Chapter 11
The Cardiovascular System

Tests of Cardiovascular
Functioning
1-The Electrocardiogram
(ECG); is the measurement of the electrical currents of the heart.
There are three currents produced in the normal ECG:

P wave; atrial depolarization.

The QRS complex (beginning of Q wave to end of S wave); depolarization of the ventricles.

T wave corresponds to repolarization of the ventricles.

2-Measurement of Cardiac
Enzymes
When cardiac muscle cells die during a myocardial infarction
(MI), they release their intracellular contents. Specific proteins and enzymes normally present only inside cardiac cells

can be measured in the blood.
This allows one to accurately diagnose the existence and frequently the extent and the timing of the infarction.
Enzymes released with cardiac cell death include :

myocardial creatine kinase
(CK),

lactic acid dehydrogenase
(LDH), and

serum glutamic oxaloacetic transaminase (SGOT).
The plasma concentration of each of these enzymes varies depending on the time since

injury and the extent of the cell damage.
3-Stress Testing
In a simple exercise stress test, the patient is asked to either walk on a treadmill or ride an exercise bike.
The pattern of the ECG is observed for alterations in rhythm; AV blocks, and STsegment changes indicative of hypoxia . Onset of physical symptoms, such as chest pain and extreme shortness of breath, is monitored.

4-Echocardiography;
U ltrasound waves directed at the chest wall that are analyzed by a computer as they bounce back from the chest. The computer generates an image that is used to calculate the chambers, the performance of the valves, and the flow of blood through the heart .
This test is highly sensitive and non-invasive and provides a visual image of the beating heart.

6-Cardiac Catheterization
In cardiac catheterization, also called coronary angiogram , a flexible tube (catheter) is inserted through a peripheral vein (femoral or brachial) into the right side of the heart, or through a peripheral artery
(femoral or brachial) into the left side of the heart. Through the catheter, the chambers of the heart can be visualized and chamber pressures and oxygen content measured.

A radiolabeled dye may be injected through the catheter, and the ability of the dye to move through the heart chambers and vessels may be monitored using x-ray techniques. Valve movement can be observed. Because cardiac catheterization is invasive, complications are possible , including tearing of the vessel wall. After the procedure, patients must lie still for 4 to 6 hours until leg vessels seal.
7-Computed Tomography Scan

Patients are given a radiolabeled dye to highlight the blood vessels, and then are exposed to a series of x-rays that create images of the heart in slices.
8-Magnetic Resonance Imaging
(MRI) utilizes a powerful magnet that sets the nuclei of atoms in the heart cells vibrating at specific, recognized frequencies. MRI is noninvasive and very sensitive, but cannot be used on patients with

pacemakers or metal implants such as stents.
Pathophysiologic Concepts
1-Thrombus
A thrombus is a blood clot that can develop anywhere in the vascular system, so blood flow is reduced or totally blocked. A thrombus can develop from any injury to the vessel.

Thrombus formation can occur when:
 blood flow through a vessel is sluggish ( venous side of the circulation)and

when blood flow is irregular ( irregular heartbeat or cardiac arrest).
2-Embolus
An embolus is a substance that travels in the bloodstream from

a primary site to a secondary site.
Types of embolism:
 blood clots
(thromboemboli)
 fat( released during the break of a long bone)
 amniotic fluid ,
 a ir and

displaced tumor cells .
Usually emboli are trapped in the first capillary network they encounter .
Venous thromboemboli, can become trapped in the coronary vessels or any of the organs

downstream, including the brain, kidneys, and lower extremities.
3-Aneurysm
An aneurysm is a dilation of the arterial wall caused by:
a congenital or atherosclerosis or infection or trauma.

Aneurysms may burst with increased pressure, leading to massive internal hemorrhage.
4- Valvular Stenosis
Stenosis of any valve usually occurs as a result of a congenital defect or an inflammatory process (e.g., after rheumatic fever).

Extra work lead to hypertrophy
(increase in size). so increases its oxygen consumption and energy demands.
5- Valve Incompetenc
Any of the cardiac valves may be incompetent. Each chamber may hypertrophy.
6-Cardiac Shunts
A shunt is a connection between the pulmonary and the

systemic circulations. After birth, any shunting is abnormal.
Blood will flow in the direction of least resistance.
*Right to Left Shunt
A right-to-left shunt delivers poorly oxygenated blood to the systemic circulation.
It is called a cyanotic shunt because it causes bluish tinge to the skin .
Fatigue results and

tachypnea . Clubbing of fingers may occur related to poor tissue perfusion.
*Left to Right Shunt
This shunt is acyanotic.
Well-oxygenated blood is directed to the right side of the heart and recirculates to the left atrium and left ventricle..


A left-to-right shunt lead to hypertrophy of pulmonary vasculature and right heart failure may develop.
 left heart failure may develop because of continual recycling of blood back into the left side of the heart from the lungs.

Conditions of Disease or
Injury
1-Atherosclerosis (hardening of the arteries), is characterized by accumulation of fatty deposits, platelets, neutrophils, monocytes and macrophages throughout the tunica intima
(endothelial cell layer) and eventually into the tunica media
(smooth muscle layer).

Arteries most often affected include the coronaries, the aorta, and the cerebral arteries.

It leads to a decrease in the diameter of the artery. The atherosclerotic area of an artery is called a plaque.
Causes of Atherosclerosis
Four hypotheses are presented.
- High Serum Cholesterol and circulating triglycerides
- High Blood Pressure
- Infection
- High Blood Iron Levels
Clinical Manifestations
- Intermittent claudicating, an aching, cramping feeling in the

lower extremities due to muscle ischemia
- Cold sensitivity occurs with inadequate blood flow to the extremities.
- The area becomes pale.
- Reduced arterial pulses
- Cell necrosis and gangrene may develop.
Diagnostic Tools
- Elevated cholesterol and triglyceride levels .Cholesterol levels >180 mg/dL of blood are considered elevated, and the

individual is considered especially at risk of coronary artery disease.
- coronary or carotid artery CT, ultrasound, or MRI.
Complications
- HTN
- Stroke
- MI
- Development of an aneurysm.
Treatment
- Diet modification can lower
LDL and improve HDL levels.

High-fiber foods (fruits, vegetables, whole grains), fatty fish (omega 3 fatty acids), and garlic have been shown to lower LDL cholesterol.
- Drug therapy is frequently used to lower total cholesterol and triglyceride levels and improve HDL.
Aspirin or anti-clotting drugs reduce risk of thrombus formation.
- A well-planned exercise program may reduce LDL, increase HDL and lower body weight. Exercise may also

stimulate development of collateral vessels around occluded sites.
- Good control of plasma glucose level is essential in diabetic patients.
- Cessation of smoking
2-Hypertension

Hypertension is abnormally high blood pressure measured on at least 3 different occasions from a person who has been at rest at least 5 minutes.

Normal Bp: 90/60 140/90 mmHg


Optimal pressures are considered less than 120 mmHg systolic and 80 mmHg diastolic, while pressures considered hypertensive are >140 / 90 mmHg.

A state of prehypertension includes blood pressures between 120 and 139 mmHg systolic and 80 and 89 mmHg diastolic.
Causes of Hypertension
- Increase in heart rate, stroke volume, and peripheral resistance

- increase in plasma volume may occur as a result of renal mishandling of salt and water, or it may result from excess salt consumption.
- increased sympathetic nervous system activity.
Types of Hypertension
- primary or essential hypertension :no known cause
- Secondary Hypertension: clear cause is present
- renal vascular hypertension, as a result of renal artery stenosis
(congenital or from atherosclerosis).

Reduced blood flow to the kidney, leads to stimulation of renin release, and production of angiotensin II which increases blood pressure . If repair of the stenosis is possible or the affected kidney is removed, blood pressure returns to normal.
- pheochromocytoma, an epinephrine-secreting tumor of the adrenal gland, which causes increased heart rate and stroke volume

- Cushing's disease, which causes increased stroke volume from salt retention
- primary aldosteronism
(increased aldosterone with no known cause)
- oral contraceptives may also cause secondary hypertension.
Clinical Manifestations
Occur after years of hypertension, and include:
- Waking headache, sometimes with nausea and vomiting.
- Blurred vision caused by hypertensive damage to the retina.

- Unsteadiness in the gait caused by central nervous system damage.
- Nocturia caused by increased renal blood flow and glomerular filtration.
- Dependent edema and swelling caused by increased capillary pressure.
Diagnostic Tools
Diagnostic measurement of blood pressure
Complications
- Stroke
- A myocardial infarct (MI)

- Renal failure -
Encephalopathy (brain damage)
Treatment
- lowering heart rate, stroke volume, or peripheral resistance.
- weight loss
- exercise, especially coupled with weight loss.
- stopping smoking
- diuretics act by causing the kidney to increase its excretion of salt and water.
- angiotensin II converting enzyme inhibitors (ACEI).

3-Raynaud's Disease

It is temporary spasm of the small arteries and arterioles, usually in the fingers or, less frequently, the toes.

Spasm leads to tissue hypoxia, which is characterized by pallor
(whiteness) or cyanosis
(bluish tinge) of the digits, followed by rubor (redness) as the local mechanisms of vasodilatation take over.

The cause of Raynaud's disease is unknown, but is

usually seen in young women in response to cold exposure.
Clinical Manifestations
Color changes of the digits with cold exposure.
Numbness of the digits, then tingling and pain as the episode ends.
Diagnostic Tools
A good physical examination and history will assist diagnosis.
Complications
- Gangrene may occur if episodes are extensive.

Treatment
Avoid unnecessary exposure to the cold.
4-Varicose veins
Veins are tortuous (twisted) distended veins occurring where blood has pooled, often in the legs.
Causes:
- long episodes of standing without muscle contraction
- valve incompetence
(weakness)
- obesity
- pregnancy.

Clinical Manifestations
Bulging, distended veins, showing prominent bluish streaks and pools in the legs.
Diagnostic Tools
Physical examination and family history will assist diagnosis.
Complications
- Blood clotting
- Chronic venous insufficiency
- Edema in the feet and ankles .
Treatment
- Weight reduction.
- Elevation of the legs

- Avoidance of tight-fitting clothes at the top of the legs or waist.
- Elastic support hose for the lower legs to compress the veins.
- Walking and exercise to increase muscle strength
- Surgical stripping of the veins or cauterization may be performed.
5-Angina Pectoris
Angina pectoris is severe pain due to an inadequate oxygen supply to the myocardial cells.
The pain may radiate down the

left arm, to the back, to the jaw, or into the abdominal area.
If the coronary arteries are narrowed with atherosclerosis and cannot dilate, ischemia occurs, and the myocardial cells begin to use anaerobic glycolysis and results in the production of lactic acid. Lactic acid decreases myocardial pH and causes the pain associated with angina pectoris.
With rest, cells revert to oxidative phosphorylation for energy production. With removal of the lactic acid, the

pain of angina goes away.
Angina pectoris is therefore a short-lived experience.
Types of Angina
There are three types of angina: stable, Prinzmetal's (variant), and unstable.
- Stable angina , also called classic angina, occurs when atherosclerotic coronary arteries cannot dilate to increase flow when oxygen demand is increased.
Increased work ,e xposure to the cold , and m ental stress may trigger classic angina.

The pain of stable angina typically goes away when the individual stops the activity.
- Prinzmetal's(variant ) angina occurs during rest or sleep. A coronary artery undergoes a spasm, causing cardiac ischemia to occur It may be related to atherosclerosis.
- Unstable angina is a combination of classic and variant angina, and is seen in an individual with worsening coronary artery disease.

Clinical Manifestations
- Constricting or squeezing pain in the pericardial or substernal area of the chest, possibly radiating to the arms, jaw, or thorax.
- In stable and unstable angina, pain is typically relieved by rest.
- In Prinzmetal's angina,pain is unrelieved by rest but usually disappears in about 5 minutes.
Diagnostic Tools
- Alteration in the ST segment of the ECG may occur.

- Areas of reduced blood flow may be observed using radioactive imaging .
- Cardiac enzymes and proteins may be measured to rule out
MI.
Treatment
- Prevention: Aspirin , avoid stressors as working in the cold, stopping smoking
- The atherosclerotic vessel is dilated by a catheter or inflated balloon.
- Bypass surgery, the diseased piece of a coronary artery is tied off, and an artery or vein (

saphenous vein and the internal mammary artery) is connected to nondamaged areas
- Placing artificial tubes, or stents, into the artery to keep it open
- Reducing energy demands:
- Nitroglycerin and other nitrates act as potent dilators of the venous system, decreasing venous return of blood to the heart. Dilation of a coronary artery also may occur with nitrates.
- Oxygen therapy eases demands on the heart.

6-Myocardial Infarction
Myocardial infarction (MI) is the death of myocardial cells that occurs following prolonged oxygen deprivation. Myocardial cells begin to die after about 20 minutes of oxygen deprivation.
After this period, the ability of the cells to produce ATP aerobically is exhausted, and the cells fail to meet their energy demands.
With the death of muscle cells and changes in the heart's electrical patterns, the heart begins to pump in a less

coordinated manner, causing contractility to decrease. Stroke volume falls, causing a fall in systemic blood pressure.
Causes of Myocardial Infarct
- long-standing coronary artery disease (CAD).
- large thrombus that totally obstruct blood flow.
- hypertrophied chambers with relative oxygen deficiency
Risk factors for developing
CAD and/or MI include a positive family history , hypertension ,

hypercholesterolemia, obesity, smoking, and diabetes .
Clinical Manifestations
Some individuals do not show any obvious signs of an MI (a silent heart attack),
However, significant clinical manifestations usually occur:
- Abrupt (usually) onset of pain, often radiates to the left arm, neck, or jaw.
- Nitrates and rest might relieve ischemia without relieving the pain of infarct completely.

- Nausea and vomiting, probably related to intense pain, are common.
- Feelings of weakness related to decreased blood flow to the skeletal muscles .
- The skin becomes cool, clammy, and pale due to sympathetic vasoconstriction.
- Urine output decreases related to decreased renal blood flow
- Tachycardia develops, due to increased cardiac sympathetic stimulation and anxiety.
Diagnostic Tools

- A good history and physical, including family history of heart disease
- Blood pressure may be decreased or normal
- Heart rate is usually increased.
- The ECG may show acute changes with elevation in the
ST segment and T wave inversion. Within 1 or 2 days of the infarct, deepening of the Q wave occurs. Although the ST and T wave changes will disappear over time, the Q wave changes remain and can be used to detect a past infarct.

- Systemic signs of inflammation occur, including fever, elevated number of leukocytes, and increased sedimentation rate. These signs begin about 24 hours after the infarct and continue for up to 2 weeks.
- Cardiac enzyme levels
(creatinine phosphokinase, serum glutamic oxaloacetic transaminase, and lactic dehydrogenase) in the serum increase as a result of myocardial cell death.
Complications

-Thromboemboli zation
-
Congestive heart failure .
- Cardiogenic shock (collapse of blood pressure).
- Myocardial rupture may occur after a large infarct. -
Pericarditis.
Treatment
-Prevention of heart disease is vital. Moderate levels of exercise (including walking), cessation of smoking, and moderate limitation of dietary fat)

- For a patient with acute coronary syndrome, the following treatment guidelines, using the acronym ABCDE, have been proposed:
A for antiplatelet therapy, anticoagulation,
B for beta-blockade and blood pressure control
C for cholesterol treatment and cigarette smoking cessation
D for diabetes management and diet
E for exercise.
7-Heart Failure

Heart failure occurs when the heart is unable to pump enough blood out to meet the oxygen and nutrient demands of the body.
Causes of Heart Failure
- Noncardiac causes such as long-standing systemic or pulmonary hypertension , kidney failure or water intoxication.
- Cardiac causes include myocardial infarct, valvular defects, and congenital malformation.

Clinical Manifestations
Clinical manifestations of heart failure are often separated into forward and backward effects:
Forward Effects of Left Heart
Failure
- Decreased systemic blood pressure -
Fatigue
- Increased heart rate
-
Decreased urine output
Backward Effects of Left
Heart Failure

- Increased pulmonary congestion, especially when lying down
- Dyspnea (difficult breathing)
- Right heart failure if the condition worsens
Forward Effects of Right
Heart Failure
- Decreased pulmonary blood flow - Decreased blood oxygenation
- Fatigue
- Decreased systemic blood pressure
- all the signs of left heart failure

Backward Effects of Right
Heart Failure
- Increased venous pooling of blood, edema of the ankles and feet
- Jugular venous distension
- Hepatomegaly and splenomegaly
Diagnostic Tools
- Radiological identification of pulmonary congestion and ventricular enlargement may indicate heart failure.
- MRI or ultrasound
Treatment

-Beta blockers and angiotensinconverting enzyme (ACE) inhibitors as the most effective therapies for heart failure .
- Oxygen therapy may be used to reduce the demands of the heart.
- Nitrates may be administered .
- Digoxin (digitalis) may be administered to increase contractility.
8-Rheumatic fever
Rheumatic fever is a serious inflammatory disease that may occur in an individual 1 to 4 weeks

following an untreated throat infection by the group A betahemolytic Streptococcus bacteria.
The acute condition is characterized by fever and inflammation of the joints, heart, nervous system, and skin.
In some cases, it can permanently affect the structure
and function of the heart, especially the heart valves .
Rheumatic fever is preventable with prompt antibiotic therapy.
Rheumatic fever can occur at any age, but mainly affects

children between the ages of 5 and 15.
Rheumatic Heart Disease
Approximately 10% of individuals who acquire rheumatic fever develop rheumatic heart disease.
Rheumatic heart disease is the major cause of acquired cardiac valve disease. The attack against self-antigens is likely related to an antigenic similarity between cardiac valves and antigens of the group A betahemolytic streptococcus.
Immune attack can occur

against any of the four cardiac valves, but is usually seen against the mitral and aortic valves.The course of rheumatic heart disease can be separated into acute and chronic stages .
In the acute stage , the valves become swollen and red as the inflammatory reaction begins.
Lesions may develop on the valve leaflets. As the acute inflammation subsides, scar tissue develops. Scar tissue may deform the valves and, in some cases, cause the leaflets to fuse together, narrowing the orifice.

A chronic stage of the disease may follow, characterized by repeated inflammation and continued scarring..
9- Mitral Valve Stenosis
Mitral valve stenosis is a narrowing in the opening of the valve between the left atrium and the left ventricle. Mitral valve stenosis usually follow rheumatic fever or another cardiac infection. It may also result from a congenital defect in valve structure.
Clinical Manifestations

-May be absent or severe, depending on the level of stenosis.
- Pulmonary congestion, with signs of dyspnea and pulmonary hypertension, may occur.
- Dizziness and fatigue due to decreased left ventricular output may occur.
Diagnostic Tools
A low-pitched murmur may be present during ventricular filling (diastole) .
Echocardiography .

Complications : Left atrial hypertrophy
Treatment : -Treatment for congestive heart failure may be required.
- Valve replacement or surgical correction of the stenosis may be attempted.
10-Aortic valve stenosis
Aortic valve stenosis is a narrowing in the opening of the valve between the left ventricle and the aorta. Like mitral valve stenosis, aortic stenosis usually follows rheumatic fever or is a congenital malformation.

Clinical Manifestations
- Clinical manifestations may be absent or severe, depending on the level of stenosis.
- Pulmonary congestion, with signs of dyspnea and pulmonary hypertension.
- Dizziness and fatigue may occur due to decreased cardiac output
Diagnostic Tools
- A systolic heart murmur may be heard as blood rushes through the narrow orifice.
- Echocardiography .
Complications

Left ventricular hypertrophy may develop, leading to congestive heart failure.
Treatment
- Treatment for congestive heart failure may be required.
- Valve replacement or surgical correction of the stenosis may be attempted.
11- Pulmonary Valve Stenosis
Pulmonary valve stenosis is a narrowing of the opening between the right ventricle and the pulmonary valve.
Pulmonary valve stenosis most

commonly occurs due to a congenital defect.
Clinical Manifestations
- Clinical manifestations may be absent or severe depending on the level of stenosis.
- Decreased pulmonary flow causes weakness and fatigue.
- Venous distention and swelling of the ankles and feet are common.
Diagnostic Tools
- Echocardiography may be used to diagnose abnormal valve structure and motion.
Complications

- Right heart hypertrophy and subsequent right heart failure may occur.
Treatment
- Treatment for heart failure may be required.
- Valve replacement or surgical correction of the stenosis may be attempted.
12-Mitral Valve
Regurgitation
Usually caused by rheumatic fever or another bacterial infection of the heart.With mitral valve regurgitation, some blood returns to the left atrium

as the left ventricle contracts.
Chronic dilation and filling of the ventricle and the atrium occur, leading to hypertrophy and, potentially, congestive heart failure. Blood backing into the pulmonary circulation causes pulmonary congestion and pulmonary hypertension.
Clinical Manifestations
- Clinical manifestations may be absent or severe, depending on the level of stenosis.
- Pulmonary congestion, with signs of dyspnea and pulmonary hypertension.

- Decreased cardiac output may cause dizziness and fatigue.
Diagnostic Tools
- A systolic heart murmur may be heard as blood is pushed through the orifice.
- Echocardiography .
Complications
-Left ventricular and left atrial hypertrophy may develop, leading to congestive heart failure.
Treatment
- Treatment for congestive heart failure may be required.

- Valve replacement or surgical correction of the incompetent valve may be attempted.
13-Aortic Valve
Regurgitation
Usually follows rheumatic fever. With blood flowing backward into the left ventricle during diastole, diastolic pressure in the aorta is reduced.
A reduction in diastolic pressure in the aorta leads to a characteristic increase in the pulse pressure = the difference between the measured systolic and diastolic pressures. Aortic

valve regurgitation leads to hypertrophy of the left ventricle, which can cause the development of congestive heart failure.
Clinical Manifestations
- A wide pulse pressure can be measured.
- Hyperkinetic (very strongly bounding) peripheral and carotid pulsations are typically present.
- Symptoms of heart failure may develop.
Diagnostic Tools

- A high-pitched diastolic heart murmur is frequently heard.
- Echocardiography .
Treatment
- Treatment for congestive heart failure may be required.
- Valve replacement or surgical correction of the incompetent valve may be attempted.
14-Congenital Heart Defects
Congenital heart defects involve abnormal shunting between the left and right sides of the heart or between the aorta and pulmonary artery.

Types of Congenital Heart
Defects
Defects may involve the atria, the ventricles, any of the valves, or the great arteries.
Atrial Septal Defect
An atrial septal defect (ASD) is an abnormal opening between the left and right atria. It is a congenital disorder that occurs when the foramen ovale fails to close after birth, or when another opening between the left and right atria is present due to improper closure of the wall

between the two atria during gestation.
Ventricular Septal Defect(VSD)
Is an abnormal opening between the left and right ventricles that occurs when the wall between the ventricles fails to close properly during gestation. VSD is the most common cardiac congenital defect. The size of the defect determines the severity of the symptoms.
Patent Ductus Arteriosus (PDA)
Occurs when the ductus arteriosus, the connection

between the pulmonary artery and the aorta, remains open after birth. Normally, the ductus closes soon after birth as a result of increased oxygenation in the pulmonary circulation. If the ductus does not close, blood will shunt between the two main arteries.
Coarctation of the Aorta
Coarctation of the aorta is a congenital defect that results in the narrowing of the aorta as it leaves the left ventricle. The narrowing can be proximal or distal to the ductus arteriosus.

Tetralogy of Fallot
Tetralogy of Fallot is a congenital heart defect characterized by four presenting abnormalities: ventricular septal defect , pulmonary artery stenosis , right ventricular hypertrophy , and a shifting of the position of the aorta so that it opens into the right ventricle (an overriding aorta). Tetralogy of Fallot is a cyanotic defect.
15-Shock
Shock is the collapse of systemic arterial blood

pressure. With a severe fall in blood pressure, blood flow does not adequately meet the energy demands of tissues and organs.
Causes of Shock
There are six major causes of shock.
- Cardiogenic shock can occur following collapse of the cardiac output, which often results from a myocardial infarct, fibrillation, or congestive heart failure.
- Hypovolemic shock can occur if there is a loss of circulating blood volume, causing a severe

drop in cardiac output and blood pressure. Hemorrhage and dehydration can cause hypovolemic shock.
- Anaphylactic shock can occur following a widespread allergic response associated with mast cell degranulation and the release of inflammatory mediators, such as histamine and prostaglandin. These inflammatory mediators cause widespread systemic vasodilatation and edema.
- Septic shock can occur following a massive systemic

infection and the subsequent release of vasoactive mediators of inflammation. These substances initiate widespread vasodilation and edema. Septic shock may occur with a bloodborne bacterial infection or result from the release of gut contents, for example, with gastrointestinal perforation or a burst appendix.
- Neurogenic shock occurs following sudden loss of vascular tone from an injury to the cardiovascular center of the brain, a spinal cord injury, or

deep general anesthesia. This type of occurrence may explain sudden fainting during a severe emotional disturbance.
- Burn shock occurs following a severe burn involving a substantial amount of total body surface area.
Clinical Manifestations
Specific manifestations will depend on the cause of shock, but all, except neurogenic shock, will include the following:
- Cool, clammy skin. -
Pallor.

- Increased heart and respiratory rate.
- Dramatically decreased blood pressure.
Individuals with neurogenic shock will have a normal or slow heart rate, and will be warm and dry to the touch.
Diagnostic Tools
- A measured severe decrease in blood pressure.
- Decreased or absent urine output.
Complications
- Tissue hypoxia, cell death, and multi-organ failure

following a prolonged decrease in blood flow.
Treatment
- The cause of shock must be identified and reversed if possible.
- Plasma volume replacement is essential, except with cardiogenic shock. What is used for replacement depends on the cause of shock.
- Supplemental oxygen or artificial ventilation may be required.

- Vasopressor agents are given in order to return blood pressure toward normal.