by

Purkinje fibers!Threshold for A.P. about -75 mV!

When reached:!•  Fast voltage-gated Na+ channels open!•  Na+ enters cell → A.P. begins!•  These channels close rapidly (in a few

msec)!

Contraction of Ventricular Muscle - 1!

Time


22!

43


2.  Plateau phase!Membrane depolarizes to +30 mV!

Fast voltage-gated Na+ channels close!•  Na+ actively pumped from cell (Na/K ATPase)!

Slow voltage-gated Ca2+ channels open!•  aka calcium-sodium channels!•  Ca2+ and Na+ enter cell from ECF!

Causes Ca2+ release from SR!i.e. ↑↑ [Ca2+] in cytoplasm!

Contraction follows !Time

44


2.  Plateau phase (continued)!•  Cell remains depolarized = plateau!

Membrane potential remains near 0 mV!Ca2+ entry from ECF = Na+ and K+ exit!K+ permeability decreases!

3. Repolarization phase!•  Slow Ca2+ channels close!•  Slow K+ channels open!•  Return to resting potential (slow K+ gates

close)!

Time

2.!

3.!


23!

45

Action Potential Cardiac Muscle Figure 20-15!

46

Slow and Fast Response A.P.s!

Fast Response •  cell depolarized by adjacent cell

Slow Response •  autorhythmicity

(Morhman and Heller 2006)

Ventricular muscle

SA node!

Action potential!

Permeability changes!


24!

47

Refractory Periods for Cardiac Muscle!

Absolute = muscle cell will not respond to any stimulus!•  Na+ channels all open, or closed and inactivated!•  About 200 msec (duration of plateau phase)!•  Continues until relaxation occurs!•  Prevents tetany → death!

Relative = larger than normal stimulus needed!•  Voltage-gated Na+ channels closed, but no longer

inactivated!Bottom line!•  A.P. lasts much longer (30X) than in skeletal muscle!•  Tetanic contractions prevented!

48

Importance of Ca2+; Energy for Contraction !

About 20% of Ca2+ enters from ECF!•  Triggers release of Ca2+ (80%) from SR!•  Interaction between Ca2+, troponin,

tropomyosin, myosin and actin occurs as in skeletal muscle!

!Energy for contraction!

•  Aerobic metabolism of fatty acids (lipid droplets) and glucose (glycogen)!

•  Myoglobin helps “store” oxygen!


25!

49

SECTION 20-3!Events during a complete heartbeat constitute a cardiac cycle!

https://www.youtube.com/watch?v=rguztY8aqpk!

Big picture!

50

The Cardiac Cycle!

Cardiac cycle: Period of time from the beginning of one heart beat to the beginning of the next!

!Recall my schematic heart handout

This is the “big picture” about how blood moves through the heart!

!Be sure you understand the information in Figures 20-16 and 20-17.!You will not be required to reproduce these figures, but you will be expected to demonstrate that you fully understand them.!


26!

51

Cardiac Cycle Terms!

Systole = contraction phase of a chamber!Chamber size decreases → ↑ pressure → eject

blood!Diastole = relaxation phase of a chamber!

Chamber size increases → ↓ pressure → chamber filling!

!Both atria and ventricles spend more time in

diastole than in systole.!(Why is this significant?)!

52

Pressure!

PRESSURE is the key to understanding blood flow patterns and the opening and closing of heart valves.!•  Blood moves from an area of higher pressure

to an area of lower pressure.!•  Valves open and close in response to

pressure gradients.!!Ventricular and atrial systole and diastole must be

coordinated to produce the correct pressure gradients that ensure efficient blood flow and heart function.!


27!

53

Introduction to the Cardiac Cycle Figure 20-16!

Isovolumetric!phase!

•  SLVs still closed!

Ejection!Phase!•  SLVs ! open!

54

Cardiac Cycle Animations!

https://www.youtube.com/watch?v=vb94rksdGlE!!https://www.youtube.com/watch?v=rguztY8aqpk!!https://www.youtube.com/watch?v=5tUWOF6wEnk!

Helpful videos!


28!

55

Pressure-volume Relationships!

Figure 20-17 details events in the Left Heart.!1.  Time scale is shown at very bottom:!

1 Cardiac Cycle = about 800 msec = .8 sec!1 beat/0.8 sec X 60 sec/min = 72 beats/min!

2. Top panel shows electrical events (ECG)!3.  Colored bars show contractile state of L. atrium

and L. ventricle!4.  Middle panel shows pressures: aorta, left

ventricle, left atrium!5.  Lower panel shows left ventricular volume!

56

Pressure and Volume Relationships Figure 20-17!

Not zero ml


29!

57

Heart Sounds Figure 20-18!

S1 = AV valve closure; S2 = SLV closure!

Time

58

SECTION 20-4!Cardiodynamics examines the factors that affect cardiac output!


30!

59

Cardiodynamics!

End-diastolic volume (EDV)!•  Volume of blood in ventricle following diastole!

End-systolic volume (ESV)!•  Volume of blood in ventricle following systole!

Stroke Volume (SV)!•  Volume of blood ejected in one beat of ventricle!•  SV = EDV - ESV!

Ejection fraction !•  % of EDV that is ejected!•  SV/EDV x 100 (about 60% at rest)!

60

Model of Stroke Volume Figure 20-19!

EDV!ESV!

SV=EDV-ESV!


31!

61

Cardiac Output (CO)!

CO = the volume of blood pumped by a ventricle in one minute (e.g. ml/min or l/min)!

!!!

= heart rate x stroke volume! = beat/min x ml/beat = ml/min!

!For example:!

75 beat/min X 80 ml/beat = 6000 ml/min != 6 l/min!

CO = HR X SV

62

Factors Affecting Cardiac Output Figure 20-20!


32!

63

Cardiac Output!

Effects on Heart Rate!

•  Autonomic Innervation!•  Cardiac Reflexes!•  Autonomic Tone!•  Neurotransmitter Effects on SA Node!•  Atrial (Bainbridge) Reflex!•  Venous Return!•  Hormonal Effects!

64

Heart receives both sympathetic and parasympathetic inputs:!•  SA and AV nodes, Atria!•  Ventricles mostly sympathetic!

Cardiac centers in medulla!Cardioacceleratory center!•  Sympathetic inputs → ↑ HR!Cardioinhibitory center!•  Parasympathetic inputs → ↓ HR!

Autonomic Innervation Figure 20-21!


33!

65

Cardiac Reflexes!

Cardiac centers (medulla) receive info from sensors:!•  Baroreceptors (BP)!•  Chemoreceptors ([CO2], [O2], pH)!

Info carried by:!•  Parasympathetic nerves (C.N. IX and X)!•  Sympathetic nerves (Cardiac plexus)!

Reflex example:!↓BP → ↑ HR → ↑ BP!

66

Autonomic Tone!

Tonic inputs to SA and AV nodes, and myocardium!•  Sympathetic (NE)!•  Parasympathetic (ACh)! ↑ or ↓ tone → change HR!

Parasympathetic inputs dominate at rest!•  Evidence:!

Cut vagus (X) → ↑ HR (Don’t try this at home.)!

!


34!

67

Neurotransmitter Effects on SA Node!

ACh: ↑ PK+ → ↓ HR!•  Binds muscarinic ACh receptors → opens K+

channels!↑  Duration of spontaneous depolarization!↓ Rate of spontaneous depolarization!↑  Duration of repolarization!

NE: ↑ PCa2+ → ↑ HR!•  Binds β-adrenergic receptors → open Ca2+

channels!↑ Rate of spontaneous depolarization!↓ Duration of repolarization!

68

Neurotransmitters and SA Node Figure 20-22!

“Normal” !

Parasympathetic!Stimulation!

↑ PK+!

Sympathetic!Stimulation!↑ PCa2+!


35!

69

Atrial Reflex!

a.k.a. Bainbridge Reflex !(A long reflex, involves the CNS.)!↑ venous return →!↑ stretch of atria →!↑ stimulation of stretch receptors →!↑ sympathetic activity to medulla →!↑ HR!

70

Venous Return and Hormonal Effects on HR!

Venous return!1.  ↑ venous return → atrial (Bainbridge) reflex!2.  ↑ venous return → !

↑ stretch on SA node → !↑ Na+ leakage into nodal cells →!↑ depolarization rate → !↑ HR!

Hormones!↑ HR via effect on SA node!

e.g. NE, E, T3 and T4!


36!

71

Cardiac Output!

Effects on Stroke Volume (SV = EDV - ESV)!

A. End Diastolic Volume (EDV)!1.  Filling Time!2.  Venous Return!

B.  End Systolic Volume (ESV)!1.  Preload!

•  Frank-Starling Principle!2.  Contractility!

•  Inotropic Effects!3.  Afterload!

•  Peripheral Resistance!

Note that preload and afterload are very similar terms that mean very different things. !

!Be sure to know the difference.!

72

Factors Affecting Stroke Volume Figure 20-23!


37!

73

A. End Diastolic Volume Effects on SV!

Changes in EDV affect SV (SV = EDV - ESV)!e.g. ↓ EDV → ↓ stroke volume!

Factors:!A. Filling time!•  Is the duration of ventricular diastole!

↑ HR → ↓ filling time → ↓ EDV → ↓ SV!B. Venous return!•  Volume of blood returning to heart during

filling time (diastole)!↓ Venous return → ↓ EDV → ↓ SV!

74

End Systolic Volume Effects on SV!

End systolic volume is the amount of blood remaining in the ventricle after systole.!•  Because SV = EDV - ESV, if ESV decreases,

SV will be greater.!Factors affecting End Systolic Volume (ESV)!

•  Preload (depends upon EDV)!•  (Myocardial) Contractility!•  Afterload!


38!

75

1. Preload and SV!

Preload = degree of stretch on ventricular muscle cells at the end of diastole!

Muscle cell length affects actin/myosin overlap and contraction strength (recall Chapter 10)!

Preload is proportional to EDV:!↑ EDV → !•  ↑ stretch (preload) → !•  More efficient actin/myosin overlap → !•  Stronger contraction → !•  ↑ SV !

76

Muscle Cell Length vs. Force of Contraction Figure 10-14

Note that this figure is for skeletal muscle, but the general principle is very similar.!


39!

77

Preload and SV at REST!

•  Relatively low venous return →!•  Small EDV →!•  Little stretch of ventricular muscle cells →!•  Short sarcomere length →!•  Suboptimal actin/myosin overlap →!•  Relatively weak contraction →!•  Large ESV (small volume of blood pumped) →!•  Low stroke volume!

(EDV - ESV = small = low stroke volume)!

78

Preload and SV during EXERCISE!

•  Increased venous return (e.g. from skeletal muscle pump) →!

•  Larger EDV →!•  Increased stretch of ventricular muscle cells →!•  Increased sarcomere length →!•  More efficient actin/myosin overlap →!•  Increased force of contraction →!•  Smaller ESV (large volume of blood pumped) →!•  Larger stroke volume!

(EDV - ESV) = large = high stroke volume!


40!

79

Preload: the Frank-Starling Principle!

a.k.a. Starling’s Law of the Heart!•  Within physiological limits, the more the heart is

filled during diastole, the greater the force of contraction and the more blood the ventricle will pump.!

Martini: “more in = more out”!Cardiac muscle normally does not stretch past its

optimal sarcomere length!Stretch is limited by:!

•  Pericardium, fibrous skeleton, CT elements within muscle!

* Balance output of R and L heart!

80

2. Contractility - Inotropic Effects on SV!

Contractility = force of contraction produced at a given preload!Affected by:!•  Autonomic input!•  Hormonal (or drug) input!

Inotropic effects:!•  Positive inotropic effect = increased force

of contraction!•  Negative inotropic effect = decreased

force of contraction!


41!

81

2A. Autonomic Inotropic Effects on SV!

Sympathetic inputs (E and NE)!•  Positive inotropic effects!•  Stimulate α1- and β1-adrenergic receptors!

Release intracellular Ca2+!Activate enzymes; increase metabolic rate!

Parasympathetic inputs (ACh from vagus)!•  Negative inotropic effects!•  Open K+ channels → hyperpolarization!

82

2B. Hormonal and Drug Inotropic Effects on SV!

Hormones: E, NE, T3, T4, and glucagon!Stimulate Ca2+ release or cellular metabolism!

Drugs:!1.  Positive inotropic effects:!•  Mimic E and NE at β1 receptors!•  Stimulate Ca2+ entry or release (e.g. isoproterenol),

or interfere with Ca2+ reuptake to SR (e.g. digitalis)!2.  Negative inotropic effects:!•  Beta-blockers (e.g. propranolol)!•  Block α and/or β; block Ca2+ release from SR or

uptake from ECF


42!

83

3. Afterload Effects on SV!

Afterload: amount of force that a ventricle must generate to force blood through a semilunar valve!

Afterload is due to peripheral resistance!E.g. increased arterial (aortic) pressure!

•  L. Ventricle must produce more force to open aortic SLV!

•  Isovolumetric contraction period is longer (see Figure 20-17)!

•  Ventricular ejection phase is therefore shorter!•  Less blood will be ejected with each beat →

decreased SV!

84

Factors Affecting Stroke Volume Figure 20-23!


43!

85

Factors Affecting CO Figure 20-24!

86

Exercise and Cardiac Output!Resting CO:!

HR ≈ 75 beat/min!SV ≈ 70 ml/beat!CO ≈ 5.25 l/min!

Mild exercise CO:!HR ≈ 100 beat/min!SV ≈ 100 ml/beat!CO ≈ 10 l/min!

Intense exercise CO:!HR ≈ 150 beat/min!SV ≈ 130 ml/beat!CO ≈ 19.5 l/min!

Recognize him?!

Dr. Rausch?!


44!

87

Cardiac Reserve!

Cardiac Reserve = maximal CO ÷ resting CO!(This is what the text refers to as the “difference”

between resting and maximal CO”.!•  Average couch potato Cardiac Reserve

= 4 or 5!•  Olympic athlete’s Cardiac Reserve

= 8 or more!Resting CO of 5 l/min, Maximal CO of 40 l/

min!Cardiac Reserve = 40/5 = 8 (or 800%)!

Documents

chapter 20 · Cardiac Muscle Cells! Contraction mechanism is similar to skeletal muscle because:! • Contraction involves Action Potential, Ca2+, troponin, tropomyosin, myosin, actin!