Unit #8 Cardiac Disorders Flashcards
What is the etiology of congenital heart disease?
- Majority of cases, the cause is unknown
- Genetic and environmental influences are probable causes
- May also be attributed to maternal rubella within the first trimester and exposure to cardiac teratogens (heavy alcohol consumption, ionizing radiation, and hypoxia).
What is the pathogenesis of congenital heart disease?
- Results in two primary pathologies; (1) Shunts- abnormal blood flow through heart or great vessels, and (2) Obstructions- Interferences with blood flow leading to increased workload of affected chamber.
- Shunts can be further characterized into right-to-left or left-to-right to indicate abnormal blood flow
- Right-to-left shunts allow un-oxygenated blood from the right side to enter the left side and systemic circulation without first passing through the lungs (cyanosis in infants because of decreased oxygen in arterial blood)
- Left-to-right shunts occurs when oxygenated blood from the left side or aorta flows back into the right side to be recirculated through the lungs (blood reaching the systemic system is oxygenated and infant is not cyanotic). However, the right side of the heart has an increased workload because of the extra shunt blood (over time cans result in right ventricular hypertrophy)
- Most common obstructive defects are stenosis or atresia (failure to develop) of the valves and coarctation of the aorta.
Describe: Atrial septal defect (ASD
- Foramen ovale is a space between a fetuses left/right atrium. This remains open to allow blood to pass from the right to the left atrium and bypass the un-inflated and non-functioning lungs.
- Higher left side pressure during birth normally causes the foramen ovale to close and thus the defect is this space not closing properly. The size of the hole can be vary from 1 cm (well toleratd) and even larger that is well tolerated and may be asymptomatic for many years as long as the shunt flow is left to right and therefore acyanotic.
Describe: Ventricular septal defect (VSD)
- Most common congenital cardiac anomaly
- Ventricular septum forms within the 5th and 6th weeks of fetal life
- Majority of defects are located in the membranous septum, close to the bundle of His.
- Functional significance depends largely on the size of the defect.
- May be apparent at birth because of rapidly developing righ-sided heart failure and a loud systolic murmur.
Describe: Patent ductus arteriosus (PDA)
- Ductus arteriosus is a normal channel between the pulmonary artery and the aorta that remains open during intrauterine life. (closes within 1-2 days after birth)
- In a fetus it allows blood to flow from the pulmonary artery into the aorta, thus bypassing the lungs.
- Low oxygen tension and local production of prostaglandin is important in maintening patency.
- After birth, flow changes from left to right because of the higher pressure in the aorta, this causes it to close because of the stimulation from oxygenated blood
- Reasos why it does not close properly in some individuals is nor well understood it may have something to do with conditions that cause low blood oxygen tension.
Describe: Coarctation of the aorta
- Narrowing or stricture that may impede bloode flow
- The coarctation is most often located just before or after the ductus arterosis
- Preductal coaraction (proximal to ductus arterosis) more severe. In some cases, aortic stricture is so severe that blood flow to the lower extremities must be maintained just by flow through the ductus arterosis (results in very high workload for righ side of heart and may lead to heart failure in early neonate period)
- Blood supply to arms/head unaffected because arteries arise proximal to stricture
- Upper extremities usually have elevated BP, whereas lower extremities have weak pulses and low BP
Describe: Pulmonary and aortic stenosis and atresia
- Often occur in conjunction with other anomalies that allow survival into the neomatal period.
- In pulmonary atresia, no communication between right ventricle and lungs, so blood must enter the lungs through a septal opening and then through a patent ductus arterosis.
- Pulmonary stenosis usually due to abnormal fusion of the valvularf cusps
- Isolated pulmonaery stenosis is easily corrected by surgery (prognosis depends in large part on health of right ventricle).
In regards to Cyanotic Congential Defects, describe what Tetralogy of fallot is.
- Four features: (1) ventricular septal defect, (2) aorta positioned above the ventricular septal opening, (3) pulmonary stenosis that obstructs right ventricular outflow, and (4) right ventricular hypertrophy.
- Severity of symptoms is associated with the degree of pulmonary stenosis
- Heart is generally enlarged because of ventricular hypertrophy
Describe what transposition of the great arteries has to do with cyanotic congential defects
- Results in the formation of two separate, noncommunicating circulations, which is incompatible with life unless mixing of blood occurs through other defects (Ex. Atrial septal defect, patent ductus arterosis).
- Right side of the heart receives blood from the systemic circulation and recirculates it through the body by way of the aorta
- Blood reaching the body has not passed through the lungs and therefore not oxygenated
Describe: Atherosclerosis
- Causes progressive narrowing of the arterial lumen and predisposes to a number of processes that can precipitate myocardial ischemia
- Risk factors of atherosclerosis include: family history, abnormal lipid levels, cigarette smoking, hypertension, diabetes, and obesity.
Describe: Arteriosclerosis
-Hardening of the arteries Pathogenesis- middle layer of the small and medium arteries (inner layer not affected) become calcified with a decrease in the ability of the artery to enlarge.
When does ischemia occur in coronary heart disease?
Occurs when oxygen supplies are insufficient to meet metabolic demand.
Describe: Angina Pectoris
- Chest pain associated with intermittent myocardial ischemia ==>oxygen demand greater than supply
- Three patterns of angina pectoris (1) Stable or typical angina-stenotic atherosclerotic coronary vessels decrease blood flow ; onset with similar stimuli; relief with rest and nitroglycerin (2) Prinzmetal variant angina-have coronary atherosclerosis but onset not related to events leading to increased myocardial demand; vasospasm usual precipitating factor with cause of vasospasm unknown (3) Unstable or crescendo angina –acute coronary syndrome.
Describe: Acute Coronary Syndrome
- Chest pain that is usually more severe and last longer than angina
- Plaque rupture with acute thrombus formation
- MI leads to drop in cardiac output (CO), triggering compensatory responses including sympathetic activation
- Sympathetic nervous system activation leads to increased myocardial workload by increasing: heart rate, contractility, and blood pressure.
Describe: Myocardial Infarction
- Complete occlusion to a blood vessel to the heart leading to tissue ischemia
- Pain not relieved by rest or nitroglycerine, lasts longer than 15 mins
- Signs and symptoms –severe chest pain, can radiate to arm, shoulder, jaw, or back **Watch silent MI (asymptomatic), or complaints like fatigue, abdomen discomfort with women and elderly
What is sudden Cardiac death?
- Unexpected death from cardiac causes within 1 hour of symptom onset
- Use of external defibrillators and CPR has increased survival
- Lethal dysrhythmia (ventricular fibrillation) is usually the primary cause
What is Chronic Ischemic Cardiomyopathy?
- Cardiomyopathy→disease of myocardium
- Heart failure develops insidiously due to progressive ischemic myocardial damage
- Typically have history of angina or MI
- More common in older adults
What is the etiology of Mitral stenosis?
- failure of the valve to open completely; results in extra pressure work for the heart
- Caused by damage by inflammation and scarring, calcification, and congenital malformations.
- Flow from the left atrium into the left ventricle is impaired.
What is the pathogenesis of Mitral stenosis?
signs/symptoms are due to congestion of blood volume and increased pressure in the left atrium and pulmonary circulation, as well as a decreased stroke volume of the left ventricle because of a deficient filling.
What are the clinical manifestations of mitral stenosis?
If uncorrected, can result in chronic pulmonaery hypertension, right ventricular hypertrophy, and right-sided heart failure.
What is Mitral regurgitation?
-Inability of a valve to close completely; results in extra volume work for the heart as blood flows backward
What is the etiology of mitral regurgitation?
can develop from valvular infection or rupture of a supporting papillary muscle.
What is the pathogenesis of mitral regurgitation?
- Backflow from the left ventricle to the left atrium during ventricular systole.
- Left ventricle must pump a greater volume to compensate for the regurgitant flow and maintain an effective stroke volume.
- Compensation can be maintained for many years before symptoms occurs.
What are the clinical manifestations of mitral regurgitation?
- Eventually leads to left-sided heart failure. Pulmonary congestion and poor cardiac output are also present.
- Common complaints of chronic weakness and fatigue
What is the etiology of Mitral valve prolapse?
-Mitral valve that balloons into the left atrium. Cause is unknown but is often associated with scoliosis and Marfan syndrome.
What is the clinical manifestation of mitral valve prolapse?
- may experience palpitations
- rhythm abnormalities
- dizziness
- fatigue
- dyspnea
- chest pain
- psychiatric manifestations (depression and anxiety)
What is the etiology of Aortic stenosis?
- Caused by age-related calcification . Calcification is common in patients with congenital bicuspid aortic valve. Postinflammatory scarring
- Calcification occurs over time and only becomes apparent between 70-90 years of age.
What is the pathogenesis of Aortic Stenosis?
With calcification on the aortic cusps, left ventricle produces high systolic pressure to overcome resistance of stenotic aortic valve.
- Slow development allows heart to maintain stroke volume by compensatory left ventricular hypertrophy.
- Combination of high left ventricular pressure and hypertrophy predisposes heart to ischemia.
What is the clinical manifestation of aortic stenosis?
Signs/Symptoms are due to diminished cardiac output, with pulmonary complications occurring later when the left ventricle fails.
-Syncope (loss of consciousness): occur when cerebral perfusion is inadequate., low systolic BP, faint pulses, anginas (relief with rest).
What is the etiology of aortic regurgitation?
- Can develop from an infection (infective endocartitis) or rupture of a supporting papillary muscle
- Postinflammatory scarring
What is the pathogenesis of aortic regurgitation?
- Left ventricle becomes volume overloaded because it contains its usual preload, received from the atrium, plus regurgitant blood from the aorta.
- Left ventricle compensates with hypertrophy and dilation
- Larger stroke volume= high systolic pressure
- Diastolic is generally lower because of rapid runoff of blood into the ventricle.
What is the clinical manifestation of aortic regurgitation?
- Patients may complain of palpations and a throbbing or pounding heart because of the large ventricular stroke volume.
- Major complication is left-sided heart failure as a result of high ventricular workload
What is the etiology of Rheumatic Fever/Heart Disease?
An acute inflammatory disease that follows infection with group A Beta-hemolytic streptococci
What is the pathogenesis of Rheumatic Fever/Heart Disease?
Damage is due to an immune attack on the individual’s own tissues
-Antibodies against the streptococcal antigens are also directed against self tissue, possibly because of an immune hypersensitivity reaction resulting from cross-reactivity between streptococcal antigens and certain tissue molecules
What is the clinical manifestation of Rheumatic Fever/Heart Disease?
- Inflammation of the heart usually includes all layers and results in carditis.
- Endocardial inflammation results in valvular swelling, erosions, and clumping of platelets and fibrin on valve leaflets. (scarring/shortening becomes progressively more severe).
- Joint inflammation, involuntary movements, and a distinctive truncal rash
What is the etiology of infective endocarditis?
- Caused by invasion and colonization of endocardial structures by microorganisms with resulting inflammation.
- Valvular lesions include growths of microorganisms enmeshed in fibrin deposits called vegetations.
