Free MCAT study guide — Biological and Biochemical Foundations of Living Systems
Cardiovascular physiology is one of the most heavily tested topics on the MCAT, appearing in both the biology and physics sections. You need to understand the anatomy of the heart (four chambers, valves, coronary circulation), the cardiac cycle (systole, diastole, pressure-volume relationships), the electrical conduction system (SA node, AV node, bundle of His, Purkinje fibers), and how to interpret ECG/EKG tracings. Blood vessel physiology covers arteries, arterioles, capillaries, venules, and veins, with emphasis on how smooth muscle tone in arterioles regulates blood pressure and flow distribution. Hemodynamics connects to physics: blood pressure, cardiac output (CO = HR x SV), total peripheral resistance, and the relationship between flow, pressure, and resistance (analogous to Ohm's law). You must also understand blood composition (plasma, red blood cells, white blood cells, platelets), the oxygen-hemoglobin dissociation curve and factors that shift it (pH, CO2, temperature, 2,3-BPG), the coagulation cascade, and blood typing (ABO and Rh systems).
The heart has four chambers: the right atrium receives deoxygenated blood from the superior and inferior venae cavae, the right ventricle pumps blood to the lungs via the pulmonary artery, the left atrium receives oxygenated blood from the pulmonary veins, and the left ventricle (the thickest-walled chamber) pumps blood to the body via the aorta. The atrioventricular (AV) valves (tricuspid on the right, mitral/bicuspid on the left) prevent backflow from ventricles to atria. The semilunar valves (pulmonic and aortic) prevent backflow from arteries to ventricles. The cardiac cycle consists of systole (contraction) and diastole (relaxation). During ventricular systole, pressure in the ventricles rises, closing AV valves (S1 heart sound), and blood is ejected through open semilunar valves. During diastole, ventricular pressure drops, semilunar valves close (S2 heart sound), AV valves open, and ventricles fill passively. The Wiggers diagram integrates pressure, volume, ECG, and heart sounds throughout the cardiac cycle.
The heart's intrinsic pacemaker is the sinoatrial (SA) node in the right atrium, which spontaneously depolarizes at 60-100 beats per minute. The signal spreads through the atrial muscle to the atrioventricular (AV) node, which delays the signal approximately 0.1 seconds to allow complete atrial contraction before ventricular contraction. From the AV node, the signal travels through the bundle of His, splits into left and right bundle branches, and reaches the Purkinje fibers, which rapidly depolarize the ventricular myocardium from apex to base. On an ECG: the P wave represents atrial depolarization, the QRS complex represents ventricular depolarization (atrial repolarization is hidden within), and the T wave represents ventricular repolarization. The PR interval reflects AV node conduction time. Pacemaker cells have unstable resting potentials due to funny (If) channels that allow slow sodium leak, producing spontaneous depolarization.
Blood pressure is the force exerted by blood on vessel walls. Systolic pressure (peak during ventricular contraction) over diastolic pressure (lowest during ventricular relaxation) is normally approximately 120/80 mmHg. Mean arterial pressure (MAP) is approximately diastolic + 1/3 (systolic - diastolic). Cardiac output (CO) equals heart rate times stroke volume (CO = HR x SV), normally about 5 L/min. Blood pressure equals cardiac output times total peripheral resistance (BP = CO x TPR). Arterioles are the primary site of resistance regulation: sympathetic stimulation and angiotensin II cause vasoconstriction (increased TPR, increased BP), while nitric oxide causes vasodilation (decreased TPR, decreased BP). The baroreceptor reflex in the carotid sinus and aortic arch provides rapid short-term blood pressure regulation. Long-term regulation involves the renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone (ADH/vasopressin).
Hemoglobin is a tetrameric protein (2 alpha, 2 beta subunits in adults) with cooperative oxygen binding that produces a sigmoidal dissociation curve. Cooperative binding means that oxygen binding to one subunit increases the affinity of the remaining subunits. The curve shifts RIGHT (decreased affinity, increased oxygen unloading to tissues) with increased temperature, increased CO2, increased H+ (decreased pH, the Bohr effect), and increased 2,3-bisphosphoglycerate (2,3-BPG). The mnemonic is: right shift means 'right where the tissues need oxygen.' The curve shifts LEFT (increased affinity, decreased oxygen unloading) with decreased temperature, decreased CO2, increased pH, decreased 2,3-BPG, and carbon monoxide (CO) or fetal hemoglobin (HbF). Fetal hemoglobin has gamma subunits instead of beta, which bind 2,3-BPG less effectively, giving HbF higher oxygen affinity than adult hemoglobin -- this facilitates oxygen transfer across the placenta. Myoglobin is a monomer with a hyperbolic dissociation curve and higher oxygen affinity than hemoglobin at all partial pressures.
Blood consists of plasma (55%, containing water, proteins like albumin, globulins, and fibrinogen, electrolytes, nutrients, and waste products) and formed elements (45%, measured as hematocrit). Red blood cells (erythrocytes) are biconcave, anucleate, and lack organelles, maximizing hemoglobin content and surface area for gas exchange. They are produced in bone marrow (erythropoiesis) stimulated by erythropoietin (EPO) from the kidneys in response to hypoxia. White blood cells (leukocytes) include neutrophils (most abundant), lymphocytes, monocytes, eosinophils, and basophils. Platelets (thrombocytes) are cell fragments from megakaryocytes that are essential for hemostasis. The coagulation cascade involves the intrinsic pathway (contact activation), extrinsic pathway (tissue factor, faster), and common pathway (both converge on factor X, which converts prothrombin to thrombin, which converts fibrinogen to fibrin). Fibrin is cross-linked by factor XIII to form a stable clot. Anticoagulants include heparin (activates antithrombin III), warfarin (inhibits vitamin K-dependent factor synthesis), and aspirin (inhibits cyclooxygenase, reducing thromboxane A2 and platelet aggregation).
The ABO blood group system is determined by carbohydrate antigens on the surface of red blood cells. Type A blood has A antigens and anti-B antibodies in plasma. Type B has B antigens and anti-A antibodies. Type AB has both antigens and no antibodies (universal recipient for RBCs). Type O has no antigens and both anti-A and anti-B antibodies (universal donor for RBCs). The antigens are determined by glycosyltransferase enzymes: the H antigen is the precursor, A transferase adds N-acetylgalactosamine, and B transferase adds galactose. Type O individuals have a nonfunctional transferase, leaving the H antigen unmodified. The Rh factor (D antigen) determines Rh+ or Rh- status. Rh incompatibility is clinically significant in pregnancy: an Rh- mother carrying an Rh+ fetus can develop anti-Rh antibodies after exposure to fetal blood (usually during delivery). Subsequent Rh+ pregnancies are at risk for hemolytic disease of the newborn (erythroblastosis fetalis). This is prevented by administering RhoGAM (anti-D immunoglobulin) to the mother.
CO = HR x SV; BP = CO x TPR. These equations are fundamental to hemodynamics.
The SA node is the pacemaker; the AV node provides the delay between atrial and ventricular contraction.
P wave = atrial depolarization, QRS = ventricular depolarization, T wave = ventricular repolarization.
The left ventricle has the thickest wall because it pumps against the highest pressure (systemic circulation).
Right shift of the O2-Hb curve (increased unloading): increased temp, CO2, H+, 2,3-BPG.
Fetal hemoglobin (HbF) has higher O2 affinity than adult hemoglobin (HbA) due to lower 2,3-BPG binding.
Carbon monoxide binds hemoglobin 200x more tightly than O2, causing a left shift and decreased O2 delivery.
Arterioles are the major site of blood pressure regulation (highest resistance vessels).
Capillaries are the site of gas, nutrient, and waste exchange (largest total cross-sectional area, slowest flow).
Veins are capacitance vessels holding 60-70% of total blood volume.
Type O is the universal RBC donor; Type AB is the universal RBC recipient.
Erythropoietin (EPO) is produced by the kidneys in response to hypoxia to stimulate RBC production.
The Frank-Starling mechanism: increased venous return stretches the ventricle, increasing stroke volume.
Confusing pulmonary and systemic circulation: pulmonary arteries carry deoxygenated blood, pulmonary veins carry oxygenated blood.
Thinking the right shift of the O2-Hb curve means increased affinity -- it means DECREASED affinity (more unloading).
Forgetting that CO poisoning does not change PaO2 (partial pressure of dissolved O2 is normal) -- it reduces O2 content by occupying hemoglobin binding sites.
Mixing up the extrinsic pathway (tissue factor, faster) with the intrinsic pathway (contact activation, slower).
Confusing universal donor (Type O, no antigens) with universal recipient (Type AB, no antibodies) for RBC transfusion.
Forgetting that the AV node delay is essential -- without it, the atria and ventricles would contract simultaneously, reducing cardiac output.
Assuming blood pressure is highest in veins -- it drops continuously from aorta to arteries to arterioles to capillaries to venules to veins.
Master the pressure-flow-resistance relationship by working through quantitative problems. If TPR doubles and CO stays constant, what happens to blood pressure? If arteriolar radius is halved, what happens to resistance (remember Poiseuille's law: resistance is proportional to 1/r^4)? These calculations bridge biology and physics and are common on the MCAT. Practice with the Wiggers diagram until you can explain every component.
For the oxygen-hemoglobin dissociation curve, practice identifying shifts and their causes from passage descriptions. A passage might describe a patient with fever, metabolic acidosis, and exercise -- all of which shift the curve right. Be prepared to compare fetal and adult hemoglobin curves side by side and explain the physiological significance. Also practice blood typing problems involving donor-recipient compatibility and Rh factor in pregnancy scenarios.
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