Heart Muscle Mechanics

7/29/2019 Heart Muscle Mechanics

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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 ventricularpreload.

NOTE: Pulmonary wedge pressure is used to estimate left atrial pressure.

Facts on Preload:

Increased preload = increased sarcomere length causing more cross-linking and more forcefulcontraction during systole.

Preload increases ventricular contraction / contractility.

This increases performance.

Performance can increase due to increased preload or contractility of both.

Cardiac Contractility:

Contractility = change in performance at a given preload / sarcomere length.

Contractility increases with increased Ca.

Cardiac Function Formulas:

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.

MAP = CO x TPR.

Cardiac Function Curves:


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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.

Increased Afterload and Hypertrophy:

Chronic exposure of ventricle to increased afterload causes it to hypertrophy, which maintains strokevolume.

Control of Heart Rate:

110 beats/min.


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Parasympathetic:

Right vagus n. = SA node.

Left vagus N. = AV node.

Sympathetic:

Stimulation causes tachycardia, and increased cardiac output.

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.

Isovolumetric Relaxation and Contraction:

Isovolumetric relaxation (terminated by opening mitral valve) and contraction (terminated by openingaortic valve).

Mitral and bicuspid valves are closed; no change in ventricular volume.

Systolic vs Diastolic Heart Failure:

Systolic: Blood can't leave the heart.

Diastolic: Blood can't enter the heart.

Cardiac Phases:

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.


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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.


Very high left ventricular pressure, and an equally high aortic pressure. A powerful mitral is pushingblood into the left ventricle with a weak aortic valve, so the ventricle is not pushing it into the aorta withequal force. In the end, the pressure is very high in the left ventricle and equally high in the aortabecause 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 powerfulbut stenosed mitral valve is pushing blood into the left ventricle.


Hence, normal left ventricular pressure + increased ventricle-aortic pressure gradient = mitralstenosis.

Mitral Insufficiency:

Blood regurgitates from LV to LA. Systolic murmur.


Hence, slightly higher left ventricular pressure + equal ventricle-atria pressure gradient = mitralinsufficiency.

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.

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Heart Muscle Mechanics