Podcast
Questions and Answers
What is the primary cause of cellular swelling during the first 30 minutes of ischemia?
What is the primary cause of cellular swelling during the first 30 minutes of ischemia?
What histological feature is associated with early coagulative necrosis within 4-12 hours after myocardial infarction?
What histological feature is associated with early coagulative necrosis within 4-12 hours after myocardial infarction?
Which cellular change is observed 1-3 days after the onset of acute myocardial infarction?
Which cellular change is observed 1-3 days after the onset of acute myocardial infarction?
What signifies the acute phase of myocardial infarction around 3-7 days?
What signifies the acute phase of myocardial infarction around 3-7 days?
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By two weeks post-myocardial infarction, what is a characteristic change in tissue?
By two weeks post-myocardial infarction, what is a characteristic change in tissue?
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What is the primary characteristic of contraction bands observed in myocardial tissue?
What is the primary characteristic of contraction bands observed in myocardial tissue?
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What stage follows after 7-10 days of myocardial infarction in terms of tissue response?
What stage follows after 7-10 days of myocardial infarction in terms of tissue response?
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What is the final outcome expected in the myocardial tissue after two months post-infarction?
What is the final outcome expected in the myocardial tissue after two months post-infarction?
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What characterizes stable angina compared to other forms of angina?
What characterizes stable angina compared to other forms of angina?
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What is the initial phase of myocardial infarction characterized by?
What is the initial phase of myocardial infarction characterized by?
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Which of the following is NOT a complication associated with myocardial infarction?
Which of the following is NOT a complication associated with myocardial infarction?
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What is the primary mechanism by which coronary thrombosis leads to myocardial infarction?
What is the primary mechanism by which coronary thrombosis leads to myocardial infarction?
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What is a characteristic of Prinzmetal angina?
What is a characteristic of Prinzmetal angina?
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Which of the following best describes myocardial necrosis?
Which of the following best describes myocardial necrosis?
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What percentage of coronary artery obstruction is generally associated with symptoms of ischemic heart disease during exertion?
What percentage of coronary artery obstruction is generally associated with symptoms of ischemic heart disease during exertion?
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What is the primary sign of myocardial infarction detectable through EKG/ECG changes?
What is the primary sign of myocardial infarction detectable through EKG/ECG changes?
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What substance is often elevated in the bloodstream following a myocardial infarction?
What substance is often elevated in the bloodstream following a myocardial infarction?
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Which of the following is a significant risk factor for the development of ischemic heart disease?
Which of the following is a significant risk factor for the development of ischemic heart disease?
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What would be a likely finding at autopsy for a patient who developed a ventricular bulge post-myocardial infarction?
What would be a likely finding at autopsy for a patient who developed a ventricular bulge post-myocardial infarction?
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What characterizes a true ventricular aneurysm following a myocardial infarction?
What characterizes a true ventricular aneurysm following a myocardial infarction?
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Which papillary muscle is most susceptible to rupture due to its precarious blood supply?
Which papillary muscle is most susceptible to rupture due to its precarious blood supply?
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What is the typical clinical presentation of a patient with a ruptured papillary muscle leading to mitral valve incompetence?
What is the typical clinical presentation of a patient with a ruptured papillary muscle leading to mitral valve incompetence?
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What is a common late complication of a myocardial infarction that occurs weeks to months later and does not involve communication with pericardium?
What is a common late complication of a myocardial infarction that occurs weeks to months later and does not involve communication with pericardium?
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What is primarily responsible for the hypercontraction observed during reperfusion injury in myocardial infarction?
What is primarily responsible for the hypercontraction observed during reperfusion injury in myocardial infarction?
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Which of the following is NOT a contributing factor to reperfusion injury?
Which of the following is NOT a contributing factor to reperfusion injury?
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What characteristic is observed in myocardial fibers experiencing contraction band necrosis?
What characteristic is observed in myocardial fibers experiencing contraction band necrosis?
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What is a likely immediate complication of myocardial infarction occurring within one hour?
What is a likely immediate complication of myocardial infarction occurring within one hour?
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What is indicated by the acute formation of a mural thrombus in the context of a ventricular aneurysm?
What is indicated by the acute formation of a mural thrombus in the context of a ventricular aneurysm?
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Which complication indicates a low ejection fraction following a massive myocardial infarction?
Which complication indicates a low ejection fraction following a massive myocardial infarction?
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What symptom is associated with acute fibrinous pericarditis following myocardial infarction?
What symptom is associated with acute fibrinous pericarditis following myocardial infarction?
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Which complication might occur as a result of a left ventricular to right ventricular shunt due to rupture?
Which complication might occur as a result of a left ventricular to right ventricular shunt due to rupture?
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What is a common clinical presentation of a patient with a ruptured ventricular septum?
What is a common clinical presentation of a patient with a ruptured ventricular septum?
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What significant effect does contractile dysfunction have on the heart?
What significant effect does contractile dysfunction have on the heart?
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What are heart failure cells and where are they found?
What are heart failure cells and where are they found?
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Which treatment is NOT typically used in managing myocardial infarction?
Which treatment is NOT typically used in managing myocardial infarction?
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What is the primary consequence of a thrombus in the LAD coronary artery?
What is the primary consequence of a thrombus in the LAD coronary artery?
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During the initial stages of congestive heart failure, what percentage of the left ventricle is typically infarcted?
During the initial stages of congestive heart failure, what percentage of the left ventricle is typically infarcted?
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What physiological change is associated with nitrates when treating angina?
What physiological change is associated with nitrates when treating angina?
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In a patient with cardiogenic shock, what immediate concern arises due to decreased cardiac output?
In a patient with cardiogenic shock, what immediate concern arises due to decreased cardiac output?
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Study Notes
Ischemic Heart Disease
- Most significant form of IHD: myocardial infarction, where ischemia causes death of cardiac muscle
- Myocardial infarction is often preceded by angina pectoris
- Angina is not severe enough to cause infarction
- Chronic IHD can progress to heart failure
- Sudden cardiac death is also a consequence of IHD
Pathogenesis of IHD
- Over 90% of patients with IHD have atherosclerosis within one or more coronary arteries
- Obstructions occupying 75% or more of the lumen cause symptoms induced by exertion
- 90% obstruction can lead to insufficient coronary blood flow even at rest
- Acute coronary syndrome is the #1 source of MI
- Acute coronary syndrome typically involves acute plaque rupture of vulnerable or unstable plaque with thrombus formation
- Rupture, erosion, ulceration, and/or deep hemorrhage contribute to acute coronary syndrome
- Intralesional inflammation, which mediates plaque disruption is often associated with acute coronary syndrome
Myocardial Infarction
- Necrosis of cardiac myocytes
- Myocardial infarction typically results from rupture of an atherosclerotic plaque with thrombus
- Complete occlusion of the coronary artery
- Leading cause of death in the US
Myocardial Infarction - Morphological & Pathophysiological Changes
- Initial phase - subendocardial necrosis involving:
- 2 months - Scarring complete
- Dense collagen scar
- Cellular swelling - reversible:
- Occurs in the first 30 minutes
- Decreased oxidative phosphorylation and decreased ATP
- Decreased function of Na+ pump and subsequent influx of H2O and Na+ resulting in cell swelling
- Wavy fibers:
- Seen from 30 minutes to about 4 hours
- Early Coagulative Necrosis:
- Edema occurs between 4 to 12 hours
- Gross changes usually not visible unless aided by TTC staining
- Loss of dehydrogenases
- TTC stains normal myocardium brick-red, leaving infarcted areas pale
- Early Acute MI: 24 hours
- Increased loss of cross striations
- Some contraction bands are also seen
- Nuclei are undergoing karyolysis
- Some neutrophils beginning to infiltrate the myocardium
- Acute MI: 1-3 days
- Coagulative necrosis with loss of nuclei and striations
- Interstitial infiltration of neutrophils
- Acute MI: 1-3 days
- Yellowish center with necrosis and inflammation surrounded by a hyperemic border
- Acute MI: 3-7 days
- Disintegration of dead myofibers
- Early phagocytosis of dead cells by macrophages
- Acute MI: 7-10 days
- Macrophages with numerous capillaries and little collagenization
- Formation of early granulation tissue
- Acute MI: 2 weeks
- Healing MI
- Increase in collagen with decreased cellularity or vascularity
- Grey-white scar from border to center of infarct
- Acute MI: 2 months
- Dense collagen scar
Contraction Bands - Pathophysiological Changes
- Very eosinophilic transverse bands made of closely packed hypercontracted sarcomeres
- Associated with reperfusion injury
- Seen at the margin of infarct
- Represent the effects of hypercontraction due to massive calcium influx across plasma membranes
- Increase in actinomyosin interactions
- Sarcomeres cannot relax in the absence of ATP and “get stuck” in an agonal tetanic state
Complications of Myocardial Infarction (Gross and microscopic)
- Cardiogenic shock (massive infarction)
- Congestive heart failure (low EF)
- Arrhythmia (conduction disturbances and myocardial irritability)
- Acute fibrinous Pericarditis with chest pain and friction rub
- Rupture of Ventricular free wall leading to cardiac tamponade
- Rupture of the Septum leading to a LV->RV shunt
- Rupture of papillary muscle– severe, acute mitral regurgitation
- Ventricular Aneurysm - Mural thrombus formation
- Dressler syndrome - autoimmune pericarditis
True Ventricular Aneurysm
- Late complication of MI
- Weeks to months after MI
- Does NOT involve communication between the LV and the pericardium
- Usually does not rupture
Rupture: Papillary Muscle Rupture
- Leads to incompetent mitral valve (MR)
- Clinical Presentation including: Blood backs up into the lungs, transudation of fluid, shortness of breath, pansytolic murmur
- Posteromedial LV papillary muscle most susceptible due to a precarious blood supply
- Occlusion of RCA, in right dominant heart patients ischemia to posterior LV and 1/3 septum
- Posterior leaflet of mitral valve attaches
Rupture: Ventricular Septum
- Analogous to LV free wall rupture
- Consequence and patient presentation differ
- Blood shunted LV → RV
- Patient presents with right-sided heart failure, JVD, pedal edema, loud systolic murmur at the left sternal border
- Most often associated with the LAD coronary artery thrombosis
Contractile Dysfunction
- Congestive heart failure
- Left ventricular failure
- Decreased contractility
- Cardiogenic shock
- Severely decreased cardiac output
- Hypotension
- Inadequate perfusion of peripheral tissues
- Congestive heart failure develops when more than 40% of the LV has infarcted
Pulmonary Edema and Congestion with Heart Failure Cells
- Blood is phagocytosed by alveolar macrophages
- Hemosiderin accumulates in alveolar macrophages called heart failure cells
MI Treatment
- Aspirin and, or heparin – limits thrombosis
- Supplemental oxygen – minimize ischemia
- Nitrates – vasodilate coronary arteries (decrease preload = decrease stress)
- Beta-Blockers – slows heart rate, decreasing oxygen demand and risk for arrhythmia
- ACE Inhibitors – decrease LV dilation
- Fibrinolysis or angioplasty – opens blocked vessel
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Description
This quiz explores Ischemic Heart Disease (IHD), focusing on myocardial infarction, angina pectoris, and their implications. It addresses the pathogenesis of IHD, including the role of atherosclerosis and acute coronary syndromes. Test your knowledge on the causes, symptoms, and consequences of this critical cardiovascular condition.
