Notes on Heart Muscle Mechanics
Rahul's Noteblog
Notes on Cardiology
Notes on Heart Muscle Mechanics
Systolic performance:
• Force of ventricular muscles during systole.
• Depends on preload and contractility.
Preload:
• Load on muscle during relaxation.
• Cannot be measured directly, rather, indices are used: LVEDV and LVEDP.
• However, preload is estimated clinically by measuring the pulmonary wedge pressure.
• Swan-Ganz catheter: used to measure pulmonary wedge pressure; used to measure ventricular preload.
• NOTE: Pulmonary wedge pressure is used to estimate left atrial pressure.
Increased preload = increased sarcomere length causing more cross-linking and more forceful contraction during systole.
Preload increases ventricular contraction / contractility.
This increases performance.
Performance can increase due to increased preload or contractility of both.
Contractility = change in performance at a given preload / sarcomere length.
Contractility increases with increased Ca.
Ejection Fraction = SV/EDV.
SV = EDV – ESV = CO/HR.
Cardiac Output = (oxygen consumption) / (aortic oxygen content – pulmonary artery oxygen content).
EF can be estimated using noninvasive techniques.
Cardiac function curves:
• Provide information on preload vs contractility.
Vector I (lower left): loss in preload due to hemorrhage, etc.; increased contractility compensates.
Vector II (lower right): loss of contractility due to congestive HF, etc.; increased preload compensates.
Vector III (upper left): acute increase in contractility; decreased preload.
Vector IV (upper right): acute increase in preload; contractility decreases.
Afterload:
• Load on muscle during contraction.
• Indices: mean arterial pressure and peak left ventricular pressure.
Chronic exposure of ventricle to increased afterload causes it to hypertrophy, which maintains stroke volume.
Control of HR:
• 110 beats/min.
Parasympathetic:
• Right vagus n. = SA node.
• Left vagus N. = AV node.
Sympathetic:
• Stimulation causes tachycardia, and increased CO.
Brainbridge reflex: right atrium stretch causes increased HR.
Baroreceptor reflex and BP control:
Baroreceptor reflex: short term blood pressure management.
Renin-angiotensin-aldosterone system: long term blood pressure management.
Carotid sinus: monitor wall-stretch and arterial blood pressure
Medulla: measures arterial blood pressure.
MAP = CO x TPR.
Isovolumetric relaxation (terminated by opening mitral valve) and contraction (terminated by opening aortic valve).
Mitral and bicuspid valves are closed; no change in ventricular volume.
Ejection phase: left ventricular ejection.
Filling phase: left ventricular filling.
Heart sounds:
Systolic:
• S1: Mitral / Tricuspid valve closure.
• S2: Aortic / Pulmonic valve closure.
• S2 splitting: delayed closing of pulmonic valve.
Diastolic:
• 3rd and 4th: ventricular filling.
• Jugular pulse is generated by changes on the right side of heart.
NOTE: Any type of stenosis creates an increased pressure gradient.
Aortic stenosis:
• Aortic stenosis causes concentric hypertrophy.
• Overall pressure inside the left heart is very high.
• High-pressure gradient between left ventricle and aorta.
• Essential hypertension.
• Pressure ~ 160 mmHg.
• Aortic valve acts as resistance in series.
• Very high left ventricular pressure, but aortic pressure remains relatively low. A powerful but blocked aortic valve is pushing blood out the left ventricle.
• Hence, high left ventricular pressure + increased ventricle-aortic pressure gradient = aortic stenosis.
Aortic insufficiency:
• Overall pressure inside the left heart is very high.
• Aortic valve does not close properly.
• Causes: increased preload, increased ventricular and aortic systolic pressures, decreased aortic diastolic pressure, increased aortic pulse pressure, diastolic murmur, and eccentric hypertrophy.
• Pressure ~ 160 mmHg.
• Very high left ventricular pressure, and an equally high aortic pressure. A powerful mitral is pushing blood into the left ventricle with a weak aortic valve, so the ventricle is not pushing it into the aorta with equal force. In the end, the pressure is very high in the left ventricle and equally high in the aorta because the left ventricle and aorta connection has been compromised.
• Hence, high left ventricular pressure + equal ventricle-atrial pressure gradient = aortic insufficiency.
Mitral stenosis:
• Diastolic murmurs are present. Pressure is high in the left atria, but low in the left ventricle. A powerful but stenosed mitral valve is pushing blood into the left ventricle.
• Pressure ~ 100 mmHg.
• Hence, normal left ventricular pressure + increased ventricle-aortic pressure gradient = mitral stenosis.
Mitral insufficiency:
• Blood regurgitates from LV to LA. Systolic murmur.
• Pressure ~ 100 mmHg.
• Hence, slightly higher left ventricular pressure + equal ventricle-atria pressure gradient = mitral insufficiency.
Pressure-volume loops:
• Highest energy consumption: isovolumetric contraction.
• Most work done: ejection phase.
• Heart failure: loop shifts to right.
• Increased contractility: loop shifts to left.
Additional Reading:
Basic Cardiology
1. Electrical Activity of the Heart
2. Heart Muscle Mechanics
3. Heart Sounds and Murmurs
Related Topics
1. Thorax Anatomy
2. Vascular Disorders
3. Heart Disorders
4. Histology of the Cardiovascular System
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Page accessed on: July 29, 2010, 11:40 am.