CIRCULATORY SHOCK CARDIAC OUTPUT, VENOUS RETURN AND THEIR REGULATION CARDIAC OUTPUT VENOUS RETURN Quantity of blood pumped into the aorta Quantity of blood each minute by the flowing from the veins heart, that which flows into the right atrium through the circulation each minute being the sum of the blood flows to all the tissues of the body FACTORS DIRECTLY AFFECTING CARDIAC OUTPUT 1) Basic level of body metabolism The average cardiac output 2) Whether the person is exercising for the resting adult is 3) The person’s age around 5L/min 4) Size of the body Increased pumping effectiveness caused by heart hypertrophy A long term increased workload causes the heart muscle to increase in mass and contractile strength (like skeletal muscles) E.g: Marathon runners hearts can increase in mass by 50-75% Combined effect of nervous excitation of the heart and hypertrophy can allow the heart to pump as much as 30 to 40 L/min (2½ times average person) This is one of the most important factors determining the runner’s running time. FACTORS THAT CAUSE A HYPOEFFECTIVE HEART 1) Increased arterial pressure against which the heart has to pump, e.g HTN 2) Inhibition of nervous excitation of the heart 3) Pathological factors that cause abnormal heart rhythm or rate of heart beat 4) Coronary artery blockage 5) Valvular heart disease 6)Congenital heart disease 7) Myocarditis 8) Cardiac hypoxia VENOUS RETURN CURVES Three principal factors that affect venous return to the heart from the systemic circulation: 1. Right atrial pressure, which exerts a backward force on the veins to impede flow of blood from the veins into the right atrium 2. Degree of filling of systemic circulation measured by the mean systemic filling pressure which forces the systemic blood towards the heart. 3. Resistance to blood flow between the peripheral vessels and the right atrium.
Plateau in the venous return curve at negative Atrial pressures caused by
collapse of the large veins
1) When the right atrial pressure falls below zero – below atmospheric pressure – there will be almost no increase in venous return 2) When the right atrial pressure has fallen to about -2 mmHg, the venous return will have reached a plateau even if it falls to -20 mmHg or -50 mmHg. Resistance to venous return SPECIFIC ANATOMICAL STRUCTURE OF THE FETAL CIRCULATION The lungs are mainly nonfunctional and the liver partially functional during fetal life and do not require much blood. The fetal heart pumps much blood through the placenta.
1) Blood returning from the placenta through the umbilical vein passes through the ductus venosus, mainly bypassing the liver. 2) Most of the blood entering the right atrium from the inferior vena cava is directed in a straight pathway across the posterior aspect of the right atrium.
• This blood is pumped by
the left ventricle mainly into the arteries of the head and the forelimbs. 3) The blood entering the right atrium from the superior vena cava is directed downwards through the tricuspid valve into the right ventricle and is mainly deoxygenated blood from the head region of the fetus.
This blood is pumped by the right
ventricle into the pulmonary artery and then through the ductus arteriosus into the descending aorta, then through the two umbilical arteries into the placenta, where the deoxygenated blood becomes oxygenated. CHANGES IN FETAL CIRCULATION AT BIRTH ⚫ At birth, there is closure of foramen ovale, ductus arteriosus and ductus venosus.
⚫ Also there is decreased pulmonary
vascular resistance and increased systemic vascular resistance.
⚫ Circulatory adjustments at birth allow
adequate blood flow to the lungs and the liver. CORONARY CIRCULATION ⚫ The heart receives its nutritive blood supply entirely through coronary arteries penetrating the cardiac muscles from the surface of the heart.
⚫ Blood inside the cardiac chambers only provides
nutrition to the endocardial surface. BLOOD CIRCULATION IN THE CORONARIES ⚫ The left coronary artery supplies mainly the anterior and left lateral portions of the left ventricle.
⚫ The right coronary artery supplies most
of the right ventricle, as well as the posterior part of the left ventricle in 80-90% of people.
⚫ Coronary venous flow from left ventricle
returns to right atrium by way of the coronary sinus (75% of total coronary blood flow) and from the right ventricle through small anterior cardiac veins that flow directly into the right atrium.
• The besian veins empty directly into all chambers of the heart Normal Coronary Blood flow: During Strenuous exercise: The resting coronary blood flow in the resting human being The coronary blood flow averages 70 ml/min/100 g heart increases threefold to fourfold to weight or 225ml/min (4-5 % of supply extra nutrient’s needed by the total cardiac output) the heart.
Phasic changes in coronary blood flow during systole and Diastole –
effect of Cardiac muscle compression
Control of Coronary Blood flow
1) Local muscle metabolism is the primary controller of coronary flow where oxygen demand is a major factor in local coronary blood flow regulation.
2) Nervous control of Coronary blood flow both directly and
indirectly by stimulation of autonomic nerves THE CEREBRAL BLOOD FLOW Blood flow of the brain is supplied by four large arteries – two carotids and two vertebral arteries which merge to form the circle of Willis at the base of the brain.
NORMAL RATE OF CEREBRAL
BLOOD FLOW
Normal blood flow through the brain
of the adult person averages 50 to 65 ml/min/100 g of brain tissue.
For the entire brain, this amounts to 750
to 900ml/min. The brain comprises only about 2% of the body weight but receives 15 % of the resting cardiac output.
Regulation of cerebral blood flow
⚫ Several metabolic tissue factors contribute to cerebral blood flow regulation:
1) Carbon dioxide concentration
2) Hydrogen ion concentration 3) Oxygen concentration 4) Substances released from astrocytes GASTROINTESTINAL BLOOD FLOW - SPLANCHNIC CIRCULATION Splanchnic circulation includes the blood flow through the gut itself plus blood flows through the spleen, pancreas, and the liver.
The celiac artery provides
blood supply to the stomach.
The superior and the
inferior mesenteric arteries supply the walls of the small and the large intestines. Blood that courses through the gut, spleen and pancreas flows immediately into the liver by way of the portal vein from where it leaves the liver by way of hepatic veins that empty into the vena cava.
Flow of blood through the liver allows the reticulo endothelial cells lining the liver sinusoids to remove bacteria and other particulate matter that might enter the circulation from the GIT. Nonfat water soluble nutrients (carbohydrates and proteins) absorbed from the gut are transported in the portal venous blood to the liver sinusoids from where both the reticuloendothelial cells and the principal parenchymal cells of the liver absorb and store temporarily one half to three quarters of the nutrients.
Much intermediary processing of nutrients
occurs in the liver cells
Almost all the fats absorbed from the
intestinal tract are not carried in the portal blood but are absorbed in the intestinal lymphatics and then are conducted into the systemic circulating blood by way of the thoracic duct bypassing the liver. CUTANEOUS BLOOD FLOW •Skin is the largest organ of the body and serves as a heat exchanger for thermoregulation. •Skin blood flow is adjusted to keep deep body at 37°C: . By arterial dilation or constriction and activity of arteriovenous anastomoses which control blood flow through surface capillaries.
•Sympathetic activity closes surface beds
during cold & fight or flight and opens them in heat and exercise. The Triple Response of Lewis ⚫ The triple response of Lewis is a cutaneous response that occurs from firm stroking of the skin, which produces an initial red line, followed by a flare around that line, and then finally a wheal. ⚫ The triple response of Lewis is due to the release of histamine. ⚫ The characteristics of the response are due to: 1) Red line: due to capillary dilatation 2) Flare: redness in the surrounding area due to arteriolar dilatation mediated by axon reflex. 3) Wheal: due to exudation of fluid from capillaries and venules CIRCULATORY SHOCK Generalized inadequate blood flow through the body leading to tissue damage due to inadequate oxygen and nutrient supply with inadequate removal of cellular waste products from the tissues leading to deterioration of organ systems PHYIOLOGICAL CAUSES OF SHOCK 1) Circulatory shock caused by decreased cardiac output
a) Cardiac abnormalities that b) Factors that decrease venous
decrease the ability of the heart to return also decrease cardiac output: 1) Diminished blood volume pump blood: 2) Decreased vascular tone 1) Myocardial infarction especially of veins 2) Toxic states of the heart 3) Obstruction to blood flow 3) Severe heart valve dysfunction especially in the venous return 4) Heart arrhythmias pathway 2) Circulatory shock that occurs without diminished cardiac output 1) Excessive metabolic rate so that even a normal cardiac output is inadequate 2) Abnormal tissue perfusion patterns , so most of the cardiac output is passing through blood vessels besides those that supply the local tissues with nutrition
STAGES OF SHOCK 1) A non progressive stage (compensated stage) , in which the normal circulatory compensatory mechanisms eventually cause full recovery without help from outside therapy
2) A progressive stage, in which , without therapy , the shock becomes
steadily worse until death.
3) An irreversible stage, in which shock progresses to such an extent that all
forms of known therapy are inadequate to save the person’s life, even though he is still alive. TYPES OFSHOCK 1) Cardiogenic shock 4) Neurogenic shock 2) Hypovolemic shock 5) Anaphylacticshock 3) Septic shock
CARDIOGENIC SHOCK – LOW CARDIAC OUTPUT FAILURE
1) After acute MI’s and prolonged periods of slow progressive cardiac deterioration, the heart becomes incapable of pumping even the minimal amount of blood required to keep the body alive. 2) Inadequate blood flow deteriorates the heart and the circulatory system itself causing an even greater decrease in cardiac output. 3) In a heart that already has a major coronary vessel blocked, deterioration begins when the arterial pressure falls below 80-90mm Hg instead of 45mm Hg in the case of a healthy heart. 4) Death can result within a few hours to a few days and survival rate is less than 30% SHOCK CAUSED BY HYPOVOLEMIA – HEMORRHAGIC SHOCK
Hemorrhage is the most common cause of hypovolemic shock.
HEMORRHAGE
Filling pressure of the circulation
venous return Cardiac ouput
SHOCK
Sympathetic Reflex compensations in shock –
their special value in maintaining arterial pressure Hypovolemic shock caused by plasma loss Severe plasma loss can occur in the following conditions:
1) Intestinal obstruction in which plasma protein rich fluid leaks
out of the intestinal capillaries into the intestinal wall and intestinal lumen 2) Severe burns or denuding conditions of the skin 3) Dehydration: fluid loss from all fluid compartments of the body in a) Excessive sweating b) Fluid loss in excessive diarrhea or vomiting c) Excess loss of fluid by kidneys d) Inadequate intake of fluid and electrolytes e) Destruction of adrenal cortices with loss of aldosterone secretion
Hypovolemic shock caused by trauma – Excessive contusion of the body can damage the capillaries sufficiently to allow excessive loss of plasma into the tissues. NEUROGENIC SHOCK – INCREASED VASCULAR CAPACITY
Shock without loss of blood volume resulting from increase in vascular capacity when even the normal amount of blood becomes incapable of filling the circulatory system adequately.
BASIC CAUSE: Sudden loss of vasomotor tone throughout the body resulting in massive dilation of the veins Diminished venous return caused by vascular dilation is called venous pooling of blood.
CAUSES OF NEUROGENIC SHOCK
1) Deep general anesthesia often depresses the vasomotor center enough to cause vasomotor paralysis 2) Spinal anesthesia extending all the way up to the spinal cord, blocks the sympathetic nervous outflow from the nervous system 3) Brain damage is often a cause of vasomotor paralysis – prolonged ischemia results in total inactivation of vasomotor neurons ANAPHYLACTIC AND HISTAMINE SHOCK In Anaphylaxis, the cardiac output and arterial pressure both decrease drastically. During this allergic condition, histamine is released which causes: 1) Increase in vascular capacity because of venous dilation, causing a marked decrease in venous return. 2) Dilation of the arterioles, resulting in greatly reduced arterial pressure 3) Greatly increased capillary permeability, with rapid loss of fluid and protein into the tissue spaces. Net effect is great reduction in venous return
SEPTIC SHOCK Disseminated bacterial infection causing extensive tissue damage Causes: 1) Peritonitis caused by spread of infection from uterus and fallopian tubes, from rupture of GI system 2) Spread of skin infection 3) Generalized gangrenous infection spreading to internal organs 4) Infection spreading into the blood from the kidney or urinary tract, often caused by colon bacilli. SPECIAL FEATURES OF SEPTIC SHOCK
2) Often marked vasodilation
1) High fever throughout the body especially in the infected tissues
3) Bacterial toxin stimulation 4) Sludging of the blood,
of cellular metabolism and caused by red cell vasodilation leading to high agglutination in response to cardiac output degenerating tissues
