Cardiac Output Cheatsheet

Cheatsheet Content

Cardiac Output (CO) Definition: The volume of blood pumped by each ventricle per minute. Formula: $CO = HR \times SV$ $HR$: Heart Rate (beats/min) $SV$: Stroke Volume (mL/beat) Normal Adult Range: Approximately $4.0 - 8.0 \, L/min$ at rest. Factors Determining Stroke Volume (SV) 1. Preload (End-Diastolic Volume - EDV) Definition: The degree of stretch of cardiac muscle cells just before they contract. It's related to the venous return filling the ventricles. Frank-Starling Law of the Heart: Within physiological limits, the force of contraction is directly proportional to the initial length of the cardiac muscle fiber. Increased preload $\rightarrow$ increased stretch $\rightarrow$ increased force of contraction $\rightarrow$ increased SV. Factors Affecting Preload: Venous Return: Blood volume (hydration, hemorrhage) Skeletal muscle pump (activity, immobility) Respiratory pump (breathing) Venous tone (vasoconstriction/vasodilation) Ventricular Filling Time: Heart rate (tachycardia reduces filling time) 2. Afterload Definition: The pressure that the ventricles must overcome to eject blood into the aorta (left ventricle) or pulmonary artery (right ventricle). It is the resistance against which the heart pumps. Relationship to SV: Increased afterload $\rightarrow$ increased resistance $\rightarrow$ decreased SV. Decreased afterload $\rightarrow$ decreased resistance $\rightarrow$ increased SV. Factors Affecting Afterload: Total Peripheral Resistance (TPR) / Systemic Vascular Resistance (SVR): Arteriolar constriction/dilation Blood viscosity Length and diameter of blood vessels Aortic/Pulmonic Valve Stenosis: Narrows the opening, increasing resistance. Hypertension: Chronically increases afterload. 3. Contractility (Inotropy) Definition: The intrinsic contractile strength of the cardiac muscle, independent of muscle stretch (preload). Relationship to SV: Increased contractility $\rightarrow$ increased force of contraction at any given preload $\rightarrow$ increased SV. Decreased contractility $\rightarrow$ decreased force of contraction $\rightarrow$ decreased SV. Factors Affecting Contractility: Positive Inotropic Agents (Increase Contractility): Sympathetic nervous system stimulation (norepinephrine, epinephrine) Digitalis (cardiac glycosides) Increased intracellular $Ca^{2+}$ Negative Inotropic Agents (Decrease Contractility): Parasympathetic nervous system stimulation (acetylcholine - modest effect) Beta-blockers Calcium channel blockers Acidosis, hypoxia Factors Determining Heart Rate (HR) 1. Autonomic Nervous System Sympathetic Nervous System (SNS): Releases norepinephrine (NE) at cardiac nerve endings and epinephrine (EPI) from adrenal medulla. Acts on $\beta_1$-adrenergic receptors in SA node. Increases rate of depolarization $\rightarrow$ increases HR (positive chronotropic effect). Parasympathetic Nervous System (PNS): Releases acetylcholine (ACh) via vagus nerve. Acts on muscarinic M2 receptors in SA node. Decreases rate of depolarization $\rightarrow$ decreases HR (negative chronotropic effect). Dominant at rest (vagal tone). 2. Hormones and Ions Epinephrine/Norepinephrine: Released by adrenal medulla, similar effects to SNS. Thyroxine: Increases metabolic rate and heart rate. Ions: $Ca^{2+}$: Excess or deficiency can alter HR and contractility. $Na^{+}$ and $K^{+}$: Imbalances can lead to arrhythmias. 3. Other Factors Age: HR generally decreases with age. Sex: Females typically have slightly higher resting HR. Fitness Level: Athletes often have lower resting HR. Body Temperature: Fever increases HR. Emotions: Stress, anxiety increase HR. Drugs: Many medications affect HR (e.g., stimulants, sedatives). Regulation of Cardiac Output The body continuously adjusts HR and SV to match metabolic demands. Baroreceptor Reflex: Located in carotid sinuses and aortic arch. Sense changes in blood pressure. Increased BP $\rightarrow$ increased baroreceptor firing $\rightarrow$ increased PNS activity / decreased SNS activity $\rightarrow$ decreased HR and SV $\rightarrow$ decreased CO and BP. Decreased BP $\rightarrow$ decreased baroreceptor firing $\rightarrow$ decreased PNS activity / increased SNS activity $\rightarrow$ increased HR and SV $\rightarrow$ increased CO and BP. Chemoreceptor Reflex: Located in carotid and aortic bodies. Sense changes in blood $O_2$, $CO_2$, and pH. Hypoxia, hypercapnia, acidosis $\rightarrow$ increased SNS activity $\rightarrow$ increased HR and SV. Other Reflexes: Atrial (Bainbridge) reflex, higher brain centers (hypothalamus, cerebral cortex).