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Cardiovascular Disorders Study Guide

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Describe 4 general treatment measures for cardiac measures:
Dietary modification
exercise program
stop smoking
drug therapy
Give 9 risk factors for developing atherosclerosis. Which ones are modifiable and which ones aren't?
Age-can't be changed
Gender- can't be changed
genetics-can't be changed
obesity-modifiable
cigarette smoking-modifiable
sedentary lifestyle-modifiable
diabetes mellitus-modifiable
poorly controlled htn-modifiable
oral contraceptives & smoking in combo-modifiable
high cholesterol and htn-modifiable
Describe the process of atheroma formation from the initial fatty streaks in the arterial wall intima to a complicated plaque:
-endothelial injury in the artery often at a young age
-inflammation and elevation of C reactive protein
-laccumulation of white blood cells especially monocytes and macrophages
-lipid accumulates in the intima or inner lining of the artery and media or muscle layer
-a plaque forms and inflammation persists
-platelets adhere to damaged surface, forming a thrombus and partial obstruction
-continued lipid buildup at the site of injury along with fibrous tissue (atheroma)
-platelets adhere, prostaglandins release, causing further inflammation and vasospasm
-process continues with larger thrombus formation and potential total occlusion and possibility of embolism
Describe the significance of plaque formation, including five potential complications of atherosclerosis:
Development of atheromatous plaques narrows the lumen of arteries, restricting flow, causing turbulence, thromus formation,and potential embolism. The atheroma also damages the arterial wall, weakening the structure and decreasing elasticity, and ultimately may calcify, causing further rigidity.Complications include thrombus formation with partial angina or total occlusion, and precipitation a MI, embolism and infarction (stroke and peripheral vascular damage), aneurysm, or rupture and hemorrhage
Which vessels are affected by artherosclerosis?
Primarily large arteries particularly at bifurcations--aorta, coronary, iliac, carotids
Describe common therapeutic interventions, to include lifestyle changes, used in the treatment of atherosclerosis:
1. Maintain weight at healthy levels to reduce the risk of metabolic syndrome, htn, and atherosclerosis
2. lower serum cholesterol and LDL in diet by reducing the intake of saturated fats and using unsaturated veggie oils; high dietary fiber intake also decreases LDL
3. sodium intake minimized for control of hypertension
4. control of primary disorders such as diabetes and htn
5. stop smoking
6. exercise appropriate for age and health status to promote collateral circulation and reduce LDL levels
7. oral anticoagulant therapy in case of thrombus formation concern
8. surgical intervention
why would you prescribe antilipidemics or lipid lowering drugs?
lower cholesterol and LDL levels
why would you prescribe platelet inhibitors?
lower platelet aggregation leading to a lower chance of thrombosis and thus leading to a lower chance of heart attack and stroke
why would you prescribe anticoagulants?
interfere with clotting factor synthesis (warfarin) or inhibit thrombin formation (heparin), leading to a lower chance of thrombosis and a lower chance of heart attacks and strokes
why would you prescribe antihypertensives?
help decrease cardiac workload
what type of surgical interventions can be used in advanced atheromas?
Percutaneous transluminal coronary angiplasty (PTCA)
Coronary artery bypass grafting
Laser Angioplasty
Define Angina Pectoris:
Chest Pain
What is the underlying pathology involved in angina pectoris?
when there is decreased blood supply (oxygen) to the heart due to either arterial obstruction or spasm OR
when there is increased demand for oxygen by the heart OR
when there is a combination of factors
Identify disorders that may cause or predispose an individual to angina:
atherosclerosis
arteriosclerosis
vasospasm
myocardial hypertrophy
severe anemias
respiratory disease
what is the most serious complication of angina pectoris?
myocardial infarction
Why does smoking cause an attack in an individual with history of angina?
smoke causes vasoconstriction, leading to increased venous return and increased heart rate
Why does going from a warm environment into the cold cause an attack in an individual with a history of angina?
vasoconstriction, leading to increased venous return and increased heart rate
Why does engaging in an argument or other stressful behavior cause an attack in an individual with a history of angina?
sympathetic stimulation increases heart rate
Why does exercise (like climbing stairs or rushing to catch bus) cause an attack in an individual with a history of angina?
increases heart rate due to increased O2 demands
Describe the classic manifestations of an anginal attack. What is the usual duration of an anginal attack?
The classic manifestations are recurrent, intermittent brief episodes of substernal chest pain, described as tightness or pressure that may radiate to the neck or left arm. An anginal attack usually lasts a few seconds or minutes
What type of drug is used to treat an anginal attack? How do these drugs relieve chest pain?
Coronary vasodilators, such as nitroglycerine, which act by reducing systemic resistance, thus decrease the demand for oxygen. Some vasodilators also relieve arterial vasospasm. Nitroglycerin has an immediate onset of action
In an emergency angina attack how would you administer nitroglycerin?
sublingual
Outline the management of an anginal attack:
1. let pt rest, stop activity
2. seat pt in an UPRIGHT position
3. give nitroglycerine sublingually
4. check pulse and respiration
5. give oxygen if necessary
6. for a pt with known angina the AHA recommends a second dose of ntg if pain persists for more than 5 minutes. After 3 doses w/in a 10 minute period and no relief it should be treated as MI. Call for emergency medical intervention
7. For pt w/o hx of angina emergency medical aid should be sought after 2 minutes w/o relief
what are the:
Actions/Effects
Adverse Effects
of Beta Adrenergic Blockers? (to control angina)
Block Beta adrenergic receptors, slowing the heart rate, reducing the workload of the heart. They cause dizziness and fatigue. An example is lopressor
what are the:
Actions/Effects
Adverse Effects
of Calcium Channel Blockers?(to control angina)
Vasodilator, blocks calcium channel, reducing cardiac contractility and work. They cause dizziness, fainting, and headache
what are the:
Actions/Effects
Adverse Effects
of nitrates (vasodilators; transdermal or oral)
(to control angina)
Reduces cardiac workload; decreases peripheral resistance by vasodilation
List other types of medications that might be prescribed for an individual with angina and explain the rationale for each.
-antihypertensive to lower blood pressure and cardiac workload
-diuretic to help control blood pressure and prevent edema
-platelet inhibitor to lower platelet aggregation and the chance of thrombus formation
-antihyperlipidemic to lower blood cholesterol and LDL levels and hopefully slow or arrest progression of atherosclerosis
What are the surgical interventions that might be used to treat angina?
Angioplasty and stent insertion; coronary bypass graft
Describe nonpharmacological interventions that could help control angina:
-avoid situations known to precipitate attack (stress)
-stop smoking
-consume diet low in saturated and trans-fats
-restrict sodium intake
-lose wt if overweight
-engage in a consistent exercise program
-reduce stress
A patient states that he has angina pectoris. Identify additional information that should be obtained from this individual.
How long has he had angina?
How frequent are the attacks?
When was the last one?
What are the known precipitating factors?
What is the response to ntg?
Does he have ntg with him?
Has he had an MI?
Identify measures that would help decrease the chance of an individual experience of an anginal attack?
Stress reduction-explanations and reassurance
Short appointments
prophylactic use of ntg
Define myocardial infarction (MI):
death of cardiac muscle resulting from prolonged ischemia
State 3 causes of MI and indicate which one occurs most frequently.
Infarction may develop in 3 ways:
1. thrombus buildup to obstruct the artery due to atherosclerosis (most common)
2. vasospasm in the presence of a partial occlusion
3. embolization of a thrombus to a smaller artery that is totally obstructed
List the warning signs of an MI:
pallor, anxiety, fear, diaphoresis, shortness of breath and tightness in chest, weakness, indigestion, or nausea
Differentiate between a transmural and intramural infarction:
Transmural infarction involves all 3 layers of the heart and subendocardial infarction involves the inner one-third to one-half of the wall
What is the most common site of an MI?
Left Ventricle
Describe the pathophysiology of an MI
Myocardial infarction occurs when a coronary artery is totally occluded, causing prolonged ischemia and cell death or infarction of the myocardium. at the point of obstruction, heart tissue becomes necrotic, and an area of injury inflammation, and ischemia develops around the necrotic zone. Functions of myocardial contractility and conduction are lost quickly. There is irreversible damage unless blood supply can be restore within the first 10-30 minutes. Inflammation subsides after 48 hours. the area of necrosis is gradually replaced by fibrous (nonfunctional) tissue. The size of the infarct is determined by the location of arterial blockage and presence of collateral circulation.
Describe the manifestations of an MI
Signs and symptoms include sudden, severe, steady, and crushing substernal chest pain that radiates to the left arm, shoulder, jaw, or neck. Other manifestations may occur even if pain is not present, including pallor, diaphoresis, nausea, dizziness, weakness, dyspnea, anxiety, fear, hypotension, and low-grade fever.
How could a diagnosis of MI be confirmed?
Diagnosis is confirmed through ECG changes and serum enzyme and isoenzyme levels. Serum levels of myosin and cardiac troponin are elveated; serum electrolyte levels may be abnormal; leukocytosis and elevated CRP and erythrocyte sedimentation rate are common; arterial blood gas will be altered. Conduct pulmonary artery pressure measurements to determine ventricular function.
What are serum enzymes? What is their significance in someone who has suffered an MI? Differentiate between enzymes and isoenzymes.
Serum enzymes are intracellular enzymes diffused from necrotic cells into the serum in a typical and predictable pattern that can be measured. Isoenzymes are subgroups of a specific enzyme that are found primarily in one type of tissue. Levels of serum enzymes and isoenzymes can be used to identify the site of the infarction, confirm an MI, and also to assess the size/severity of infarction.
Explain why the electrocardiogram would change after an MI:
Electrical activity of myocardium will be altered in areas of severe ischemia or necrosis.
What complication of an MI is responsible for the greatest number of deaths. Why is this complication so serious?
Arrhythmias account for the greatest number of deaths because the impair the efficiency of the heart, resulting in decreased perfusion to vital organs as well as the heart itself; leading to shock
Briefly describe other complications that may accompany an MI
Other complications include cardiogenic shock, CHF, and less frequently the rupture of necrotic heart and tissue and embolism
Identify the treatments used in the treatment of an MI and include the rationale for each.
Treatment includes rest, oxygen therapy, analgesics, anticoagulants, antiarrhythmic drugs, digoxin, specific measure to treat shock if present, and bypass surgery
Identify differences between angina pectoris and MI
-Angina is usually precipitated by something that increases heart rate; MI may occur at rest or even while aslep
-Anginal pain is relieved by ntg and rest; the pain of an MI is not relieved by NTG and rest
-there is no tissue death with angina; MI causes cell death
-Cardiac enzymes and isoenzymes are elevated with MI; there are no changes with angina. There are permanent ECG changes with MI; no permanent changes with angina
-There is leukocytosis with MI, which is not elevated with angina
-CRP is elevated with MI; it isn't with angina
-ESR is elevated with MI but not with angina
-There are elevated serum levels of myosin and troponin with MI
Describe the pathway of impulses in the cardiac conduction system, starting at the pacemaker of the heart.
SA node to AV node to AV bundle to right and left bundle branches to Purkinje fibers
SA-AV-HIS-RL Bundle Branches-Purkinje
What does the P Wave represent?
Atrial Depolarization
What does the QRS complex represent?
Ventricular depolarization
What does the T Wave Represent?
Ventricular Repolarization.
Remember that we don't like to do things to the heart in T wave b/c it's irritable
Define Dysrhythmia
alteration of cardiac rate or rhythm
list several condition in which cardiac arrhythmias occur
Cardiac arrhythmias may occur due to damage to the heart's conduction system or systemic causes such as an electrolyte abnormalities, fever, hypoxia, stress, infection, or drug toxicity
fibrillation
heart rate greater than 350 beats per minute
premature ventricular contraction
extra heartbeat arising in the ventricles
bradycardia
heart rate less than 60 beats per minute
heart block
slowing or no transmission of impulses between atria and ventricles
premature atrial contraction (PAC)
additional heartbeat originating in the atria
cardioversion
restoration of normal cardiac rhythm by electrical shock
flutter
heart rate between 150 and 350 beats per minute
ectopic beat
extra beat originating outside the SA node
tachycardia
heart rate between 100 and 160 beats per minute
Why is a rapid (resting) heart rate undesirable?
It interferes with normal ventricular filling and decreases both period of ventricular diastole and perfusion
Why is an excessively slow heart rate undesirable?
It results in decreased cardiac output which results in decreased perfusion of vital organs
what are the:
Actions/Effects
Adverse Effects
of Beta Adrenergic Blockers?
(to control dysrhythmias)
Blocks Beta Adrenergic receptors slowing heart rate, prevents SNS stimulation and increased demand on heart. Causes dizziness and fatigue. Lopressor is exp
what are the:
Actions/Effects
Adverse Effects
of Calcium Channel Blockers?
(to control dysrhythmias)
Vasodilator, blocks calcium channel. Dizziness, fainting, headache. Exp. Adalat
what are the:
Actions/Effects
Adverse Effects
of Digitalis/Digoxin?
(to control dysrhythmias)
Slows conduction through the AV node, increases force of contraction (cardiotonic) to increase efficiency
An individual who has been diagnosed with cardiac arrhythmias may have a history of atherosclerosis and other heart-related problems, such as angina or a previous MI. Identify other meds that such an individual may be taking to control these conditions.
-antihypertensive to decrease blood pressure and cardiac workload
-diuretic to help control blood pressure and prevent edema
-platelet inhibitor to decrease platelet aggregation and decrease the chance of thrombus formation
-anticoagulant to decrease the chance of thrombus formation
-antihyperlipidemic to decrease blood cholesterol and LDL levels and hopefully slow or arrest progress of atherosclerosis
-ntg
What type of pacemaker can be used by paramedics as an immediate life saving treatment of an MI?
device that provides electrical stimulation directly to the heart muscle to stimulate heart contraction as needed or for overall control of heart rate
Why is it important to know whether a client has a pacemaker?
use of electronic equipment may interfere with normal functioning of a pacemaker
Define cardiac arrest:
cessation of all activity in the heart; no impulse conduction, thus a flat ECG
Identify the causes of CHF
causes of chf include a problem in the heart itself (valve defect or MI) or a condition that increases the workload of the heart (eg hypertension)
Describe the compensatory mechanisms that are recruited in early heart failure to maintain cardiac output
reduced blood flow into systemic circulation to include kidneys; increased rennin and aldosterone secretion-resulting in vasoconstriction and increased blood volume. SNS response increases heart rate and peripheral resistance. Chambers of the heart tend to dilate, cardiac muscle becomes hypertrophied
The consequences of heart failure are often referred to as the backward and forward effects. Explain what is meant by these terms.
Backward Effects: the chamber and blood vessels behind or 'upstream' from the failing ventricle will not empty properly resulting in the accumulation or congestion of blood and therefore an increased pressure in these areas.
Forward Effects: there will be decreased output of blood flowing from the failing ventricle into the vessels in front of it or down stream.
Right Sided Heart Failure
Cause
Backward Effects
Forward Effects
Manifestations
Cause: Infarction of right ventricle, pulmonary valve stenosis, pulmonary disease (cor pulmonale
Backward Effects: Dependent edema in feet, hepatomegaly and splenomegaly, ascites, distended neck veins, headache, flushed face
Forward Effects: Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance
Manifestations: Compensations/tachycardia and pallor, secondary polycythemia, daytime oliguria
Left Sided Heart Failure
Cause
Backward Effects
Forward Effects
Manifestations
Cause: infarction of left ventricle, aortic valve, stenosis, hypertension, hyperthyroidism
Backward Effects: orthopnea, cough, sob, paroxysmal nocturnal dyspnea, hemopytsis, rales
Forward Effects: fatigue, weakness, dyspnea, exercise intolerance, cold intolerance
Manifestations: Compensations/tachycardia and pallor, secondary polycythemia, daytime oliguria
Explain why the following manifestation occurs with CHF: Splenomegaly
venous congestion in inferior vena cava ad other veins draining abdominal organs
Explain why the following manifestation occurs with CHF: ascites
venous congestion i inferior vena cava and other veins draining abdominal organs
Explain why the following manifestation occurs with CHF: orthopnea
due to pulmonary edema- fluid shifts into upper lobes when head is lowered, causing dyspnea and anxiety, and more fluid shifts from tissues into blood when recumbent, thus increasing vascular volume and pressure in pulmonary capillaries
Explain why the following manifestation occurs with CHF: cough
due to fluid congestion in lungs and pulmonary edema
Explain why the following manifestation occurs with CHF: hemoptysis
as congestion increased in pulmonary circulation red blood cells are pushed out of capillaries into alveoli, causing rusty colored sputum or blood-specked sputum
Explain why the following manifestation occurs with CHF: Distended neck veins
due to increased congestion and pressure in the superior vena cava
Explain why the following manifestation occurs with CHF: decreased urine output
occurs during day...vas fluid accumulates in dependent regions, there is decreased renal perfusion; late in disease, oliguria reflects decreased cardiac output and renal failure.
Explain why the following manifestation occurs with CHF: nocturia
when individual is in supine position, edema in dependent areas is mobilized, resulting in increased cardiac output, renal perfusion, and therefore glomerular filtration rate
Explain why the following manifestation occurs with CHF: polycythemia
Impaired gas exchange due to pulmonary congestion causes chronic hypoxia that in turn stimulates release of erythropoietin-increased RBC poduction
Why is a low sodium diet used to treat CHF?
It helps prevent fluid retention
Why is a low cholesterol diet used to treat CHF?
Hopefully helps arrest progression of atherosclerosis
Why are compression stocking used to treat CHF?
Prevent venous stasis and thrombophlebitis
Why is continuous oxygen therapy used to treat CHF?
Decreases dyspnea and improves arterial blood gases
Why are diuretics used to treat CHF?
mobilizes edema and promotes excretion of excess fluid leading to decreased plasma volume and therefore decreased cardiac workload
Why are potassium supplements used to treat CHF?
Prevents hypokalemia which is a common side effect of diuretic therapy
Why are ACE inhibitors used to treat CHF?
ACE inhibitors decrease renin secretion and therefore prevent both vasoconstriction and aldosterone secretion (which causes salt and water retention)
Why is digoxin used to treat CHF?
It increases the strength of myocardial contractions that increase cardiac output
Why are platelet inhibitors or anticoagulants used to treat CHF?
They decrease thrombosis, particularly in the legs
Why are sedatives or antianxiety agents used to treat CHF?
Decreases anxiety, which can contribute to increased heart and respiratory rates
List factors that may contribute to the development of congenital heart defects
most defects are multifactorial and reflect both genetic and environmental influences. EG chromosomal abnormalities in Down Syndrome. Environmental factors include viral infections such as rubella and maternal alcoholism (fetal alcohol syndrome and maternal diabetes
Define Septal defect
hole or defect in the atrial or ventricular septa
define valvular incompetence
failure of a valve to close completely
define regurgitation
backward flow or leaking of blood due to valvular incompetence
define prolapse:
abnormally enlarged and floppy valve leaflets that balloon backward with pressure or posterior displacement of the valve cusp
Define Stenosis
narrowing of a valve
define heart murmur
abnormal heart sounds due to leaky valves
How are most congenital heart defects deteceted?
by presence of a heart murmur
Distinguish between a left to right shunt and a right to left shunt. Describe the composition of systemic blood, and explain the implications in each case
Left to right shunt means that blood from the left side of the heart is recycled to the right side and to the lungs, resulting in increased volume in the pulmonary circulation, a decreased cardiac output, and an inefficient system--an acyanotic condition.
Right to lef shunt means that unoxygenated blood from the right side of the heart bypasses the lung directly and enters the left side of the heart and hence the systemic circulation producing varying degrees of cyanosis; death may occur in infancy in severe cases
Outline the signs and symptoms of large congenital heart defects:
Signs and symptoms include
-pallor and cyanosis
-tachycardia, with very rapid sleeping pulse frequently a pulse deficit
-dyspnea on exertion and tachypnea
-in toddlers and older children, frequently assuming a squatting position to modify blood flow
-clubbed fingers developed in time
-marked intolerance for exercise and exposure to cold
-delayed growth and development
explain the consequences of a large ventricular-septal defect, including the complications that develop if the defect is not corrected.
ventricular septal defect is the most common congenital heart defect. "Hole in the heart" Large openings; left to right shunt, reducing the flow of blood from the left ventricle, reducing stroke volume and cardiac output in systemic circulation. More blood enters the pulmonary circulation, compromising its efficiency, and in time, overloads and irreversibly damages the pulmonary vessels, causing htn. This complication if untreated would lead to abnormally high pressure in the right ventricle and reversal of the shunt to a right to left shunt including cyanosis.
What's the pathophysiology of: mitral stenosis?
Behind the valve: Left atrial hypertrophy, atrial arrhythmias, mural thrombi, pulmonary cogestion, Pulmonary htn
In front of the valve: decreased cardiac output
Manifestations: Dyspnea, orthopnea, cyanosis, fatigue, arrhythmais, heart murmur, increased risk of stroke due to emboli originating in the left atrium
What's the pathophysiology of: mitral reguritation
Behind the valve: left atrial hypertrophy, atrial arrhythmias, mural thrombi, pulmonary congestion, pulmonary congestion, pulmonary hypertension
In front of the valve: decreased cardiac output
Manifestations: dyspnea, orthopnea, cyanosis, fatigue, dizziness, arrhythmias, heart murmur.
name 2 conditions that are usually associated with heart murmurs
Valvular Defect and Septal Defect
Describe the four defects that are present in Tetralogy of Fallot. Outline the direction of blood flow and describe the implications of altered blood flow.
1. Pulmonary Valve Stenosis: restricts outflow from the right ventricle, leading to right ventricular hypertrophy and high pressure in the right ventricle leading to the right left shunt
2. Ventricular septal deficit: an opening in the ventricular septum allows blood to flow between the ventricles
3. Dextroposition of the aorta: promotes blood flow directly from the right ventricle into the general circulation.
4. Right ventricular hypertrophy: thickening of the ventricular wall because of increased work.
The most common cyanotic congenital heart disorder, tetralogy of Fallot is a right to left shunt of blood through the VSD with marked systemic effects. This means that unoxygenated blood from the right side of the heart bypasses the lungs and enters the left side of the heart and general circulation. The high proportion of unoxygenated blood produces a bluish color in the skin and mucous membranes (cyanosis) and marked systemic effects resulting from hypoxemia
Describe therapeutic interventions used in the treatment of heart defects:
Treatments include surgical repair of the defect, valve replacement, or drug therapy (those drugs used to tx heart failure)
A client states that he previously had a heart murmur but the defective valve was replaced with a prosthetic valve. What meds will he be taking and why? what meds will he require if he is undergoing an invasive procedure and why
1. He will be taking antiplatelet inhibitors such as ASA or an anticoagulant because despite replacement of the damaged valve platelets will still aggregate on the replacement. These could become emboli therefore increasing the risk of stroke
2. He will require an antibacterial agent preferably penicillin for prophylaxis, because invasive procedures provide a portal of entry for bacteria that may then colonize on the prosthetic valve causing infective endocarditis
Which Microorganism generally causes rheumatic fever?
group a Streptococci
Identify individuals who are at high risk for developing rheumatic fever
those between 5 and 15 years old
Describe the pathophysiology of rheumatic fever.
An acute systematic inflammatory condition resulting from abnormal immune reaction of an untreated infection usually B Streptococci. Results in acute cardiac inflammation involving one or more layers of the heart: Pericarditis, myocarditis, and or endocarditis. Other sites of inflammation include large joints, particularly in the legs; migratory polyarthritis; nonpruritic skin rash; nontender subcutaneous nodules on the extensor surfaces of the wrist, elbows, knees, or ankles; and inflammation of the basal nuclei in the brain causing involuntary jerky movements. Rheumatic heat disease can develop years later.
Describe the manifestations of rheumatic fever under the following: general indication of systemic inflammation
low-grade fever, leukocytosis, malaise, anorexia, and fatigue
Describe the manifestations of rheumatic fever under the following: pericarditis
inflammation of the outer layer of the heart; may include effusion
Describe the manifestations of rheumatic fever under the following: myocarditis
inflammation develops as localized lesions in heart muscle, called Aschoff bodies
Describe the manifestations of rheumatic fever under the following: endocarditis
inflammation of the inner lining of the heart, especially the valves, which become edematous; verrucae (small wort like lesions) form
Describe the manifestations of rheumatic fever under the following: polyarthritis
migratory inflammation of many joints, especially in the legs
Describe the manifestations of rheumatic fever under the following: skin manifestations
erythema marginatum (red macules or papules)
Describe the manifestations of rheumatic fever under the following: subcutaneous nodules
nontender lesions on the extensor surfaces of writsts, elbows, knees
Describe the manifestations of rheumatic fever under the following: Sydenham's chorea
inflammation of the basal nuclei in the brain causing involuntary jerky movements of the face, arms, and legs
Endocarditis is the most common pathophysiological change associate with rheumatic fever and my be the most serious problem. Why?
Endocarditis may lead to permanent scaring of heart valves which leads to rheumatic heart disease. If Rheumatic Heart Disease develops the individual is now at high risk for infective endocarditis.
Identify the measures used to diagnose rheumatic fever:
CBC and serology for identifying leukocytosis and anemia; monitoring antistreptolysin O antibody titer; ecg to identify characteristic changes
What affect does the following class of drug have on rheumatic fever; ANTIBIOTICS
Eradicate bacteria and prevent future infection: penicillin
What affect does the following class of drug have on rheumatic fever; NSAIDS
Decrease acute inflammation to prevent heart complications
Relieves joint symptoms
Lowers fever
What affect does the following class of drug have on rheumatic fever; CORTICOSTEROIDS
decrease immune response and acute inflammation to prevent heart complications
What affect does the following class of drug have on rheumatic fever; ANTIPYRETICS
Decrease fever
What affect does the following class of drug have on rheumatic fever; ANTIARRHYTHMICS
improve efficiency of heart function, prevent complications
What affect does the following class of drug have on rheumatic fever; MUSCLE RELAXANTS
decrease muscle spasms
What are other measures used in the treatment of rheumatic fever?
Restrictions of physical activities; maintenance of nutrition and hydration
Distinguish between rheumatic fever and rheumatic heart disease:
rheumatic fever is an acute, inflammatory disorder caused by abnormal immune response, following an infection. Indication of rheumatic fever involves permanent scarring of one or mover valves; the individual is at high risk of endocarditis. Scar tissue in the myocardium may cause arrhythmias
Which heart valve is most commonly affected by heart disease?
Mitral Valve
Why is aspirin often prescribed for individuals with a history of rheumatic heart disease?
Damaged heart valves stimulate platelet aggregation, leading to increased risk of emboli and stroke
Why are individuals with a history of rheumatic heart disease at an increased risk of developing infective endocarditis?
Damaged endocardial surface provides an environment for bacterial colonization
Explain why individuals with a history of rheumatic heart disease require prophylactic antibiotic coverage before any invasive procedure...such as dental surgery:
Some individuals should be premedicated with antimicrobial drugs before invasive procedures to avoid bacteremia. There are 2 predisposing factors for subacute infective endocarditis: damaged endocardium and portal of entry for bacteria or other organisms. Someone with RHD has damaged heart valves and the invasive procedure provides a portal of entry
Why does someone with a prosthetic heart valve still need to take ASA or platelet inhibitor?
Despite replacing the damaged valve, there is an increased susceptibility to thrombus formation requiring pt's to take daily asa
Differentiate between subacute and acute infective endocarditis. Identify the microbial agents involved in each:
Subacute: defective heart valves infected by organisms ith low virulence (streptococcus viridans
Acute: normal vales attacked by highly virulent pathogens..ie staphylococcus aureus
Identify individuals who are at high risk for developing each type of infective endocarditis:
Those with: congenital defects
rheumatic fever
mitral prolapse
prosthetic heart valves
septal defects
recent stent insertion
indwelling catheters
immunosuppression or immunodeficiency
Outline the pathophysiology of infective endocarditis
-infection of normal or defective heart valves
-inflammation of the valves and formation of vegetations on the cusps
-defective opening and closing of the valves
-potential for septic emboli causing infarction or infection
-Additional scarring and destruction of valve leaflets and chordae tendinea
Describe the manifestations and complications of infective endocarditis
subacute infective endocarditis has an insidious onset. Various new heart murmurs are common. AN initial low grade fever and fatigue may be signs. Anorexia, splenomegaly, and Osler's nodes on the fingers are often present. There are signs of vascular occlusion or infection (abcesses) in remote locations. An intermittent high fever may develop and in severe cases, CHF develops. Acute endocarditis has sudden onset with sudden, spiked fever, chills, and drowsiness. Heart valves are badly damaged and may be torn, causing severe impairment of heart function. As in the subacute form, septic emboli may cause infarctions and abscesses in remote sites with corresponding signs of symptoms and infections
How is a diagnosis of endocarditis confirmed?
Blood culture
Describe the treatment for infective endocarditis:
Antimicrobial drugs, usually for a minimum of 4 weeks, other medication to support heart function is usually required.
Rheumatic Fever
-Causative Agent: Group A B-hemolytic streptococci
-predisposing factors: Age 5-15, economically disadvantaged, living in crowded conditions
-manifestations: general...fever, leukocytosis, malaise, fatigue, anorexia. Heart: pericarditis, myocarditis, endocarditis, tachycardia, heart murmur, arrhythmias, heart failure
-polyarthritis, skin manifestations (rash) chorea, subcutaneous nodules, epistaxis, abdominal pain
Infective Endocarditis:
Causeative agent: Acute-- Staphylococcus aureus
Subacute--Streptococcus Viridans
Gram-negative bacilli, enterococci, Fungi
Predisposing factors: damaged endocardium: rheumatic heart disease, previous endocarditis, congenital heart defects, prosthetic heart valves. Portal of entry for microbes: IV drug users, indwelling cath, recent joint replacement
Manifestations/Complications: fever, leukocytosis, fatigue, elevated ESR
positive blood culture
change in heart murmur, septic emboli
Caugh, dyspnea, arthralgia, arthritis, petechial hemorrhages in skin, mucosa, nail bed, chest pain, confusion, paralysis, stroke, blindness, hematuria, abdominal pain
name the possible causes of acute pericarditis:
Acute pericarditis may involve simple inflammation of the pericardium or may be secondary to open heart surgery, MI, rheumatic fever, systemic lupus erythematosus, cancer, renal failure, trauma, viral infection
Define Hypertension. Include the numerical values for blood pressure in definition. How does age affect the criteria for hypertension?
High blood pressure, when the systolic pressure is above 120 and the diastolic pressure is above 70 when an individual is at rest. Essential htn develops when blood pressure is consistently above 140/90mm Hg. Men are more likely to have htn before55, after which women have a greater incidence. Differences in systolic and diastolic pressure increase with age, as the elasticity of arteries is lost
Differentiate between essential and secondary hypertension
Essential htn is idiopathic. Secondary HTN results from renal or endocrine disease or phenochromocytoma
What is meant by the term malignant hypertension
Hypertension that is uncontrollable, severe, and rapidly progressive with many complications and characterized by high diastolic pressure
Identify predisposing factors for hypertension, including those that are modifiable. Note that these parallel the risk factors or artherosclerosis and heart disease
Genetic Factors: nonmodifiable
Excessive alcohol intake: modifiable
High sodium intake: modifiable
obesity: modifiable
prolonged or recurrent stress: modifiable
describe the pathophysiology and complications of undiagnosed or uncontrolled hypertension.
there is an increase in arteriolar vasoconstriction, possibly due to increased susceptibility to various stimuli. There is a major increase in peripheral resistance, reducing the capacity of the system and increasing diastolic pressure. Decreased renal blood flow causes an increase in renin, angiotensin, and aldosterone secretion. Resulting increases in vasoconstriction. Chronic hypertension causes arterial wall damage, sclerosis, and stenosis. Aneuryms or atheromas may form, reducing blood flow to involved area. There is ischemia and necrosis of involved tissues. The areas most frequently damaged are kidneys, brain, and retina. The end result of poorly controlled hypertension can be chronic renal failure, stroke, vision loss, or chf.
Explain why hypertension is often referred to as the silent killer:
it is often asymptomatic in the early stage, and initial symptoms are usually vague until complications arise.
Differentiate between hypertension in the early stages and established hypertension.
In the early stages hypertension are frequently asymptomatic but initial signs may include fatigue, malaise, and morning headache. Essential hypertension develops when the blood pressure is consistently greater than 140/90
Describe lifestyle and behavioral changes that are recommended in the treatment of hypertension. Explain the rationale for each modification.
Reduce salt intake, body weight, and stress and increase cardiovascular fitness
What is the greatest problem in the treatment of hypertension
patient compliance-ie willingness to consistently follow treatment plan.
Antihypertensive: Diuretics
-Mechanism of action/Effects: increased excretion of sodium and water leading to decreased blood volume
-Adverse: nausea, vomiting, Orthostatic hypotension, dizziness Xerostomia, Hypokalemia
Exp: HCTZ
Antihypertensive: ACE Inhibitors
Mechanism of action: Blocks formation of angiotensin II, decreased aldosterone secretion, prevent vasoconstriction
Adverse: headache, orthostatic hypotension, dizziness
Exp: captopril
Antihypertensive: Calcium Channel Blockers
Vasodilation, decreased myocardial infarction, conduction and contractility
adverse: dizziness, fainting, headache, orthostatic hypotension, constipation, gingival htn
Antihypertensive: B Adrenergic Blockers
Prevent increased heart rate in response to sympathetic nervous system and cholamines
Cause: bradycardia, dizziness, fatigue, orthostatic hypotension, sexual dysfunction, atenolol
Identify adverse effects that are common to all hypertensive medications
nausea, erectile dysfunction, orthostatic hypotension, dizziness
List other medications that might be prescribed, and state the rationale for each
-platelet inhibitor: to prevent heart attack and stroke
-antihyperlidemic: to arrest or slow progression of atherosclerosis
Describe the general manifestations of peripheral vascular disease
-increasing fatigue and weakness in the legs
-intermittent claudication
-sensory impairment
-weak peripheral pulse distal to the occlusion
-marked pallor or cyanosis when legs elevated; redness when they are dangling
-skin that is dry and hairless
-toenails that are thick and hard
-poorly perfused extremities that are cold
What are the therapeutic interventions used in the treatment of peripheral vascular disease
-reduction in serum cholesterol levels
-platelet inhibitors or antiocoagulants reduce thrombosis
-smoking cessation
-exercise program
-maintaining dependent position for the legs
-peripheral vasodilators
-surgical procedures to increase blood flow
-preventative measures to avoid skin trauma
-antibiotics for gangrenous ulcers
-amputations when necessary to prevent infection spread; relieve pain
Define aortic aneurysm
localized dilation of an arterial wall
Identify the causes of aneurysms
causes include atherosclerosis, trauma (possible auto accidents), syphilis, congenital defects
Describe the complications of aneurysms
rupture, leading to moderate bleeding or severe hemorrhage and death; or thrombus may develop in the aneurysm, causing obstruction
Identify factors that contribute to the development of varicose veins
inherent weakness or defect in vein walls or valves (familial tendency); long periods of standing
Describe the signs and symptoms of varicosities
-superficial varicosities on the legs appear as irregular, purplish, bulging veins in the legs
-Edema in the feet
-fatigue and aching in the legs are common
-shiny, pigmented, and hairless skin
-ulcers may develop
Differentiate between thrombophlebitis and phlebothrombosis:
Throbophlebitis: devp of a thrombus in a vein in which inflammation is present
phlebothrombosis: spontaneous thrombus development in the absence of inflammation
Identify 3 factors that contribute to the development of thrombophelebitis
-blood stasis or sluggish blood flow
-endothelial injury
-increased blood coagulability
Outline measures that could decrease the risk of developing thrombophlebitis
exercise
elevation of legs
compression or elastic stockings
what is a pulmonary embolus? where did the blood clot probably originate?
pulmonary embolus is a blood clot (or sometimes other material) that blocks a pulmonary artery or one of its branches. It typically originates in leg veins due to thrombophlebitis
Define shock
Hypotension resulting from a decreased circulating volume, resulting in decreased tissue perfusion and general hypoxia
Outline the compensatory mechanisms that are recruited as the blood pressure decreases:
-SNS and adrenal medulla stimulated to increase the rate, force of contractions, and systemic vasoconstriction
-renin secreted to activate angiotension, a vasoconstrictor, and aldosterone to increase blood volume (sodium and water retention)
-increased ADH to promote reabsorption in the kidneys and therby increase blood volume
-glucocorticoids secreted to help stabilize the vascular system
-acidosis stimulates respirations, increasing oxygen supply
Describe the general manifestations of shock, including the cause of each
-thirst, anxiety, and restless, because SNS is quickly stimulated by hypotension
-compensation follows as vasoconstriction shunts blood from the viscera and skin to the vital areas
-progressive signs include lethargy, weakness and faintness, and metabolic acidosis due to decrease in blood flow and blood pressure. Metabolic acidosis may result as anaerobic metabolism increases lactic secretion
Identify the potential complications of shock, and explain why each one occurs
If shock is prolonged, the body's responsiveness diminishes as oxygen supply decreases and wastes accumulate. Compensated metabolic acidosis progresses to decompensated acidosis. There is depression of the Central Nervous System, loss of cell meta bolism, and reduction in effectiveness of medications. The progression to irreversible shock results in acute renal failure due to tubular ischemia and necrosis and ARDS
Outline general measures in the treatment of shock
-place patient in supine position
-cover and keep warm
-call 911 or other assistance
-administer oxygen if possible
-determine underlying cause and treat if possible; eg pressure for bleeding
Hypovolemic or Hemorrhagic shock
-Etiology: blood or plasma loss, dehydration: vomiting, diarrhea, Third Spacing
-manifestations: bleeding, burns, dysphagia, nausea, vomiting, diarrhea, ascites, signs of peritonitis
-Treatment: blood/plasma transfusion, fluid and electrolyte replacement, treat specific cause (measures to stop bleeding)
Cardiogenic Shock
Etiology: Myocardial infarction, Arrhythmias
specific manifestations: warning signs of infarction, ecg changes
specific treatment: antiarrhythmic agents, ecg monitoring, tx for MI
Anaphylactic shock
Etiology: severe allergic or hypersensitivity reaction lead to generalized vasodilation
Specific Manifestations: Severe dyspnea, wheezing, chest tightness, pruritus, urticaria (hives), tingling, flushing, feeling of warmth
TX: epinephrine IM or IV, Corticosteroids, Antihistamines
Septic Shock
Etiology: severe, overwhelming infection
Specific Manifestations: high fever, possibly with chills, warm flushed dry skin, rapid strong pulse, hyperventilation
TX: antibacterial corticosteroids
Neurogenic (syncope) shock
Etiology: pain or fear, emotional upset (unpleasant sight or smell)
Specific Manifestations: sudden vertigo and loss of consciiousness Flushed, warm skin
TX: spirits of ammonia 'smelling salts' Lower head, remove stimulus
In what cardiovascular condition/conditions does the following manifestations present: Ascites
right sided heart failure
In what cardiovascular condition/conditions does the following manifestations present: positive Homan's sign:
thrombophlebitis
In what cardiovascular condition/conditions does the following manifestations present: ECG changes
myocardial infarction; arrhythmias
In what cardiovascular condition/conditions does the following manifestations present: positive blood cultures
rheumatic fever, endocarditis
In what cardiovascular condition/conditions does the following manifestations present: claudication
thrombophlebitis
In what cardiovascular condition/conditions does the following manifestations present: hemoptysis
heart failure
In what cardiovascular condition/conditions does the following manifestations present: heart murmur
congenital defects, rheumatic fever, rheumatic heart disease, tetralogy of Fallow, septal defects, valvular defects,-stenosis and regurgitation
In what cardiovascular condition/conditions does the following manifestations present: elevated cardiac enzymes
myocardial infarction
In what cardiovascular condition/conditions does the following manifestations present: subcutaneous nodules
rheumatic fever
In what cardiovascular condition/conditions does the following manifestations present: pulmonary edema
left-sided heart failure, mitral stenosis, mitral regurgitation
What's the following drug used for? Calcium Channel Blockers
antihypertensive, antiarrhythmic, prophylactic antianginal
What's the following drug used for? nitroglycerine
antianginal--prophylactic or acute
What's the following drug used for? Penicillin
scarlet fever, rheumatic fever, rheumatic heart disease
What's the following drug used for? B-Adrenergic blockers
antihypertensive antiarrhythmic, prophylactic antianginal
What's the following drug used for? digoxin
heart failure, antiarrhythmic
What's the following drug used for? diuretics
heart failure, hypertension
What's the following drug used for? antidysrhythmics
arrhythmias, post-myocardial infarction, rheumatic fever
What's the following drug used for? ACE inhibitors
antihypertensive