Cardiac Output & Stroke Volume Lecture Notes PDF

**[Lecture 4 & 5]** **End-Diastolic Volume (EDV):** The volume of blood in the ventricle when it\'s fully relaxed and filled with blood, typically around 120-130 ml. **The end of ventricular relaxation, just before it contracts.** **End-Systolic Volume (ESV):** The volume of blood remaining in...

**[Lecture 4 & 5]** **End-Diastolic Volume (EDV):** The volume of blood in the ventricle when it\'s fully relaxed and filled with blood, typically around 120-130 ml. **The end of ventricular relaxation, just before it contracts.** **End-Systolic Volume (ESV):** The volume of blood remaining in the ventricle after it has contracted, typically around 50-60 ml.   **If more blood comes back to the heart input, the output is greater; more venous return = greater Stroke volume.** Increased ventricular thickness is counterproductive to SV/, decreases pre-load. 1. **Preload and Venous Return:** - **Preload** refers to the initial stretching of the cardiac myocytes (heart muscle cells) ***[prior to contraction]***. It largely depends on the amount of blood filling the ventricles (end-diastolic volume or EDV), which is influenced by venous return---the blood returning to the heart. 2. **Frank-Starling Law:** - This law states that the force of the heart\'s contraction is directly related to the initial length (stretch) of the cardiac muscle fibers. Essentially, the more the heart muscle is stretched during filling, the stronger the subsequent contraction will be. - This is represented in the graph as the **ventricular function curve** or **Frank-Starling relationship**. 3. **Impact of Increased Stretch:** - When the ventricles fill with more blood (increased EDV), the muscle fibers stretch more. This increased stretch results in more myofilament cross-bridges forming, which enhances the heart\'s ability to contract. Additionally, the sensitivity of these myofilaments to calcium (Ca²⁺) increases, further boosting contractility. 4. **Inotropy:** - **Inotropy** refers to the strength of the heart\'s contraction. - The graph shows how stroke volume changes with varying levels of inotropy. The solid line represents normal inotropy, while the dashed and blue lines represent decreased and increased inotropy, respectively. Increased inotropy results in a higher stroke volume for a given EDV, while decreased inotropy results in a lower stroke volume. 5. **Length-Tension Relationship:** - The relationship between the length of the cardiac muscle fibers (due to EDV) and the tension they can generate is fundamental to this concept. As the length increases, the tension (and thus the force of contraction) also increases, which in turn increases stroke volume.  1. **Forces Contributing to Afterload:** - **Elastic Forces:** These relate to the stretchiness or compliance of the arteries. Less elastic (stiffer) arteries increase afterload because the heart must work harder to overcome the resistance posed by these rigid vessels. - **Kinetic Forces:** These involve the velocity and flow of blood through the circulatory system. The faster the blood flows, the more resistance it creates, adding to the afterload. 2. **Terms like \"Resistance\" or \"Impedance\":** - These terms describe the opposition to blood flow that the heart must overcome. Higher resistance (like from narrower or stiffer arteries) means a higher afterload. 3. **Main Opposing Forces:** - **Arterial Blood Pressure:** The higher the blood pressure in the arteries, the greater the force the ventricles must generate to push blood out, thus increasing afterload. - **Vascular Tone:** This refers to the degree of constriction or dilation in the blood vessels. Increased vascular tone (constriction) raises afterload because the heart has to pump against narrower vessels. 4. **Impact on Stroke Volume:** - **Increased Afterload (e.g., from Atherosclerosis):** When conditions like atherosclerosis (narrowing of the arteries due to plaque buildup) increase arterial resistance, the stroke volume (the amount of blood ejected per beat) initially decreases. This is because the heart struggles to overcome the higher resistance. - **Compensatory Mechanisms:** Over time, the heart adapts to the increased afterload through mechanisms like ventricular hypertrophy (thickening of the heart muscle) or by increasing contractility. These adaptations help to restore or maintain stroke volume and ensure sufficient blood flow despite the higher resistance. 1. **Contractility:** - Defined as the inherent strength of the heart muscle\'s contraction during systole. It\'s independent of muscle fiber length (which is influenced by preload or end-diastolic volume). 2. **Ventricular Function Curve:** - This curve represents the relationship between **ventricular end-diastolic volume (EDV)** (the amount of blood in the ventricles before contraction) and **stroke volume (SV)**. - The curve shifts based on the heart's contractility. 3. **Shifts in the Curve:** - **Shift to the Left (Positive Inotropy):** When the contractility increases (e.g., due to sympathetic stimulation, circulating catecholamines, or positive inotropic drugs like digitalis), the curve shifts to the left. This means that for any given EDV, the heart can pump out more blood, increasing stroke volume. - **Shift to the Right (Negative Inotropy):** When contractility decreases (e.g., due to factors like hypoxia, acidosis, or pharmacological depressants), the curve shifts to the right. This indicates a reduced stroke volume for a given EDV. 4. **Descending Limb:** - The **dashed line** in the diagram represents the descending limb of the Frank-Starling curve. This occurs when contractility is exceeded to the point where the heart muscle becomes overstretched, and the efficiency of contraction diminishes. Beyond this point, even if the EDV increases, the stroke volume starts to decrease because the heart can no longer contract effectively. 5. **Factors Influencing Contractility:** - **Positive Influences:** Sympathetic nerve impulses, circulating catecholamines, and positive inotropic agents (e.g., digitalis) enhance contractility. - **Negative Influences:** Conditions like hypoxia, acidosis, loss of myocardium, or the use of pharmacological depressants decrease contractility. **Summary:** Contractility is the strength of the heart\'s contraction during systole and can be influenced by various factors. The ventricular function curve shifts left with positive inotropy (increased contractility) and right with negative inotropy (decreased contractility). The dashed line on the descending limb of the curve highlights a point where the heart\'s contractile capacity is exceeded, leading to a drop in stroke volume despite increased filling.