Chapter 11The Cardiovascular System

Tests of Cardiovascular Functioning1-The Electrocardiogram (ECG) • Is the measurement of the electrical currents of the heart.

Contraction of the atria and ventricles results from action potentials occurring simultaneously in all muscle cells of the atria, followed by all muscle cells of the ventricles.

• There are three currents produced in the normal ECG: -the P wave corresponds to atrial depolarization. -The QRS complex (beginning of Q wave to end of S wave)

corresponds to depolarization of the ventricles. -The T wave corresponds to repolarization of the ventricles.

2-Measurement of Cardiac EnzymesWhen cardiac muscle cells die during a myocardial

infarct (MI), they release their intracellular contents. Specific proteins and enzymes normally present only inside cardiac cells can be measured in the blood. Their plasma concentration allows one to accurately diagnose the existence , the extent and the timing of the infarct .

• Enzymes released with cardiac cell death include : -myocardial creatine kinase (CK), - lactic acid dehydrogenase (LDH), and - serum glutamic oxaloacetic transaminase (SGOT).

3-Stress Testing 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, the presence of AV blocks, and evidence of ST-segment changes indicative of hypoxia.

- Onset of physical symptoms, such as chest pain and extreme shortness of breath, is monitored.

4-Echocardiography• Echocardiography involves ultrasound 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 size and movement of the heart 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.

5-Cardiac Catheterization (coronary angiogram)A flexible tube (catheter) is inserted through a peripheral vein (femoral or brachial) into the right side or through a peripheral artery (femoral or brachial) into the left side. The chambers of the heart can be visualized and chamber pressures and oxygen content measured. A radiolabeled dye may be injected through it, so the heart chambers and vessels may be monitored using x-ray techniques. Valve movement can be observed. Because it 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.

6-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.

7-Magnetic Resonance Imaging 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 non-invasive and very sensitive, - but cannot be used on patients with

pacemakers or metal implants such as stents.

Pathopysiologic concepts1-Thrombus It is a blood clot that can develop anywhere in the

vascular system(unbroken blood vessel), so blood flow is reduced or totally blocked.

A thrombus can develop : - from any injury to the vessel wall ,because

endothelial cell injury draws platelets and clotting factors to the area.

- 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.Most emboli are :-blood clots (thromboemboli) usually from deep leg

veins. -fat( released during the break of a long bone) -amniotic fluid, -air and -displaced tumor cells. Usually emboli are trapped in the first capillary

network they encounter.

3-Aneurysm An aneurysm is a dilation of the arterial wall caused

by a congenital or commonly, from atherosclerosis or may develop as a result of an 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 leads to hypertrophy (increase in size) of the heart, so increases its oxygen consumption and energy demands.

5-Valve Incompetence 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 delivers poorly oxygenated blood to the systemic circulation.

It is called a cyanotic shunt because it causes bluish tinge to the skin .It leads to:

-Fatigue -increased respiratory rate . -Clubbing of fingers 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 leads to hypertrophy of pulmonary vasculature and right heart failure may develop .

-In addition, 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 or 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).

It leads to a decrease in the diameter of the artery. The atherosclerotic area of an artery is called a plaque.

Arteries most often affected include the coronaries, the aorta, and the cerebral arteries .

Causes of Atherosclerosis :Four hypotheses are presented. - High Serum Cholesterol and circulating triglycerides. - High Blood Pressure. - Infection. - High Blood Iron Level. Clinical Manifestations - Intermittent claudication, an aching, cramping feeling in the lower

extremities due to muscle ischemia. - Cold sensitivity due to 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 higher

than 180 mg/dL of blood are considered elevated. - Identifying or monitoring atherosclerosis may be done using coronary or

carotid artery CT, ultrasound, or MRI.

Complications - Hypertension - 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.

- Drugs are 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 Is high blood pressure measured on at least three different

occasions from a person who has been at rest at least 5 minutes. Optimal pressures are considered less than 120 mmHg systolic

and 80 mmHg diastolic, while pressures considered hypertensive are higher than 140 mmHg systolic, and higher than 90 mmHg diastolic.

A state of prehypertension is 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 as: a - renal vascular hypertension: renal artery stenosis,

(congenital or a result of atherosclerosis)leads to 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.

b- pheochromocytoma, an epinephrine-secreting tumor of the adrenal gland causes increased heart rate and stroke volume.

c - Cushing's disease, which causes increased stroke volume from salt retention.

d - primary aldosteronism (increased aldosterone with no known cause).

e- oral contraceptives .

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 (ACE

inhibitors) .

3-Raynaud's Disease It is temporary spasm ( unknown cause) 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.

-It 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.

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 AnginaThere are three types of angina:• - Stable angina, also called classic angina, occurs when

atherosclerotic coronary arteries cannot dilate to increase flow when oxygen demand is increased. Increased work ,exposure to the cold, and mental 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 .

• - 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 (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), - 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. - 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 family history of heart disease may be present.• - 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• -Thromboembolization • - 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 angiotensin-converting 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 Is a serious inflammatory disease that may occur in an

individual 1 to 4 weeks following an untreated throat infection by the group A beta-hemolytic 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. It is the major cause of acquired cardiac valve disease.

Immune attack can occur against any of the four cardiac valves due to antigenic similarity between it and that bacteria, but is usually seen against the mitral and aortic valves.

The course can be separated into acute and chronic: -In the acute stage, the valves become swollen and red

and scar tissue develops. Scar tissue cause the leaflets to fuse together, narrowing the orifice.

- A chronic stage may follow, characterized by repeated inflammation and continued scarring.

9- Mitral Valve Stenosis Is a narrowing in the opening of the mitral valve ,

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 is a narrowing in the opening of the aortic valve.

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 Is a narrowing of the opening of the pulmonary

valve. It 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 .

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 .Blood

backing into the pulmonary circulation causes pulmonary congestion and pulmonary hypertension.

Clinical Manifestations Clinical manifestations may be absent or severe: - 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.

Defects may involve the atria, the ventricles, any of the valves, or the great arteries.

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 : follow collapse of the cardiac output, which often results from a myocardial infarct, fibrillation, or CHF. .

• Hypovolemic shock follow a loss of circulating blood volume (Hemorrhage and dehydration ),

causing a severe drop in cardiac output and blood pressure • - Anaphylactic shock follow a widespread

allergic response associated with mast cell degranulation and the release of histamine and prostaglandin. These inflammatory mediators cause widespread systemic vasodilatation and edema.

• Septic shock follow a massive systemic infection and the release of vasoactive mediators of inflammation that initiate widespread vasodilation and edema. Septic shock may occur with a blood-borne 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 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 of shock 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.