Cardiovascular Pathophysiology and Heart Function

• HR is the Heart Rate.
• SV is the Stroke Volume.

Because a large person requires more blood than a small person, clinicians often use the Cardiac Index (CI), which scales the cardiac output to the patient's body surface area (BSA): $CI = \frac{CO}{BSA}$

Stroke Volume (SV) and Ejection Fraction (EF)

Stroke volume is the amount of blood ejected from the left ventricle during a single contraction. It is the difference between the volume of blood in the ventricle at its fullest and its emptiest: $SV = EDV - ESV$ Where:

• End-Diastolic Volume (EDV) is the maximum blood volume at the end of the relaxation phase.
• End-Systolic Volume (ESV) is the minimum blood volume remaining after contraction.

A vital clinical measure of how well the heart is pumping is the Ejection Fraction (EF). This represents the percentage of the total EDV that is actually ejected with each beat: $EF = \frac{EDV - ESV}{EDV}$

Mean Arterial Pressure (MAP)

Blood pressure is the force required to perfuse organs. The Mean Arterial Pressure (MAP) is the average pressure in a patient's arteries during one cardiac cycle and can be calculated using the relationship between CO and Systemic Vascular Resistance (SVR): $MAP = CO \times SVR$ Alternatively, using blood pressure readings, MAP can be estimated as: $MAP = \frac{(2 \times \text{diastolic pressure}) + \text{systolic pressure}}{3}$

Determinants of Stroke Volume

The efficiency of the heart's contraction (Stroke Volume) is influenced by three primary mechanical factors: preload, contractility, and afterload.

1. Preload: This is the degree of stretch of the myocardial fibers at the end of diastole. It is primarily dependent on venous return (the amount of blood returning to the heart).
2. Contractility (Inotropy): This refers to the intrinsic force of the myocardial contraction at any given preload. This relationship is described by the Frank-Starling Mechanism, which states that as the initial muscle fiber length increases (due to increased preload), the force of the subsequent contraction also increases.
3. Afterload: This is the resistance or "wall stress" the ventricle must overcome to eject blood during systole. A major contributor to afterload is the SVR. According to LaPlace’s Law, the tension on the ventricular wall is influenced by ventricular pressure, the radius of the chamber, and the thickness of the wall: $\text{Tension} = \frac{\text{ventricular pressure} \times \text{radius}}{2 \times \text{wall thickness}}$

Exam Tip: Remember that "Inotropy" refers to the force of contraction (contractility), while "Chronotropy" refers to the heart rate. Some drugs can affect both, but they are distinct physiological concepts.

Clinical Pathophysiology: Atherosclerosis and Ischemia

The Process of Atherosclerosis

Atherosclerosis is the "hardening" of the arteries caused by an inflammatory response to injury. The "Response to Injury" hypothesis suggests that risk factors like hypertension, diabetes, and smoking injure the endothelial lining. This injury leads to the accumulation of oxidized LDL, which attracts monocytes that migrate into the subendothelial space and become macrophages. These macrophages ingest the lipids to become foam cells, forming a fatty streak.

Over time, this develops into a fibroproliferative plaque consisting of two main parts:

• Fibrous Cap: A hard, collagen-rich tissue that stabilizes the plaque.
• Lipid Core: A soft, lipid-rich center that is highly dangerous because it can destabilize the plaque.

Ischemic Heart Disease (IHD) and Acute Coronary Syndromes (ACS)

Ischemia occurs when there is an imbalance between myocardial oxygen supply and demand.

• Stable Ischemic Heart Disease (Stable Angina): Occurs when an atherosclerotic plaque narrows the lumen by more than 70%, causing predictable chest pain during exertion (increased demand) that is relieved by rest.
• Acute Coronary Syndromes (ACS): Occurs when a plaque ruptures, exposing the lipid core to the blood and triggering thrombus (clot) formation. ACS is categorized into:
  • Unstable Angina: Plaque rupture with less obstructive thrombi; no evidence of myocardial necrosis (no rise in troponin).
  • NSTEMI (Non-ST Segment Elevation MI): More severe plaque rupture resulting in myocardial necrosis (positive troponin).
  • STEMI (ST Segment Elevation MI): Complete or near-complete occlusion of a coronary artery, causing acute injury and significant ECG changes.

Prevention Strategies

Managing cardiovascular risk involves two distinct approaches:

1. Primary Prevention: Aimed at patients who do not yet have cardiovascular disease. It focuses on treating risk factors such as obesity, smoking, inactivity, diabetes, and dyslipidemia to prevent the onset of disease.
2. Secondary Prevention: Aimed at patients who already have established cardiovascular disease. The goal is to treat the condition to decrease further damage, morbidity, and mortality.

Clinical Pearl: In the case of a STEMI, "Time is Tissue." Rapid intervention is required because, within 20 to 60 minutes of an occlusion, ATP stores are depleted and irreversible cell damage begins.