Download ANPS 020 Black 02-01

ANPS020
February 1, 2012
CARDIODYNAMICS: The movement and force generated by cardiac contractions
Some basic terms to know:
End-diastolic volume EDV): the amount of blood in the ventricle just before contraction
End-systolic volume (ESV): the amount of blood left in the ventricle after contraction (it
doesn’t get pumped)
Stroke volume (SV): the amount pumped out of ventricle during systole
SV=EDV-ESV
Ejection fraction: the percentage of EDV represented by SV important clinical measure:
weak heart pumps less
-normal 60%
Cardiac output (CO): the volume pumped by the left ventricle in 1 minute important
value: this determines oxygen available to tissue
CARDIODYNAMICS: MEASUREMENT OF CARDIAC OUTPUT
CO = cardiac output (mL/min)
CO = HR x SV
CO + HR x (EDV-ESV) expanded form
HR = heart rate (beats/min)
SV = stroke volume (ML/beat)
At rest, CO=5 liters/min
During strenuous activity, CO can rise to 30 liters/min
Cardiac output can be adjusted by changes in either heart rate, EDV or ESV
CARDIO DYNAMICS: FACTOR AFFECTING HEART RATE
Autonomic innervation:
-cardiac plexuses contain the nerves that innervate the heart, including both sympathetic
and parasympathetic axons
-a cardiac center in the medulla oblongata of the brainstem drives the autonomic system:
--cardioacceleratory center controls sympathetic neurons to the heart which increase heart
rate
--cardioinhibitory center controls parasympathetic neurons which slow heart rate
AUTONOMIC INNERVATION OF THE HEART
Note that parasympathetic fibers innervate the SA and AV nodes as well as the atrial
muscle
Sympathetic fibers innervate both nodes, atrial muscle and ventricular muscle
CARDIODYNAMICS
Cardiac reflexes automatically adjust cardiac output
Sensory input to cardiac reflexes
-barioreceptors are sensory receptors monitoring blood pressure
-chemoreceptors are sensory receptors monitoring arterial oxygen and carbon dioxide
levels
Cardiac center integrates sensory inputs and adjusts cardiac activity appropriately: turns
UP one pathway and turns DOWN the other
Output of the cardiac center is through the autonomic nervous system
-dual innervation
-fine adjustments meet needs of the body
HOW IST HE HEART RATE CONTROLLED
Autonomic axons adjust heart rate by slowing down or speeding up rate of spontatneous
depolarization of pacemaker cells
CARDIODYNAMICS: FACTOS AFFECTING STROKE VOLUME
Recall that stroke volume is determined by EDV and ESV
1. Changing the EDV:
- Filling time: duration of ventricular diastole
- -longer fill time results in larger fill volume
- Venous return: rate of blood flow during ventricular diastole
- -factors that cause more blood to return to heart result in larger fill volume
(vasoconstriction for example)
2. Changing the ESV
- Preload: ventricular stretching during diastole
- contractility: force produced during contraction, at a given period
- afterload: tension the ventricle produces to open the semilunar valve and eject
blood
Preload: the degree of ventricular stretching to EDV
-directly proportional to EDV: more blood in ventricle = more stretch
-stretch affects the ability of muscle cells to produce tension
This property of cardiac muscle cells is known as Frank-Starling Principle:
-as EDV increases, stroke volume increase
(translation: the heart pumps whatever it gets. The more blood in the ventricle, the greater
the stretch on the ventricle wall and stronger the contraction)
However, there are physical limits that limit extensive ventricular expansion:
-Myocardial connective tissue in and around the heart cells
-The cardiac (fibrous) skeleton – the connective tissue of framework of the heart
-The pericardial sac outside the heart
Contractility – how hard the ventricle contracts is affected by:
Autonomic activity: sympathetic stimulation causes the ventricles to contract with m ore
force, pumping out more blood (increasing ejection fraction and thus decreasing ESV)
-NE released by postganglionic fibers of cardiac nerves
-Epinephrine and NE released by the adrenal gland into the blood
-Parasympathetic system does not innervate ventricles so had no significant effect on
contractility
Hormones:
-Many hormones affect heart contraction (epinephrine, norepinephrine, thyroid hormore)
-Pharmaceutical drugs mimic hormone actions
-some drugs stimulate or block beta receptors to increased or decreased sympathetic
effect
--beta blockers are commonly used class of drugs to reduce heart work
--some drugs alter levels of calcium ions )e.g. calcium channel blockers and calcium
levels within the muscle cells determine contraction level
-given to keep from putting too much load on heart
Afterload: the aortic pressure that must be overcome in order for the ventricle to eject
blood – is affected by any factor that restricts arterial blood flow
-any factor that increases peripheral resistance affects afterload
As afterload increases, less blood is ejected
-ESV increases, so stroke volume decreases
(indirect relationship)
THE CIRCULATORY SYSTEM: REGULATING BLOOD FLOW
Organs must receive a steady supply of oxygen and nutrients in order to survive.
Maintaining a steady flow of blood to the organs is the job of the cardiovascular system.
Both the heart and the blood vessels are capable of change in order to adjust the flow of
blood.
There are only 5 liters of blood in the body, and it is constantly being redistributed
between different organ systems
PRESSURE AND RESISTANCE
Blood flow into tissue = difference in blood pressure between heart and
capillaries/peripheral resistance
Blood flow from a region of high pressure to one of lower pressure, the greater the
pressure difference driving the movement, the greater the flow
The heart generates pressure to overcome resistance
The pressure different across the systemic circuit – from left ventricle back to right atrim
– is about 100 mmHG
Blood pressure (BP): Arterial pressure (mmHg)
Capillary hydrostatic pressure: Pressure within the capillary beds
Venous pressure in the venous system
3 sources contribute to peripheral resistance
1. Vascular Resistance
- Due to friction between blood and the vessel wall
- Depends on vessel length (constant) and diameter (adjustable)
2. Viscosity
- Resistance caused by molecules and suspended materials in a liquid
- Whole blood viscosity is about 4 times that of water
- Can change with dehydration
3. Turbulence
-
Swirling action that disturbs smooth flow
PRESSURE IN THE CARDIOVASCULAR SYSTEM
Systolic pressure:
-peak arterial pressure during ventricular systole
Diastolic pressure:
-minimum arterial pressure during diastole
Pulse pressure:
-difference between systolic and diastolic pressure
Hypertension: abnormally high blood pressure
Hypotension: abnormally low blood pressure
CHANGE IN PRSSURE AND RESISTNACE IN THE CIRCUIT
Although capillaries have the smallest diameter, there are so many of them that the crosssectional area increases at that point of the circulation, causing a drop in pressure and a
decrease in flow velocity. These features enhance exchange in the capillary beds,
providing high surface area and sufficient time for exchange of materials between blood
and tissue.
PRESSURE IS PULSATILE IN LARGER ARTERIES
Pulse pressure creates the “throbbing” feeling in an artery
During systole, the heart forces blood into the vessels and exerting great pressure on the
vessel walls.
During diastole, the heart is not pushing blood, the recoil of the walls of the elastic
arteries continues to push blood and exert pressure.