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What is the primary consequence of chronic pressure overload on the cardiac myocyte?
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 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?
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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?
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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?
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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.
