Transcript AP151 HEART SLIDES-

Figure 22.6
CARDIAC MUSCLE CELLS
• Branched
• joined by intercalated discs
– desmosomes: tightly bind cells & transfer of tension
– gap junction: electrical synapses that directly transfer electrical
activity/AP from one cell to the next
• Contractile/myocardial Cells => contract and conduct AP’s
• Conductile/autorhythmic cells => produce and conduct action
potentials
AP in SA conductile/nodal/autorhythmic cells
VG Na+ channels
• HCN channels: VG ion channels, open due to hyperpolarization,
– allow Na+ in
• VG Ca channels cause depolarization of AP
• VG K channels cause repolarization
Fig. 13.20
Conduction System
• AP/Stimulus begins in SA node
• Transmitted through conduction
system and from cell to cell via gap
junctions
• Both Atria contract, then both
ventricles contract
AP in Contractile/Myocardial Cells
•Plateau cause by slow VG Ca+ channels & Ca+
inflow
• this prolonged state of depolarization results in
long period of refractory.
•Long refractory prevents heart from entering tetanus
(which is a good thing as heart needs to relax to fill)
AP and Excitation-Contraction Coupling in Myocardial cells (contractile cells)
•
•
•
•
AP formation and
propagation as in axons and
skeletal muscle
opening of VG Ca+  Ca+
flows in
Ca+ entering cytoplasm
causes Ca release channels
to open
massive Ca release from
SR
–
Fig. 12.34
“calcium induced calcium
release”
•
actin and mysin interact as
in skeletal muscle
•
Extracellular calcium plays
bigger role in myocardial
contraction than in skeletal
muscle fiber contraction
Fig. 13.10
Table 13.6
Fig. 13.11
Fig. 13.13
Cardiac Cycle:
• the repeating sequence of
contraction and relaxation of
the heart.
• Diastole = relaxation
– filling
• Systole = contraction
– ejection of blood
Fig. 13.14
Fig. 13.14
1.
Isovolumetric
contraction
2.
Ejection
3.
Isovolumetric
relaxation
4.
Rapid refilling
5.
Atrial contraction
ECG: measures overall electrical
activity of the whole heart
PR interval:
time it takes for
depolarization that begins
in SA to spread to
ventricles
Long PR represent
damage to atria
conductive system or AV
note
QT interval:
time of ventricles to
depolairze and
repolarize.
Can Ax electrolytes
imbalance, tissue
damage, ischemia
Fig. 13.25
Maintenance of proper blood pressure (BP) is
critical for proper CVS function
BP is influenced by:
1. cardiac output (CO)
– heart function
2. peripheral resistance
– vessel activity and blood characteristics
Cardiac Output = Heart Rate (HR) x stroke volume (SV)
Page 470
Relationship among factors that determine cardiac output
Heart activity is regulated by
1. Autonomic Nervous System (ANS)
– Sympathetic Nerves
– Parasympathetic nerves—vagus nerve
2. Hormones
3. Intrinsic Regulation
Fig. 14.27
• Cardiac Control Centers is in
medulla
– influenced by higher brain centers
• Cardiac centers recieve sensory
input from
–
–
–
–
vagus nerve
hypoglossal nerve
barroreceptors—pressure
chemoreceptors—blood chemistry
• Medulla Signals heart via
– vagus nerve-parasympathetic
– sympathetic cardiac nerves
Fig. 14.27
Regulation of Heart Rate
• Nervous system
– SD and PD inneration of SA node
• Endocrine System
– hormone affects on SA node
• Intrinsic (autoregulation)
– stretch of nodal cells directly increases rate of depolarization
Vagus Nerve (parasympathetic)
• Ach—muscarinic receptors (g-proteins—ion channels)
• innervates atria/SA node & AV node
Sympathetic Nerves (sympathetic)
• Norepinephrine (NE)—Beta 1 (β1) receptors
• innervates atria/SA node & AV node
• innervates ventricles
•
sympathetic nervous system also signals the heart via the endocrine system/epinephrine
Autonomic Innervation
• Parasymphathetic division slows heart rate
– slows rate of SA node depolarization
• Sympathetic division increases heart rate
– speeds up rate of SA node depolarization
Heart receives constant input from BOTH systems
• balance of SD and PD determines if HR goes up or down
• At rest Parasympathetic signals predominate and this depresses the heart
rate below the SA nodes intrinsic rate of ~100 bpm
Nervous Regulation of HR
/ Natural rate
Parasympathic:
• Ach-muscarinic receptors
• opens K+ gates
• slows pacemaker potential
– decreases HR
Sympathetic:
• NE-- β1 opens Na-Ca+
channels
• speeds up pacemaker
potential
– increases HR
Interplay between PD and SD activity
• Increasing PD—slows heart
• decreasing PD—speeds heart
• increasing SD—speeds heart
• decreasing SD—slows heart
Hormones and HR
• N.E., Epinephrine (E), and Thyroid Hormones
delivered through blood can also increase HR
– increasing levels increase HR
– decreasing levels decrease HR
– mechanism similar to nervous system mechanisms (alters
rate of pacemaker potential)
Atrial Reflex (SD regulation of heart)
• Atrial Reflex (Bainbridge reflex)
– Increased filling of atria (i.e., increased venous return or
increased blood volume) stretches atrial wall
– sensory neurons relay stretch to medulla
– medulla increase rate of SD signaling of heart (or
decreasin PD, literature is unclear)
– HR increases (in either case).
Intrinsic Regulation (autoregulation) of the Heart
Rate
– Increased filling of atria (i.e., increased venous return or
increased blood volume) stretches nodal cells of atrial
wall
– stretching of the cells directly causes their rate of
depolarization to increase
Regulation of Stroke Volume
• Stroke Volume influenced by:
– ESV
– EDV
– SV
– Preload (directly related to EDV)
– Afterload (equivalent to peripheral resistance/arterial blood
pressure)
EDV: the amount of blood
in each ventricle at the
end of diastole (i.e.,
how much blood fills
ventricles)
ESV: amount of blood in
each ventricle at end of
systole (how much
blood is left after
ejection/contraction
SV: how much blood is
ejected from each
ventricle during systole
EDV-ESV=SV
Interactions between EDV, Preload, SV and CO
•
•
•
•
Preload: amount of stretching of ventricular wall
Caused by filling of ventricle and directly related to EDV
↑ EDV  ↑ Preload
↓ EDV  ↓ Preload
• EDV is influenced by venous return (rate of blood return to heart
through veins)
• ↑ venous return  ↑ EDV/ Preload
• ↓ venous return  ↓ EDV/Preload
Interactions between EDV, Preload, SV and CO:
Frank-Starling
• ↑ venous return  ↑ EDV/ Preload  increased ventricular stretching
 ↑ ventricular contraction strength  ↑ SV  ↑ CO
• “more in, more out”
• intrinsic regulation that makes output match return (also keeps two
circuits in synch by making sure amount through systemic circuit
keeps pace with amount through pulmonary
• Increased contraction strength due to lengthening of sarcomeres to a
more optimum overlap length  stronger contraction
Fig. 14.3
Contractility:
↑ contractility--↑ SV, ↓ contractility-- ↓ SV
• Contractility=Increase in contraction strength due to ionotropic effects
(i.e., for reasons other than fiber length/overlap)
– due to Ca+ availability in cytoplasm
Causes of Increased Contractility
• SD fibers to ventricles—NE– Beta 1-- ↑ contractility-- ↑ SV
• Adrenal medulla—E-- Beta 1(in venricles)-- ↑ contractility-- ↑ SV
• Although PD technically innervates ventricles their role is negligable
Hormones (other than E)
• Thyroid hormone and glucagon also increase contractility
Topics Related to contractility
• Beta 1 stimulators or drugs that increase intracellular
calcium (like digitalis) increase contractility/CO
• Beta blockers drugs decrease Ca+, decrease
contractility, decrease CO
– used to treat hypertension
• Ca+ channels blockers (nifedipine): Ca+, decrease
contractility, decrease CO
– used to treat hypertension
Afterload and CO
• Afterload: amount of pressure ventricles need to
produce/overcome to eject blood
• directly related to arterial blood pressure (i.e., peripheral resistance)
• ↑ afterload  ↓ ejection  ↓ SV  ↓ CO
• chronic high blood pressure = chronic high afterload causing
heart to work excessively hard/stress to maintain CO
• weakened or diseased heart may be unable to overcome
relatively small increases in afterload causing significant
problems in maintain CO/BP
~TPR
Table 14.1
Fig. 14.2
Table 14.3
Fig. 14.7
Fig. 14.5
P.R.