Lecture Notes on Blood Volume, Anemia, and Cardiovascular Dynamics

A set of flashcards based on the lecture notes covering various aspects of blood volume, anemia, and cardiovascular dynamics.

What is the total blood volume in men and women?

75.5 mL/kg in men and 66.5 mL/kg in women.

How much of body weight does blood volume constitute?

7% to 8% of body weight. 5 to 6 L

What is the percentage composition of blood cells and plasma in total blood volume?

Blood cells make up ~40-45% and plasma makes up ~55-60%.

What energy production method do red blood cells rely on?

Glycolysis, because they lack mitochondria.

What is the normal range for arterial blood oxygen partial pressure (PaO2)?

80-100 mmHg.

What physiological response compensates for tissue hypoxia?

Increased heart rate, increased cardiac output, and increased flow to vital organs.

What is Thalassemia?

An inherited stem cell disorder globin chains (alpha or beta) characterized by the increased destruction of red blood cells.

What differentiates α-thalassemia from β-thalassemia?

They are classified by the polypeptide chain(s) with deficient synthesis.

What are the laboratory features of Sickle Cell Anemia?

Presence of sickled red blood cells in blood smear and severe anemia. Sickled cells cause vascular occlusion.

What is the treatment of choice for Sickle Cell Anemia?

Stem cell transplant.

What mechanism leads to antibody-mediated drug reactions?

Exposure to a drug causes destruction and lysis of the sensitized person’s own RBCs.

What is Polycythemia?

Excess red blood cells resulting in increased blood viscosity.

What causes Secondary Polycythemia?

Secondary Polycythemia is caused by chronic hypoxemia, which stimulates the kidneys to increase erythropoietin production. This heightened erythropoietin level, in turn, stimulates the bone marrow to produce more red blood cells. Common causes of chronic hypoxemia include chronic lung diseases (e.g., COPD), living at high altitudes, sleep apnea, and certain cardiac shunts.

What determines vascular resistance?

Vessel length, vessel radius, and blood viscosity.

What are the types of blood flow?

Laminar flow and turbulent flow.

What are the clinical features of chronic venous insufficiency?

Swelling, edema, venous stasis, inflammation, ulcers, and pain.

What does systemic arterial blood pressure depend on?

Cardiac output and resistance to ejection of blood from the heart.

What is the formula for cardiac output (CO)?

CO = Stroke volume (SV) x Heart rate (HR).

What causes short-term regulation of blood pressure?

Rapid adjustments related to position changes, exercise, and emotions.

a large, stable plaque alters what

coronary perfusion

What are the characteristics of vulnerable plaques?

Large lipid core, thin cap, high shear stress, and inflammation.

What is rheumatic heart disease?

An acute inflammatory disease following infection with group A β-hemolytic streptococci. connective tissue damage in heart joints skin- cause valve swelling

What are the outcomes of myocardial infarction?

Complete occlusion can cause irreversible damage to myocardial cells.

What is the difference between stable angina and unstable angina?

Stable angina occurs predictably with exertion; unstable angina is a sign of acute coronary syndrome.

What changes occur in coronary vessels during acute occlusion?

Plaque disruption and thrombus formation lead to acute coronary syndromes.

Shunts?

Shunts are abnormal pathways of blood flow through the heart or great vessels.

What results from increased pulmonary blood flow in Atrial Septal Defect?

Pulmonary hypertension and potential ventricular hypertrophy. Reversal ( right to left)

Heme reduction and globin reuse

Heme is reduced to bilirubin. Globin and iron portions are conserved and reused.

Partial pressure of oxygen in venous blood (PvO2)

35-40 mmHg

Thalassemia severity classifications

Most clinically severe form: Thalassemia major (homozygous). Thalassemia minor (heterozygous) is less severe.

Factors initiating thrombosis

• Blood flow: slow or turbulent flow

• Blood vessel wall: damage or inflammation to the intimal wall of vessel

• Blood coagulability: emergence of a hypercoagulable state

Varicose veins

Superficial veins affected, often associated with chronic venous insufficiency.

Systemic Vascular Resistance (SVR) determinants and alternative name

SVR is determined by: Radius of arteries and degree of vessel compliance. SVR is also known as cardiac afterload.

Long-term regulation of blood pressure (BP)

Increase in extracellular fluid volume causes increased CO and SVR, which then causes elevated BP. This causes kidneys to excrete (lose) excess sodium and water (fluid).

Secondary hypertension and its most common cause

Secondary hypertension has an identifiable cause. Hyperaldosteronism is the most common cause

Major determinants of coronary vascular resistance

1. Artery diameter

2. Varying degrees of external compression by myocardial contraction and relaxation

Patients with chest pain and ST-segment elevation (STEMI) on ECG

Candidates for acute reperfusion therapy.

Patients with symptoms of unstable angina and no ST elevation (non-STEMI, NSTEMI) on ECG:

Do not benefit from reperfusion therapy; candidates for clot removal (stents) and antiplatelet drugs.

Mitral valve location

Valve between the left atrium and left ventricle.

Aortic valve location and function

Valve allowing outflow from the left ventricle to the aorta.

Stenosis effects

Blood flow from left atrium to left ventricle impaired during ventricular diastole. Can lead to chronic pulmonary hypertension, right ventricular hypertrophy, and right-sided heart failure.

Regurgitation effects

Backflow of blood from the left ventricle to the left atrium during ventricular systole. May lead to left-sided heart failure.

Cardiac Tamponade

When fluid accumulation in the pericardial sac is large or sudden, it can lead to external compression of the heart chambers such that filling is impaired.

Chronic Pericarditis and its two principal forms

Healing of the acute form that results in chronic dysfunction. Two principal forms:

1. Adhesive mediastino-pericarditis: pericardial sac is destroyed, and the external aspect of the heart adheres to surrounding mediastinal structures.

2. Constrictive pericarditis: pericardial sac becomes dense, nonelastic, fibrous, and scarred.