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Questions and Answers
What is the primary consequence of chronic pressure overload on the cardiac myocyte?
What is the primary consequence of chronic pressure overload on the cardiac myocyte?
Which of the following is a characteristic feature of pathologic hypertrophy?
Which of the following is a characteristic feature of pathologic hypertrophy?
What is the primary mechanism underlying the transition from adaptive hypertrophy to maladaptive hypertrophy?
What is the primary mechanism underlying the transition from adaptive hypertrophy to maladaptive hypertrophy?
What is the effect of altered calcium handling on cardiac function?
What is the effect of altered calcium handling on cardiac function?
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What is the primary function of the sarcoplasmic reticulum (SR) Ca-pump in cardiac myocytes?
What is the primary function of the sarcoplasmic reticulum (SR) Ca-pump in cardiac myocytes?
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What is the consequence of upregulation of the sarcolemmal Na-Ca exchanger activity in cardiac myocytes?
What is the consequence of upregulation of the sarcolemmal Na-Ca exchanger activity in cardiac myocytes?
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What is the primary mechanism underlying diastolic dysfunction in heart failure?
What is the primary mechanism underlying diastolic dysfunction in heart failure?
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What is the consequence of impaired activation of ryanodine receptors in cardiac myocytes?
What is the consequence of impaired activation of ryanodine receptors in cardiac myocytes?
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Which of the following is a characteristic feature of eccentric hypertrophy?
Which of the following is a characteristic feature of eccentric hypertrophy?
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What is the primary consequence of ventricular wall thinning in cardiac remodeling?
What is the primary consequence of ventricular wall thinning in cardiac remodeling?
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Study Notes
Adaptive Response to Physiologic Stress and Increased Workload
- The adaptive response to physiologic stress and increased workload involves the Frank-Starling mechanism, neurohormonal response, and cardiac remodeling.
- The neurohormonal response includes increased sympathetic activity, increased activation of the renin-angiotensin-aldosterone system (RAAS), and cardiac remodeling.
Regulation of Cardiac Output
- Cardiac output (CO) is regulated by heart rate, contractility, afterload, and preload.
- CO = heart rate (HR) x stroke volume (SV).
- Factors affecting CO include sympathetic and parasympathetic activity, contractility, afterload, and preload.
LV Pressure Volume Loop
- The LV pressure volume loop is a graphical representation of the cardiac cycle.
- The loop consists of four phases: diastolic ventricular filling, isovolumetric contraction, systole, and isovolumetric relaxation.
- The end-diastolic pressure volume relationship (EDPVR) and end-systolic pressure volume relationship (ESPVR) are important components of the LV pressure volume loop.
Heart Failure
- Heart failure is a syndrome resulting from any structural or functional cardiac disorder that impairs the ability of the ventricles to fill with or eject blood.
- Hemodynamic changes in heart failure include decreased output, decreased filling, and neurohormonal changes.
- Cellular changes in heart failure include inefficient intracellular calcium handling, adrenergic desensitization, myocyte hypertrophy, re-expression of fetal phenotype proteins, cell death, and fibrosis.
Causes of Heart Failure
- Mechanical damage, including pressure overload and volume overload, can lead to heart failure.
- Myocardial damage, including dilated cardiomyopathy, hypertrophic cardiomyopathy, and myocarditis, can also lead to heart failure.
- Other causes of heart failure include coronary heart disease, pericardial disease, and restrictive cardiomyopathy.
HFrEF and HFpEF
- Heart failure with reduced ejection fraction (HFrEF) is characterized by impaired contractile function, inadequate CO, and hypoperfusion.
- Heart failure with preserved ejection fraction (HFpEF) is characterized by impaired ability of the ventricles to relax and fill during diastole, leading to decreased SV and CO.
Maladaptive Response
- Chronic RAAS activation can lead to maladaptive changes, including elevated arteriolar resistance, excess fluid retention, and myocardial remodeling.
- Chronic heart failure is characterized by an imbalance of neurohormonal mechanisms, leading to impaired contractility, adverse cardiac remodeling, excessive vasoconstriction, and excess fluid buildup.
Preload and Afterload
- Preload is the volume of blood in the ventricles at the end of diastole, and it increases with increased fluid volume.
- An increase in preload leads to an increase in SV and CO, and results in an increase in the width of the PV loop.
- Afterload is the pressure that the ventricle must eject blood against, and it increases with increased aortic pressure.
- An increase in afterload leads to a decrease in SV and CO, and results in a decrease in the width of the PV loop.
Contractility
- An increase in contractility shifts the PV loop upward and to the left, resulting in an increase in stroke volume.
- A decrease in contractility shifts the PV loop to the right, resulting in ventricular wall thinning, scar formation, and infarct expansion.
Cardiac Remodeling
- Physiologic hypertrophy is a response to chronic exercise training, and it is characterized by increased myocyte size, formation of new sarcomeres, and adequate vasculature.
- Pathologic hypertrophy is a response to pressure and volume overload, and it is characterized by increased myocyte size, formation of new sarcomeres, cardiac fibrosis, myocyte necrosis, and apoptosis.
- Concentric hypertrophy is a response to pressure overload, and it is characterized by increased systolic wall stress, leading to the addition of sarcomeres in parallel.
- Eccentric hypertrophy is a response to volume overload, and it is characterized by increased diastolic wall stress, leading to the addition of sarcomeres in series.
Altered Calcium Handling
- Altered calcium handling is a key feature of heart failure, and it is characterized by decreased function of the sarcoplasmic reticulum (SR) Ca-pump, upregulation of the sarcolemmal Na-Ca exchanger activity, and impaired activation of ryanodine receptors.
- This leads to impaired excitation-contraction coupling, systolic dysfunction, and diastolic dysfunction.
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Description
This quiz covers the adaptive response to physiologic stress, including the Frank-Starling mechanism, neurohormonal response, and cardiac remodeling. It also explores the pathophysiologic steps in response to increased workload.
