Quick Review: Hemodynamics

Tisha K. Fujii DO
Dept. of Trauma & Critical Care
Boston University School of Medicine
Boston Medical Center

Address:
Boston
Ma.
USA

Bradley J. Phillips MD
Dept. of Trauma & Critical Care
Boston University School of Medicine
Boston Medical Center

Address:
Boston
Ma.
USA

Citation: T. K. Fujii & B. J. Phillips : Quick Review: Hemodynamics . The Internet Journal of Academic Physician Assistants. 2003 Volume 3 Number 1

---

Abstract

Before discussing basic hemodynamics, we should remind ourselves of the systemic circuit:
1. Cardiac Anatomy
2. Circulatory Pathways
This brief review discusses the basics of hemodynamics.

---

Cardiac Anatomy

The Heart: 2 Separate Volume Pumps !

• RA & RV - Low Pressure “Bellows”
• LA & LV - High Pressure “Drive”

The in-series nature of these two systems implies that the output of the Right Heart becomes the input of the Left Heart, and therefore, the output of the Left Heart becomes the input of the Right Heart

Flow via Series: Demonstrated by William Harvey, 1628

• The Heart is a muscular organ enclosed in a fibrous sac (the Pericardium)
• Cardiac Muscle is termed the Myocardium
• The inner surface of the myocardium (the one icontact with the blood) is lined by a thin layer of Endothelium
• The Heart is divided into Right & Left Halves
• Each consisting of an atrium & ventricle
• Separated by the Atrioventricular Valves: Tricuspid, Mitral
• Openings of the RV into the Pulmonary Trunk & the LV into the Aorta are also regulated by Valves: Pulmonic, Aortic

Valve Function is a Passive Process ! Function of Papillary Muscles

Desaturated Blood returns from the Systemic Vessels via the SVC & IVC

• Is displaced passively (and actively with atrial contraction) through the Tricuspid Valve - into the Right Ventricle.
• Contraction of the RV ejects this volume through the Pulmonic Valve and into the Low-Pressure Pulmonary Artery, (PAP 5 - 12) then through the associated end-capillaries where gas-exchange occurs !

Saturated Blood is then returned to the Left Atrium via the Pulmonary Veins !

• In the LA, the blood is displaced to the LV (15 - 20 % Atrial “Kick”)
• With LV Contraction, blood is forced through the aortic valve into the high-pressure aorta (SBP 120 - 160) thus perfusing the brain, kidneys, abdominal viscera, and extremities

Myocardial Perfusion occurs primarily during Diastole

Myocardial Blood Flow:

Flow is provided by the Right & Left Coronary Arteries which are the first branches of the aorta, arising from the Sinuses of Valsalva RCA - supplies the RV Wall, Sinus Node, and AV Node in 90 % of pts, the RCA terminates as the Posterior Descending Artery (Right Coronary Dominance)The Left Main Coronary gives rise to both LAD & Circumflex The LAD is usually the largest of all coronary arteries and supplies the anterior / apical LV, the majority of the IV Septum, and the left side of the RVThe Circumflex supplies the lateral LV and in 10 % of pts provides the Posterior Descending Coronary (Left Coronary Dominance) Venous Drainage of the Heart: Occurs mainly via the Coronary Sinus (into the RA).
also: Anterior Cardiac Veins, Thebesian Channels, Sinusoidal Paths
Total Coronary Flow: 0.7 - 0.9 ml/min/g myocardium

Myocyte Contraction

Chemical Energy ..............................  Mechanical Energy
(Oxygen & Substrate)			   	(Pressure & Flow)

At the cellular level, electrical depolarization of the myocardial cell membrane allows ionized calcium flux into the cytoplasm - leading to hydrolysis of ATP by Myosin.

This leads to a conformational change in the Actin-Myosin Cross Bridge producing sliding of myosin filaments relative to actin & overall shortening of the sarcomere [Sliding Filament Theory]

Calcium is then removed from the cell by Active Transport in the Sarcoplasmic Reticulum - allowing Relaxation, while ATP is regenerated by Metabolic Processes

Over the physiologic range of sarcomere length (1.6 - 2.0 um), the amount of metabolic energy converted to mechanical work is dependent on the available Surface Area of Cross-Bridge Interactions !

Work is directly proportional to End-Diastolic Sarcomere Length

This “Length Dependency” is the fundamental basis for the Frank-Starling Law !

Otto Frank, 1885 (Frog Heart Preparations):“the output of a normal heart is influenced primarily by the volume of blood in the ventricle at the end of diastole”

• Ernest Starling, 1914 (extended this basic principle to mammalian hearts)

• Relationship: EDV to SP

• The Steep Ascending Portion of the Curve ! This area indicates the importance of PreLoad (i.e. Volume) for augmenting Output

• The “Descending Limb”
• As EDV becomes Excessive, Pressure begins to Fall
• WHY ?
• Is it clinically significant?

Cardiac Output

CO = HR x SV “the amount of blood pumped by the heart per unit time”

Normal C.O. : 3.5 - 8.5 L/min

Manipulation of the factors can lead to augmentation of CO at the lowest possible energy cost !

Determinants of Cardiac Performance & Output

Preload: EDV (the load that stretches a muscle prior to contraction)
Afterload: SVR (the load that must be moved during muscle contraction)
Contractility: the velocity of muscle shortening at a constant preload and afterload
Compliance: the length that a muscle is stretched by a given preload. Determined by the inherent Elasticity !
Heart Rate: several effects on overall Cardiac Function : Tachycardia/Bradycardia

Preload

• At the cellular level, Preload is defined as end-diastolic sarcomere length which is linearly related to EDV.
• Problem: We can not measure Ventricular Volume in the Clinical Setting (rather impractical !)
• LVEDP represents the Distending Pressure (the Filling Pressure) of the Ventricle and can be used as an index of EDV
• However, this Relationship is Exponential, NOT Linear!
• In Normal Hearts, LA Pressure correlates with LV Pressure and thus, becomes the closest approximation of Preload
• Can Measure LA Pressure by using a Left Atrial Catheter! But tubes are tubes and series are series !!
• In Clinical Practice, Pulmonary Capillary Wedge Pressure is used as an index of LAP & LVEDP

PCWP = LAP = LVEDP (best approximation)

But Remember, the relationship between LVEDP & LVEDVis NOT Linear!!
PCWP is by definition an ESTIMATE of EDV& thus, an ESTIMATE of Preload

• At Filling Pressures of 15 - 18 mm Hg (PCWP), the ventricle operates on the very steep portion of the Diastolic Compliance Curve where further increases in PCWP lead to little change in EDV (and CO)
• Issues:
• Potential Injury / Relative Ischemia
• Hyperdynamic Resuscitation
• Also, the Relationship between PCWP & EDV is NOT Constant !
• It is Affected by Changes in Compliance, Wall Thickness, HR, Ischemia, & Medications
• This is a “One-Point-in-Time” Effect
• Right-sided Filling Pressure: CVP
• has been used as a rough estimate of LV Preload, but it may be an unreliable indicator of ventricular function (especially in the critically ill patient)
• can be used to guide Volume Status
• i.e. what is returning to the right atrium/right ventricle ?
• may also be useful in patients with suspected cardiac tamponade or constrictive pericarditis

Elevation of CVP to Equal PAD& PCWP
Square Root Sign : characteristic RA waveform in patients with Constrictive Pericarditis

Afterload

The impedance to LV Ejection and is usually estimated by the Systemic Vascular Resistance. Remember: changes in afterload have no effect on the contractility of a normal heart

• The Normal Heart: SW performed at a given EDV is Insensitive to changes in SVR
• The Impaired Heart: Increasing afterload MAY decrease SW output for a given EDV, and thus impair myocardial performance
• when faced with this situation, if you reduce LV Impedance you may be able to increase CO !
• Sodium Nitroprusside
• Intra-Aortic Balloon Pump

SVR = {(MABP - CVP)/CO} x 80

MBAP (Mean Arterial Blood Pressure) = DBP + [1/3(SBP - DBP)]

SVR units: dynes-second/cm⁵

Decreasing Afterload exchanges Pressure Work for Flow Work and serves to increase vital organ perfusion !

Pressure Work................................................Flow Work

Plus, since pressure work is more costly than flow work in terms of myocardial oxygen consumption, by decreasing afterload - you also decrease the overall energy requirement

PVR = {(MPAP - PWP)/CO} x 80

Remember:

Preload must be Optimized PRIOR to Afterload ReductionA Low Arterial Pressure may preclude SVR ManipulationRV Afterload = PVR
• only a massive change in PVR can induce primary heart dysfunction
• the vast majority of RV Failure is Secondary to LVF and usually responds to measures directed at the LV
• Isolated RVF :
• Massive PE, Severe COPD (post-op),
• Isolated RV Infarct

Contractility

the inotropic state: an intrinsic property of myocardial muscle which is manifested as a greater force of contraction for a given preload

In terms of pressure & volume, the ventricle performs the same SW for a given EDV when the inotropic state is held constant.When the inotropic state is augmented, more SW is produced at the same EDV. Clinically, this translates into Increased CO & MAP at a given Filling Pressure !

By increasing intropic state, you increase both Pressure Work & Flow Work - thus, the cost in myocardial oxygen consumption may be high !!

• An increased inotropic state may lead to a delay in recovery of function following myocardial injury!
• Inotropic Agents should only be used with caution & only AFTER other factors have been optimized!
• Preload
• Afterload
• Heart Rate

Compliance & Elasticity

“Compliance”: the tendency of an object to return to it's original shape when it has been deformed or altered

(Compliance = change in Volume / change in Pressure)

The more elastic the muscle, the less it will be stretched by preload (i.e. the less compliant it is)Elasticity is the Reciprocal of Compliance!

Heart Rate

Heart Rate can Influence Cardiac Function in Several Ways:

Increasing the Contraction Frequency limits Diastolic Filling Time, Coronary Perfusion Time, & Reduces overall EDVIncreasing Rate increases Work Output from the ventricle per unit time at a given EDV. [An Inotropic Effect]Increasing Rate increases Myocardial O2 ConsumptionBradycardia significantly decreases CO

Cardiac Physiology is based on a thorough understanding of the underlying mechanics !

Anatomy & CirculationFlow & Perfusion Myocyte ContractionThe Frank-Starling RelationshipCardiac Output & the Determinant Factors

---

This article was last modified on Fri, 13 Feb 09 13:19:27 -0600

This page was generated on Tue, 09 Feb 10 08:12:01 -0600, and may be cached.