Cardiac Physiology Flashcards
What is Ohm’s law? How does it relate to blood flow in the human body?
Ohm’s law characterizes the relationship between current and voltage across a resistor:
I = ΔV/R
I, current; ΔV, voltage gradient; R, resistance
This law can be applied to calculate the total electrical current through an electrical circuit, or it can be
used to calculate the localized current through a specific resistor in a circuit. An analogy of Ohm’s law can be made for blood flow in the human body. Where the pressure gradient (Δ P ), across the resistance (R), of a vascular bed acts as a driving force for blood flow (Q), through the said vascular bed. The relationship between blood flow, pressure, and systemic vascular resistance (SVR) can be characterized by the following analogous equation:
Q =ΔP/R
Q, flow; ΔP, pressure gradient; R, resistance
This equation can be applied to various “resistors” or “circuits” within the human body. Recall, two circuits in
series will have the same amount of current or blood flow (i.e., pulmonary and systemic circulation), whereas two resistors in parallel (e.g., mesenteric vs. musculoskeletal circulation) will have varying degrees of blood flow, depending upon their relative resistance. Thus the human body can be described as two circuits in series (i.e., pulmonary and systemic) with multiple resistors in parallel for each circuit. Moreover, the regional blood flow can vary between parallel vascular beds by modulating vascular resistance between sympathetic and parasympathetic tone (i.e., systemic circulation) or by hypoxic pulmonary vasoconstriction (i.e., pulmonary circulation).
Therefore using Ohm’s law, cardiac output can be calculated for the pulmonary and systemic “circuits”, respectively:
CO = mPAP - LAP / PVR
Pulmonary circulation
CO = MAP-CVP /SVR
Systemic circulation
CO, cardiac output; mPAP, mean pulmonary artery pressure; LAP, left atrial pressure; PVR, pulmonary vascular resistance; MAP, mean arterial pressure; CVP, central venous pressure; SVR, systemic vascular resistance
What is the Fick principle?
Over 150 years ago, Dr. Fick introduced the principle that the uptake of a substance (e.g., oxygen) is equal to
the product of blood flow and the difference between arterial venous concentration of that substance. Most commonly, this equation is solved for cardiac output by calculating the difference between arterial and venous oxygen content and measuring (or approximating) oxygen consumption, V̇ O2. The V̇ O2 is generally estimated by body weight, or BSA, and not directly measured in a clinical setting. Therefore this is usually the greatest source of error.
The Fick principle can be used to calculate cardiac output by the following equation:
CO =VO2 / CaO2-CvO2
CO, cardiac output (mL of blood/min); V̇O2, O2 consumption (mL of O2 /min); CaO2 –CvO2, difference between arterial and venous O2 content
What is oxygen content? How do you calculate it?
Oxygen content is the amount of O2 in arterial or venous blood per unit volume. The arterial oxygen content can be calculated from an arterial blood gas, whereas the venous oxygen content is calculated from a mixed venous blood gas using a pulmonary artery catheter to sample blood from the pulmonary artery.
Arterial oxygen content, for example, can be calculated by the following equation:
O2 content = 1.36 x Hgb x SaO2 +0.003 x PaO2(mL of O2/dL of blood)
What is the most important factor in determining oxygen content?
The most important factor in oxygen content is the hemoglobin concentration and hemoglobin oxygen saturation. Oxygen partial pressure is a minor contributor to oxygen content.
What is a typical V̇ O2? What are the determinants of myocardial oxygen demand?
Total body oxygen consumption in a healthy adult at rest, a metabolic equivalent equal to one, is 3 to 4 mL O2/kg/min or about 250 mL O2/min for a 70-kg person. Metabolic equivalents (MET) are categorized by multiples of the baseline oxygen consumption, V̇ O2, at rest. For example, to safely undergo major surgical operations, a patient should have the physiologic reserve to climb greater than one flight of stairs or walk greater than two city blocks (i.e., MET >/= 4), which yields the following:
Vo2 >/= 250 mL O2/min x 4 = 1000mL O2/min
Myocardial oxygen demand depends on the amount of work performed by the heart (primarily the ventricles). The primary determinants of myocardial oxygen demand are wall tension (e.g., increases in afterload) and heart rate. Other factors include contractility and ventricular chamber size; however, fundamentally both of these factors are related to wall tension (see question on Laplace’s law).
What is Laplace’s law and how does it apply to myocardial oxygen demand?
The law of Laplace characterizes the relationship between pressure, wall radius, and wall thickness in determining wall tension as depicted subsequently:
σ = Pr/2h
σ, wall tension; P, pressure within the chamber; r, chamber radius; h, chamber wall thickness
This explains the pathophysiological adaptation of the heart to chronic hypertension or aortic stenosis, which
cause concentric hypertrophy of the left ventricle. The ventricular wall thickens as an adaptive mechanism to minimize wall tension (i.e., afterload) and hence oxygen demand. It is important to emphasize that afterload can be defined as anything that increases wall tension on the ventricle as depicted by this equation.
What is the equation for coronary perfusion pressure?
Coronary perfusion pressure can be explained by the following equation:
CPP = Paorta - Pventricle
CPP, coronary perfusion pressure; Paorta, aortic pressure; Pventricle, ventricular pressure
Although this equation is true for the right heart in both systole and diastole, the left heart is only perfused during diastole, where the equation can be simplified to the following:
CPP = dBP - LVEDP
CPP, coronary perfusion pressure; dBP, aortic diastolic blood pressure; LVEDP, left ventricular end-diastolic pressure
What happens to coronary blood flow during systole and diastole?
The left heart is only perfused during diastole when the aortic pressure (Paorta) is greater than the ventricular pressure (Pventricle). Therefore it is important to avoid tachycardia to maintain coronary perfusion to the left heart. The right heart, however, is perfused during systole and diastole, as the aortic pressures are generally higher than the right ventricular pressures in both systole and diastole.
Describe the determinants of myocardial oxygen supply and their relationship.
Oxygen delivery to the myocardium is the product of coronary blood flow (CBF) and the oxygen content of arterial blood (CaO2):
Myocardial O2 Supply = CBF x CaO2
Recall, that oxygen content (CaO2) is determined by the following:
CaO2 = 1.36 x Hg x SaO2 + 0.003 x PaO2
CorBF is governed with the same relationship as I = ΔV/R, where ΔV is the coronary perfusion pressure:
CorBF = (Paorta - Pventricle) /CorVR
Paorta, aortic root pressure; Pventricle, ventricular chamber pressure; CVR, coronary vascular resistance
Therefore myocardial oxygen supply can be rewritten as the following:
MyocardialO2supply =
(Paorta-Pventricle) x CaO2
CVR
How can you increase myocardial oxygen supply and delivery?
From the earlier equation, the myocardial oxygen supply (CaO2) can be increased by any of the following:
1) Increase [Hg] by transfusing red blood cells.
2) Maintain an SaO2 of 100% with supplemental oxygen.
3) Maintain an adequate coronary perfusion pressure (Paorta – Pventricle) with vasopressors (i.e., phenylephrine) to
increase Paorta.
4) Reduce ventricular pressure (Pventricle) with diuretics and/or venodilators (e.g., nitroglycerin).
5) Avoid tachycardia, as ventricular pressure (Pventricle) increases during systole, causing coronary blood flow to the
left ventricle to approach or equal zero.
How can this be used to understand coronary ischemia? How does this pertain to
coronary artery disease, aortic stenosis, and right heart failure because of a pulmonary embolism?
In referring to the aforementioned equations for coronary blood flow, anything that decreases aortic blood pressure, increases ventricular pressure, increases coronary resistance (e.g., coronary stenosis or thrombosis), or
decreases oxygen delivery (e.g., anemia) can cause coronary ischemia.
In patients with coronary artery disease, it is important to avoid tachycardia as the left heart is only perfused
during diastole. Further, any medical condition associated with an excessively high ventricular filling pressure (e.g., congestive heart failure, end-stage renal disease, aortic stenosis, pulmonary embolism) can decrease coronary perfusion.
Recall, if Pventricle increases, then coronary perfusion pressure decreases, where CorPP = Paorta – Pventricle.
Therefore management of patients with these conditions (e.g., aortic stenosis, right heart failure because of pulmonary embolism) include strategies to optimize coronary perfusion (e.g., diuretics to decrease Pventricle or vasopressors to increase Paorta).
What is Poiseuille’s law and how does it relate to blood flow in the human body?
R = (8ηL) / (πr4)
R, resistance; η, viscosity of blood; L, blood vessel length; r, blood vessel radius
Poiseuille’s law explains the various factors that affect resistance of flow provided flow is laminar and
nonturbulent. For example, low hematocrit blood flowing through a short, wide caliber vessel would have low resistance, whereas high hematocrit blood flowing through a long, narrow caliber vessel would have high resistance to flow. The most important factor affecting resistance to flow is radius, as doubling this parameter will decrease resistance by a factor of 16. The resistance of the arterial vasculature is significantly higher than the venous system, especially at the level of the arterioles.
What is compliance and how does it affect blood flow in the human body?
C = ΔV / ΔP
C, compliance; ΔV, volume; ΔP, pressure
Compliance reflects the ability of a vessel to distend for a given pressure. Veins are much more compliant
than arteries because they lack muscular stiffness. Arteries (and veins) often become stiff with age
(i.e., arteriosclerosis) causing decrease compliance. This may contribute or even cause hypertension and will reduce a patient’s physiologic reserve in the setting of hemorrhage. Classically, patients with noncompliant, stiff arteries have a larger pulse pressure.
Veins are approximately 20 to 30 times more compliant than arteries and store approximately two-thirds
of the entire blood volume. An important concept to appreciate is that this large volume of blood, stored in
the venous vasculature, can be recruited in situations associated with hypovolemia or hemorrhagic shock through increased sympathetic tone. In the setting of hypovolemia, increased sympathetic tone stimulates α1 adrenergic receptors causing venoconstriction, which deceases venous compliance and facilitates venous return to maintain preload.
What is the physiological response to hemorrhage? How does age affect this response?
In the setting of hemorrhage, sympathetic tone increases to prevent decreases in blood pressure and cardiac output to ultimately preserve oxygen delivery to tissues.
Increased sympathetic tone causes the release of norepinephrine and epinephrine, which stimulate α1 adrenergic receptors on the arteries (primarily the arterioles) to increase SVR.
These same catecholamines also stimulate α1 adrenergic receptors on the veins to decrease venous compliance, facilitating venous return to maintain preload and cardiac output.
Finally, these catecholamines also increase heart rate (i.e., chronotropy) and contractility (i.e., inotropy) to maintain normal cardiac output.
Young, healthy patients tend to have greater physiological reserve and can tolerate relatively large volumes of blood loss before their vitals become abnormal (i.e., tachycardia and hypotension).
However, older patients tend to have diminished physiological reserve because of atherosclerosis (decrease venous compliance and ability to recruit blood), decreased cardiac contractility and response to catecholamines, and often are on medications, such as β blockers that blunt their physiological response to hemorrhage.
Describe the basic structure and function of the heart.
The heart is a muscular organ whose primary purpose is to generate a pressure gradient to drive nutrient and oxygen- rich blood delivery to other organs. The heart consists of four chambers: two atria and two ventricles (Fig. 5.1). The heart is customarily split into two halves: the right side of the heart and the left side. Each successive chamber is separated from the next by a one-way pressure-regulated valve.
All four chambers of the heart contract in a coordinated fashion to generate the movement of blood throughout the entire cardiovascular system. Most of its mass is composed of a continuous band of muscle that is wrapped about the ventricular chambers of the heart to facilitate coordinated contraction.
The left and right sides of the heart are separated by a fibromuscular wall called a septum. The septum at the level of the atria is termed the interatrial septum and between the ventricles as the interventricular septum. The right side of the heart receives deoxygenated blood from the venous system into the right atrium. Blood flows passively and is actively moved across the tricuspid valve (TV) into the right ventricle (RV). This blood is actively pumped across the pulmonic valve (PV) into the pulmonary vascular bed and returns, oxygenated, to the left atrium. Left atrial blood is passively and actively moved across the mitral valve (MV) into the left ventricle (LV). The LV then contracts with enough pressure to pump the oxygenated blood via the aortic valve (AV) throughout the entire cardiovascular system of the body and back to the right atrium.
