Ch.19 Common Cardiovascular Disorders Flashcards
Describe the pericardium. What are the different layers? How much fluid is in the pericardial space?
There are two layers: the tough fibrous lay and the inner serous layer
Inner serous layer has two sublayers: the parietal and visceral (epicardium)
The pericardial space holds anywhere from 10-50ml of serous fluid.
What is pericarditis? What defines any pericarditis as being an acute event?
Pericarditis is the inflammation of the percardium
Any pericarditis that lasts no longer than 1-2 weeks is considered acute.
Is most pericarditis (90%) found to be idiopathic?
YES YES YES
What is dressler syndrome?
pericarditis, malaise, fever, and elevated WBC count weeks to months after an MI
What is constrictive pericarditis? How is this treated? is this effective?
the formation of adhesions after repeated bouts of pericarditis that dont allow the heart to fill properly during diastole.
it is treated by removing the diseased portion of the pericardium, and it isnt very effective, most people even with successful removal dont have a long term survival rate.
What is the biggest symptom that occurs in patients with pericarditis?
chest pain that seems pleuritic and worsens by breathing deeply or lying supine, relieved by sitting up, leaning forward, and shallow breaths.
What can confirm but not rule out the diagnosis of pericarditis?
pericardial friction rub (rasping or scraping high-pitched sound that varies with cardiac cycle)
Where is a pericardial friction rub best heard?
diaphragm of stethescope over the lower to middle left sternal edge.
What are some complications of pericarditis to watch out for?
constrictive pericarditis
pericardial effusion possibly leading to tamponade
What labs would be ran to see about possible pericarditis?
CBC, cardiac enzymes (inflammation may extend to myocardium), CRP, sed rate, rheumatoid factors, antinuclear antibody titers, blood culture if evidence of infection, viral study if diagnostic workup is negative.
When do most cases of pericarditis abate? is recurrence common?
after 2-6 weeks
recurrence is rare
What is the basic treatment of pericaridits?
NSAIDS (aspirin or ibuprofen)
Colchicine
steroids (if seemingly autoimmune)
What is myocarditis?
myocarditis is the inflammation of the myocardium.
What is the difference between primary and secondary myocarditis?
Primary: acute viral infection or autoimmune response to the infection
Secondary:related to a specific organism
Why is myocarditis so devastating?
its prevalence is unknown because its clinical presentation is subacute most often. It is a progressive disease with a poor prognsis becuase of the high risk for dysrhythmias, CHF, and death.
it is a leading cause of sudden death in young athletes.
How is myocarditis definitively diagnosed, but not ruled out?
endomyocardial biopsy
What things could indicate a diagnosis of myocarditis?
Do these differ from viral?
fatigue, dyspnea, palpitations, precordial discomfort, slight rise in serum enzyme levels, non-specific ST-T wave changes
with viral there is typically a delay of onset of cardiac symptoms (CHF, dysrhythmias)
How is myocarditis treated and managed?
it is very similar to the treatment for heart failure.
Help the family deal with reality of the potentially lethal disease that often doesnt resolve.
heart transplant or mechanical circulation may be the end result.
If an athlete has myocarditis,can they return to competitive sports, is so, when?
withdraw from competitive sports for at least 6 months following the onset of the disease.
returning to sports depends on normalizing cardiac function and no clinical signs of abnormal function, such as dysrhythmias
Describe endocarditis.
an infection of the endocardial surface of the hear including the valves
caused by bacteria. viral, or fungal agents.
What are some risk factors for infectious endocarditis
prior cardiac condition (including congenital heart disease)
Bloodstream infection
Mitral valve prolapse
rheumatic heart disease
IV drug use (illicit)
patients with prosthetic valves or long-term indweling devices
VALVE DISEASE
> 60 y/o
Why might there be such a rise in incidence of IE in pediatrics?
an increase in pediatric survival of congenital heart disease
Briefly describe the pathophysiology of the development of IE.
enodothelial damage creates turbulent blood flow
This blood flow aggregates platelets (especially in patients in hypercoagulable state)
platelet or fibrin clot on valve leaflet forms
clot is exposed to bacteria in the blood (commonly from dental or urologic procedures)
bacteria proliferates and interferes with normal valve function and eventually damages structure
these non-functioning valves can eventually lead to heart failure an particles from the vegetations or valves can become thrombii.
How does bacteria manage to proliferate on vegetations and valves?
turbulent blood flow concentrates number of bacteria by vegetation
vegetation itself covers bacteria with layers of platelets and fibrin protecting the colony from bodies defenses
When will symptoms of endocarditis usually occur within in relation to a precipitating event?
2 weeks
What are the possible processes that can cause symtpoms of endocarditis in a 2 week period?
bacteremia
fungemia
valvulitis
immunologic response (?)
peripheral emboli
What are some initial, nonspecific complaints that someone presenting with endocarditis may have?
malaise
anorexia
fatigue
weight loss
night sweats
FOCUS ON HISTORY AND PHYSICAL EXAM WHEN NONSPECIFIC SYMPTOMS APPEAR
What is the one thing that is most common in all patients presenting with endocarditis?
fever and a new or changed heart murmur
20% of patients with IE have a presenting symptom of what?
stroke from septic emboli
What are some more specific features of endocarditis?
box 19-4!
What offer a definitive diagnosis of I.E.?
Persistent bacteremia caused by common pathogens of I.E. And evidence of myocardial involvement, like echocardiographic imaging of vegetation or a new or worsening murmur
This is Duke criteria
How many separate cultures are drawn to diagnose I.E.?
Two or three
Take extra care in preparation to avoid contamination.
How is I.E. Treated?
Antibiotics based on culture results
Look out for resistance, most therapies have been modified to account for this
Treat before specimens are identified, as soon as cultures are drawn
When is surgery recommended for I.E.?
Presence of native or prosthetic valve dysfunction or dehiscence, severe CHF secondary to valve dysfunction, and uncontrolled infections
How is I.E. Cured most often cured?
Prolonged antibiotic therapy
Entire colony needs to be eradicated from vegetation
What is the difference between cardiomyopathy and myocarditis?
Myocarditis is inflammatory in its cause of damage while cardiomyopathy continues to have an idiopathic cause.
What is the definition of cardiomyopathy?
Diseases of the heart muscle that cause cardiac dysfunction such as heart failure, dysrhythmias, or sudden death.
What are the different categories and sub-categories for cardiomyopathy?
Dilated - ischemic and nonischemic
Hypertrophic
Describe dilated cardiomyopathy.
An increase in myocardial cavity size because of ventricular wall thinning leading to impaired systolic function. As the cavity gets bigger the heart takes a globular shape.
What can cause a decrease in myocardial contractility which may be the cause of the dilation of the chamber and thinning of the ventricular wall in the first place?
Ischemia, alcohol abuse, endocrine disorders, pregnancy, viral infections, muscular dystrophy, valvular disease, Ect…
Describe the pathophysiology of dilated cardiomyopathy.
Decrease in contractility (EF less than 40%) leads to increased end systolic volume. This increase in preload eventually causes the hearts ventricles to dilate to accommodate. This further decreases strike volume. Eventually the mitral and tricuspid valves become insufficient.
What is the third most common cause of heart failure, the most common cause of heart failure in the young, and the most common cause of heart transplantation?
DCM
Is DCM familial?
Yes, 30-50% of cases are
What is the most prevalent toxic cause of DCM?
Alcohol abuse
What are the two different types of DCM?
Ischemic and nonischemic
Describe ischemic cardiomyopathy.
Oxygen levels are inadequate enough to meet metabolic demands of myocardial cells. Decrease in oxygen = less ATP. Electrolyte pumps stop working which leads to mechanical and electrical dysfunction
What can happen to myocardial tissue if it becomes very ischemic, but doesn’t die?
It can hibernate. Restoring the flow to this hibernating tissue can greatly increase myocardial function.
What may happen if the chordae tendineae are damaged after an infarct?
This can lead to acute mitral regurge that may be life threatening if large enough
Describe the pathophysiology of cardiogenic shock and how the body compensates.
Left ventricle empties poorly
End-diastolic pressure increases
Pulmonary artery pressure increases
Pulmonary edema results
Organ damage begins
Respiratory rate increases to supply more oxygen to blood because of poor gas exchange because of edema, also because of metabolic acidosis because of lactic acid production with damaged organs
What is azotemia? What is it a sign of?
High levels of nitrogen containing products (like BUN and creatinine), higher than 20:1
Pre renal Azotemia indicates that the kidneys have started to have decreased perfusion or function, what can happen if it is prolonged? What is this known as?
The ratio may be normalized, however creatinine and BUN will continue to rise. This is known as tubular necrosis.
Other than damage to the kidneys, what else can happen with prolonged episodes of low cardiac output?
Ileus, bowel infarction, liver failure, pneumonia, skin breakdown
How does nonischemic DCM develop?
Many times it is idiopathic, but there are many other causes that directly damage the heart muscle that arent due to ischemia.
Can both ischemic and nonischemic DCM be acute or chronic?
Yes they can, both of which in chronic the symptoms come on more subtle and the body has time to compensate in most cases (for a while), acute not so much
What may cause acute nonischemic DCM?
Myocarditis
What may cause chronic nonischemic DCM?
Alcoholism and HTN
When do people most often get treatment for their DCM?
After HF becomes uncompensated (interferes with daily activities)
Can medications slow progression of DCM?
No, they will treat symptoms, structural changes are progressive in most cases (unless hyperthyroidism, hypothyroidism, hemochromatosis, valvular disease, and tachycardia are causes it may be reversed)
What are the final treatments for advanced DCM?
Heart transplant or ventricular assist devices
When would an ICD be placed?
If there is a risk for sudden death due to dysrhythmias.
Describe hypertrophic cardiomyopathy.
This is due to a dysfunction in diastole because of limited space in the dilated ventricle that doesn’t fully relax in diastole.
Sometimes the septal wall can hyper trophy, causing a dysfunction in the outflow of blood from the left ventricle during systole
Is HCM genetic?
Yes, it is the most common genetic cardiovascular disorder.
Is HCM a secondary disorder?
NO
What is HCM the leading cause of in the US?
Sudden death in athletes in competitive and recreational sports. Due to the risk for sudden death from ventricular dysrhythmias.
How is HCM often found?
Investigation of a murmur or during a family screening.
What is the most common symptom of HCM?
Dyspnea especially on exertion
How is HCM confirmed?
LVH on echo, borderline LVH may be normal in competitive athletes
Do patients with HCM get ICDs?
Yes, if they have had ventricular dysrhythmias before or have survived sudden death.
What can be done with septal hypertrophy?
Ablation or surgical removal of portion of septum.
