Lecture Notes on Preload, Contractility, Blood Pressure, and Circulation
Hemodynamics and Perfusion
Preload
- Preload is the volume of blood in the ventricles at the end of diastole (end-diastolic volume).
- Dehydration leads to decreased preload.
- Signs of decreased preload in dehydrated patients include a thready pulse.
- Fixing Preload: Increasing volume (e.g., with IV fluids).
- Typically, low preload is the problem.
Contractility
- Contractility refers to the force of ventricular contraction (the "swish").
- Impact of Heart Attack (Myocardial Infarction - MI):
- Can impair the muscle of the heart.
- Can disrupt the electrical activity of the heart.
- Either issue will compromise contractility (the "squish").
Stroke Volume and Cardiac Output
Stroke volume is influenced by preload, afterload, and contractility.
Compensation for Dehydration: In dehydrated patients, heart rate increases to maintain cardiac output.
- Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV).
- When stroke volume decreases (due to dehydration), the heart rate increases to compensate.
- Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV).
Myocardial Infarction (MI): Also known as a heart attack.
Blood Pressure and Perfusion
Arterial blood pressure is essential for organ perfusion.
Formula for Mean Arterial Pressure (MAP):
Organ Response to Low Blood Pressure: If blood pressure drops too low, organs will not perfuse adequately, leading to organ damage or death.
Vulnerable Organs: Kidneys are often among the first to suffer damage from inadequate perfusion.
Body's Response to Hypotension: The body prioritizes blood flow to the brain, heart, and kidneys, potentially sacrificing perfusion to extremities, the gut, and the liver.
- Cold extremities are a sign of this compensatory mechanism.
Shock: Prolonged inadequate perfusion leads to shock and multisystem organ failure.
- Organ damage from shock may be irreversible.
Blood Pressure Regulation
Blood pressure is regulated by multiple mechanisms.
Neurological Control: Neurons in the brain regulate blood pressure via the sympathetic and parasympathetic nervous systems.
- Sympathetic nervous system increases blood pressure and heart rate.
- Parasympathetic nervous system decreases blood pressure and heart rate.
Kidney's Role: Receptors in the kidneys monitor blood pressure and fluid balance.
- The kidneys activate the renin-angiotensin-aldosterone system (RAAS) to increase blood pressure when perfusion is inadequate.
- Kidney injury or failure often leads to blood pressure dysregulation (either too high or too low).
ACE Inhibitors: Angiotensin-converting enzyme (ACE) inhibitors are medications that block the conversion of angiotensin I to angiotensin II, thus lowering blood pressure.
- These medications target the renin-angiotensin system.
Aldosterone: A hormone produced by the adrenal glands and kidneys that promotes sodium and water retention to increase blood pressure.
Altered Perfusion: Causes and Mechanisms
Altered perfusion refers to impaired blood flow to tissues and organs.
Underlying Respiratory Issues: Inadequate oxygenation due to respiratory problems impairs perfusion.
Circulation Problems: Hemorrhage or blood clots obstruct blood flow.
Inadequate Pumping: Heart failure or other cardiac conditions reduce cardiac output.
Excessive Demand: Increased metabolic demands can outstrip the body's ability to perfuse tissues adequately.
Anemia: Reduced oxygen-carrying capacity impairs oxygen delivery to organs.
- Anemia reduces the amount of oxygen that can be delivered to organs, impacting perfusion.
VQ Mismatch: VQ mismatch is a condition in which ventilation and perfusion are not properly matched in the lungs.
Impaired Circulation
- Hemorrhage:
- Injury to a blood vessel results in hemorrhage.
- The "Stop the Bleed" campaign aims to educate people on how to control bleeding from deep wounds, particularly in mass shooting events.
- Death from deep wounds is often due to exsanguination (bleeding out).
- Controlling hemorrhage helps maintain preload and cardiac output.
- Obstruction:
- Obstructions impair circulation by impeding blood flow.
- Thrombus: A blood clot that forms in a blood vessel.
- Pulmonary Embolus (PE): A blood clot that travels to the lungs, blocking pulmonary circulation.
- If a clot detaches, it becomes a thromboembolus.
- Venous Stasis: Stagnant blood flow in the veins, promoting clot formation.
- Prolonged standing can lead to venous stasis and varicose veins.
- Compression socks prevent venous stasis by promoting venous return.
- Sequential compression devices (SCDs) mimic the effect of compression socks in hospitalized patients.
- Veins have valves to prevent backflow, but prolonged pressure can damage these valves, leading to varicose veins.
- Hypercoagulability: Increased tendency to form blood clots.
- Thrombocythemia: An abnormally high number of platelets in the blood.
- Platelets are involved in blood clotting.
- Virchow's Triad: Describes the three broad categories of factors that are thought to contribute to thrombosis
- Endothelial injury (damage to the blood vessel lining).
- Hypercoagulability (increased tendency to clot).
- Venous stasis (slow or stagnant blood flow).
- All three contribute to increase risk of clot formation.
- Atherosclerosis: Deposition of fat in the arteries.
- Aneurysms and Bifurcations: Weakened blood vessel walls or abnormal branching can impede blood flow.
Cardiac Output Impairment
- Inadequate cardiac output results in inadequate perfusion.
- Factors that Change Cardiac Output:
- Blood volume and viscosity.
- Electrical and pumping function of the heart.
- Heart rate and rhythm.
- Blood pressure regulation.
- Structural defects in the heart (e.g., atrial septal defect (ASD) or ventricular septal defect (VSD)).
- ASD: Hole between the atria.
- VSD: Hole between the ventricles.
- Structural defects cause abnormal blood flow patterns.