Block 3 Cardio Physio BRS

Contractility of myocardial cells depends on the intracellular [Ca2+], which is regulated by Ca2+ entry across the cell membrane during the plateau of the action potential and by Ca2+ uptake into and release from the sarcoplasmic reticulum (SR). Ca2+
binds to troponin C and removes the inhibition of actin–myosin interaction, allowing contraction
(shortening) to occur.

The atrioventricular (AV) delay (which corresponds to the PR interval)
allows time for filling of the ventricles from the atria. If the ventricles contracted before
they were filled, stroke volume would decrease.

If the radius of the artery decreased by 50% (1/2), then resistance would increase by 2(4th) , or 16 (R = 8nl /(pi)r4).
Because blood flow is inversely proportional to resistance (Q = (delta)P/R),
flow will decrease to 1/16th, the original value.

Propranolol, a 13- adrenergic antagonist, blocks all
sympathetic effects that are mediated by a 13 1 or p2 receptor. The sympathetic effect on the sinoatrial
(SA) node is to increase heart rate via a p i receptor; therefore, propranolol decreases heart
rate. Ejection fraction reflects ventricular contractility, which is another effect of 13 1 receptors;
thus, propranolol decreases contractility, ejection fraction, and stroke volume. Splanchnic and
cutaneous resistance are mediated by a 1 receptors.

Turbulent flow is predicted when the Reynold's number is increased.
Factors that increase the Reynold's number and produce turbulent flow are decreased
viscosity (hematocrit) and increased velocity. Partial occlusion of a blood vessel increases the
Reynold's number (and turbulence) because the decrease in cross-sectional area results in increased
blood velocity (v = Q/A).

An increase in arteriolar resistance will increase total peripheral
resistance (TPR). Arterial pressure = cardiac output x TPR, so arterial pressure will also increase.
Capillary filtration decreases when there is arteriolar constriction because P c decreases.
Afterload of the heart would be increased by an increase in TPR.

In anticipation of exercise, the central command increases sympathetic
outflow to the heart and blood vessels, causing an increase in heart rate and contractility.
Venous return is increased by muscular activity and contributes to an increase in cardiac output
by the Frank-Starling mechanism. Pulse pressure is increased because stroke volume is increased.
Although increased sympathetic outflow to the blood vessels might be expected to increase
total peripheral resistance (TPR), it does not because there is an overriding vasodilation
of the skeletal muscle arterioles as a result of the buildup of vasodilator metabolites (lactate, K+,
adenosine). Because this vasodilation improves the delivery of 0 2, more 02 can be extracted and
used by the contracting muscle.

A negative inotropic effect is one that decreases myocardial contractility.
Contractility is the ability to develop tension at a fixed muscle length. Factors that decrease
contractility are those that decrease the intracellular [Ca 2-1. Increasing heart rate increases
intracellular [Ca2+] because more Ca2± ions enter the cell during the plateau of each
action potential. Sympathetic stimulation and norepinephrine increase intracellular [Ca2+] by
increasing entry during the plateau and increasing the storage of Ca 2+ by the sarcoplasmic reticulum
(SR) [for later release]. Cardiac glycosides increase intracellular [Ca 2÷] by inhibiting the
Na+–K+ pump, thereby inhibiting Na+–Ca21- exchange (a mechanism that pumps Ca2+ out of the
cell). Acetylcholine (ACh) has a negative inotropic effect on the atria.

The absent P wave indicates that the atrium is not depolarizing and,
therefore, the pacemaker cannot be in the sinoatrial (SA) node. Because the QRS and T waves
are normal, depolarization and repolarization of the ventricle must be proceeding in the normal
sequence. This situation can occur if the pacemaker is located in the atrioventricular (AV) node.
If the pacemaker were located in the bundle of His or in the Purkinje system, the ventricles would
activate in an abnormal sequence (depending on the exact location of the pacemaker) and the
QRS wave would have an abnormal configuration. Ventricular muscle does not have pacemaker
properties.

The PR segment (part of the PR interval) and the ST segment are
the only portions of the electrocardiogram (ECG) that are isoelectric. The PR interval includes
the P wave (atrial depolarization) and the PR segment, which represents conduction through the
atrioventricular (AV) node; during this phase, the ventricles are not yet depolarized. The ST segment
is the only isoelectric period when the entire ventricle is depolarized.

The second heart sound is associated with closure of the aortic and
pulmonic valves. Because the aortic valve closes before the pulmonic valve, the sound can be split
by inspiration.

During exercise, local metabolites accumulate in the exercising
muscle and cause local vasodilation and decreased arteriolar resistance of the skeletal muscle.
Because muscle mass is large, it contributes a large fraction of the total peripheral resistance
(TPR). Therefore, the skeletal muscle vasodilation results in an overall decrease in TPR, even
though there is sympathetic vasoconstriction in other vascular beds.

A decrease in blood pressure causes decreased stretch of the
carotid sinus baroreceptors and decreased firing of the carotid sinus nerve. In an attempt to restore
blood pressure, the parasympathetic outflow to the heart is decreased and sympathetic outflow
is increased. As a result, heart rate and contractility will be increased. Mean systemic pressure
will increase because of increased sympathetic tone of the veins (and a shift of blood to the
arteries).

Cardiac output of the left and right sides of the heart is equal. Blood
ejected from the left side of the heart to the systemic circulation must be oxygenated by passage
through the pulmonary circulation.

The gap junctions occur at the intercalated disks between cells
and are low-resistance sites of current spread.

When a person moves to a standing position, blood pools
in the leg veins, causing decreased venous return to the heart, decreased cardiac output, and decreased
arterial pressure. The baroreceptors detect the decrease in arterial pressure, and the vasomotor
center is activated to increase sympathetic outflow and decrease parasympathetic outflow.
There is an increase in heart rate (resulting in a decreased PR interval), contractility, and
total peripheral resistance (TPR). Because both heart rate and contractility are increased, cardiac
output will increase toward normal.

Myocardial 02 consumption is determined by the amount of tension
developed by the heart. It increases when there are increases in aortic pressure (increased afterload),
increased heart rate or stroke volume (which increase cardiac output), or when the size
(radius) of the heart is increased (T = P x r). Influx of Na + ions during an action potential is a
purely passive process, driven by the electrochemical driving forces on Na + ions. Of course, maintenance
of the inwardly directed Na + gradient over the long term requires the Na +–K+ pump,
which is energized by adenosine triphosphate (ATP).

Histamine causes vasodilation of the arterioles, which increases
Pc and capillary filtration. It also causes constriction of the veins, which contributes to
the increase in Pc. Acetylcholine (ACh) interacts with muscarinic receptors (although these are
not present on vascular smooth muscle).

Blood flow to the brain is autoregulated by the PCO2.
If metabolism increases (or arterial pressure decreases), the PCO2 will increase and cause cerebral
vasodilation. Blood flow to the heart and to skeletal muscle during exercise is also regulated
metabolically, but adenosine and hypoxia are the most important vasodilators for the heart.
Adenosine, lactate, and K+ the are the most important vasodilators for exercising skeletal muscle.
Blood flow to the skin is regulated by the sympathetic nervous system rather than by local
metabolites.

An increase in contractility produces an increase in cardiac output
for a given end-diastolic volume, or pressure. The Frank-Starling relationship demonstrates
the matching of cardiac output (what leaves the heart) with venous return (what returns to the
heart). An increase in contractility (positive inotropic effect) will shift the curve upward.

In a left-to-right ventricular shunt, a defect in the ventricular septum
allows blood to flow from the left ventricle to the right ventricle instead of being ejected into the
aorta. The "shunted" fraction of the left ventricular output is therefore added to the output of the
right ventricle, making pulmonary blood flow (the cardiac output of the right ventricle) higher
than systemic blood flow (the cardiac output of the left ventricle). In normal adults, the outputs
of both ventricles are equal in the steady state. In the fetus, pulmonary blood flow is near zero.
Right ventricular failure results in decreased pulmonary blood flow. Administration of a positive
inotropic agent should have the same effect on contractility and cardiac output in both ventricles.

The decrease in pressure at any level of the cardiovascular
system is caused by the resistance of the blood vessels (AP = Q x R). The greater the resistance,
the greater the decrease in pressure. The arterioles are the site of highest resistance in the vasculature.
The arterioles do not have the greatest surface area or cross-sectional area (the capillaries
do). Velocity of blood flow is lowest in the capillaries, not in the arterioles.

Edema occurs when more fluid is filtered out of the
capillaries than can be returned to the circulation by the lymphatics. Filtration is increased by
changes that increase Pc or decrease are. Arteriolar constriction would decrease P, and decrease
filtration. Dehydration would increase plasma protein concentration (by hemoconcentration)
and thereby increase ire and decrease filtration. Increased venous pressure would increase Pe
and filtration.

Ventricular volume is at its lowest value while the ventricle is relaxed
(diastole), just before ventricular filling begins

Orthostatic hypotension is a decrease in arterial pressure that occurs
when a person moves from a supine to a standing position. A person with a normal baroreceptor
mechanism responds to a decrease in arterial pressure through the vasomotor center by
increasing sympathetic outflow and decreasing parasympathetic outflow. The sympathetic component
helps to restore blood pressure by increasing heart rate, contractility, total peripheral resistance
(TPR), and mean systemic pressure. In a patient who has undergone a sympathectomy,
the sympathetic component of the baroreceptor mechanism is absent

Cardiac output is calculated by the Fick principle if whole body oxygen
(02) consumption and [02] in the pulmonary artery and pulmonary vein are measured. Mixed
venous blood could substitute for a pulmonary artery sample, and peripheral arterial blood could
substitute for a pulmonary vein sample. Heart rate is not needed for this calculation.

Cardiac output = 500 ml/min_______________
0.24 ml 02/ml – 0.16 ml 02/ml
= 6250 ml/min or 6.25 L/min

Phase 4 depolarization is responsible for the pacemaker property
of sinoatrial (SA) nodal cells. It is caused by an increase in Na + conductance and an inward
Na+ current (If), which depolarizes the cell membrane.

Propranolol is an adrenergic antagonist that blocks
both B1and B2 receptors. When propanolol is administered to reduce cardiac output, it inhibits
B1 receptors in the sinoatrial (SA) node (heart rate) and in ventricular muscle (contractility).

An increase in ejection fraction means that a higher fraction of the
end-diastolic volume is ejected in the stroke volume (e.g., because of the administration of a positive
inotropic agent). When this situation occurs, the volume remaining in the ventricle after
systole, the end-systolic volume, will be reduced. Cardiac output, pulse pressure, stroke volume,
and systolic pressure will be increased.

The a l receptors for norepinephrine are excitatory
on vascular smooth muscle and cause vasoconstriction. There are also B2 receptors on the arterioles
of skeletal muscle, but they produce vasodilation.

Angiotensin I, angiotensin II, and aldosterone are increased
in response to a decrease in renal perfusion pressure. Antidiuretic hormone (ADH) is released
when atrial receptors detect a decrease in blood volume. Of these, only aldosterone increases Na+
reabsorption. Atrial natriuretic peptide is released in response to an increase in atrial pressure,
and an increase in its secretion would not be anticipated after blood loss.

The post-extrasystolic contraction produces increased pulse
pressure because contractility is increased. Extra Ca 2+ enters the cell during the extrasystolic
beat. Contractility is directly related to the amount of intracellular Ca 2+ available for binding to
troponin C.

Pulse pressure is the difference between the highest (systolic) and
lowest (diastolic) arterial pressures. It reflects the volume ejected by the left ventricle (stroke volume).
Pulse pressure increases when the capacitance of the arteries decreases, such as with aging.

Circulation of the skin is controlled primarily by the sympathetic
nerves. The coronary and cerebral circulations are primarily regulated by local metabolic
factors. Skeletal muscle circulation is regulated by metabolic factors (local metabolites) during
exercise, although at rest it is controlled by the sympathetic nerves.

Because 0 2, CO2, and CO are lipophilic, they cross capillary
walls primarily by diffusion through the endothelial cell membranes. Glucose is water-soluble;
it cannot cross through the lipid component of the cell membrane and is restricted to the waterfilled
clefts, or pores, between the cells.

Pressures on the venous side of the circulation (e.g., central
vein, right atrium, renal vein) are lower than pressures on the arterial side. Pressure in the pulmonary
artery (and all pressures on the right side of the heart) are much lower than their counterparts
on the left side of the heart. In the systemic circulation, systolic pressure is actually
slightly higher in the downstream arteries (e.g., renal artery) than in the aorta because of the reflection
of pressure waves at branch points.

On the extrasystolic beat, pulse pressure decreases because there
is inadequate ventricular filling time—the ventricle beats "too soon." As a result, stroke volume
decreases.

A pattern of two P waves preceding each QRS complex indicates
that only every other P wave is conducted through the atrioventricular (AV) node to the
ventricle. Thus, conduction velocity through the AV node must be decreased.

The upstroke of the action potential in the atria, ventricles,
and Purkinje fibers is the result of a fast inward Na + current. The upstroke of the action
potential in the sinoatrial (SA) node is the result of an inward Ca 2+ current. The plateau of the
ventricular action potential is the result of a slow inward Ca 2+ current. Repolarization in all cardiac
tissues is the result of an outward K + current.

Diarrhea causes a loss of extracellular fluid volume, which produces a decrease in arterial pressure. The decrease in arterial pressure activates the baroreceptor mechanism, which produces an increase in heart rate when the patient is supine. When she stands up, blood pools in her leg veins and produces a decrease in venous return, a decrease in cardiac output (by the Frank-Starling mechanism), and a further decrease in arterial pressure.
The further decrease in arterial pressure causes further activation of the baroreceptor mechanism
and a further increase in heart rate.

Acetylcholine (ACh) causes slowing of the heart via
muscarinic receptors in the sinoatrial (SA) node.
.
BLOCKING the B1 slows the heart, (this is pharmacy NOT physiology)

In this patient, hypertension is most likely caused by left renal artery
stenosis, which led to increased renin secretion by the left kidney. The increased plasma renin activity
causes an increased secretion of aldosterone, which increases Na + reabsorption by the renal
distal tubule. The increased Na+ reabsorption leads to increased blood volume and blood pressure.
The right kidney responds to the increase in blood pressure by decreasing its renin secretion. Right
renal artery stenosis causes a similar pattern of results, except that renin secretion from the right
kidney, not the left kidney, is increased. Aldosterone-secreting tumors cause increased levels of aldosterone,
but decreased plasma renin activity (as a result of decreased renin secretion by both kidneys).
Pheochromocytoma is associated with increased circulating levels of catecholamines, which
increase blood pressure by their effects on the heart (increased heart rate and contractility) and
blood vessels (vasoconstriction); the increase in blood pressure is sensed by the kidneys and results
in decreased plasma renin activity and aldosterone levels.

Aortic pressure reaches its highest level immediately after the
rapid ejection of blood during left ventricular systole. This highest level actually coincides with
the beginning of the reduced (slow) ventricular ejection phase.

The mitral [atrioventricular (AV)] valve opens when left atrial pressure
becomes higher than left ventricular pressure. This situation occurs when the left ventricular
pressure is at its lowest level—when the ventricle is relaxed, blood has been ejected from
the previous cycle, and before refilling has occurred.