The Cardiovascular System

Comprehensive practice flashcards covering the anatomy, histology, hemodynamics, circulation circuits, blood components, coagulation cascades, and cardiovascular pathologies from the lecture notes.

What are the primary physical properties, normal pH, and total volume of blood in the human body?

1. Tissue Classification

   • Blood is a specialized fluid connective tissue consisting of cellular elements suspended in a liquid extracellular matrix called plasma.

2. Normal pH

   • Blood is slightly alkaline with a normal physiological pH of $7.4$.

3. Total Volume

   • Adults: Approximately $4\text{--}5\,\text{dm}^3$.

   • Newborns: Approximately $300\,\text{cm}^3$.

What are the five primary physiological functions of blood?

1. Nutrient and Gas Transport

   • Carries oxygen from the lungs to peripheral tissues and distributes absorbed nutrients, hormones, and enzymes throughout the body.

2. Waste Elimination

   • Transports carbon dioxide to the lungs and nitrogenous metabolic wastes (such as urea) to the excretory organs for filtration and excretion.

3. Immune Protection

   • Transports leukocytes and circulating antibodies to neutralize pathogens, combat infection, and target foreign antigens.

4. Hemostasis and Clotting

   • Initiates vascular spasm and coagulation cascades to seal damaged vessels, preventing fluid and blood loss after injury.

5. Thermoregulation

   • Distributes and regulates heat throughout the body by shifting blood flow between core organs and the cutaneous vascular bed.

What proportion of total blood volume is plasma, and what are its key components?

1. Volume Proportion

   • Plasma constitutes approximately $55\%$ of whole blood volume.

2. Primary Solvent

   • Composed of $90\text{--}92\%$ water, serving as the medium for suspension and transport.

3. Plasma Proteins ($7\text{--}8\%$)

   • Albumin: Maintains colloidal osmotic pressure.

   • Globulins: Serve as transport proteins and immunoglobulins (antibodies).

   • Fibrinogen and Prothrombin: Essential inactive precursors for blood coagulation.

4. Dissolved Solutes ($1\text{--}2\%$)

   • Electrolytes/mineral salts ($\text{Na}^+$, $\text{K}^+$, $\text{Ca}^{2+}$), absorbed nutrients (glucose, amino acids, lipids), dissolved metabolic wastes (urea), regulatory hormones, enzymes, and dissolved gases ($\text{O}_2$, $\text{CO}_2$).

What are the structural dimensions, cellular lifespan, and organ sites of breakdown for human erythrocytes?

1. Morphology and Dimensions
   • Biconcave discs measuring roughly $7\,\mu\text{m}$ in diameter and $2\,\mu\text{m}$ in thickness; this shape provides an optimal surface-area-to-volume ratio for gas diffusion.
2. Cellular Composition
   • Mature red blood cells lack nuclei and mitochondria to maximize space for hemoglobin and prevent internal oxygen consumption. Each cell carries approximately $270\text{ million}$ hemoglobin molecules.
3. Cell Count
   • Approximately $5 \times 10^6\,\text{cells per mm}^3$ of blood.
4. Lifespan and Degradation
   • Erythrocytes circulate for approximately $120\,\text{days}$, after which damaged or aged cells are phagocytosed and degraded in the spleen and liver.

How are leukocytes classified into granular and agranular forms, and what are the primary roles of each cell type?

1. Granular Leukocytes (possess visible cytoplasmic granules and lobed nuclei)
   • Neutrophils: Multilobed nucleus; phagocytose and destroy invading bacteria and fungal pathogens.
   • Basophils: Bi- or tri-lobed nucleus; release histamine and heparin to mediate inflammatory reactions.
   • Eosinophils: Bilobed nucleus; attack multicellular parasites and modulate allergic responses.
2. Agranular Leukocytes (lack distinct cytoplasmic granules)
   • Monocytes: Large kidney-shaped nucleus; differentiate into macrophages to engulf cellular debris and foreign invaders.
   • Lymphocytes: Round, eccentric nucleus with thin rim of cytoplasm; mediate adaptive immunity through antibody production (B cells) and cytotoxic destruction of infected cells (T cells).

What three structural tissue layers compose the wall of the heart?

1. Endocardium
   • The smooth, thin innermost layer composed of simple squamous endothelial tissue and underlying connective tissue; lines the chambers and covers the heart valves.
2. Myocardium
   • The thick, contractile middle layer composed of specialized cardiac muscle tissue; responsible for the pumping action of the heart.
3. Pericardium
   • The protective fibroserous sac encasing the heart, comprising an external tough fibrous pericardium and an internal two-layered serous pericardium (parietal and visceral layers) with pericardial fluid in between.

What unique physiological and histological properties characterize cardiac muscle tissue?

1. Involuntary Control
   • Regulated unconsciously by the autonomic nervous system and intrinsic pacemaker tissues.
2. Intercalated Discs
   • Interwoven branching fibers connected by gap junctions that allow rapid ion passage, enabling synchronous contraction as a functional syncytium.
3. Impulse Conduction
   • Myocardial cells can propagate electrical action potentials across the cardiac chambers.
4. Fatigue Resistance
   • Packed with dense mitochondria and rich capillary beds, making cardiac tissue reliant on aerobic metabolism and incapable of sustaining an oxygen debt under normal conditions.

What structural differences distinguish the atrioventricular (AV) and semilunar (SL) valves, and what prevents AV valve prolapse?

1. Atrioventricular (AV) Valves
   • Tricuspid Valve: Positioned between the right atrium and right ventricle (features three flaps/cusps).
   • Bicuspid (Mitral) Valve: Positioned between the left atrium and left ventricle (features two flaps/cusps).
2. Inversion Prevention Mechanism
   • Fibrous tendinous cords called chordae tendineae anchor the AV valve cusps to papillary muscles in the ventricular walls, preventing the flaps from inverting into the atria during ventricular systole.
3. Semilunar (SL) Valves
   • Crescent-shaped, pocket-like valves situated at the arterial exits (pulmonary valve and aortic valve); close passively when arterial backpressure exceeds ventricular pressure during diastole.

What is the pathway of cardiac electrical conduction, and why is the AV nodal delay essential?

1. Conduction Sequence
   • Sinoatrial Node (SAN): Pacemaker in the upper right atrium; spontaneously generates action potentials spreading across both atria.
   • Atrioventricular Node (AVN): Receives the atrial wave of depolarization.
   • Bundle of His & Bundle Branches: Run down the interventricular septum.
   • Purkinje Fibres: Rapidly deliver the impulse upward through the ventricular myocardium from apex to base.
2. Physiological Significance of the Nodal Delay
   • An intrinsic pause of roughly $0.1\,\text{s}$ at the AVN ensures the atria contract and fully empty their blood into the ventricles before ventricular systole commences.

What are the three distinct phases and associated timings of a single cardiac cycle at a normal heart rate?

1. Atrial Systole ($0.1\,\text{s}$)
   • Atria contract, pushing remaining blood through open AV valves into the relaxed ventricles; semilunar valves remain closed.
2. Ventricular Systole ($0.3\,\text{s}$)
   • Ventricles contract; AV valves snap shut (producing the first heart sound, $S_1$), and intraventricular pressure opens the semilunar valves to eject blood into the aorta and pulmonary trunk.
3. Complete Cardiac Diastole ($0.4\,\text{s}$)
   • Both atria and ventricles relax; semilunar valves close to prevent arterial backflow (producing the second heart sound, $S_2$), and blood passively fills the atria and ventricles. Total cycle duration is approximately $0.8\,\text{s}$.

What resting heart rate ranges define normal sinus rhythm, tachycardia, and bradycardia?

1. Normal Sinus Rhythm
   • A resting heart rate between $60\text{--}100\,\text{bpm}$.
2. Tachycardia
   • An abnormally elevated resting heart rate exceeding $100\,\text{bpm}$; triggered by exercise, fever, sympathetic activation, hyperthyroidism, or emotional stress.
3. Bradycardia
   • An abnormally low resting heart rate below $60\,\text{bpm}$; found naturally in conditioned endurance athletes, or pathologically in hypothermia, hypothyroidism, jaundice, and conduction blocks.

How do pulmonary and systemic circulation differ in their structural circuits and functional roles?

1. Pulmonary Circulation
   • Circuit: Right ventricle $\rightarrow$ pulmonary trunk and pulmonary arteries $\rightarrow$ alveolar capillary networks in the lungs $\rightarrow$ four pulmonary veins $\rightarrow$ left atrium.
   • Function: Offloads carbon dioxide from venous blood and re-oxygenates erythrocytes.
2. Systemic Circulation
   • Circuit: Left ventricle $\rightarrow$ ascending aorta and systemic arterial tree $\rightarrow$ systemic tissue capillaries $\rightarrow$ systemic veins and venae cavae $\rightarrow$ right atrium.
   • Function: Delivers oxygenated blood, hormones, and nutrients to all peripheral tissues while picking up metabolic wastes.

How does coronary circulation supply the heart myocardium, and where does it drain?

1. Arterial Inflow
   • Right and left coronary arteries emerge directly from the base of the ascending aorta just superior to the aortic semilunar valve, branching across the epicardial surface to penetrate the thick myocardial tissue.
2. Capillary Perfusion
   • Myocytes extract oxygen primarily during ventricular diastole when the heart muscle is relaxed and myocardial vessels are not compressed.
3. Venous Drainage
   • Deoxygenated blood is gathered by cardiac veins that converge into the coronary sinus, which empties directly into the right atrium.

What dual blood supply serves the liver, and what proportion is delivered by the portal venous system?

1. Hepatic Artery ($25\%$)
   • Delivers oxygen-rich arterial blood originating from the celiac trunk to provide oxygen to hepatic parenchyma and bile duct structures.
2. Hepatic Portal Vein ($75\%$)
   • Supplies the majority of liver blood flow, delivering deoxygenated, nutrient-rich venous blood from the stomach, intestines, pancreas, and spleen.
3. Functional Significance
   • Directs absorbed monosaccharides, amino acids, and toxins through the liver sinusoids for metabolic processing, storage, detoxification, and protein synthesis before reaching the inferior vena cava via the hepatic veins.

What are the three vascular shunts of the fetal circulation, their functions, and their postnatal remnants?

1. Foramen Ovale
   • Fetal Function: An interatrial shunt routing oxygen-rich blood from the right atrium directly to the left atrium to bypass unexpanded lungs.
   • Postnatal Remnant: Closes upon first breath due to left atrial pressure rise, forming the fossa ovalis.
2. Ductus Arteriosus
   • Fetal Function: Connects the pulmonary trunk to the aortic arch, diverting right ventricular output away from high-resistance pulmonary beds.
   • Postnatal Remnant: Fibroses within weeks after birth into the ligamentum arteriosum.
3. Ductus Venosus
   • Fetal Function: Connects the umbilical vein directly to the inferior vena cava, bypassing the fetal liver.
   • Postnatal Remnant: Obliterates to form the ligamentum teres (or ligamentum venosum).

What histological and hemodynamic differences distinguish arteries from veins?

1. Arteries
   • Direction & Pressure: Transport blood away from the heart under high, pulsatile pressure.
   • Wall Architecture: Thick, muscular walls with prominent elastic fibers in the tunica media; narrow, rigid lumens; no internal valves.
   • Lumen & Flow: Round cross-section with rapid, surging flow reflecting ventricular systole.
2. Veins
   • Direction & Pressure: Transport blood back toward the heart under low, non-pulsatile pressure.
   • Wall Architecture: Thinner tunica media with fewer smooth muscle and elastic elements; large, irregular, collapsible lumens.
   • Special Features: Contain unidirectional semilunar pocket valves to prevent retrograde flow against gravity, supported by skeletal muscle contractions.

What local chemical, neural, and physical stimuli trigger arteriolar vasoconstriction versus vasodilation?

1. Arteriolar Vasoconstriction (Narrows lumen, increases peripheral resistance)
   • Chemical/Metabolic: Elevated local $\text{O}_2$, decreased $\text{CO}_2$, endothelin.
   • Hormonal/Neural: Sympathetic nerve stimulation (noradrenaline), circulating adrenaline, vasopressin (ADH), and angiotensin II.
   • Physical: Cold exposure.
2. Arteriolar Vasodilation (Widens lumen, lowers peripheral resistance and increases local perfusion)
   • Chemical/Metabolic: Decreased $\text{O}_2$, elevated $\text{CO}_2$, increased lactic acid and metabolites, nitric oxide (NO), histamine release.
   • Neural/Physical: Decreased sympathetic tone and local heat exposure.

What are the structural features and anatomical locations of continuous, fenestrated, and sinusoid capillaries?

1. Continuous Capillaries
   • Features: Complete, uninterrupted endothelial lining with narrow intercellular clefts allowing diffusion of water, ions, and small solutes.
   • Locations: Skeletal muscle, adipose tissue, central nervous system, lungs, and skin.
2. Fenestrated Capillaries
   • Features: Endothelial walls perforated by small pores (fenestrations) that enhance permeability to fluids, small proteins, and solutes.
   • Locations: Kidney glomeruli, small intestinal villi, choroid plexus, and endocrine glands.
3. Sinusoid (Discontinuous) Capillaries
   • Features: Wide, irregular vascular channels with large intercellular gaps and an incomplete basement membrane allowing cell and large protein migration.
   • Locations: Liver, spleen, bone marrow, and lymph nodes.

How can arterial, venous, and capillary hemorrhage be differentiated by flow dynamics and appearance?

1. Arterial Bleeding
   • Appearance: Bright red blood due to high oxyhemoglobin saturation.
   • Flow Dynamics: Rapid, forceful spurts synchronized with the cardiac pulse; poses rapid risk of hypovolemic shock.
2. Venous Bleeding
   • Appearance: Dark bluish-red blood due to deoxygenated hemoglobin.
   • Flow Dynamics: Steady, smooth, non-pulsatile stream under low hydrostatic pressure.
3. Capillary Bleeding
   • Appearance: Intermediate red color.
   • Flow Dynamics: Slow, uniform oozing across superficial abrasions; typically clots spontaneously.

What are the three major arterial branches originating directly from the aortic arch?

1. Brachiocephalic Trunk (Innominate Artery)
   • The first and largest branch; divides into the right common carotid artery (to the right side of the head and neck) and the right subclavian artery (to the right shoulder and upper limb).
2. Left Common Carotid Artery
   • The second branch; ascends the left side of the neck to supply the left cranium and brain.
3. Left Subclavian Artery
   • The third branch; courses beneath the clavicle to supply the left upper limb and left thoracic wall.

Which paired arterial systems are responsible for supplying blood to the brain?

1. Internal Carotid Arteries
   • Arise from the bifurcation of the common carotid arteries; enter the skull base through the carotid canals to provide arterial inflow to the anterior and middle cerebral circulations.
2. Vertebral Arteries
   • Arise from the subclavian arteries; ascend through the transverse foramina of cervical vertebrae ($\text{C}_6\text{--}\text{C}_1$) and enter through the foramen magnum to merge into the basilar artery, supplying the brainstem, cerebellum, and posterior cerebrum.

Which segments of the gastrointestinal tract are vascularized by the superior versus inferior mesenteric arteries?

1. Superior Mesenteric Artery (SMA)
   • Arises from the anterior abdominal aorta below the celiac trunk.
   • Territory: Vascularizes the entire midgut, including the jejunum, ileum, caecum, appendix, ascending colon, and the proximal two-thirds of the transverse colon.
2. Inferior Mesenteric Artery (IMA)
   • Arises from the anterior abdominal aorta superior to its bifurcation.
   • Territory: Vascularizes the hindgut, including the distal third of the transverse colon, descending colon, sigmoid colon, and the upper rectum.

How does venous blood from the head and neck drain into the superior vena cava?

1. External Jugular Veins
   • Collect blood from the face, scalp, and superficial cervical tissues, emptying into the subclavian veins.
2. Internal Jugular Veins
   • Collect venous outflow from the dural venous sinuses of the brain and deep neck structures, traveling alongside the common carotid artery.
3. Brachiocephalic Veins and SVC
   • On each side, the internal jugular vein unites with the subclavian vein to form the brachiocephalic (innominate) vein; both brachiocephalic veins merge in the superior mediastinum to create the superior vena cava (SVC) entering the right atrium.

What five physiological variables directly govern arterial blood pressure?

1. Cardiac Output ($\text{CO}$)
   • The volume of blood ejected per minute ($\text{CO} = \text{Heart Rate} \times \text{Stroke Volume}$); increases directly raise blood pressure.
2. Total Peripheral Resistance ($\text{TPR}$)
   • The frictional resistance encountered by blood in the systemic arterioles; arteriolar vasoconstriction elevates resistance and blood pressure.
3. Total Blood Volume
   • Hypovolemia (e.g., hemorrhage, dehydration) lowers venous return and arterial pressure, whereas fluid retention increases it.
4. Blood Viscosity
   • The internal friction of blood; elevated hematocrit or hyperproteinemia increases resistance and pressure.
5. Arterial Wall Elasticity
   • Distensible elastic arteries cushion systolic surge; loss of compliance (arteriosclerosis) increases systolic blood pressure.

What systolic and diastolic pressure parameters define Normal BP, Prehypertension, Stage 1, and Stage 2 Hypertension?

1. Normal Blood Pressure
   • Systolic $<120\,\text{mmHg}$ and diastolic $<80\,\text{mmHg}$.
2. Prehypertension
   • Systolic $120\text{--}139\,\text{mmHg}$ or diastolic $80\text{--}89\,\text{mmHg}$.
3. Stage 1 Hypertension
   • Systolic $140\text{--}159\,\text{mmHg}$ or diastolic $90\text{--}99\,\text{mmHg}$.
4. Stage 2 Hypertension
   • Systolic $\ge 160\,\text{mmHg}$ or diastolic $\ge 100\,\text{mmHg}$.

What are the three consecutive physiological stages of hemostasis following vascular injury?

1. Vascular Spasm
   • Immediate, reflex contraction of circular smooth muscle in the injured vessel wall, triggered by pain receptors, mechanical trauma, and endothelin; reduces lumen diameter to limit blood loss.
2. Platelet Plug Formation
   • Endothelial disruption exposes subendothelial collagen fibers. Platelets adhere via von Willebrand factor, become activated, degranulate (secreting ADP and thromboxane $\text{A}_2$), and aggregate to form a mechanical primary plug.
3. Blood Coagulation (Clotting)
   • A sequential enzymatic cascade (intrinsic and extrinsic pathways) activating clotting factors in the presence of $\text{Ca}^{2+}$ and Vitamin K, culminating in a stable secondary fibrin mesh.

What enzymatic reactions occur in the final common pathway of the blood coagulation cascade?

1. Prothrombinase Activation
   • Activated Factor X ($\text{Factor X}_a$), together with activated Factor V ($\text{Factor V}_a$) and calcium ions ($\text{Ca}^{2+}$), forms the prothrombinase enzyme complex.
2. Thrombin Generation
   • Prothrombinase converts the inactive plasma protein prothrombin (Factor II) into the active enzyme **thrombin (Factor II}_a).\n3. **Fibrin Polymerization**\n - Thrombin cleaves soluble **fibrinogen (Factor I)** into insoluble **fibrin monomers (Factor I}_a) that polymerize into long strands.
3. Fibrin Cross-linking
   • Thrombin activates Factor XIII ($\text{Factor XIII}_a$), which covalently cross-links the fibrin polymers into a stabilized, durable clot framework.

Why is blood type O negative considered the universal red cell donor, and AB positive the universal recipient?

1. Type $\text{O}^-$ (Universal Donor)
   • Erythrocytes express no A, B, or Rh (D) antigens on their surface membranes.
   • When transfused, recipient anti-A, anti-B, or anti-Rh antibodies cannot bind to the donor cells, preventing immune agglutination and acute hemolysis.
2. Type $\text{AB}^+$ (Universal Recipient)
   • The recipient's plasma contains no anti-A, anti-B, or anti-Rh antibodies.
   • Consequently, they can receive red blood cells of any ABO or Rh phenotype without triggering antibody-mediated destruction of transfused erythrocytes.

What immunological mechanism causes Rhesus incompatibility in pregnancy, and how is it managed?

1. Sensitization During First Pregnancy
   • An $\text{Rh}^-$ mother carries an $\text{Rh}^+$ fetus. During parturition, fetal red cells enter the maternal circulation, stimulating maternal B cells to produce anti-Rh antibodies. The first baby is delivered unaffected.
2. Pathology in Subsequent Pregnancies
   • In a subsequent $\text{Rh}^+$ pregnancy, maternal IgG anti-Rh antibodies cross the placenta into fetal circulation, binding to and lysing fetal erythrocytes (causing hemolytic disease of the newborn or erythroblastosis fetalis).
3. Clinical Prophylaxis
   • Administering RhoGAM (anti-Rh immunoglobulin) to the mother at $28\,\text{weeks}$ of gestation and within $72\,\text{hours}$ of delivery neutralizes fetal Rh antigens before maternal immunization can take place.

What is the genetic and cellular basis of sickle cell anemia, and what evolutionary advantage does the sickle trait provide?

1. Genetic Basis
   • Caused by a single point mutation in the beta-globin gene, resulting in an abnormal hemoglobin variant ($\text{HbS}$).
2. Cellular Pathophysiology
   • Deoxygenation causes $\text{HbS}$ molecules to polymerize into rigid rod-like fibers, distorting erythrocytes into stiff sickle-shaped cells. These fragile cells rupture easily (hemolytic anemia) and aggregate in microvessels, producing painful vaso-occlusive crises and ischemia.
3. Evolutionary Advantage
   • Individuals with the heterozygous sickle cell trait are protected against severe malaria because the malaria parasite (Plasmodium) cannot complete its intracellular reproductive cycle inside sickled red cells.

What causes varicose veins, and what are their four progressive clinical stages?

1. Etiology and Pathogenesis
   • Incompetence or structural damage of the semilunar valves in superficial veins allows retrograde blood flow and pooling; this produces sustained venous hypertension, causing veins to become dilated, elongated, and tortuous.
2. Stage 1
   • Reticular veins or spider veins (fine superficial telangiectasias).
3. Stage 2
   • Dilated, palpable varicose veins or prominent venous nodes.
4. Stage 3
   • Dependent subcutaneous edema of the lower leg and ankle.
5. Stage 4
   • Trophic skin changes, including stasis dermatitis (varicose eczema), hyperpigmentation, induration, and ulceration.

What is the pathogenesis of atherosclerosis, and what are its established clinical risk factors?

1. Pathological Mechanism
   • A chronic progressive inflammatory disease of medium and large arteries. Initiated by endothelial injury, followed by subendothelial accumulation of low-density lipoproteins (LDL), recruitment of monocytes/macrophages into lipid-laden foam cells, smooth muscle proliferation, and fibrous cap formation (atheroma). Plaque rupture triggers thrombosis, luminal occlusion, angina, myocardial infarction, or stroke.
2. Primary Risk Factors
   • Tobacco smoking, chronic hypertension, dyslipidemia/hypercholesterolemia, diabetes mellitus (hyperglycemia), obesity, oxidative stress, sedentary lifestyle, and positive family history.