N715 Exam 3 New Pt 2

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Questions and Answers

Which statement accurately describes a characteristic of myocardial hibernation?

It leads to complete necrosis of the cardiac myocytes.

It causes significant regional wall motion abnormalities without any compensatory mechanisms.

It is characterized by altered contractility but preserved ejection fraction. (correct)

It results in irreversible damage to the myocardium due to prolonged ischemia.

What is the primary effect of oxidative stress mechanisms on cardiomyocytes during an MI?

It enhances mitochondrial efficiency, improving ATP production.

It leads to increased production of reactive oxygen species, damaging cellular components. (correct)

It stimulates myocardial regeneration and repair processes.

It promotes vasodilation and increased coronary perfusion.

In the context of calcium handling in cardiomyocytes during heart failure, which of the following statements is correct?

Increased calcium uptake by the sarcoplasmic reticulum enhances muscle relaxation.

Calcium handling abnormalities contribute to impaired contractility and arrhythmogenesis. (correct)

Calcium overload leads to decreased cardiac contraction in all heart failure types.

Differences in calcium handling have no impact on cardiac output.

What distinguishes NSTEMI from STEMI regarding myocardial tissue damage?

In NSTEMI, only a portion of the ventricular wall is necrotic, retaining some contractile ability. Signup and view all the answers

Which of the following is a consequence of reperfusion injury following an MI?

Increased inflammatory response and oxidative stress leading to additional myocardial damage. Signup and view all the answers

What primarily contributes to myocardial stunning following brief ischemic events?

Increased formation of reactive oxygen species Signup and view all the answers

Which cellular source is a primary origin of reactive oxygen species in the context of myocardial stunning?

Cardiomyocytes Signup and view all the answers

What role does calcium overload play in myocardial stunning?

It contributes to mitochondrial dysfunction and ROS formation. Signup and view all the answers

Which of the following best describes the phenomenon that occurs during myocardial stunning?

Reversible contractile dysfunction after myocardial ischemia. Signup and view all the answers

What is the significance of the sarcoplasmic reticulum dysfunction in myocardial stunning?

It induces calcium overload into the cytosol. Signup and view all the answers

Which treatment approach can be utilized to mitigate the severity of myocardial stunning?

Inotropic agents and antioxidants Signup and view all the answers

Which of the following conditions does not characterize myocardial stunning?

Hemodynamically compromising alterations Signup and view all the answers

What is the role of the feedback loop between reactive oxygen species and calcium overload in myocardial stunning?

It perpetuates the stunning phenomenon. Signup and view all the answers

What is the primary cause of reperfusion injury in cardiovascular conditions?

Restoration of blood flow after ischemia Signup and view all the answers

How does impaired calcium handling in cardiomyocytes affect heart function?

Leads to reduced myocardial efficiency Signup and view all the answers

Which characteristic is associated with myocardial hibernation?

Reversible state of myocardial dysfunction Signup and view all the answers

What mechanism does oxidative stress primarily invoke in cardiomyocytes during ischemic conditions?

Increased production of reactive oxygen species Signup and view all the answers

Which of the following conditions is most likely to contribute to calcium overload in cardiomyocytes?

Sodium-potassium pump dysfunction Signup and view all the answers

Which statement about oxidative stress mechanisms in heart conditions is accurate?

It contributes to cellular injury and cardiac dysfunction. Signup and view all the answers

What is a characteristic feature of myocardial hibernation?

Reduction in myocardial contractility due to prolonged ischemia Signup and view all the answers

How does oxidative stress specifically influence calcium handling in cardiomyocytes?

Promotes dysfunction of calcium regulatory proteins Signup and view all the answers

Study Notes

Myocardial Remodeling

Myocardial Remodeling: Structural and functional changes in the heart after a myocardial infarction (MI), the body's response to damage.
Mediators: Angiotensin II (Ang II), aldosterone, catecholamines, adenosine, and inflammatory mediators contribute to remodeling.
Effects: Myocyte hypertrophy, loss of contractile function, and increased myocardial dysfunction, potentially leading to heart failure.

Phases of Remodeling

Initial Phase: Inflammatory response where damaged cells are degraded, macrophages remove dead cells, and scar tissue forms over 6 weeks.
Potential for Re-injury: Activity during this phase may stress the newly formed scar tissue.

Functional Impairment

Reduced Contractility: Abnormal wall motion.
Altered Compliance and Function: Reduced stroke volume, increased end-diastolic pressure.
SA Node Malfunction and Dysrhythmias: Potential for heart failure.

Consequences of MI and Remodeling

Ventricular Dysfunction: Decreased ejection fraction (EF), increased ventricular end-diastolic volume (VEDV).
Vasoconstriction and Coronary Spasm: Due to Ang II release, impacting fluid retention and remodeling.
Electrolyte Abnormalities: Disruptions in potassium, calcium, and magnesium balance.

Long-term Outcomes

Chronic Heart Failure: Due to sustained functional impairment.
Sudden Cardiac Death: Result of severe dysrhythmias after MI.

Therapeutic Interventions

Reperfusion Therapy: Crucial to reduce infarct size, but can cause reperfusion injury.
Medications: Renin-angiotensin-aldosterone blockers and beta-blockers to inhibit remodeling and restore coronary flow.
Emerging Therapies: Investigation into ischemia-reperfusion injury reduction in cardioprotection, alongside stem cell therapy for cardiac muscle repair and regeneration.

Symptoms

Typically involves severe, sudden chest pain, unlike angina.
Other symptoms may include nausea, vomiting, radiation of pain, and sensation resembling indigestion.
Silent infarction: Some individuals experience no pain.

Cardiovascular Changes

Sympathetic Nervous System activation: Compensatory mechanism leading to increased heart rate and blood pressure.
Extra Heart Sounds: Indicate left ventricular dysfunction.
Pulmonary Congestion: Dull percussion and inspiratory crackles, symptomatic if heart failure develops.
Peripheral Vasoconstriction: Causes cool, clammy skin.

Postinfarction Complications

Severity and number depend on necrosis extent, prior condition, and promptness of treatment.
Common complications include heart failure, arrhythmias, pericarditis, and thromboembolism.

Risk Factors and Sudden Cardiac Death

Myocardial ischemia, with or without infarction.
Interplay between ischemia, left ventricular dysfunction, and electrical instability.

Myocardial Stunning

Myocardial stunning: Prolonged yet reversible post-ischemic contractile dysfunction.
Reperfusion injury: Reflects increased reactive oxygen species (ROS) formation and decreased calcium responsiveness.

Key Mechanisms

Reactive Oxygen Species (ROS): Major contributor to myocardial stunning during reperfusion.
Calcium Overload: Ischemia-reperfusion results in increased cytosolic calcium, impairing mitochondrial function and ROS formation.

Myocardial Hibernation

Myocardial hibernation: Reversible reduction in myocardial contractile function due to chronic ischemia.
Metabolic adaptations: Enable myocardial viability in response to chronic reduced blood flow.
Flow-Function Matching: Hibernating myocardium demonstrates a state of metabolic adaptation to decreased blood flow and function.

Molecular Adaptations

Downregulation of proteins for calcium handling.
Expression of heat shock proteins.
Modifications to mitochondrial and cytoskeletal proteins.

Prevention and Treatment

Addressing the underlying causes (such as hypertension and coronary artery disease).
Treatments to restore myocardial perfusion and function, including revascularization, stem cell procedures, and pharmacological interventions (statins, and others).

Heart Failure

Heart failure (HF) or congestive heart failure (CHF): Characterized by the heart’s inability to pump sufficient blood, potentially chronic or acute.
Chronic Heart Failure: Results from conditions like untreated hypertension and coronary artery disease.

Acute Heart Failure

Sudden onset of heart failure, often caused by conditions like myocardial infarction (MI), pulmonary embolism (PE), or acute left-sided heart failure.

Types of Heart Failure

Heart Failure with Reduced Ejection Fraction (HFrEF): Ejection fraction less than 40%.
Heart Failure with Preserved Ejection Fraction (HFpEF): Ejection fraction greater than 50%; obesity linked, more common in women

Clinical Manifestations

Often asymptomatic initially
Headaches
Shortness of breath (dyspnea).
Swelling (edema) in legs, ankles, and feet.
Fatigue and weakness.

Cardiovascular Conditions

Conditions that affect the heart, including its structure and function.

Diagnosis

Symptoms
Structural abnormalities
Lab findings.

Causes of Heart Failure

MI, valve damage, high heart rate
Ejection Fraction: percentage of blood pumped out per heartbeat.

Mechanisms of Heart Failure

Contractile dysfunction
Neurohormonal reactions.
Renal perfusion changes.

Types and Pathophysiology of Cardiomyopathy

Dilated
Hypertrophic
Restrictive

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Description

This quiz explores the structural and functional changes in the heart following a myocardial infarction (MI). It covers the phases of remodeling, mediators involved, and the consequences such as reduced contractility and potential for heart failure.