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Reminders . Review heart anatomy for quiz in lab . No PreLab . HW 19: Cardiovascular Homework due in lab THE CARDIOVASCULAR SYSTEM
Part 2 PROPERTIES OF CARDIAC MUSCLE
Cardiac muscle Skeletal muscle . Striated . Striated . Short . Long . Wide . Narrow . Branched . Cylindrical . Interconnected
PROPERTIES OF CARDIAC MUSCLE
Intercalated discs passage of ions Numerous large mitochondria . 25–35% of cell volume Able to utilize many food molecules . Example: lactic acid
Nucleus Intercalated discs Cardiac muscle cell
Gap junctions Desmosomes
(a)
Figure 18.11a Cardiac muscle cell Mitochondrion
Intercalated Nucleus disc
T tubule Mitochondrion Sarcoplasmic reticulum Z disc
Nucleus Sarcolemma I band I band (b) A band
Figure 18.11b PROPERTIES OF CARDIAC MUSCLE
Some cells are myogenic . Heart contracts as a unit or not at all . Sodium channels leak slowly in specialized cells . Spontaneous deoplarization . Compare to skeletal muscle Action Potential in Myogenic Cells of the Heart
Action Threshold potential
2 2
3
1 Pacemaker potential 2 Depolarization The 3 Repolarization is due to This slow depolarization is action potential begins when Ca2+ channels inactivating and due to both opening of Na+ the pacemaker potential K+ channels opening. This channels and closing of K+ reaches threshold. allows K+ efflux, which brings channels. Notice that the Depolarization is due to Ca2+ the membrane potential back membrane potential is influx through Ca2+ channels. to its most negative voltage. never a flat line.
Figure 18.13 Action Potential of Contractile Cardiac Muscle Cells
Action 1 Depolarization is potential due to Na+ influx through Plateau fast voltage-gated Na+ channels. A positive
feedback cycle rapidly
2 opens many Na+ Tension channels, reversing the development membrane potential.
(contraction) Channel inactivation ends this phase. 1 3 2 Plateau phase is due to Ca2+ influx through Tension (g) Tension slow Ca2+ channels. This keeps the cell depolarized because few K+ channels Absolute Membrane(mV) potential are open. refractory period 3 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which Time (ms) brings the membrane potential back to its resting voltage.
Figure 18.12 CONDUCTION SYSTEM OF THE HEART
Terms . Systole versus diastole Specialized cardiac cells . Initiate impulse . Conduct impulse CONDUCTION SYSTEM OF THE HEART
Conduction pathway
SA node (pacemaker) atrial depolarization and contraction
AV node bundle of His right and left bundle branches
purkinje fibers myocardium contraction of ventricles Superior vena cava Conduction Pathway Right atrium 1 The sinoatrial (SA) node (pacemaker) generates impulses. Internodal pathway
2 The impulses Left atrium pause (0.1 s) at the atrioventricular (AV) node. 3 The atrioventricular Purkinje (AV) bundle fibers connects the atria to the ventricles. 4 The bundle branches conduct the impulses Inter- through the interventricular septum. ventricular septum 5 The Purkinje fibers depolarize the contractile cells of both ventricles. (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation (Intrinsic Innervation) Figure 18.14a CONDUCTION SYSTEM OF THE HEART
1. Sinoatrial (SA) node (pacemaker) . Generates impulses about 70-75 times/minute (sinus rhythm) . Depolarizes faster than any other part of the myocardium
2. Atrioventricular (AV) node . Delays impulses approximately 0.1 second . Depolarizes 50 times per minute in absence of SA node input
CONDUCTION SYSTEM OF THE HEART
3. Atrioventricular (AV) bundle (bundle of His) . Only electrical connection between the atria and ventricles
4. Right and left bundle branches . Two pathways in the interventricular septum that carry the impulses toward the apex of the heart
5. Purkinje fibers . Complete the pathway into the apex and ventricular walls CONDUCTION SYSTEM OF THE HEART
Intrinsic innervation External influences Normal: . Average = 70 bpm . Range = 60-100 bpm
The vagus nerve Dorsal motor nucleus of vagus (parasympathetic) Cardioinhibitory center decreases heart rate.
Medulla oblongata Cardio- acceleratory Sympathetic trunk ganglion center Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction.
AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons
Figure 18.15 HOMEOSTATIC IMBALANCES
Defects in the intrinsic conduction system may result in 1. Arrhythmias: irregular heart rhythms 2. Bradycardia < 60 bpm 3. Tachycardia >100 bpm 4. Maximum is about 300 bpm ELECTROCARDIOGRAPHY
A composite of all the action potentials generated by nodal and contractile cells at a given time . Represents movement of ions = bioelectricity . Three waves 1. P wave: electrical depolarization of atria 2. QRS complex: ventricular depolarization 3. T wave: ventricular repolarization QRS complex Sinoatrial node
Ventricular depolarization Atrial Ventricular depolarization repolarization
Atrioventricular node P-Q S-T Interval Segment Q-T Interval
Figure 18.16 SA node R Depolarization Repolarization
R P T
Q P T S 1 Atrial depolarization, initiated Q by the SA node, causes the S P wave. 4 Ventricular depolarization AV node R is complete. R
P T P T Q S Q 2 With atrial depolarization S complete, the impulse is 5 Ventricular repolarization delayed at the AV node. begins at apex, causing the R T wave. R
P T P T Q S Q 3 Ventricular depolarization S begins at apex, causing the 6 Ventricular repolarization QRS complex. Atrial is complete. repolarization occurs.
Figure 18.17 (a) Normal sinus rhythm. (b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min.
(c) Second-degree heart block. (d) Ventricular fibrillation. These Some P waves are not conducted chaotic, grossly irregular ECG through the AV node; hence more deflections are seen in acute P than QRS waves are seen. In heart attack and electrical shock. this tracing, the ratio of P waves to QRS waves is mostly 2:1.
Figure 18.18 THE CARDIAC CYCLE
All events associated with blood flow through the heart during one complete heartbeat . Systole—contraction (ejection of blood) . Diastole—relaxation (receiving of blood)
THE CARDIAC CYCLE
Three events 1) Recordable bioelectrical disturbances (EKG) 2) Contraction of cardiac muscle 3) Generation of pressure and volume changes
Blood flows from areas of higher pressure to areas of lower pressure . Valves prevent backflow
THE CARDIAC CYCLE
Ventricular filling → ventricular systole . Backpressure closes AV valves = isovolumetric contraction . Ventricular pressure > aorta & pulmonary valve pressure →semilunar valves open . Portion of ventricular contents ejected Left heart QRS P T P Electrocardiogram 1st 2nd EKG Heart sounds
Dicrotic notch
Aorta
Pressure Left ventricle
changes Atrial systole Left atrium
Pressure (mmPressure Hg)
EDV
Changes in SV Ventricular volume volume (ml) ESV
Atrioventricular valves Open Closed Open Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1
Left atrium Contraction Right atrium Left ventricle Right ventricle
Ventricular Atrial Isovolumetric Ventricular Isovolumetric Ventricular filling contraction contraction phase ejection phase relaxation filling 1 2a 2b 3
Ventricular filling Ventricular systole Early diastole (mid-to-late diastole) (atria in diastole)
Figure 18.20 HEART SOUNDS
Two sounds associated with closing of heart valves . First sound occurs as AV valves close and signifies beginning of systole = Lub . Second sound occurs when SL valves close at the beginning of ventricular diastole = Dub Heart murmurs = abnormal heart sounds . Most often indicative of valve problems Aortic valve sounds heard in 2nd intercostal space at right sternal margin
Pulmonary valve sounds heard in 2nd intercostal space at left sternal margin
Mitral valve sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle
Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space
Figure 18.19 Left heart QRS P T P Electrocardiogram Heart sounds 1st 2nd
Dicrotic notch
Aorta
Pressure Left ventricle
changes Atrial systole Left atrium
Pressure (mmPressure Hg)
EDV
Changes in SV Ventricular volume volume (ml) ESV
Atrioventricular valves Open Closed Open Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1
Left atrium Right atrium Left ventricle Right ventricle
Ventricular Atrial Isovolumetric Ventricular Isovolumetric Ventricular filling contraction contraction phase ejection phase relaxation filling 1 2a 2b 3
Ventricular filling Ventricular systole Early diastole (mid-to-late diastole) (atria in diastole)
Figure 18.20 HEART SOUNDS
Mitral stenosis HEART SOUNDS
Valvular insufficiency (regurgitation)
CARDIAC OUTPUT (CO)
Definition: volume of blood pumped by each ventricle in one minute . AKA: Minute volume 2 major factors . Stroke volume (SV) . Heart rate (HR) CARDIAC OUTPUT
CO (ml/min) = heart rate (HR) x stroke volume (SV) . HR = number of beats per minute . SV = volume of blood pumped out by a ventricle with each beat (ml/min)
CARDIAC OUTPUT
Stroke volume . Difference between EDV and ESV . EDV-ESV=SV . Average is about 75 ml
Left heart QRS P T P Electrocardiogram 1st 2nd EKG Heart sounds
Dicrotic notch
Aorta
Pressure Left ventricle
changes Atrial systole Left atrium
Pressure (mmPressure Hg)
EDV
Changes in SV Ventricular volume volume (ml) ESV
Atrioventricular valves Open Closed Open Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1
Left atrium Right atrium Left ventricle Right ventricle
Ventricular Atrial Isovolumetric Ventricular Isovolumetric Ventricular filling contraction contraction phase ejection phase relaxation filling 1 2a 2b 3
Ventricular filling Ventricular systole Early diastole (mid-to-late diastole) (atria in diastole)
Figure 18.20 CARDIAC OUTPUT (CO)
At rest . CO (ml/min) = HR (75 beats/min) SV (70 ml/beat) = 5.25 L/min
. Maximal CO is 4–5 times resting CO in nonathletic people . CO may reach 30 L/min in trained athletes . Cardiac reserve . Difference between resting and maximal CO REGULATION OF STROKE VOLUME
Stroke volume . Three main factors affect SV . Preload . Contractility . Afterload REGULATION OF STROKE VOLUME
Preload . Frank-Starling law of the heart . Degree of stretch of cardiac muscle cells before they contract . At rest, cardiac muscle cells are shorter than optimal length . Slow heartbeat and exercise increase venous return . Increased venous return distends (stretches) the ventricles and increases contraction force REGULATION OF STROKE VOLUME
Contractility . Contractile strength at a given muscle length, independent of muscle stretch and EDV . Agents increasing contractility . Increased Ca2+ influx . Sympathetic stimulation Increase SV Decrease ESV . Hormones . Thyroxin, glucagon, and epinephrine . Agents decreasing contractility . Calcium channel blockers REGULATION OF STROKE VOLUME
Afterload . Pressure that must be overcome for ventricles to eject blood . Hypertension increases afterload . Results in increased ESV and reduced SV CONTROL OF HEART RATE
Sympathetic nervous system . Norepinephrine . Increased SA node firing rate . Faster conduction through AV node . Increases excitability of heart
Parasympathetic nervous system . Vagus nerve . Decreases HR
Who dominates at rest?
Exercise (by Heart rate Bloodborne Exercise, skeletal muscle and (allows more epinephrine, fright, anxiety respiratory pumps; time for thyroxine, see Chapter 19) ventricular excess Ca2+ filling)
Venous Sympathetic Parasympathetic Contractility return activity activity
EDV ESV (preload)
Stroke Heart volume rate
Cardiac output
Initial stimulus Physiological response Result
Figure 18.22 The vagus nerve Dorsal motor nucleus of vagus (parasympathetic) Cardioinhibitory center decreases heart rate.
Medulla oblongata Cardio- acceleratory Sympathetic trunk ganglion center Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction.
AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons
Figure 18.15 CONTROL OF HEART RATE
Other factors… QUESTIONS?
Activity: Cardiovascular 24