PHYSIOLOGY

1.8 CARDIAC OUTPUT REGULATION AND CIRCULATORY SHOCK PHYSIOLOGY

MARIA CHRISTINA JOY IRORITA, MD | OCTOBER 01, 2020

OUTLINE • Effect of Age on CO

I. Cardiac Output and Venous V. Cardiac Failure → CI rises rapidly to a level greater than 4L/min/m² at age 10 yrs. and
Return A. Circulatory Dynamics in CF declines to about 2.4L/min/m² at age 80 yrs.
A. Cardiac Index VI. Heart Valves and Heart
II. Blood Flow during Exercise Sounds
III. Coronary Circulation VII. Circulatory Shock Physiology
A. Physiologic Anatomy of the
Coronary Blood Supply
IV. Ischemic Heart Disease
LEGENDS
Remember Lecturer Book Presentation

I. CARDIAC OUTPUT AND VENOUS RETURN

• Anatomy of the Heart

• Control of CO by VR – Frank-Starling Mechanism of the Heart

→ F-S Mechanism of the heart is the intrinsic ability of the heart to adapt
to increasing volumes of inflowing blood
→ Within physiological limits, the heart pumps all the blood that returns
to it by way of the veins
Main reason of peripheral factors is important in controlling CO is
that the heart has a built-in mechanism that normally allows to pump
the blood that flows into the RA from the veins
F-S Mechanism: increased blood flow in the heart, increased blood
stretches the walls of the heart chamber.
→ Stretching the heart (stretching of the sinus node) causes the heart
to pump faster, resulting in an increased heart rate as much as 10 to
15 percent
→ Bainbridge reflex
▪ The stretched right atrium initiates a nervous reflex passing first to
the vasomotor center of the brain and then back to the heart by
way of the sympathetic nerves and vagi to also increase the HR
Under most normal unstretched conditions, CO is controlled mainly
by peripheral factors that determine venous return
• Control of CO by VR
Flow of Blood in the Heart: Systemic circulation → Inferior and Superior → Under most normal unstressed conditions, the CO is controlled
vena cava → Right atrium → Tricuspid valve → Right ventricle → mainly by peripheral factors that determine VR
Pulmonary artery → Lungs → Pulmonary vein → Left atrium → Mitral
valve → Left ventricle → Aorta → Systemic circulation • CO is the sum of all tissue blood flows

• Cardiac Output
→ Quantity of blood pumped into the aorta each minute by the heart
→ Also, the quantity of blood that flows through the circulation
→ Is the sum of the blood flows to all the tissues of the body
All the blood going out of the heart through the aorta

• Venous Return
→ Quantity of blood flowing from the veins into the right atrium each
minute
→ Venous return = cardiac output
▪ Except: at a time when blood is temporarily stored in or
removed from the heart and lungs
All blood going to right atrium

• Factors affecting CO
→ Level of body metabolism
→ Level of activity
→ Age
→ Body size
▪ Young, healthy men: resting CO average = 5.6 L/min.
▪ Women: 4.9 L/min
▪ Adult: 5 L/min

A. Cardiac Index Figure 20-2: CO is equal to venous return and is the sum of tissue
• Cardiac Index = CO per square meter of body surface area and organ blood flows. Except when the heart is severely weakened
• CO increases approx. in proportion to the surface area of the body and unable to adequately pump the venous return, cardiac output
• Average human being who weighs 70kg has a body surface area of about (total tissue blood flow) is determined mainly by the metabolic needs
1.7 square meters of the tissues and organs of the body.
→ If the average adult CO is 5L/min, the normal average CI for adults Increasing level of work output during exercise, oxygen consumption
is about 3L/min/m² of body surface area and CO increase in parallel to each other

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1.8 CARDIAC OUTPUT REGULATION AND CIRCULATORY SHOCK PHYSIOLOGY

• CO and Peripheral Vascular Resistance • Causes of Hypoeffective Heart

→ When arterial pressure is unchanged, CO is inversely proportional to → Increased in arterial pressure against which the heart must pump,
total peripheral vascular resistance such as in severe hypertension
If total peripheral resistance is normal (100% mark), CO is also → Inhibition of nervous excitation of the heart
normal → Pathological factors that cause abnormal heart rhythm or rate of
→ Increase in cardiac output = decrease in peripheral resistance. (E.g. heartbeat
beriberi, hyperthyroidism, anemia, pulmonary disease, Paget’s → Coronary artery blockage, causing a “heart attack”
disease) → Valvular heart disease
→ Increase peripheral resistance = decrease cardiac output. (E.g. → Congenital heart disease
hypothyroidism, removal of arm and lungs) → Myocarditis – inflammation of the heart muscle
→ Ohm’s Law: → Cardiac hypoxia
𝐴𝑟𝑡𝑒𝑟𝑖𝑎𝑙 𝑃𝑟𝑒𝑠𝑠𝑢𝑟𝑒
𝐶𝑂 =
𝑇𝑜𝑡𝑎𝑙 𝑃𝑒𝑟𝑖𝑝ℎ𝑒𝑟𝑎𝑙 𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 • Nervous System role in CO Control
During exercise:
▪ Increase in skeletal muscle metabolism
− Arterial dilatation for adequate tissue oxygenation
▪ Autonomic nervous centers of the brain will cause large vein
constriction, increased HR, and increased contractility of the heart
▪ All these changes acting together increase the arterial pressure
above normal, which in turn forces still more blood flow through the
active muscles

• Conditions that Decrease the Peripheral Resistance and Increase

the CO to above Normal
a. Beriberi
Caused by insufficient quantity of the vitamin thiamine (Vitamin
B1) in the diet. Its diminished ability of the tissues to use some
cellular nutrients, local tissue blood flow mechanisms in turn
cause marked compensatory peripheral vasodilation.
Figure 20-4: Chronic effect of different levels of total peripheral b. Arteriovenous fistula or shunt
resistance on cardiac output, showing reciprocal relationship Large amounts of blood flow directly from the artery into the
between total peripheral resistance, CO and Atrioventricular vein. Increase TPR, decrease VR and CO
c. Hyperthyroidism
• The Heart has Limits for the CO that it can achieve Increased of metabolism of most tissues. TPR decreases; VR
Plateau level of this normal CO curve is 13L/min, 2.5 times the and CO often increase to 40-80% above normal
normal CO of about 5L/min d. Anemia
→ The normal human heart can pump a VR up to about 2.5 times the Two peripheral effects greatly decrease of TPR;
normal VR before the heart becomes a limiting factor in the control 1. Reduced viscosity of the blood
of CO 2. Decreased concentration of RBC

Figure 20-5: CO curves for the normal heart and for hypoeffective
(pumping at levels below normal) and hypereffective (pumping
better than normal)
Figure 20-7: LOW CARDIAC OUTPUT. Shows that far right several
• Factors that Cause HYPERACTIVE Heart conditions that cause abnormally low CO. Two conditions; (1)
→ Nervous stimulation abnormalities that decrease pumping effectiveness (2) decrease VR
→ Heart muscle hypertrophy
• Nervous Excitation increases CO • Causes of Low CO
→ Combination of sympathetic stimulation and parasympathetic → Decreased pumping effectiveness of the heart
inhibition increase the pumping effectiveness of the heart ▪ Severe coronary blood vessel blockage and consequent
▪ Increasing the HR (young people, normal level of 72beats/min myocardial infarction
up to 180-200 beats/min ▪ Severe valvular heart disease
▪ Increasing the strength of heart contraction (increased ▪ Myocarditis
contractility) twice its normal strength Cardiac tamponade – presence of blood or fluid in the pericardial
space
• Heart Hypertrophy effect on CO ▪ Cardiac metabolic derangements
→ Long-term increased workload Cardiac shock: CO falls so low that the tissues throughout
▪ Heart muscle increase in mass and contractile strength the body begin to suffer nutritional deficiency
→ This increases the plateau level of the CO curve, sometimes 60 to → Decreased VR
100%, and therefore allows the heart to pump much greater than ▪ Decreased blood volume
usual amounts of CO Most common noncardiac peripheral factor that leads to
→ In marathon runners, the total effect can allow the heart to pump as decreased CO is decreased blood volume
much 30 to 40L/min, about 2.5 times the level that can be achieved Acute venous dilatation
in the average person

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Sympathetic nervous system suddenly become inactive (Ex. • Anterior Cardiac Veins
Fainting) → Receives most of the coronary venous blood from the right
▪ Obstruction of large veins ventricular muscle
Large veins leading into the heart become obstructed and the Thebesian Veins
blood in the peripheral vessels cannot flow into the heart → Very small amount of coronary venous blood flows back into the
▪ Decreased tissue mass (decreased skeletal mass) heart through this.
▪ Decreased metabolic rate of the tissue
Hypothyroidism- reduce metabolic rate and therefore tissue • Normal Coronary Blood Flow
blood flow and CO → At rest:
▪ 70ml/min/100g of heart weight
II. BLOOD FLOW DURING EXERCISE ▪ 225ml/min (4 to 5 percent of the total CO)
• Rate of blood flow through the muscles
→ At rest: 3 to 4ml/min/100g of muscle • Coronary Blood Flow during Exercise
→ During extreme exercise in the well-conditioned athlete: 100 - 200 Cardiac Output: increase 4 to 7 times
ml/min/100g of muscle (25 to 50-fold) → Work output: increase 6 to 9 times
→ Coronary blood flow: increases 3 to 4 times to supply the extra
• Control of Blood flow in Skeletal Muscles nutrients by the heart
→ Local arteriolar vasodilation → The “efficiency” of cardiac utilization of energy increases to make up
▪ Due to decreased oxygen for the relative deficiency of coronary blood supply
Arteriolar walls cannot maintain contraction in the absence of
oxygen → release of vasodilator substances (e.g. Adenosine) • Phasic Changes in Coronary Blood Flow during Systole and Diastole
Other vasodilator factors maintaining increased capillary blood
flow as long as the exercise continues: (1) potassium ions, (2)
adenosine triphosphate (ATP), (3) lactic acid (4) carbon dioxide
→ Sympathetic vasoconstriction nerve fibers
▪ Norepinephrine release
Decrease blood flow to as little as ½ to 1/3 normal
Vasoconstriction: physiologic importance in decreasing of
arterial pressure in circulatory shock and increase BP in periods
of stress
→ Medullae of adrenal gland release of norepinephrine and
epinephrine

• Circulatory Readjustments during Exercise

→ During Exercise:
▪ Sympathetic Nervous System activation
▪ Increase in arterial pressure
▪ Increase in CO
→ Effects of Sympathetic Activation: → Figure 21-4: Coronary capillary blood flow in the left ventricle muscle
▪ Increased HR and contractility falls to a low value during systole. This is due to strong compression
▪ Strong contraction of most of the peripheral arterioles except in of the intramuscular blood vessels by the left ventricular muscle
the active muscles, coronary and cerebral systems during systolic contraction
− These are important systems that should not have → During diastole, the cardiac muscle relaxes → blood flows rapidly
decreased blood flow. during all of diastole
Blood flow:  required by the muscle;  by non-muscular → Blood flow through the coronary capillaries of the right ventricle also
areas (“lending” blood to the muscles as much as 2 L/min) undergoes phasic changes during the cardiac cycle, but the inverse
Coronary and cerebral systems: spared from phasic changes are only partial
vasoconstrictor effect because of poor vasoconstrictor ▪ Force of contraction of the right ventricular muscle is far less than
innervation that of the left ventricular muscle – because right ventricle pumps
▪ Contraction of the muscle walls of veins and other capacitative to the pulmonary circulation which has less resistance compared
areas of the circulation greatly increases the mean systemic to the systemic circulation
filling pressure
Important in  venous return of blood to the heart, • Epicardial VS. Subendocardial Coronary Blood Flow
therefore,  the cardiac output.
CO must increase to 4-5x in the nonathlete, or to 6-7x times in
well-trained athlete, to satisfy the metabolic needs of the exercising
muscles.

III. CORONARY CIRCULATION

A. Physiologic Anatomy of the Coronary Blood Supply
→ The first branches of the aorta are the coronary arteries.
• Left coronary artery
→ Supplies mainly the
anterior and left lateral
portions of the left
ventricle
• Right coronary artery Figure 21-5:
→ Supplies most of the → Epicardial Coronary arteries
right ventricle as well as ▪ Supplies most of the muscle
the posterior part of the → Intramuscular Arteries
left ventricle in 80 to 90 ▪ Derived from the Epicardial arteries penetrate the muscle,
percent of people supplying the needed nutrients
→ Right Dominant Pattern → Subendocardial arterial plexus
• Coronary sinus ▪ Immediately beneath the endocardium
→ Receives about 75% of During systole, blood flow through the subendocardial plexus of
the coronary venous the left ventricle, where the intramuscular coronary vessels are
blood flow from the left compressed greatly by ventricular muscle contraction, tends to
ventricular muscle return be reduced.
→ Empties into the right atrium
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1.8 CARDIAC OUTPUT REGULATION AND CIRCULATORY SHOCK PHYSIOLOGY

• Control of Coronary Blood Flow ▪ Occasionally, the clot breaks away from its attachment on the
→ Local muscle metabolism atherosclerotic plaque and flows to a more peripheral branch of the
▪ Primary controller of coronary flow coronary arterial tree where it blocks the artery at that point –
▪ Blood flow through the coronary system coronary embolus
− Regulated mostly by local arteriolar vasodilation ▪ Local muscular spasm of a coronary artery. Spasm might result
− In response to the nutritional needs of cardiac muscle from direct irritation of smooth muscle of arterial wall by edges of
▪ Major factor: Cardiac musculature demand for oxygen the plaques

→ Nervous control • Life Saving Value of Collateral Circulation in the Heart

▪ Stimulation of the autonomic nerves to the heart affect → The degree of damage to the
coronary blood flow both directly and indirectly heart muscle caused either by
− Direct effects: from action of the nervous transmitter slowly developing atherosclerotic
substances acetylcholine from the vagus nerves and constriction of the coronary
norepinephrine from the sympathetic nerves on the arteries or by sudden coronary
coronary vessels occlusion is determined to a
− Indirect effects: from secondary changes in coronary blood great extent by the degree of
flow caused by increased or decreased activity of the heart collateral circulation that has
▪ Sympathetic Stimulation already developed or that can
− Releases norepinephrine from the sympathetic nerves and open within minutes after the
epinephrine + norepinephrine from the adrenal medullae occlusion
o Increases both HR and heart contractility and → A life-saving mechanism
increases the rate of metabolism of the heart When occlusion occurs in one of the larger coronary arteries, the
o Increased metabolism of the heart sets off local blood small anastomoses begin to dilate → diameters of the collateral
flow regulatory mechanisms for dilating the coronary vessels do not enlarge much more for the next 8 to 24 hours →
vessels, and the blood flow increases approx. in collateral flow begins to increase, doubling by the second or third day
proportion to the metabolic needs of the heart muscle and often reaching normal coronary flow within about 1 month.
Vagal stimulation and Ach Release: slows the heart
and has depressive effect on heart contractility • Myocardial Infarction
→ Immediately after an acute coronary occlusion, blood flow ceases in
→ Direct Effects of Nervous Stimuli on the Coronary Vasculature the coronary vessels beyond the occlusion except for small amounts
▪ Norepinephrine and Epinephrine of collateral flow from surrounding vessels
− Vascular constrictor or dilator effects: depending on the → The area of muscle that has either zero or little flow is said to be
presence of constrictor or dilator receptors in the blood infarcted
vessel walls After the onset of the infarction, small amounts of collateral blood
▪ Alpha receptors: constrictor receptors begin to seep into the infarcted area & combining with progressive
▪ Beta receptors: dilator receptors dilation of blood vessels → Area is overfilled with stagnant blood →
▪ Both alpha and beta receptors exist in the coronary vessels muscle fibers uses up O2 → Hgb become deoxygenated → infarcted
▪ In general, the epicardial coronary vessels have a area takes on a bluish-brown hue and blood vessels engorges.
preponderance of alpha receptors In later stages, vessel walls become highly permeable and leak fluid
▪ The intramuscular arteries may have a preponderance of beta → local muscle tissue becomes edematous → cardiac muscle cells
receptors swell because of diminished cellular metabolism → Within a few
hours of almost no blood supply, the cardiac muscle cells die
→ Metabolic factors
▪ Major controllers of myocardial blood flow • Causes of Death after Acute Coronary Occlusion
▪ Myocardial oxygen consumption – main metabolic factor that 1. Decreased Cardiac Output
control blood flow → Due to loss of ability to contract
▪ Whenever the direct effects of nervous stimulation reduce Systolic stretch: ischemic portion → instead of contracting, it
coronary blood flow, the metabolic control of coronary flow is forced outward by the pressure that develops inside the
usually overrides the direct coronary nervous effects within ventricle. Therefore, much of the pumping force of the
seconds ventricle is dissipated by bulging of the area of non-
functional cardiac muscle.
IV. ISCHEMIC HEART DISEASE When Heart becomes incapable of contracting to pump
→ Significantly causes morbidity and mortality worldwide enough blood into the peripheral arterial tree → cardiac
failure and death of peripheral tissues as a result of
• Atherosclerosis peripheral ischemia
→ Frequent cause of diminished coronary blood flow
→ At risk individuals: 2. Damming of blood in the pulmonary blood vessels and then death
▪ Genetic predisposition resulting from pulmonary edema
▪ Overweight or obese and have a sedentary lifestyle
▪ High blood pressure 3. Fibrillation of the Ventricles after MI
▪ With damage to the endothelial cells of the coronary blood Occur during
vessels - First 10 minutes after the infarction occurs
→ Large quantities of cholesterol gradually become deposited beneath - Period of cardiac irritability beginning 1 hour or so
the endothelium at many points in arteries throughout the body Factors that makes heart fibrillate
→ These areas of deposit are invaded by fibrous tissue and frequently ▪ Acute loss of blood supply to the cardiac muscle → rapid
become calcified depletion of K from the ischemic musculature.
→ The net result is the development of atherosclerotic plaques that ▪ Ischemia of the muscle causes an “injury current”
actually protrude into the vessel lumens and either block or partially ▪ Powerful sympathetic reflexes → heart does not pump
block blood flow an adequate volume of blood into the arterial tree →
Common site for development of atherosclerotic plaques: first few cm reduced blood pressure
of the major coronary arteries. ▪ Cardiac muscle weakness caused by the myocardial
infarction causes the ventricle to dilate excessively →
• Acute Coronary Occlusion excess prolongation of conduction pathway in ventricles
→ Frequently occurs in a person who already has underlying → circus movement cycle of new excitation
atherosclerotic coronary heart disease
→ May result from; 4. Rupture of the Infarcted Area
▪ The atherosclerotic plaque can cause a local blood clot called a Rupture of ventricles → Loss of blood into the pericardial
thrombus that occludes the artery space causes rapid development of cardiac tamponade

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• Recovery from Acute M.I • Management of M.I

→ When the area of → Drugs:
ischemia is large, ▪ Vasodilator drugs
some of the − administered during an acute anginal attack to provide
muscle fibers in immediate relief from the pain
the center of the − Short-acting vasodilators are nitroglycerin (NTG) and
area die rapidly, other nitrate drugs
within 1 to 3 hrs, − For chronic stable angina pectoris: Other vasodilators,
where there is such as angiotensin-converting enzyme inhibitors,
total cessation of angiotensin receptor blockers, calcium channel blockers
coronary blood ▪ Beta blocker
supply. − prevents sympathetic enhancement of HR and cardiac
Immediately metabolism during exercise or emotional episodes
around the dead
area is a → Aortic-Coronary bypass or
nonfunctional coronary artery bypass graft
area, with failure (CABG)
of contraction and Done if drugs alone do not
usually failure of impulse conduction work
→ Extending circumferentially around the nonfunctional area is an area Usually via the saphenous
that is still contracting but only weakly because of mild ischemia vein
→ Shortly after the occlusion, the muscle fibers in the center of the
ischemic area die → Coronary Angioplasty
→ During the ensuing days, this area of dead fibers becomes bigger When an area is blocked by a
because many of the marginal fibers finally succumb to the plaque, a catheter is inserted
prolonged ischemia via the radial or femoral
→ At the same time, because of enlargement of collateral arterial artery.
channels supplying the outer rim of the infarcted area, much of the Compresses the plaque increasing the lumen allowing the blood to
nonfunctional muscle recovers flow.
→ After a few days to 3 weeks, most of the nonfunctional muscle
become functional again or dies Difference:
→ Fibrous tissue begins developing among the dead fibers because − CABG: An open heart surgery (oxygenation is done using heart-
ischemia can stimulate growth of fibroblasts and promote lung machine)
development of greater than normal quantities of fibrous tissue – − Coronary angioplasty: Done in catheterization laboratory and
dead muscle tissue is gradually replaced by fibrous tissue target blood vessel is accessed through other arteries using a
→ Fibrous tissue undergoes progressive contraction and dissolution, malleable catheter/wire with a balloon in the stent, opening the
the fibrous scar may grow smaller over a period of several months blocked area.
to a year
→ Finally, the normal areas of the heart gradually hypertrophy to
compensate at least partially for the lost dead cardiac musculature
→ By these means, the heart recovers either partially or almost
completely within a few months
▪ Essential to place the patient on bedrest

• Value of Rest in Treating M.I

→ The degree of cardiac cellular death is determined by the degree of
ischemia and the workload on the heart muscle
→ When the heart becomes excessively active
▪ The vessels of the normal musculature become greatly dilated V. CARDIAC FAILURE
▪ Allows blood flow into the coronary vessels to flow through the • Result from any heart condition that reduces the ability of the heart to
normal muscle tissue, thus, leaving little blood to flow through pump enough blood to meet the body’s needs
the small anastomotic channels into the ischemic area – the • Ischemic heart disease: most common cause of heart failure
ischemic condition worsens – coronary steal syndrome Other causes:
▪ Treatment of M.I: observance of absolute body rest during the ▪ Damaged heart valves
recovery process ▪ External pressure around the heart
In the presence of a coronary embolus that occludes a certain ▪ Vitamin B deficiency
area, collateral circulation helps to supply blood to the rest of that ▪ Primary cardiac muscle disease
area. However, if person becomes active immediately after the ▪ Any other abnormality that makes the heart a hypo effective pump.
infarction. More blood will flow to other areas with no infarction,
compromising the area that needs more blood flow. A. Circulatory Dynamics in Cardiac Failure
Putting the patient on bedrest will increase the chance of blood • Acute Effects of Moderate Cardiac Failure
flowing to the infarcted area. 1. Reduced Cardiac Output
It is very important to have bedrest after an infarction. 2. Increased Venous Pressure: damming of blood in the veins
• Angina Pectoris (Cardiac Pain) 2 STAGES
→ Begins to appear whenever the load on the heart becomes too great 1. Acute Stage
in relation to the available coronary blood flow 2. Chronic Stage
→ Usually felt beneath the upper sternum over the heart
→ Often referred to distant surface areas of the body, most commonly After myocardial infarction, look at the graph, Line A is the Normal Heart.
to the left arm and left shoulder but also frequently to the neck and Line B is the acutely damaged heart
even to the side of the face To compensate, to get the required 5 L/min cardiac output, the right atrial
→ Exacerbated by cold temperatures or by having a full stomach, both pressure will try to increase caused by sympathetic stimulation.
of which increase the workload of the heart With sympathetic stimulation, right atrial pressure will slightly increase
→ The pain is frequently described as hot, pressing, and constricting and then in partially recovered heart, the cardiac output will approximate
and is of such quality that it usually makes the patient stop all normal which is 5 L/min but in return, the heart has to increase the atrial
unnecessary body activity pressure to give that cardiac output.

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• Acute Heart Failure: Sympathetic Nervous Reflexes → Achieves most of its final state of recovery within 5 to 7 weeks,
The response is from although mild degrees of additional recovery can continue for
the Sympathetic months.
Nervous reflexes
→ Sympathetic reflexes • Changes that Occur After Acute Cardiac Failure — Compensated
become maximally Heart Failure
developed in about 30 Dynamics of circulatory changes after an acute, moderate heart
seconds attack, we can divide the stages into:
→ The parasympathetic 1. Instantaneous effect of the cardiac damage;
nervous signals to the 2. Compensation by the sympathetic nervous system, which
heart become occurs mainly within the first 30 seconds to 1 minute
inhibited at the same 3. Chronic compensations resulting from partial heart recovery
time and renal retention of fluid.
→ So for it to work, the In compensated heart failure, meaning the heart is able to give
sympathetic reflex enough volume for the body to be supplied of the nutrients they need
should increase but Figure 22-1:
the parasympathetic ▪ Point A: Normal state of circulation
should be inhibited. ▪ Point B: secs after the heart attack but before sympathetic
→ The normal muscle is reflexes have occurred
strongly stimulated by ▪ Point C: rise in cardiac output toward normal caused by
sympathetic sympathetic stimulation
stimulation → ▪ Point D: increase in right atrial pressure can maintain the
compensate for the nonfunctional muscle cardiac output at a normal level despite continued weakness
→ Increases venous return of the heart
▪ Increases the tone of most of the blood vessels of the circulation → Any attempt to perform heavy exercise causes immediate return of
When there is damaged muscle, the functional area of the heart the symptoms of acute heart failure because the heart is not able to
will compensate for the non-functional muscle. increase its pumping capacity to the levels required for the exercise
→ The cardiac reserve is reduced in compensated heart failure
• Chronic Stage Of Failure
→ 2 Main Events: • Dynamics of Severe Cardiac Failure — Decompensated Heart Failure
▪ Fluid retention → Severely damaged heart:
▪ Varying degrees of recovery of the heart itself over a period of ▪ No amount of compensation, either by sympathetic nervous
weeks to months reflexes of by fluid retention, can make the excessively
weakened heart pump a normal cardiac output
• Circulatory Dynamics In Cardiac Failure: Chronic → The cardiac output cannot rise high enough to make the kidneys
→ Renal fluid retention and increase in blood volume excrete normal quantities of fluid
▪ Occur for hours of days → Fluid continues to be retained → more edema → eventually leads to
▪ If CO decreases to 50-60%, acute kidney injury happens → death
anuria (no urination) → fluid retention In compensated, the heart is still able to give enough cardiac output
▪ Urine output does not return all the way to normal until the for bodily functions but in decompensated, there’s also dysfunction
cardiac output and arterial pressure rise almost to normal of other organ systems, especially the renal — the kidneys are
levels affected, because the heart cannot pump enough cardiac output.

→ Moderate fluid retention can be beneficial

▪ The increased blood volume, increases venous return
1) Increases the mean systemic filling pressure which
increase the pressure gradient for causing venous flow
of blood toward the heart
2) Distends the veins → reduce the venous resistance and
allows even more ease of flow of blood to the heart
▪ When the heart’s pumping capability is reduced further, blood
flow to the kidneys finally becomes too low or the kidneys to
excrete enough salt and water to equal salt and water intake
▪ Fluid retention begins and continues indefinitely. Unless major
therapeutic procedures are used to prevent this outcome
▪ Fluid retention continues unless the patient is given medication
to improve urination
Figure 22 -2:
▪ At this point, the heart is already pumping at its maximum
capacity, this excess fluid no longer has a beneficial effect on → Straight line in Figure 22.2 is at a cardiac output level of 5L/min.
the circulation instead, the fluid retention increases the This level is approximately the critical cardiac output; the cardiac
workload on the already damaged heart. Severe edema output level that is required in the normal adult person to make
the kidneys re-establish normal fluid balance
develops throughout the body → can lead to death.
Remember before compensated heart failure, the right atrial
pressure will continue to rise however in decompensated, even
• Detrimental effects of excess fluid retention in severe cardiac failure
with the increase in right atrial pressure, it cannot reach the
▪ Increasing the workload on the damaged heart
required cardiac output so it increases from +4, +8, to +10 even
▪ Overstretching of the heart → further weakens the heart +16 but it cannot reach the 5L/min critical level.
▪ Filtration of fluid into the lungs → pulmonary edema and This happens when there is greatly depressed cardiac output
consequent deoxygenation of the blood indicating decompensated heart so:
There is no good exchange of oxygen in the lungs
− From point B to D: RA pressure continues to rise; Fluid
▪ Development of extensive edema in most parts of the body
is continuously being retained
− At point F: cardiac output now less than 2.5 L/min and
• Recovery Of The Heart After Myocardial Infarction the right atrial pressure 16 mmHg
→ Processes to restore the normal cardiac function
− After another few days of fluid retention the right atrial
▪ New collateral blood supple
pressure has risen still further, cardiac function is
▪ Undamaged portion of the heart musculature hypertrophies to beginning to decline toward a lower level
compensate
→ The heart ordinarily recovers rapidly during the first few days and
weeks.

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• Decompensated Heart Failure • Cardiac Reserve

→ Decompensated heart failure: state of heart failure which the failure → Maximum percentage that the cardiac output can increase above
continues to worsen normal
→ Failure of the cardiac output (and arterial pressure) to rise to the → In persons with severe heart failure, there is no cardiac reserve
critical level required for normal renal function results in: As we have mentioned before, the order is decreased or there is no
▪ Progressive retention of more and more fluid → causes cardiac reserve
progressive elevation of the mean systemic filling pressure and Healthy young adult: Cardiac reserve is 300 to 400 percent.
progressive elevation of the right atrial pressure Athletically trained persons: 500 to 600 percent or more.
▪ Until finally the heart is so overstretched or so edematous that it Persons with severe heart failure, there is no cardiac reserve.
cannot pump even moderate quantities of blood and, therefore, Exercise test – diagnosis of low cardiac reserve
fails completely Since there is no cardiac reserve, if you give them stress, you have
→ Clinically seen as progressing edema, especially edema of the lungs them run the treadmill so that would need additional work on the
which leads to bubbling rales (a crackling sound) in the lungs and to heart and they don’t have any cardiac reserve and they have heart
dyspnea (air hunger) failure so they will decompensate.

• Treatment Of Decompensation VI. HEART VALVES AND HEART SOUNDS

→ Stop decompensation by:
▪ Strengthening the heart
− administering a cardiogenic drug or inotropes, such as digitalis
▪ Administering diuretic drugs to increase kidney excretion
− at the same time reducing water and salt intake
→ Both methods stop the decompensation process by re-establishing
normal fluid balance so that at least as much fluid leave the body
enters it
Maintain Balance
→ Mechanism of action of the cardiogenic drugs (ex. Digitalis)
▪ Increase the quantity of calcium ions in muscle fibers
▪ Digitalis depress the sodium-calcium exchange pump and raise
calcium ion concentration in cardiac muscle provides the extra
calcium needed to increase the muscle contractile force
Digitalis and other cardiotonic glycosides are believed to
strengthen heart contractions by increasing Ca ions in muscle • Heart Sounds
fibers. Effect is likely due to inhibition of Na-K ATP in cardiac cell → “lub” is associated with closure of the atrioventricular (A-V) valves at
membranes. Inhibition of the sodium-potassium pump increases the beginning of systole
intracellular Na concentration and slows the Na-Ca exchange ▪ First heart sound
pump, which extrudes Ca from the cell in exchange for Na “dub” is associated with closure of the semilunar (aortic and
pulmonary) valve sat the end of systole
• Unilateral Left Heart Failure ▪ Second heart sound
Remember that left ventricle gives blood to the Aorta which delivers → 3rd heart sound
blood to your systemic organs ▪ Occurs at the beginning of the middle third o diastole
When the left side of the heart fails without concomitant failure of the ▪ Oscillation of blood back and forth between the walls of the
right side, blood continues to be pumped into the lungs (from the ventricles initiated by inrushing blood from the atria
body, blood will enter the right atrium; the right ventricle, goes to the ▪ Normally present in children, adolescents, and young adults but
lungs and then from lungs will enter through the pulmonary vein, then generally indicates systolic heart failure in older adults
left atrium, left ventricle then to the Aorta) with the usual right heart → 4th heart sound
vigor, whereas it is not pumped adequately out of the lungs by the ▪ Atrial contraction
left heart into the systemic circulation In persons who derive benefit from atrial contraction for
So if you have left heart failure and your right heart failure is still okay, ventricular filling as a result of decreased ventricular wall
the right will still continue to pump with your lungs but left heart not compliance and increased resistance to ventricular filling
functioning. So blood will be retained in the lungs. ▪ In patients with left ventricular hypertrophy
→ Mean pulmonary filling pressure rise because of the shift of large
volumes of blood from the systemic circulation into the pulmonary • Valvular Lesions
circulation → Rheumatic valvular lesions
→ As the volume of blood in the lungs increases, the pulmonary By far the greatest number of valvular lesions results from
capillary pressure increases rheumatic fever
▪ And pressure rises above a value approximately equal to the ▪ Autoimmune disease in which the heart valves are likely to be
colloid osmotic pressure of the plasma (about 28 mmHg) fluid damaged or destroyed
begins to filter out of the capillaries into the lung interstitial ▪ Preliminary Streptococci infection caused specifically by Group
spaces and alveoli → pulmonary edema A hemolytic Streptococci
→ Most important problems of left heart failure: ▪ Antibodies produced by the body react not only with the
▪ Pulmonary vascular congestion streptococcal protein but also with other protein tissues of the
▪ Pulmonary edema body, often causing severe immunologic damage
▪ Rheumatic fever particularly causes damage in certain
→ In severe, acute left heart failure, pulmonary edema occasionally
susceptible areas, such as the heart valves
occurs so rapidly that it can cause death by suffocation in 20 to 30
▪ The degree of heart valve damage is directly correlated with the
minutes
concentration and persistence of the antibodies
If this happens so fast and the body won’t be able to compensate
▪ Mitral valve – most frequently damaged
and in severe, acute and there’s no time for the body to compensate,
▪ Aortic valve – second most common valve to be damaged
the patient may die.
▪ The free edges of the leaflets, which are normally filmy and free-
lapping, often become solid, scarred mass
• Low Output Cardiac Failure – Cardiogenic Shock/Simple Cardiac
▪ Leaflets adhere to one another so extensively that blood cannot
Shock
flow through it normally → stenosed
→ Caused by inadequate cardiac pumping
▪ When the valve edges are so destroyed by scar tissue that they
It is called Cardiogenic since the problem is with the Heart
cannot close as the ventricles contract → regurgitation
→ Once cardiogenic shock develops, the survival rate is often less than
(backflow) of blood occurs when the valve should be closed
30 percent even with appropriate medical care
Other Causes of Valvular Lesions: Stenosis or lack of one or
→ Viscous cycle of cardiac Deterioration: Low arterial pressure that more leaflets of a valve also occurs occasionally as a congenital
occurs during shock →  the coronary blood supply → weakens the defect. Complete lack of leaflets is rare; congenital stenosis is
heart → makes the arterial pressure fall still more → shock more common
progressively worsens
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1.8 CARDIAC OUTPUT REGULATION AND CIRCULATORY SHOCK PHYSIOLOGY

• HEART MURMURS arterial blood will flow through the ductus arteriosus (special
Many abnormal heart sounds, known as “heart murmurs,” occur artery present in the fetus that connects the pulmonary artery
when abnormalities of the valves are present with the aorta) → bypassed lungs → immediate recirculation of
→ Normal the blood through the systemic arteries of the fetus without the
→ Aortic stenosis blood going through the lungs.
→ Mitral regurgitation − Newborn infant with PDA: quantity of reverse blood flow through
→ Aortic regurgitation the ductus may be insufficient to cause a heart murmur → no
→ Mitral stenosis abnormal heart sounds are heard.
→ Patent ductus − As the baby grows older (1-3y/o): a harsh, blowing murmur
arteriosus begins to be heard in the pulmonary artery area of the chest.
▪ more intense: systole when the aortic pressure is high
▪ less intense: diastole when the aortic pressure falls low, so
that the murmur waxes and wanes with each beat of the
heart, creating the so-called “machinery murmur”
− This lack of blood flow through the lungs is not detrimental to the
fetus because the blood is oxygenated by the placenta.

Closure of the ductus arteriosus after birth:

→ O2 constricts the muscle in the ductus wall.
→ In about 1 of every 5500 babies, the ductus does not close (“patent
ductus arteriosus”)
→ Early months: a patent ductus usually does not cause severely
Mitral Regurgitation abnormal function
− Mitral valve should close however its incompetent, this is during → As the child grows older, the differential between the high pressure
systolic phase but its incompetent so blood will flow back to the left in the aorta and the lower pressure in the pulmonary artery
atrium and then that’s when you will hear the murmur. progressively increases, with corresponding increase in backward
flow of blood from the aorta into the pulmonary artery. Also, the
Mitral stenosis high aortic blood pressure usually causes the diameter of the
− If the mitral valve closes during systolic phase, then the mitral valve partially open ductus to increase with time, making the condition
should open during diastole because you need the valve to open so even worse.
that blood will flow from the left atrium to the left ventricle, however Older child with a patent ductus
the mitral valve stenos its obstructed because rheumatic heart → People with this condition do not show cyanosis until later in life
disease happen so the valve is obstructed blood cannot flow from (when the heart fails, or the lungs become congested)
the left atrium to left ventricle, since this valve stenos you will be → Early in life, the arterial blood is often better oxygenated than
hearing the murmur during diastole because that’s when the valve normal because of the extra times it passes through the lungs.
should have open but its obstructed therefore you hear the turbulent
of blood flow from the left atrium to the left ventricle. Major effects of PDA:
→  cardiac and respiratory reserve. The left ventricle is pumping
First heart sounds opening of the av valve, Second heart sounds about 2 or more times the normal cardiac output, and the maximum
opening of the aortic and pulmonary valve. that it can pump after hypertrophy of the heart has occurred is
about 4 to 7x normal → net blood flow through the remainder of
Semilunar valve the body can never increase to the levels required for strenuous
− Aortic and pulmonary valve stenosis if its stenos you will hear during activity.
systole because its obstructed and blood cannot flow out of the aorta → Even moderately strenuous exercise → person become weak and
or pulmonary artery, on the other hand for the av valve if stenos so may faint from momentary heart failure.
you will hear the murmur during diastole because it’s when the av → Excess flow through the lungs → ↑ pressures in the pulmonary
valve should open, but since its obstructed because of rheumatic vessels → pulmonary congestion and pulmonary edema →
heart disease then you will hear the murmur. progressively more severe with age
→ Most patients with uncorrected patent ductus die from heart
▪ Pulmonary stenosis, aortic stenosis - systolic
disease between ages 20 and 40 years.
▪ Pulmonary regurgitation, aortic regurgitation - diastolic Treatment or Surgery
▪ Mitral regurgitation, tricuspid regurgitation- systolic ▪ Ligate the patent ductus
▪ Stenosis if stenos mitral or tricuspid you hear it during ▪ Divide it and then close the two ends. (this procedure was one
diastolic of the first successful heart surgeries ever performed.)

(PDA) PATENT DUCTUS ARTERIOSUS TETRALOGY OF FALLOT (R-L shunt) (tetRaLogy of Fallot)
− One murmur which is continuous → Most of the blood bypasses the lungs (as much as 75%) → aortic
− Connects your aorta and pulmonary artery blood is mainly unoxygenated venous blood → “blue baby”
− Machinery murmur sound → In this condition, four abnormalities of the heart occur simultaneously:
3 major types of congenital anomalies of the heart and its associated (SHOP)
vessels: •Septal defect (VSD)
1. Stenosis of the channel of blood flow at some point in the heart •Hypertrophy of the R ventricle
or in a closely allied major blood vessel •Overriding aorta
2. Anomaly that allows blood to flow backward from the left side •Pulmonary stenosis
of the heart or aorta to the right side of the heart or pulmonary → Diagnosis is based on:
artery → failing to flow through the systemic circulation (left-to- • Cyanotic (“blue”) skin
right shunt) • ↑ systolic pressure in the R ventricle (recorded through a catheter)
3. Anomaly that allows blood to flow directly from the right side of
• Characteristic changes in the radiological silhouette of the heart,
the heart into the left side of the heart → failing to flow through showing an enlarged R ventricle
the lungs (right-to left shunt)
• Angiograms showing abnormal blood flow through the
PDA (L-R shunt) (“ligaw → relationship → pda”) interventricular septal hole and into the overriding aorta, but much
− During fetal life, the lungs & the elastic compression of the lungs less flow through the stenosed pulmonary artery.
(keeps the alveoli collapsed) keeps most of the lung blood → Treatment or Surgery
vessels collapsed → ↑ resistance to blood flow through the lungs ▪ Open the pulmonary stenosis, close the septal defect, and
→ ↑pulmonary arterial pressure reconstruct the flow pathway into the aorta.
−  resistance to blood flow from the aorta through the large - If successful, the average life expectancy
vessels of the placenta →  pressure in the aorta of the fetus increases from only 3 to 4 years to 50 or more
(lower than in the pulmonary artery) → almost all pulmonary years.

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1.8 CARDIAC OUTPUT REGULATION AND CIRCULATORY SHOCK PHYSIOLOGY

Causes of congenital anomalies: • Circulatory Shock Physiology

a) viral infection in the mother during the first trimester of pregnancy → Tissue deterioration – end result of circulatory shock
(when the fetal heart is being formed) → Inadequate blood flow causes the body tissues to begin
b) Defects are particularly prone to develop when the expectant deteriorating, including the heart and circulatory system
mother contracts German measles This deterioration causes an even greater decrease in cardiac
c) Hereditary output, and a vicious cycle ensues, with progressively increasing
d) Children of patients surgically treated for congenital heart circulatory shock, less adequate tissue perfusion, more shock, and
disease have about a 10x greater chance of having congenital so forth until death occurs.
heart disease than do other children. - During this late stage of circulatory shock, appropriate
physiological treatment can often reverse the rapid slide to
VII. CIRCULATORY SHOCK PHYSIOLOGY death
If there is Cardiogenic shock the end result of circulatory shock is
Tissue Deterioration because there will be no nutrients flowing to
the tissues and the inadequate blood flow therefore will cause the
body tissues begin to deteriorate including the heart and the
circulatory system.

• Stages Of Shock
→ Nonprogressive stage (sometimes called the compensated stage)
▪ In which the normal circulatory compensatory mechanisms
eventually cause full recovery without help from outside therapy
Shock of lesser degree

→ Progressive stage
▪ Without therapy, the shock becomes steadily worse until death
occurs
• Circulatory Shock
→ Irreversible stage
→ Generalized inadequate blood flow through the body to the extent ▪ The shock has progressed to such an extent that all forms of
that the body tissues are damaged unknown therapy are inadequate to save the person’s life even
→ Too little oxygen and other nutrients are delivered to the tissue cells though, for the moment, the person is still alive
During that part anything you do won’t help the patient because
• Physiological Causes Of Shock the shock is already irreversible.
→ Circulatory shock caused by decreased cardiac output
▪ Cardiac abnormalities that decrease the ability of the heart to • Hemorrhagic Shock
pump blood (e.g. MI, toxic states of the heart, severe heart valve → Shock caused by hypovolemia
dysfunction, heart arrhythmias, and other conditions) → → Hypovolemia – means diminished blood volume
Cardiogenic shock → Hemorrhage – most common cause o hypovolemic shock
As many as 70% of people who experience cardiogenic
→ Hemorrhage decreases the filling pressure of the circulation →
shock do not survive
decreases venous return → cardiac output falls below normal →
shock may ensue
▪ Factor that decrease venous return also decrease cardiac output
Hemorrhage usually happen in trauma patients
because the heart cannot pump blood that does not flow into it
The most common cause: diminished blood volume
Venous return can be reduced as result of decreased • Sympathetic Reflex Compensations In Shock
vascular tone, especially of the venous blood reservoirs, → Value in maintaining arterial pressure
or obstruction to blood flow at some point in the circulation, → The decrease in arterial pressure after hemorrhage, cause powerful
especially in the venous return pathway to the heart. sympathetic reflexes (initiated mainly by the arterial baroreceptors
and other vascular stretch receptors)
• Oxygen Delivery ▪ The arterioles constrict in most parts of the systemic circulation
Is affected by − Increasing the total peripheral resistance
cardiac output and ▪ The veins and venous reservoirs constrict
the arterial oxygen − Maintain adequate venous return despite diminished
content, the cardiac volume
output is affected ▪ Heart activity increases markedly
by heart rate and Sympathetic reflexes:
stroke volume. − Geared more for maintaining arterial pressure than for
maintaining cardiac output.
−  the arterial pressure mainly by  total peripheral resistance,
which has no beneficial effect on cardiac output; however, the
sympathetic constriction of the veins is important to keep venous
• Stroke Volume return and cardiac output from falling
− Extend the amount of blood loss that can occur without causing
death to about twice that which is possible in their absence

→ Protection of blood flow through the coronary and cerebral

circulations
▪ Special value of the maintenance of normal arterial pressure
even in the presence of decreasing cardiac output
The sympathetic stimulation does not cause significant
constriction of either the cerebral or the cardiac vessels.
In both vascular beds, local blood flow autoregulation is
excellent → prevents moderate decreases in arterial pressure
from significantly decreasing their blood flows.
• 3 Factors mainly affect stroke volume: Therefore, blood flow through the heart and brain is maintained
→ Affected by preload the amount/volume of blood that goes into the essentially at normal levels as long as the arterial pressure
heart, the heart will contract myocardial contractility, and the does not fall below about 70 mm Hg.
pressure that the heart will contract against that’s afterload
(systemic vascular resistance).

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1.8 CARDIAC OUTPUT REGULATION AND CIRCULATORY SHOCK PHYSIOLOGY

• Compensated Shock ▪ Increased capillary permeability

→ Mechanisms of the circulation to maintain cardiac output Hours of capillary hypoxia and lack of other nutrients →
▪ Baroreceptor reflexes – elicit powerful sympathetic stimulation of permeability of the capillaries gradually increases → large
the circulation quantities of fluid begin to transude into the tissues →
▪ Central nervous system ischemic response decreases blood volume even more → further decrease in
− elicits a powerful sympathetic stimulation throughout the cardiac output → shock worsens.
body Capillary hypoxia does not cause increased capillary
− but is not activated significantly until the arterial pressure permeability until the late stages of prolonged shock
falls below 50mmHg
▪ Reverse stress-relaxation of the circulatory system ▪ Release of toxins from ischemic tissue
− causes the blood vessels to contract around the diminished Toxins: histamine, serotonin, and tissue enzymes → further
blood volume so that the blood volume that is available more deterioration of the circulatory system
adequately ills the circulation
▪ Increased secretion of renin by the kidneys and formation of ▪ Cardiac depression caused by endotoxin
angiotensin II Endotoxin: released from the bodies of dead gram-negative
− which constricts the peripheral arterioles bacteria in the intestines; can play a major role in some types
− causes decreased output of water and salt by the kidneys of shock, especially “septic shock”
▪ Increased secretion by posterior pituitary gland of vasopressin Diminished blood flow to the intestines → enhanced formation
(antidiuretic hormone), which constricts the peripheral arterioles and absorption of this toxic substance → increased cellular
and veins and greatly increases water retention by the kidneys. metabolism despite inadequate nutrition of the cells, which has
▪ Increased secretion by the adrenal medullae of epinephrine and a specific effect on the heart muscle → cardiac depression
norepinephrine, which constricts the peripheral arterioles and veins
and increases the heart rate ▪ Generalized cellular deterioration
▪ Compensatory mechanisms that return the blood volume back Liver is affected mainly because of lack of enough nutrients to
toward normal, including absorption of large quantities of fluid from support the normally high rate of metabolism in liver cells; also,
the intestinal tract, absorption of fluid into the blood capillaries from partly because of the exposure of the liver cells to any vascular
the interstitial spaces of the body, conservation of water and salt by toxin or other abnormal metabolic factor occurring in shock.
the kidneys and increased thirst and increased appetite for salt. Among the damaging cellular effects that are known to occur
The sympathetic reflexes and increased secretion of in most body tissues are the following:
catecholamines become maximally activated within 30 seconds to ▪ Active transport of Na and K through the cell membrane is
a few minutes after hemorrhage. (rapid help) diminished → Na and Cl accumulate in the cells and K is
The angiotensin and vasopressin mechanisms, and the reverse lost from the cells → cells begin to swell.
stress-relaxation that causes contraction of the blood vessels and ▪ Mitochondrial activity in the liver cells and other tissues of
venous reservoirs, all require 10 minutes to 1 hour to respond the body, becomes severely depressed.
completely, but they aid greatly ↑ arterial pressure or ↑ circulatory ▪ Lysosomes in the cells in widespread tissue areas begin
filling pressure → ↑return of blood to the heart. to break open, with intracellular release of hydrolases →
Readjustment of blood volume by absorption of fluid from the further intracellular deterioration.
interstitial spaces and intestinal tract, oral ingestion and absorption ▪ Cellular metabolism of nutrients, such as glucose,
of additional quantities of water and salt, may require from 1 to 48 eventually becomes greatly depressed in the last stages
hours, but recovery eventually takes place, provided the shock does of shock. The actions of some hormones are depressed as
not become severe enough to enter the progressive stage. well

• Progressive Shock • Irreversible Shock

Even if the body is doing all the compensatory mechanisms but shocks Progressive shock continuous the patient will go now to irreversible
will still progress shock
→ Causes: → After shock has progressed to a certain stage transfusion or any other
▪ Cardiac depression type of therapy becomes incapable of saving the person’s life
Heart does not contract well → In severe shock a stage is eventually reached at which the person will
Arterial pressure falls low enough → coronary blood flow die even though vigorous therapy might still return the cardiac output
decreases below that required for adequate nutrition of the to normal for short periods
myocardium → weakens the heart muscle →  CO more Even if you give all the inotrope and the cardiac output will go to normal
Thus, positive feedback cycle has developed, whereby the shock but the damage has been extensive, and cannot be repaired so you
becomes more and more severe. cannot revive that patient, you cannot bring that patient back, there are
a certain point where in that the patient has cross.
▪ Vasomotor Failure The high-energy phosphate reserves in the tissues of the body,
Veins do not constrict especially in the liver and the heart, are greatly diminished in severe
When diminished blood flow to the brain’s vasomotor center shock.
depresses the center so much that it becomes progressively less Essentially all the creatine phosphate has been degraded, and almost
active and finally totally inactive. all the adenosine triphosphate has downgraded to adenosine
During the first 4 to 8 minutes, complete circulatory arrest to the diphosphate, adenosine monophosphate, and, eventually, adenosine.
brain causes most intense of all sympathetic discharges, but by → adenosine diffuses out of the cells into the circulating blood →
the end of 10 to 15 minutes, the vasomotor center becomes so converted into uric acid, a substance that cannot reenter the cells to
depressed reconstitute the adenosine phosphate system.
The vasomotor center usually does not fail in the early stages of Once the high-energy phosphate stores of the cells are depleted, they
shock if the arterial pressure remains above 30 mm Hg are difficult to replenish. Thus, one of the most devastating end results
in shock, and the one that is perhaps most significant for development
▪ Blockage of very small vessels by “sludge blood” → caused by local of the final state of irreversibility, is this cellular depletion of these high-
blood agglutination due to acidosis energy compounds
Initiating cause: sluggish blood flow in the micro vessels
Tissue metabolism continues despite the low flow → large • Other Causes Of Hypovolemic Shock
amounts of acid, both carbonic acid and lactic acid, continue to → Plasma loss
empty into the local blood vessels → increase the local acidity of ▪ Intestinal obstruction
the blood → local blood agglutination → minute blood clots → − Distention of the intestine in intestinal obstruction partly
very small plugs in the small vessels. blocks venous blood flow in the intestinal walls, which
Even if the vessels do not become plugged, an increased increases intestinal capillary pressure
tendency for the blood cells to stick to one another makes it more o Cause fluid to leak from the capillaries into the intestinal
difficult for blood to flow through the microvasculature (“sludged walls and also into the intestinal lumen
blood”) → Severe burns or other denuding conditions of the skin
→ Dehydration
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1.8 CARDIAC OUTPUT REGULATION AND CIRCULATORY SHOCK PHYSIOLOGY

• Neurogenic Shock Because the gravity will pull blood toward the heart
Usually in neurogenic shock there is extreme vasodilation you First essential step in the treatment of many types of shock
cannot fill the circulatory system Usually in neurogenic shock there
is extreme vasodilation you cannot fill the circulatory system • Circulatory Arrest
→ Vascular capacity increases so much that even the normal amount → All blood flow stops
of blood is incapable of filling the circulatory system adequately → As a result of cardiac arrest or ventricular fibrillation
→ Sudden loss of vasomotor tone throughout the body, resulting → More than 5 to 8 minutes of total circulatory arrest can cause at least
especially in massive dilation of the veins some degree of permanent brain damage in more than half of
→ The resulting condition is known as neurogenic shock patients
→ Causes of neurogenic shock: → 10 to 15 minutes almost permanently destroys significant amounts
▪ Deep general anesthesia of mental power
Depresses the vasomotor center → vasomotor paralysis
→ shock REFERENCES
▪ Spinal anesthesia • Dr. Irorita’s PowerPoint
When this extends all the way up the spinal cord, blocks • Guyton and Hall
the sympathetic nervous outflow from the nervous system • Internet Pictures
→ can be a potent cause of neurogenic shock
▪ Brain damage - cause of vasomotor paralysis APPENDIX

• Anaphylactic Shock And Histamine Shock

→ Anaphylaxis – allergic condition in which cardiac output and arterial
pressure often decreased drastically
Vasodilation, there is decrease in preload and sometimes
therefore the cardiac output is affected
Results primarily from an antigen-antibody reaction → basophils in
the blood and mast cells in the pericapillary tissues will release
histamine or a histamine-like substance.
Histamine causes (1) an increase in vascular capacity because of
venous dilation → a marked decrease in venous return; (2) dilation
of the arterioles → in greatly reduced arterial pressure; and (3)
greatly increased capillary permeability, with rapid loss of fluid and
protein into the tissue spaces.
The net effect is a great reduction in venous return and sometimes
such serious shock that the person may die within minutes.

• Septic Shock
→ Bacterial infection widely disseminated to many areas o the body.
With the infection causing extensive damage
Causing decrease also in cardiac output, sometimes there is a lot of
mechanism vasodilatation or vasoconstriction depending and
sometimes it also affects the cardiac output.
Most cases of septic shock are caused by Gram-positive bacteria,
followed by endotoxin-producing Gram-negative bacteria
Most frequent cause of shock-related death in the modern hospital
Early stages of septic shock: no signs of circulatory collapse but only
signs of the bacterial infection.
Infection becomes more severe: circulatory system usually
becomes involved either because of direct extension of the infection
or secondarily as a result of toxins from the bacteria → loss of
plasma into the infected tissues through deteriorating blood capillary
walls.

• Treatment Of Shock
What causes shock is decrease in contractility or sometimes if
there’s extensive vasodilation since decrease in preload volume is
the problem:
→ Replacement therapy
▪ Blood and plasma transfusion
▪ Plasma substitute (dextran)
Plasma
− Can usually substitute adequately for whole blood
because it increases the blood volume and restores
normal hemodynamics.
− Cannot restore a normal hematocrit
− it is reasonable to use plasma (EMERGENCY
CONDITIONS) in place of whole blood for treatment of
hemorrhagic or most other types of hypovolemic shock.

→ Sympathetic drugs: epinephrine and norepinephrine

▪ Beneficial for neurogenic and anaphylactic shock
Sympathomimetic drugs: if we need the heart to contract
better, usually this is what we give in neurogenic and
anaphylactic shock.

→ Other supportive treatment:

▪ Oxygen therapy
▪ Head-down position
− Placing the patient with the head down at least 12 inches
lower than the feet helps in promoting venous return
PHYSIOLOGY 11 of 11