CARDIOVASCULAR SHOCK

PRESENTER:DR MTONGWE

FACILITATOR: DR.F. BUKACHI

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•Definition•Basic Physiology•Classification •Causes •Symptoms and Sings•Treatment•complication

DEFINITION

• generalized inadequate blood flow, to the extent that the body tissues are damaged, especially because too little oxygen and other nutrients delivered to the tissue cells. Even the cardiovascular system itself- the heart musculature, walls of the blood vessels, vasomotor system and other circulatory parts begin to deteriorate. So shock, once begun, is prone to become progressively worse.

DEFINITION

• Profound hemodyamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vital organs

Physiological causes of shock.

• Circulatory shock caused by decreased cardiac output.

• Shock usually results from inadequate cardiac out put. Two types of factors reduce this:

1. Cardiac abnormality that decrease the ability of the heart to pump blood- these include myocardial infarction, toxic states of the heart, valve dysfunction, arrhythmias etc

2. Factors that reduce the venous return. Egdiminished blood vol. decreased vascular tone, obstruction to the blood flow

Circulatory shock that occur without diminished blood cardiac output

Occasionally, cardiac output is normal or even greater than normal, yet the person is in circulatory shock. This can result from (1) excessive metabolic rate, so even a normal cardiac output is inadequate, or (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.

• What Happens to the Arterial Pressure in Circulatory Shock?

• In the minds of many physicians, the arterial pressure level is the principal measure of adequacy of circulatory function. However, the arterial pressure can often be seriously misleading. At times, a person may be in severe shock and still have an almost normal arterial pressure because of powerful nervous reflexes that keep the pressure from falling. At other times, the arterial pressure can fall to half of normal, but the person still has normal tissue perfusion and is not in shock.

• In most types of shock, especially shock caused by severe blood loss, the arterial blood pressure decreases at the same time the cardiac output decreases.

Tissue Deterioration Is the End Result of Circulatory Shock

• Once circulatory shock reaches a critical state of severity, regardless of its initiating cause, the shock itself leads to more shock. That is, the inadequate blood flow causes the body tissues to begin deteriorating, including the heart and circulatory system itself. This causes an even greater decrease in cardiac output, and a vicious circle ensues, with progressively increasing circulatory shock, less adequate tissue perfusion, more shock, and so forth until death. It is with this late stage of circulatory shock that we are especially concerned, because appropriate physiologic treatment can often reverse the rapid slide to death.

Stages of Shock

• Because the characteristics of circulatory shock change with different degrees of severity, shock is divided into the following three major stages:

• A nonprogressive stage (sometimes called the compensated stage), in which the normal circulatory compensatory mechanisms eventually cause full recovery without help from outside therapy.

• A progressive stage, in which, without therapy, the shock becomes steadily worse until death.

• An irreversible stage, in which the shock has progressed to such an extent that all forms of known therapy are inadequate to save the person's life, even though, for the moment, the person is still alive

Cardiovascular shock classification

• The causes are divided into four groups: 1. inadequate volume of blood to fill the vascular system

(hypovolemic shock);2. increased size of the vascular system produced by

vasodilatation in the presence of a normal blood volume (distributive, vasogenic, or low-resistance shock);

3. inadequate output of the heart as a result of myocardial abnormalities (cardiogenic shock);

4. inadequate cardiac output as a result of obstruction of blood flow in the lungs or heart (obstructive shock).

• Hypovolemic shock (decreased blood volume) Hemorrhage Trauma Surgery Burns Fluid loss associated with vomiting or diarrhea

• Distributive shock (marked vasodilation; also called vasogenic or low-resistance shock) Fainting (neurogenic shock) Anaphylaxis Sepsis (also causes hypovolemia due to increased capillary permeability with loss of fluid into tissues) Cardiogenic shock (inadequate output by a diseased heart) Myocardial infarction Congestive heart failure Arrhythmias

• Obstructive shock (obstruction of blood flow) Tension pneumothorax Pulmonary embolism Cardiac tumor Pericardial tamponade

DIAGNOSIS

• Recognizing the cause of shock is more important than categorizing the type.

• Often, the cause is obvious or can be recognized quickly based on the history and physical examination, aided by simple testing.

• Specific diagnosis criteria include obtundation, heart rate > 100, respiratory rate > 22, hypotension (systolic BP < 90 mm Hg) or a 30-mm Hg fall in baseline BP, and urine output < 0.5 mL/kg/h. Laboratory findings that support the diagnosis include lactate > 3 mmol/L, base deficit < −4 mEq/L, and Paco2< 32 mm Hg. However, none of these findings alone is diagnostic, and each is evaluated by its trend (ie, worsening or improving) and in the overall clinical context, including physical signs.

Hypovolemic shock

• characterized by hypotension; a rapid, threadypulse; cold, pale, clammy skin; intense thirst; rapid respiration; and restlessness or, alternatively, torpor. Urine volume is markedly decreased. Hypovolemic shock is commonly subdivided into categories on the basis of cause. The use of terms such as hemorrhagic shock, traumatic shock, surgical shock, and burn shock

• In hypovolemic and other forms of shock, inadequate perfusion of the tissues leads to increased anaerobic glycolysis, with production of large amounts of lactic acid. In severe cases, the blood lactate level rises from a normal value of about 1 mmol/L to 9 mmol/L or more. The resulting lactic acidosis depresses the myocardium, decreases peripheral vascular responsiveness to catecholamines, and may be severe enough to cause coma.

Compensatory Reactions Activated by Hypovolemia.

• Vasoconstriction • Tachycardia• Venoconstriction• Tachypnea Increased thoracic pumping• Restlessness Increased skeletal muscle pumping (in some

cases)• Increased movement of interstitial fluid into capillaries• Increased secretion of vasopressin• Increased secretion of glucocorticoids• Increased secretion of renin and aldosterone• Increased secretion of erythropoietin• Increased plasma protein synthesis

Hypovolemic Shock Caused by Body Fluid LossSite of Fluid Loss Mechanism of LossSkin Thermal or chemical burn, sweating due to

excessive heat exposure

GI tract Vomiting, diarrheaKidneys Diabetes mellitus or insipidus, adrenal

insufficiency, salt-losing nephritis, the polyuric phase after acute tubular damage, use of potent diuretics

Intravascular fluid lost to the extravascular space

Increased capillary permeability secondary to inflammation or traumatic injury (eg, crush), anoxia, cardiac arrest, sepsis, bowel ischemia, acute pancreatitis

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sympathetic

innervation of

myocardium

sympathetic innervation of

arterioles

Baroreceptors on aorta and carotid

sinus send information about

changes in BP to cardiovascular

centre

cardiovascular centre

sympathetic and

parasympathetic innervation

of Sino-atrial node

Control of Blood Pressure via the Baroreceptor Reflex

brain

key

parasympathetic nerves

sympathetic nerves

afferent sensory nerves

arterioles

heart

© Roger McFadden – University of Central England 2003

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Renin – Angiotensin – Aldosterone Pathway

THIRST

ANGIOTENSIN II

ADRENAL

CORTEX

KIDNEYS increase Na+

reabsorption from filtrate

BP

VASOCONSTRICTION

BLOOD

PRESSURE

ALDOSTERONE

BLOOD

VOLUME

ANGIOTENSIN CONVERTING

ENZYME

JUXTAGLOMERULAR cells in the

kidney respond to a REDUCTION

IN BLOOD VOLUME from

EXCESS VOMITING, SWEATING,

& HAEMORRHAGE etc.

RENIN released into

blood

ANGIOTENSINOGEN ANGIOTENSIN I

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osmoreceptors in hypothalamus detect

increase in osmolarity of blood

and release ADH

into blood stream

ADHFILTRATE

ADH

water

urine blood

nephron capillary

ADH increases the

amount of water

reabsorbed from the

filtrate to the blood

urine output is reduced as more water is returned to

the blood

Role of ADH in dehydration

• decrease in pulse pressure or mean arterial pressure decreases the number of impulses ascending to the brain from the arterial baroreceptors, resulting in increased vasomotor discharge. The resulting vasoconstriction is generalized, sparing only the vessels of the brain and the heart. The coronary vessels are dilated because of the increased myocardial metabolism secondary to an increase in heart rate. Vasoconstriction in the skin accounts for the coolness and pallor, and vasoconstriction in the kidneys accounts for the shutdown in renal function.

• The immediate cardiac response to hypovolemia is tachycardia. With more extensive loss of volume tachycardia can be replaced by bradycardia, whereas with very severe hypovolemia tachycardia reappears. Bradycardia may be due to unmasking of a vagally mediated depressor reflex, perhaps related to limiting blood loss.

• Vasoconstriction in the kidney reduces glomerular filtration. This reduces water loss, but it reaches a point at which nitrogenous products of metabolism accumulate in the blood (prerenal azotemia). If hypotension is prolonged, there may be severe renal tubular damage, leading to acute renal failure.

• The fall in blood pressure and the decreased O2-carrying power of the blood caused by the loss of red cells results in stimulation of the carotid and aortic chemoreceptors. This not only stimulates respiration but increases vasoconstrictor discharge. In severe hypovolemia, the pressure is so low that there is no longer any discharge from the carotid and aortic baroreceptors. This occurs when the mean blood pressure is about 70 mm Hg. Under these circumstances, if the afferent discharge from the chemoreceptors via the carotid sinus and vagus nerves is stopped, there is a paradoxic further fall in blood pressure rather than a rise.

• Hypovolemia causes a marked increase in the circulating levels of the pressor hormones angiotensin II, epinephrine, norepinephrine, and vasopressin. ACTH secretion is also increased, and angiotensin II and ACTH both cause an acute increase in aldosteronesecretion. The resulting retention of Na+ and water helps re-expand blood volume.

• Forms of Hypovolemic Shock• Hemorrhagic shock is probably the most carefully studied

form of shock because it is easily produced in experimental animals. With moderate hemorrhage (5–15 mL/kg body weight), pulse pressure is reduced but mean arterial pressure may remain normal. With more severe hemorrhage, blood pressure always falls.

• After hemorrhage, the plasma protein lost in shed blood is gradually replaced by hepatic synthesis, and the concentration of plasma proteins returns to normal in 3–4 days. The increase in circulating erythropoietin increases red blood cell formation, but it takes 4–8 weeks to restore red cell counts to normal.

Sympathetic Reflex Compensations in Shock-Their Special Value to Maintain

Arterial Pressure• The decrease in arterial pressure after

hemorrhage, as well as decreases in pressures in the pulmonary arteries and veins in the thorax, causes powerful sympathetic reflexes (initiated mainly by the arterial baroreceptorsand other vascular stretch receptors.

• These reflexes stimulate the sympathetic vasoconstrictor system in most tissues of the body, resulting in three important effects:

• (1) The arterioles constrict in most parts of the systemic circulation, thereby increasing the total peripheral resistance.

• (2) The veins and venous reservoirs constrict, thereby helping to maintain adequate venous return despite diminished blood volume.

• (3) Heart activity increases markedly, sometimes increasing the heart rate from the normal value of 72 beats/min to as high as 160 to 180 beats/min.

Protection of Coronary and Cerebral Blood Flow by the Reflexes

• A special value of the maintenance of normal arterial pressure even in the presence of decreasing cardiac output is protection of blood flow through the coronary and cerebral circulatory systems. The sympathetic stimulation does not cause significant constriction of either the cerebral or the cardiac vessels.

• In addition, in both vascular beds, local blood flow auto regulation is excellent, which prevents moderate decreases in arterial pressure from significantly decreasing their blood flows. Therefore, blood flow through the heart and brain is maintained essentially at normal levels as long as the arterial pressure does not fall below about 70 mm Hg, despite the fact that blood flow in some other areas of the body might be decreased to as little as one third to one quarter normal by this time because of vasoconstriction.

The factors that cause a person to recover from moderate degree of

shock• are all the negative feedback control mechanisms

of the circulation that attempt to return cardiac output and arterial pressure back to normal levels. They include the following:

1. Baroreceptor reflexes, which elicit powerful sympathetic stimulation of the circulation.

2. Central nervous system ischemic response,which elicits even more powerful sympathetic stimulation throughout the body but is not activated significantly until the arterial pressure falls below 50 mm Hg.

3. Reverse stress-relaxation of the circulatory system, which causes the blood vessels to contract around the diminished blood volume so that the blood volume that is available more adequately fills the circulation.

4. Increased secretion of renin by the kidneys and formation of angiotensin II, which constricts the peripheral arteries and also causes decreased output of water and salt by the kidneys, both of which help prevent progression of shock.

5. Increased secretion by the posterior pituitary gland of vasopressin (antidiuretic hormone),which constricts the peripheral arteries and veins and greatly increases water retention by the kidneys.

6. Increased secretion by the adrenal medulla of epinephrine and norepinephrine, which constricts the peripheral arteries and veins and increases the heart rate.

7. Compensatory mechanisms that return the blood volume back toward normal, including absorption of large quantities of fluid from the intestinal tract, absorption of fluid into the blood capillaries from the interstitial spaces of the body, conservation of water and salt by the kidneys, and increased thirst and increased appetite for salt, which make the person drink water and eat salty foods if able.

Progressive Shock/Vicious Circle and Cardiovascular Deterioration

• Cardiac Depression; When the arterial pressure falls low enough, coronary blood flow decreases below that required for adequate nutrition of the myocardium. This weakens the heart muscle and thereby decreases the cardiac output more. Thus, a positive feedback cycle has developed, whereby the shock becomes more and more severe.

• Vasomotor Failure -brain's vasomotor center depresses so much that it, too, becomes progressively less active and finally totally inactive. For instance, complete circulatory arrest to the brain causes, during the first 4 to 8 minutes, the most intense of all sympathetic discharges, but by the end of 10 to 15 minutes, the vasomotor center becomes so depressed that no further evidence of sympathetic discharge can be demonstrated. Fortunately, the vasomotor center usually does not fail in the early stages of shock if the arterial pressure remains above 30 mm Hg.

• Blockage of Very Small Vessels-"SludgedBlood." In time, blockage occurs in many of the very small blood vessels in the circulatory system and this also causes the shock to progress

• Increased Capillary Permeability After many hours of capillary hypoxia and lack of other nutrients, the permeability of the capillaries gradually increases, and large quantities of fluid begin to transude into the tissues

• Release of Toxins by Ischemic Tissue shock causes tissues to release toxic substances, such as histamine, serotonin, and tissue enzymes

• Traumatic shock develops when there is severe damage to muscle and bone. This is the type of shock seen in battle casualties and automobile accident victims. Bleeding into the injured areas is the principal cause of such shock. The amount of blood that can be lost into a site of injury that appears relatively minor is remarkable; the thigh muscles can accommodate 1 L of extravasatedblood, for example, with an increase in the diameter of the thigh of only 1 cm.

• Breakdown of skeletal muscle is a serious additional problem when shock is accompanied by extensive crushing of muscle (crush syndrome). When pressure on tissues is relieved and they are once again perfusedwith blood, free radicals are generated, which cause further tissue destruction (reperfusion-induced injury). Increased Ca2+ in damaged cells can reach toxic levels. Large amounts of K+ enter the circulation. Myoglobin and other products from reperfused tissue can accumulate in kidneys in which glomerularfiltration is already reduced by hypotension, and the tubules can become clogged, causing anuria.

• Surgical shock is due to combinations, in various proportions, of external hemorrhage, bleeding into injured tissues, and dehydration.

• In burn shock, there is loss of plasma from burn surfaces and the hematocrit rises rather than falls, producing severe hemoconcentration. There are, in addition, complex metabolic changes. For these reasons, plus the problems of easy infection of burned areas and kidney damage, the mortality rate when third-degree burns cover more than 75% of the body is close to 100%.

Distributive Shock

• In distributive shock, most of the symptoms and signs described previously are present. However, vasodilation causes the skin to be warm rather than cold and clammy.

• Anaphylactic shock is a good example of distributive shock. In this condition, an accelerated allergic reaction causes release of large amounts of histamine, producing marked vasodilation. Blood pressure falls because the size of the vascular system exceeds the amount of blood in it even though blood volume is normal.

• neurogenic shock, a sudden burst of autonomic activity results in vasodilation and pooling of blood in the veins. The resulting decrease in venous return reduces cardiac output and frequently produces fainting, or syncope, a sudden transient loss of consciousness. A common form is postural syncope, which occurs on rising from a sitting or lying position.

• This is common in patients taking drugs that block sympathetic discharge or its effects on the blood vessels. Falling to the horizontal position restores blood flow to the brain, and consciousness is regained. Pressure on the carotid sinus produced, for example, by a tight collar can cause sufficient bradycardia and hypotension to cause fainting (carotid sinus syncope).

• Fainting brought on by a variety of activities has been given appropriate names such as micturition syncope, cough syncope, deglutition syncope, and effort syncope

septic shock

• This is the most common cause of death in ICUs. It is a complex condition that includes elements of hypovolemic shock resulting from loss of plasma into the tissues ("third spacing") and cardiogenic shock resulting from toxins that depress the myocardium. It is associated with excess production of NO, and therapy with drugs that scavenge NO may be beneficial.

• The hallmark of septic shock is a decrease in peripheral vascular resistance that occurs despite increased levels of vasopressorcatecholamines. Before this vasodilatoryphase, many patients experience a period during which oxygen delivery to tissues is compromised by myocardial depression, hypovolemia, and other factors.

• During this "hypodynamic" period, the blood lactate concentration is elevated, and central venous oxygen saturation is low. Fluid administration is usually followed by the hyperdynamic, vasodilatory phase during which cardiac output is normal (or even high) and oxygen consumption is independent of oxygen delivery.

• The blood lactate level may be normal or increased, and normalization of the central venous oxygen saturation (SvO2) may reflect either improved oxygen delivery or left-to-right shunting.

VASODILATORS

• Prominent hypotensive molecules include nitric oxide, -endorphin, bradykinin, PAF, and prostacyclin.

• However, in clinical trials, neither a PAF receptor antagonist nor a bradykininantagonist improved survival rates among patients with septic shock, and a nitric oxide synthetase inhibitor, L-NG-methylarginine HCl, actually increased the mortality rate.

Severe Sepsis: A Single Pathogenesis?

• In some cases, circulating bacteria and their products almost certainly elicit multiorgandysfunction and hypotension by directly stimulating inflammatory responses within the vasculature. In patients with fulminantmeningococcemia, for example, mortality rates have correlated well with blood endotoxin levels and with the occurrence of DIC.

• In most patients with nosocomial infections, in contrast, circulating bacteria or bacterial molecules may reflect uncontrolled infection at a local tissue site and have little or no direct impact on distant organs; in these patients, inflammatory mediators or neural signals arising from the local site seem to be the key triggers for severe sepsis and septic shock

SITE OF SEPSIS Vs SEVERITY

• In a large series of patients with positive blood cultures, the risk of developing severe sepsis was strongly related to the site of primary infection: bacteremia arising from a pulmonary or abdominal source was eightfold more likely to be associated with severe sepsis than was bacteremic urinary tract infection, even after the investigators controlled for age, the kind of bacteria isolated from the blood, and other factors.

• Some of the typical causes of septic shock include the following:

• Peritonitis caused by spread of infection from the uterus and fallopian tubes, sometimes resulting from instrumental abortion performed under unsterile conditions.

• Peritonitis resulting from rupture of the gastrointestinal system, sometimes caused by intestinal disease and sometimes by wounds.

• Generalized bodily infection resulting from spread of a skin infection such as streptococcal or staphylococcal infection.

• Generalized gangrenous infection resulting specifically from gas gangrene bacilli, spreading first through peripheral tissues and finally by way of the blood to the internal organs, especially the liver.

• Infection spreading into the blood from the kidney or urinary tract, often caused by colon bacilli.

• A third pathogenesis may be represented by severe sepsis due to superantigen-producing Staphylococcus aureus or Streptococcus pyogenes, since the T cell activation induced by these toxins produces a cytokine profile that differs substantially from that elicited by gram-negative bacterial infection.

• In summary, the pathogenesis of severe sepsis may differ according to the infecting microbe, the ability of the host's innate defense mechanisms to sense it, the site of the primary infection, the presence or absence of immune defects, and the prior physiologic status of the host

• Genetic factors may also be important. For example, studies in different ethnic groups have identified associations between allelic polymorphisms in TLR4, caspase 12L, TNF-, and IFN- genes and the risk of developing severe sepsis.

Cardiogenic Shock

• When the pumping function of the heart is impaired to the point that blood flow to tissues is no longer adequate to meet resting metabolic demands, cardiogenic shockresults. This is most commonly due to extensive infarction of the left ventricle but can also be caused by other diseases that severely compromise ventricular function.

• The symptoms are those of hypovolemicshock plus congestion of the lungs and viscera resulting from failure of the heart to put out all the venous blood returned to it. Consequently, the condition is sometimes called "congested shock." The incidence of shock in patients with myocardial infarction is about 10%, and the mortality rate is 60–90%.

• Cardiogenic shock (CS) is characterized by systemic hypoperfusion due to severe depression of the cardiac index [<2.2 (L/min)/m2] and sustained systolic arterial hypotension (<90 mmHg), despite an elevated filling pressure [pulmonary capillary wedge pressure (PCWP) > 18 mmHg]. It is associated with in-hospital mortality rates >50%.

CAUSES

• Circulatory failure based on cardiac dysfunction may be caused by primary myocardial failure, most commonly secondary to acute myocardial infarction (MI), and less frequently by cardiomyopathy or myocarditisor cardiac tamponade.

• *Intrinsic causes:• Hearth muscle damage• Acute MI• CHF• Obstructive• Dysrhthmia• Valvular distruption

• *Extrinsic causes(cause obstructive shock):• Cardiac Tamponade• Tension Pneumothorax• *Symptoms and Signs• Cool, clammy, pale, cyanotic skin, BP drop, capillary refill.

Mechanisms of Cardiogenic and Obstructive ShockType Mechanism CauseObstructive Mechanical interference

with ventricular fillingTension pneumothorax, cava compression, cardiac tamponade, atrial tumor or clot

Interference with ventricular emptying

Pulmonary embolism

Cardiogenic Impaired myocardial contractility

Myocardial ischemia or MI, myocarditis, drugs

Abnormalities of cardiac rhythm

Tachycardia, bradycardia

Cardiac structural disorder

Acute mitral or aortic regurgitation, ruptured interventricular septum, prosthetic valve malfunction

• Etiologies of Cardiogenic Shock or Pulmonary Edema• Acute myocardial infarction/ischemia• LV failure• VSR• Papillary muscle/chordal rupture—severe MR• Ventricular free wall rupture with subacute

tamponade• Other conditions complicating large MIs• Hemorrhage• Infection•

• Excess negative inotropic or vasodilator medications

• Prior valvular heart disease

• Hyperglycemia/ketoacidosis

• Post-cardiac arrest

• Post-cardiotomy

• Refractory sustained tachyarrhythmias

• Acute fulminant myocarditis

• End-stage cardiomyopathy

• Left ventricular apical ballooning • Takotsubo cardiomyopathy• Hypertrophic cardiomyopathy with severe outflow

obstruction• Aortic dissection with aortic insufficiency or tamponade• Pulmonary embolus• Severe valvular heart disease• Critical aortic or mitral stenosis• Acute severe aortic or MR• Toxic-metabolic• Beta-blocker or calcium channel antagonist overdose

• Other Etiologies of Cardiogenic Shock

• RV failure due to:

• Acute myocardial infarction

• Acute co-pulmonale

• Refractory sustained bradyarrhythmias

• Pericardial tamponade

• Toxic/metabolic

• Severe acidosis, severe hypoxemia

Pathophysiology of cardiogenic shock.

• CS is characterized by a vicious circle in which depression of myocardial contractility, usually due to ischemia, results in reduced cardiac output and arterial pressure (BP), which result in hypoperfusion of the myocardium and further ischemia and depression of the cardiac output. Systolic myocardial dysfunction reduces stroke volume and, together with diastolic dysfunction, leads to elevated LV end-diastolic pressure and PCWP as well as to pulmonary congestion.

• Reduced coronary perfusion leads to worsening ischemia and progressive myocardial dysfunction and a rapid downward spiral, which, if uninterrupted, is often fatal. A systemic inflammatory response syndrome may accompany large infarctions and shock. Inflammatory cytokines, inducible nitric oxide synthase, and excess nitric oxide and peroxynitrite may contribute to the genesis of CS as they do to other forms of shock.

• Lactic acidosis from poor tissue perfusion and hypoxemia from pulmonary edema may result from pump failure and then contribute to the vicious circle by worsening myocardial ischemia and hypotension. Severe acidosis (pH < 7.25) reduces the efficacy of endogenous and exogenously administered catecholamines. Refractory sustained ventricular or atrial tachyarrhythmias can cause or exacerbate CS.

• Autopsy specimens often reflect the stuttering course and piecemeal necrosis of the LV, showing varying stages of infarction. Reinfarction is apparent as new areas of necrosis contiguous with or remote from a slightly older infarct. Infarctions that extend through the full myocardial thickness and result in rupture of the interventricularseptum, papillary muscle, or ventricular free wall may result in shock.

Obstructive Shock(extracardiac)

• The picture of congested shock is also seen in obstructive shock. Causes include massive pulmonary emboli, tension pneumothoraxwith kinking of the great veins, and bleeding into the pericardium with external pressure on the heart (cardiac tamponade).

• In the latter two conditions, prompt surgery is required to prevent death. Pulsus paradoxusoccurs in cardiac tamponade. Normally, blood pressure falls about 5 mm Hg during inspiration.

• In pulsus paradoxus, this response is exaggerated, and blood pressure falls 10 mm Hg or more as a result of increased pressure of the fluid in the pericardial sac on the external surface of the heart. However, pulsusparadoxus also occurs with labored respiration in severe asthma, emphysema, and upper airway obstruction.

Treatment:

* Aims

- Correct the cause

- Assist compensatory mechanism to restore an adequate level of tissue perfusion

* Volume resuscitation

- Enternal route

* Intervenous route

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• Cardiogenic shock is an emergency requiring immediate resuscitative therapy before shock irreversibly damages vital organs. The key to a good outcome in patients with cardiogenicshock is an organized approach, with rapid diagnosis and prompt initiation of pharmacologic therapy to maintain blood pressure and cardiac output.

• PROCEDURES:• Central venous line placement- ressussitation,

monitoring• Pulmonary artery catheter• Intraaortic baloon pump• Pci and CARBG- PCI or coronary artery bypass is the

treatment of choice for cardiogenic shock and that each has been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation.

• Thrombolytics

• Consultation with a cardiologist.

• echocardiographic support, placement of an intra-aortic balloon pump (IABP), and transfer to more definitive care (eg, cardiac catheterization suite, ICU, operating room). In severe cases, also consider discussing the case with a cardiothoracic surgeon.

• Pharmacotherapy

• Ionotropics augment coronary and cerebral blood flow (dopamine,bobutamine,norepinephrinemilrinone, inamrinone)

• Vasodilators decrease preload and afterload-nitroglyceride- This agent causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production

• Antiplatelets

• Analgesia-opiods decrease sympathetic stress and provide preload reduction.

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Irreversible Shock (complication) leads to:

• Renal failure

• Hepatic failure

• Multiple organ systems failure

• Adult respiratory distress syndrome

• Death

EFFECTS ON CO,PCWP AND SVR

Etiology CO PCWP SVR

cardiogenic decreased increased increased

hypovolemic decreased decreased increased

distributive increased decreased decreased

obstructive decreased Increased increased

REFERENCES

• Guyton and hall textbook of medical physiology

• Medical Physiology-Ganong

• Emedicine -http://emedicine.medscape.com/article/152191-overview

• Harrison internal medicine

• Merck Manuals