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Cardiovascular System
HARDIAN
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Heart Anatomy
Figure 18.1
Coverings of the Heart: Anatomy
The pericardium:
Protects and anchors the heart
Prevents overfilling of the heart with blood
Allows for the heart to work in a relatively friction-
free environment
Pericardial Layers of the Heart
Figure 18.2
Heart Wall
Figure 18.4b
External Heart: Major Vessels of the Heart
(Posterior View)
Figure 18.4d
Gross Anatomy of Heart: Frontal Section
Figure 18.4e
Circulation Reviewed
Figure 18.5
Coronary Circulation
Figure 18.7a
Coronary Circulation: Venous Supply
Figure 18.7b
Heart Valves
Figure 18.8a, b
Heart Valves
Figure 18.8c, d
Atrioventricular Valve Function
Figure 18.9
Semilunar Valve Function
Figure 18.10
Heart Sounds
33
Microscopic Anatomy of Heart Muscle
Figure 18.11
Cardiac Muscle Cells:
Myocardial Autorhythmic Cells
Membrane potential “never
rests” pacemaker potential.
Myocardial Contractile Cells
Have a different looking action
potential due to calcium
channels.
General cardiac cell stuff:
Intercalated discs
Allow branching of the
myocardium
Gap Junctions (instead of
synapses)
Fast Cell to cell signals
Many mitochondria
Large T tubes
: Cardiac muscle
Coordinating the Pump: Electrical Signal Flow
Figure 18.13
Sympathetic and Parasympathetic
Sympathetic – speeds heart rate by Ca++ & I-f
channel flow
Parasympathetic – slows rate by K+ efflux &
Ca++ influx
Heart muscle:
Is stimulated by nerves and is self-excitable
(automaticity)
Contracts as a unit
Has a long (250 ms) absolute refractory period
Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker
potentials
Use calcium influx (rather than sodium) for rising
phase of the action potential
The Heart: Conduction System
Figure 18.14a
Heart Excitation Related to ECG
Figure 18.17
Extrinsic Innervation of the Heart
Heart is stimulated
by the sympathetic
cardioacceleratory
center
Heart is inhibited by
the parasympathetic
cardioinhibitory
center
Figure 18.15
Electrocardiography
Electrical activity is recorded by electrocardiogram
(ECG)
P wave corresponds to depolarization of SA node
QRS complex corresponds to ventricular
depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger
QRS complex
Electrocardiograms (EKG/ECG)
• Three formations
– P wave: impulse across atria
– QRS complex: spread of impulse down septum,
around ventricles in Purkinje fibers
– T wave: end of electrical activity in ventricles
The electrocardiogram
Cardiac muscle polarization & ECG
SA node
AV node
Electrocardiography
Figure 18.16
Electrocardiograms (EKG/ECG)
Figure 8.15B, C
Cardiac Cycle
Ventricular systole
Atria relax
Rising ventricular pressure results in closing of AV
valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar valves
Filling of Heart Chambers
Figure 11.6
Phases of the Cardiac Cycle
Figure 18.20
Phases of the Cardiac Cycle
Figure 18.20
Summary
Figure 18.21
Extrinsic Factors Influencing Stroke Volume
Sympathetic
stimulation
releases
norepinephrine
and initiates a
cyclic AMP
second-
messenger
system
Figure 18.22
Regulation of Heart Rate
87
Cardiac pressor reflex
stretch receptors(baroreceptors)
aortic baroreceptor- location aorta
carotid baroreceptor -location common carotid
Cardiac pressor reflex
effector- SA node
stimulus for reflex- Sudden raise in heart rate and
or BP
Result of stimulation- Heart rate decreases, blood
pressure decreases
cellular mechanism
when K+ ion leave hyperpolarized cardiac muscle cells
heart rate decreases
The Heart: Regulation of Heart Rate
Figure 11.7
Factors Involved in Regulation of Cardiac
Output
Figure 18.23
STARLING LAW OF THE HEART
arteriole runoff
blood going from arteries to
arterioles
the greater the resistance the
less the runoff
blood viscosity
the more RBC and the more
protein the greater the
resistance
the greater the viscosity the
higher the resistance
vasomotor control mechanism
integrator
activation of vasomotor center
causes a decrease in stroke volume
decrease cardiac output which leads to
reduced BP
END RESULT- blood pressure returns to
normal
Vasomotor pressoreceptor reflexes
emergency mechanism
active when oxygen is low to brain stem
Sensors- osmotic receptors in the medulla
integrator- vasomotor center
effector- lungs- increase blood flow to the lung
VENOUS RETURN TO HEART
Respiratory pump
decreased thoracic pressure (during inspiration)
pulls blood into central veins
increasing thoracic pressure (during expiration)
pushes blood in central veins into heart
deeper respirations increase venous return to heart
VENOUS RETURN TO HEART
Figure 11.8b
Blood Vessels: Anatomy
Pressure Gradient
Figure 11.9
Capillary Beds
Capillary beds
consist of two
types of vessels
Vascular shunt –
directly connects an
arteriole to a venule
Figure 11.10
Capillary Beds
True capillaries –
exchange vessels
Oxygen and
nutrients cross to
cells
Carbon dioxide
and metabolic
waste products
cross into blood
Figure 11.10
Diffusion at Capillary Beds
Figure 11.20
Vital Signs
Arterial pulse
Blood pressure
Repiratory Rate
Body Temperature
All indicate the efficiency of the system
Pulse
Pulse –
pressure wave
of blood
Monitored at
“pressure
points” where
pulse is easily
palpated
Figure 11.16
Blood Pressure
Figure 11.18
Blood Pressure: Effects of Factors
Neural factors
Autonomic nervous system adjustments
(sympathetic division)
Renal factors
Regulation by altering blood volume
Renin – hormonal control
Blood Pressure: Effects of Factors
Temperature
Heat has a vasodilation effect
Cold has a vasoconstricting effect
Chemicals
Various substances can cause increases or
decreases
Diet
Variations in Blood Pressure