Cardiac Output and Blood Flow Flashcards

Cardiac Output and Frank-Starling Law

• At homeostasis, cardiac output equals venous return.

Frank-Starling Law

• Developed by Otto Frank and Ernest Starling (1895-1914).
• Describes the relationship between stroke volume and end-diastolic volume (EDV).
• Stroke volume increases in response to increased blood volume in the ventricles before contraction (EDV).
• A larger volume causes the cardiac muscle to stretch.
• Increased stretch of cardiac muscle leads to a greater force of contraction.
• Cardiac output is synchronized with venous return.
• Analogous to the length-tension relationship in striated muscles.
• Greater muscle stretch results in greater tension.
• Unlike skeletal muscle, cardiac muscle's force is dependent on increasing calcium sensitivity.

Blood Vessel Structure

• Artery: Contains tunica intima (endothelium, loose connective tissue, internal elastic lamina), tunica media (smooth muscle, elastic fibers, external elastic lamina), and tunica externa (collagen fibers).
• Vein: Contains tunica intima (endothelium, basement membrane), tunica media (smooth muscle, elastic fibers), tunica externa (collagen fibers), and valves.
• Arterioles branch from arteries and venules merge into veins; capillaries form a network between arterioles and venules.

Blood Pressure Regulation

• Factors influencing blood pressure:
  • Heart rate (HR): beats per minute.
  • Peripheral resistance (PR): constriction of arteries.
  • Stroke volume (SV): blood volume ejected per beat.
  • Blood volume (BV): total blood available.
  • Blood viscosity: thickness of blood.
  • Cardiac output (CO): mL ejected from the ventricle per minute.
• Formulas:
  • Cardiac\ Output = Heart\ Rate \times Stroke\ Volume (CO = HR \times SV)
  • Stroke\ Volume = End\ Diastolic\ Volume - End\ Systolic\ Volume (SV = EDV - ESV)
  • Blood\ Pressure = Cardiac\ Output \times Peripheral\ Resistance (BP = CO \times PR)

Mechanism of Blood Pressure Regulation

• A decrease in blood volume (BV) leads to a decrease in blood pressure (BP).
• Decreased BP stimulates baroreceptors in the carotid arteries, aortic arch, and kidneys.
• Baroreceptor stimulation activates the cardiac center in the medulla.
• The medulla stimulates the sympathetic nervous system, releasing norepinephrine (nor) and epinephrine (epi).
• This increases cardiac function.

Heart Rate Regulation

• Epinephrine and norepinephrine bind to 𝛽 receptors on the sinoatrial (SA) node of the heart.
• Potassium (K+) leak gates close more frequently, triggering action potentials.
• Calcium (Ca2+) is released more often, increasing heart rate.
• Increased HR leads to increased cardiac output (CO = HR \times SV), resulting in increased blood pressure (BP = CO \times PR).

Peripheral Resistance Regulation

• Epinephrine and norepinephrine bind to 𝛼 receptors on smooth muscle surrounding arteries.
• This opens calcium gates on the membrane.
• Ca2+ diffuses in, increasing actin and myosin binding.
• Arteries vasoconstrict, potentially halving the original diameter and increasing peripheral resistance fourfold.
• Peripheral resistance is the friction of blood against the artery walls.
• Increased peripheral resistance raises blood pressure (BP = PR \times CO).

Stroke Volume - End Diastolic Volume

• Mechanism 1
  • Epinephrine and norepinephrine bind to receptors on smooth cardiac and skeletal muscle, increasing Ca2+ diffusion into the cell.
  • Excess Ca2+ causes muscle twitching.
  • Veins in muscle are “milked” by twitching.
  • Blood returns to the heart, increasing end-diastolic volume (EDV).
  • Increased EDV increases stroke volume (SV = EDV - ESV).
  • Increased SV increases cardiac output (CO = SV \times HR).
  • Increased CO increases blood pressure (BP = CO \times PR).
• Mechanism 2
  • Epinephrine and norepinephrine bind to respiratory muscles, expanding the thoracic cage and decreasing intrathoracic pressure.
  • Blood pressure in extremities becomes higher than in the heart, promoting venous return.
  • Increased venous return increases EDV.
  • Increased EDV increases SV.
  • Increased SV increases CO.
  • Increased CO increases BP.

Stroke Volume - End Systolic Volume

• Mechanism 1
  • Epinephrine and norepinephrine bind to myocardial cells, opening Ca2+ gates on the membrane.
  • Ca2+ diffuses into the cell, increasing actin and myosin binding and contractility.
  • Increased ventricular force decreases end-systolic volume (ESV).
  • Decreased ESV increases stroke volume (SV = EDV - ESV).
  • Increased SV increases cardiac output (CO = SV \times HR).
  • Increased CO increases blood pressure (BP = CO \times PR).
• Mechanism 2 (Frank-Starling Law)
  • Increased venous return to the heart stretches ventricular muscle.
  • Stretching aligns actin and myosin, increasing contraction force.
  • This decreases end-systolic volume.
  • Decreased ESV increases stroke volume (SV = EDV - ESV).
  • Increased SV increases cardiac output (CO = SV \times HR).
  • Increased CO increases blood pressure (BP = CO \times PR).

Blood Volume Regulation

• Epinephrine and norepinephrine bind to receptors on juxtaglomerular (JG) cells in the kidneys.
• JG cells release renin.
• Renin converts angiotensinogen to angiotensin I.
• Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE).
• Angiotensin II:

Angiotensin II Effects

• Causes arteries to vasoconstrict, increasing BP (BP = PR \times CO).
• Stimulates the adrenal cortex to secrete aldosterone.
• Aldosterone stimulates the kidneys to increase reabsorption of sodium.

Sodium and Blood Volume

• Increased sodium in the blood causes water to move by osmosis into the blood.
• This increases blood volume.
• Increased blood volume increases cardiac output.
• Increased CO increases blood pressure (BP = CO \times PR).
• Sodium stimulates osmoreceptors in the hypothalamus.
• This stimulates thirst and the release of antidiuretic hormone, decreasing urine output.

Blood Viscosity Regulation

• Bleeding decreases the number of red blood cells (RBCs).
• Decreased RBCs reduces oxygen (O2) content.
• Chemoreceptors in the kidneys stimulate the release of erythropoietin.
• Erythropoietin stimulates erythropoiesis in bone marrow.
• Increased RBCs increase blood viscosity.
• Increased blood viscosity increases peripheral resistance.
• Increased peripheral resistance increases blood pressure (BP = PR \times CO).

Hypotension

• Orthostatic Hypotension:
  • Sudden loss of blood pressure upon standing.
  • Causes: dehydration, prolonged bed rest, pregnancy, medical conditions, medications, diabetes, arrhythmias.
  • Seek medical attention if fainting occurs.
• Severe Hypotension (Shock):
  • Causes: severe infection, sudden blood loss, heart attack, severe allergic reaction.
  • Symptoms and Blood Pressure Ranges:
    • Nausea, dizziness: 90/60 mmHg
    • Fainting, tiredness: 80/60 mmHg
    • Weakness, blurry vision: 80/50 mmHg
    • Sleepiness, confusion: 70/50 mmHg
    • Coma and death: 60/45 mmHg to 50/35 mmHg

Blood Pressure Chart

• Systolic Blood Pressure:
  • Normal: < 120 mmHg
  • Prehypertension: 120-139 mmHg
  • High Stage 1 Hypertension: 140-159 mmHg
  • High Stage 2 Hypertension: 160+ mmHg
• Diastolic Blood Pressure:
  • Normal: < 80 mmHg
  • Prehypertension: 80-89 mmHg
  • High Stage 1 Hypertension: 90-99 mmHg
  • High Stage 2 Hypertension: 100+ mmHg
• Vessel changes with hypertension include increased wall thickness and reduced interior diameter.

Hypertension

• No Hypertension: Heart pumps normally, blood flows easily through vessels.
• Hypertension: Heart pumps harder, blood may not flow easily through vessels.

Cardiac Output Factors

• Factors that Increase Cardiac Output:
  • Increased heart rate (sympathetic stimulation).
  • Increased stroke volume (increased EDV, decreased ESV due to sympathetic stimulation).
• Factors that Decrease Cardiac Output:
  • Decreased heart rate (decreased sympathetic/increased parasympathetic stimulation).
  • Decreased stroke volume.

Cardiac Output Graphs

• Cardiac output is affected by sympathetic stimulation, pathology, and right atrial pressure.
• Right atrial pressure affects venous return.

Cardiac Output and Venous Return

• Three factors affecting venous return:
  1. Right atrial pressure (backward pressure on veins).
  2. Degree of filling of systemic circulation (mean systemic filling pressure).
  3. Resistance to blood flow between peripheral vessels and right atrium.

Venous Return Curve

• Arterial and venous pressures reach equilibrium when systemic circulation ceases.
• This is called the mean systemic filling pressure.

Mean Systemic Filling Pressure

• Mean pressure in circulatory system when no blood is in motion.
• Value is approximately 7 mmHg.
• Influenced by blood volume and smooth muscle tone.
• Measured by clamping the aortic root and great veins at the right atrium.
• Indirectly measured by inspiratory holds during mechanical ventilation.
• Used to determine:
  • Additional fluid needs.
  • Vasopressor needs.
  • Effect of drugs on venous tone.
  • Determination of hemorrhage during surgery.

Cardiac Output and Venous Return Graphs

• Graphs can be used to determine cardiac output and venous return under different conditions (normal, spinal anesthesia, moderate sympathetic stimulation, maximal sympathetic stimulation).
• Also, can be used for determining the mean systemic filling pressure for each condition (pregnancy, spinal surgeries, etc.).

Exercise Impact on Cardiac Output and Venous Return

• Venous return curve rises due to:
  • Increased mean systemic filling pressure.
  • Decreased resistance to venous return in active tissues.
• Heavy exercise increases these effects (red curve compared to black curve which is normal).

Coronary Blood Flow

• Normal flow at rest averages 225 ml/min or 4-5% of total cardiac output.
• During strenuous exercise, coronary blood flow increases 3-4x to meet the heart muscle's energy needs.

Coronary Circulation

• Left Coronary Artery: Arises from the left posterior aortic sinus; gives rise to the circumflex artery and left anterior descending artery.
• Right Coronary Artery: Arises from the right anterior aortic sinus.
• Coronary Sinus.
• Anterior Cardiac Veins.

Anastomiosis

• Connection/opening between two divergent structures.
• Takes place between branches of coronary arteries.
• If a blockage occurs in one coronary artery slowly, the second artery can still supply oxygen-rich blood.
• Blockage must progress slowly for anastomoses to proliferate.

Coronary Blood Flow Regulation

• Flow occurs primarily during diastole (ventricular relaxation).
• Local flow is regulated by local arteriolar demands.
• Increases with decreased oxygen and increased adenosine.
• Decreased heart activity is accompanied by decreased coronary flow.

ANS Impact on Coronary Blood Flow During Exercise

• Parasympathetic
  • Dilates blood vessels.
  • Decreases metabolic rate.
  • Metabolic control outweighs neural control, resulting in constriction of coronary arteries.
• Sympathetic
  • Constricts blood vessels.
  • Increases metabolic rate.
  • Metabolic control outweighs neural control, resulting in dilation of coronary artery.
• Take home message: a well-conditioned heart has the best blood supply.

Burning Carbohydrates

• Exercising between moderate (60% heart rate max) to high intensity (90% heart rate max) results in carb burning.
• Glycogen stores are utilized.
• Losing “water weight” is due to decreased glycogen (as well as perspiration).
• Marathon runners “hit the wall” when glycogen is depleted.
• Carb loading improves performance during exercises lasting over 90 minutes.
• Reduction in whole body lipid oxidation.
• Eat large amounts of carbs (8-12g/kg) 24 hours pre marathon.
• To lose weight, we don’t want to burn carbs, but rather fat.

Burning Fat

• Subtract your age from 220 for maximum heart rate.

• Fat burning zone is between 50-70% of maximum heart rate.

• Example:

  • 37-year-old =
  • 220 - 37 = 183 \ bpm
  • 60% of 183 = 110 bpm

• Less intense cardio for longer duration results in burning fat.