Chapter 19: Disorders of Cardiac Function Flashcards
Describe the causes, manifestation, and complications related to pericarditis.
Pericarditis is an inflammation of the percardium
Acute pericarditis is defined as signs and symptoms resulting from inflammation of less than 2 weeks duration
Inflammation increases capillary permeability = increase fluid
Healing often progresses to deposition of scar tissue
Causes: Viral Bacterial Uremia Neoplastic Radiation Trauma Drug toxicity
MANIFESTATION: Decreased cardiac output Pericardial friction rub Chest pain -Precordial -Abrupt onset, sharp, radiates -Scapula pain -Increases with deep breath, cough -Relief when sitting forward ECG changes
Inflammation & “scarring” due to pericarditis will decrease cardiac output = Constrictive Pericarditis
Complication of Pericarditis
Pericardial Effusion
Cardiac Tamponade
Dressler Syndrome
(post heart attack)
Describe the pathophysiology that results in pericardial effusion.
The accumulation of fluid in the pericardial cavity, usually as a result of an inflammation or infectious process.
Causes: Inflammation of pericardium Infection elsewhere Neoplasms Cardiac surgery Trauma
Relate the cardiac compression that occurs with cardiac tamponade to the clinical manifestations, diagnosis, and treatment of the disorder.
Compression d/t fluid/blood.
Build up of blood or other fluid in the pericardial sac puts pressure on the heart, which may prevent it from pumping effectively
Causes: Trauma Myocardial rupture post MI Cardiac surgery Aortic dissection
MANIFESTATION:
Dependent on amount and rapidity
Limits stroke volume and CO = low SBP
CNS: change in mentation
Resp: dyspnea, tachypnea
CVS: chest pain, tachycardia
Elevated central venous pressure(right atrium) & jugular venous pressure
Circulatory shock
DIAGNOSIS/TREATMENT
Muffled heart sounds
Pulsus paradoxus**
-In tamponade, During inspiration, blood is drawn into the the thoracic cavity in which reduces blood pressure in the body causing pulsus paradoxus
>10 mmHg fall with respirations
ECG
Decreased voltage
DIAGNOSE
Echocardiogram
CT, MRI
Treatment
Immediate pericardialcentesis
Describe blood flow in the coronary circulation and relate it to the metabolic needs of the heart.
?
Discuss the risk factors associated with coronary artery disease.
NON-MODIFIABLE: Sex/Gender Post-menopausal women Age Ethnicity Genetics
MODIFIABLE: Hypertension Hyperlipidemia tobacco use Diabetes Obesity Sedentary lifestyle/physical inactivity Ability to cope with stress
What is the pathology, diagnostic measures, symptomology and treatment goals for chronic ischemic coronary artery disease
Chronic Stable Angina
Pathology - Chronic stable angina is associated with a fixed coronary obstruction that produces a disparity between coronary blood flow and metabolic demands of the myocardium
chronic stable angina is provoked by exertion or emotional stress and relieved within minutes by rest or the use of nitroglycerin. A delay of more than 5 to 10 minutes before relief is obtained suggests that the symptoms are not due to ischemia or that they are due to severe ischemia.
Manifestation - constricting, squeezing, or suffocation sensation. Pain locates at the precordial or substernal location, and may radiate to left shoulder and jaw
Silent Myocardial Ischemia
Pathology -Silent myocardial ischemia occurs in the absence of angi- nal pain. The factors that cause silent myocardial ischemia is the impaired blood flow from the effects of coronary atherosclerosis or vasospasm. Silent myocardial ischemia affects three populations—persons who are asymptomatic without other evidence of CAD, persons who have had a myocardial infarct and continue to have episodes of silent ischemia, and persons with angina who also have episodes of silent ischemia
-are more likely in the elderly
-Less myocardium involved
-neuropathy
Hypotension, low body temp, vague complaints of discomfort, mild diaphoresis, stroke-like symptoms, dizziness, sensorium changes
Treatment is dependent on findings investigative diagnostic
Variant or Vasospastic Angina (Prinzmetal) d/t spasms of coronary artery Cause is unclear Often @ night Variable symptoms
DIAGNOSTIC
- pain history
- risk factors
- lab results
- ECG
- Echocardiogram
- exercise stress testing
TREATMENT
- symptom reduction
- lifestyle modification
- smoking cessation
- stress reduction
- increase exercise
What is the pathology, diagnostic measures, symptomology and treatment goals for acute coronary syndrome.
Risk is classified based on ECG changes
Unstable Angina/Non ST-segment elevation Myocardial Infarction (non-STEMI) (when there is ischemia to the heart)
ST-segment elevation MI (STEMI)
All caused by an imbalance in myocardial
oxygen supply and demand
The classic ECG changes are T-wave inversion, ST-segment elevation, and abnormal Q wave
The T wave and ST segment represents the repolarization phase, and are usually the first to be involved during myocardial ischemia and injury
Causes:
Unstable plaque, rupturing to form a clot
Thin fibrous cap with fatty core is most unstable
Coronary vasospasm
Atherosclerotic narrowing (progressive)
Inflammation/infection
Secondary causes: Anemia Fever Hypoxemia SURGERY
Typical Pattern of Manifestations With pre-diagnosis of “Stable Angina” More severe or more often than usual Occurs at rest (or minimal exertion) Lasts 20 minutes
Unstable Angina/Non-ST MI:
Typical Pattern of Manifestations With pre-diagnosis of “Stable Angina” More severe or more often than usual Occurs at rest (or minimal exertion) Lasts 20 minutes
If biomarkers (troponin) are elevated = non-STEMI High risk of STEMI
Ischemic death of myocardial tissue
ST Elevation MI: Typical Pattern of Manifestations Crushing/constricting pain; usually abrupt Substernal with radiation to left arm, jaw, neck Epigastric distress/nausea Palpitation Cool, clammy skin SOB ANXIETY
Unrelieved by rest/nitro
Cardiac muscle wall ischemia & necrosis
Subendocardial (in one layer of the heart muscle)
Transmural = Q wave (all layers) BIG Q WAVE
“Stunned” myocardium
Cell death in 15-20 minutes
Early perfusion & revascularization can prevent necrosis
Decreased contractile force
Decreased CO
Decreased coronary artery perfusion
Increased pulmonary vasculature pressure
Interruption of conduction
Dysrhythmias
Typical Signs:
- Elevated HR
- BP changes
- Low oxygen sat
- Low grade temp, diaphoresis
DIAGNOSIS based on Serum Biomarkers:
Troponin
Rise within 2-3 hours; remains 7-10 days
Myoglobin
Rises within 1 hr, peaks at 4hrs
Also from skeletal muscle damage
Creatine Kinase MB (CK-MB)
Peaks at 4-6 hrs; gone in 2-3 days
Specific to cardiac muscle
Characterize the pathogenesis of atherosclerosis in terms of fixed atherosclerotic lesions, unstable plaque, and thrombosis with obstruction.
Fixed stable plaque
-Stable atherosclerotic plaques produce fixed obstruction of coronary blood flow with myocar- dial ischemia occurring during periods of increased metabolic need, such as in stable angina.
Unstable Plaque
- can rupture and cause platelet adhesion and thrombus formation
- sudden surge of sympathetic activity with an increase in blood pressure, heart rate, force of cardiac contraction, and coronary blood flow is thought to increase the risk of plaque disruption. Indeed, many people with myocardial infarction report a trigger event, most often emotional stress or physical activity
Thrombosis with obstruction
-Local thrombosis occurring after plaque disruption results from a complex interaction among its lipid core, smooth muscle cells, macrophages, and collagen. The lipid core provides a stimulus for platelet aggregation and thrombus formation. Both smooth muscle and foam cells in the lipid core contribute to the expression of tissue factor in unstable plaques. Once exposed to blood, tissue factor initiates the extrinsic coagulation pathway, resulting in the local generation of thrombin and deposition of fibrin
Define cardiomyopathy
Cardiomyopathies are disorders of the heart muscle and are usually associated with disorders of myocardial per- formance, which may be mechanical (e.g., heart failure) or electrical (e.g., life-threatening arrhythmias).
Discuss the pathology and manifestations associated with hypertrophic cardiomyopathy
Pathology
- unexplained left ventricular hypertrophy
- disproportionate thickening of the ventricular septum
- abnormal diastolic filling
- cardiac arrhythmias
- left ventricular outflow obstruction
Manifestation Variable Decreased stroke volume d/t impaired diastolic filling -Dyspnea -Chest pain -Syncope post exertion Atrial fibrillation Lethal ventricular arrhythmias
Discuss the pathophysiology, risk factors, manifestations and complications associated with infective endocarditis and rheumatic heart disease
INFECTIVE ENDOCARDITIS
PATHO:
Two factors contribute: a portal of entry by which the organism gains access to the circulatory system and a damaged endocardial surface. The portal of entry into the bloodstream via dental or surgical procedure that causes transient bacteremia, injection of a contaminated substance directly into the blood by intravenous drug users.
-vegetative lesions form on the heart valves
-The aortic and mitral valves T
-The infectious loci continuously release bacteria into the bloodstream and are a source of persistent bacteremia. As the lesions grow, they cause
-valve destruction
-leading to valvular regurgitation
-ring abscesses with heart block
-pericarditis
-aneurysm
-valve perforation.
The loose organization of these lesions permits the organisms and fragments of the lesions to form emboli and travel in the bloodstream, causing cerebral, systemic, or pulmonary emboli.
The bacteremia also can initiate immune responses thought to be responsible for skin manifestations, polyarthritis, glomerulonephritis, and other immune disorders
Any infection of inner lining of heart
Usually staphylococcus aureus
Vegetative
Involvement of mitral & aortic valves most common
Acute: relatively healthy individual
Sub-acute/chronic: h/o valve abnormalities
Risk Factors Infection elsewhere Dental surgery/surgery, IV drug use/contaminants Immunodeficiency/immunosuppression Valve prolapse (sudden or congenital)
Manifestation:
S&S of systemic infection*
Heart sound changes*
Symptoms related to embolism
Complications:
Emboli (lung, renal, brain)
Valve dysfunction
arrhythmias
Rheumatic Heart Disease
Pathology is unclear however it is linked to immunological response.
It is thought that antibodies directed against the M protein of certain strains of streptococci cross-react with glycoprotein antigens in the heart, joints, and other tissues to produce an autoimmune response through a phenomenon called molecular mimicry
Risk factors
- under developed countries
- inadequate health care
- poor nutrition
- crowded living
Manifestation
Acute Phase
- history of initiating streptococcal infection
- inflammatory lesions within connective tissue such as the heart, blood vessel, joints, subcutaneous tissues called Aschoff bodies
COMPLICATION Pancarditis (involving all three layers, endocardium, myocardium, or pericardium) Pericardial friction rub, murmur Mitral/aortic valve involvement arrhythmias
Diagnosis
- Evidence of GAS infection
- Elevated WBC, ESR, CRP
- Echocardiogram, Ultrasound
Treatment
-Antibiotics, prevention of complications
Recurrent Phase
-involves the extension of the cardiac effect of the disease
Chronic Phase
-characterized by permanent deformity of the heart valves and is a common cause of mitral valve stenosis.
What are the causes, pathology, manifestation and complication of valvular disease in mitral valve stenosis
Pathology
- incomplete opening of the mitral valve during diastole, with left atrial distension and impaired filling of the left ventrical
- this is characterized by fibrous replacement of valvular tissue, stiff tissue, often causing chordae tendineae to shorten
Causes:
Rheumatic Fever
Congenital
Manifestation:
- nocturnal paroxysmal dyspnea
- orthopnea
- chest pain
- weakness, fatigue
- palpitation
Complication:
Arrhythmias (atrial fibrillation, atrial tachycardias)
Mural thrombi (thrombi that adhere to the wall of a blood vessel)
What are the causes, pathology, manifestation and complication of valvular disease in mitral valve regurgitations
Pathology
incomplete closure of the mitral valve, with the left ventricular stroke volume being divided between the forward stroke volume that moves blood into the aorta and the regurgitant stroke volume that moves it back into the left atrium during systole
Causes: RHD (rheumatic heart disease) Chordae tendineae or papillary muscle rupture LVH dilates orifice Mitral valve prolapse
Manifestations: Slow process = compensation Pulmonary congestion Pansystolic murmur L Atrial and LV hypertrophy
Complications:
Atrial fibrillation
thrombus
What are the causes, pathology, manifestation and complication of valvular disease in mitral valve prolapse
Pathology
-myxedematous (mucinous) degeneration of mitral valve leaflets that causes them to become enlarged and floppy so that they prolapse or balloon back into the left atrium during systole
Associated with:
Marfan’s sydrome & Osteogensis imperfecta
Manifestations:
“snap”
Asymptomatic
Chest pain, dyspnea
Complications:
Mitral valve regurgitation, atrial fib
thrombus
What are the causes, pathology, manifestation and complication of valvular disease in aortic valve stenosis
Pathology
-narrowing of the valve orifice with increased resistance to ejection of blood from the left ventricle into the aorta.
Causes:
- congenital valve malformations
- acquired calcification of a normal tricuspid valve. (wear and tear)
- male, active inflammation
Manifestation:
- angina, syncope, and heart failure develop
- decrease in exercise tolerance
Complication
-dyspnea
