Cardiovascular System & Hypertension — Comprehensive Study Notes Summary & Study Notes

❤️ Heart: structure and function

The cardiovascular system consists of the heart, blood, and blood vessels. The heart acts as two coordinated pumps: the right (pulmonary) circuit sends deoxygenated blood to the lungs, and the left (systemic) circuit sends oxygenated blood to the tissues.

The heart is protected by the sternum, spine, and lungs, rests on the diaphragm, and is roughly the size of a fist. It is enclosed by the pericardium.

🧩 Layers of the heart wall

The heart wall has three main layers: epicardium (outer, contains vessels and nerves), myocardium (middle, cardiac muscle that generates force), and endocardium (inner endothelial lining that reduces friction).

🏛️ Chambers and valves

There are four chambers: right/left atria (receive blood) and right/left ventricles (pump blood). Valves ensure unidirectional flow: atrioventricular (AV) valves — tricuspid (right) and mitral (left) — and semilunar valves (aortic and pulmonary).

🚀 Major vessels

Great vessels include the aorta (from LV, systemic), superior/inferior vena cava (to RA), pulmonary trunk and pulmonary arteries (to lungs), and the pulmonary veins (back to LA).

💓 Cardiac output and ejection fraction

Cardiac output (CO) is the volume pumped per minute: $CO = SV \times HR$. Higher CO increases blood pressure.

Ejection fraction (EF) is the percent of EDV ejected per beat and is calculated by: $EF = \frac{SV}{EDV} \times 100$. EF helps classify heart failure.

🩸 Blood: composition and functions

Blood functions: transport oxygen/nutrients, remove wastes, carry hormones, regulate temperature and pH, and maintain fluid balance.

Major components: plasma (~55%) and cellular elements (~45%) (red blood cells, white blood cells, platelets). RBCs transport O2 with hemoglobin (lifespan ~120 days). WBCs provide immunity. Platelets are central to hemostasis (clotting, vascular spasm, plug formation).

🩺 Vascular system: vessel types and tunics

Three vessel types:

• Arteries: carry blood away from the heart; thick walls and high pressure.
• Veins: return blood to the heart; greater capacitance and lower pressure.
• Capillaries: microscopic exchange vessels forming beds for gas/nutrient exchange.

Arterial wall layers (tunics): tunica intima (endothelium), tunica media (smooth muscle — controls vasoconstriction/vasodilation), and tunica externa (collagenous support).

Arteries subdivide into elastic arteries (near heart, e.g., aorta), muscular arteries (supply organs), and arterioles (resistance vessels feeding capillary beds).

📈 Blood pressure and determinants

Blood pressure (BP) is the force of blood on vessel walls and is measured as systolic/diastolic (SBP/DBP).

BP is determined primarily by three variables: cardiac output (CO), total peripheral resistance (TPR), and blood volume. Changes in any of these affect systemic BP.

TPR is influenced by blood viscosity, vessel length, and especially vessel diameter. Vasoconstriction increases TPR and BP; vasodilation decreases them.

Mean arterial pressure (MAP) reflects perfusion pressure across the cardiac cycle; target perfusion generally requires $MAP \ge 60\ mmHg$.

🧠 Neural regulation

Baroreceptors (stretch receptors) respond to pressure changes and modulate the autonomic nervous system. Chemoreceptors sense blood PO2/PCO2/pH and influence breathing and vascular tone. The sympathetic system raises HR, contractility, and vasoconstriction (via catecholamines). The parasympathetic system conserves energy and reduces HR.

🧪 Hormonal and renal control (RAAS and others)

Hormones strongly influence BP and volume:

• Renin–angiotensin–aldosterone system (RAAS): Low perfusion causes renal renin release, converting angiotensinogen to angiotensin I; ACE converts I to angiotensin II, a potent vasoconstrictor that stimulates aldosterone (increases Na+ and water reabsorption). RAAS raises BP and blood volume.

• Antidiuretic hormone (ADH) from the hypothalamus promotes water reabsorption and vasoconstriction.

• Atrial natriuretic peptide (ANP) is secreted by atria in response to volume/pressure; it antagonizes RAAS, promotes natriuresis and vasodilation, and lowers BP.

• Epinephrine and norepinephrine from adrenal medulla increase HR, contractility, and cause vasoconstriction in many vascular beds.

Renal handling of salt and water is central to long-term BP regulation.

⚠️ Hypertension: pathophysiology and consequences

Hypertension (HBP) makes the heart work harder, leading to left ventricular hypertrophy, increased risk of myocardial infarction (MI), heart failure (HF), stroke, chronic kidney disease (CKD), and peripheral arterial disease (PAD).

High BP damages the endothelium of arteries, enabling lipid infiltration, foam cell formation, and atherosclerotic plaque development. Plaque rupture can cause thrombosis and acute ischemia (STEMI or NSTEMI in coronary arteries).

🧠 Stroke types

• Ischemic: occlusion (thrombus/embolus).
• Hemorrhagic: vessel rupture.
• Transient ischemic attack (TIA): brief ischemia with transient deficits.

🫀 Heart failure: definitions and classification

Heart failure (HF) occurs when the heart cannot supply sufficient blood to meet tissue demands. Symptoms include dyspnea, fatigue, edema, and tachycardia. Common causes: MI, coronary artery disease, and longstanding hypertension.

EF-based categories:

• HFrEF: reduced EF, typically $<40$; systolic dysfunction.
• HFmrEF: mildly reduced EF, $41$.
• HFpEF: preserved EF, $\ge 50$; diastolic dysfunction.

Right-sided vs left-sided failure differ by congestion patterns (systemic vs pulmonary).

🧾 Diagnosis and prognosis

HF is evaluated by history, physical exam, blood tests, ECG, imaging (echocardiography for EF), and functional tests. Prognosis remains serious: 5-year mortality and readmission rates are high.

🔧 Management principles of HF

Management includes lifestyle modification, pharmacotherapy, device therapy (pacemakers, ICDs), and surgery (CABG, valve repair, transplant) when needed.

Cornerstone HF medications recommended across guidelines:

• RAAS inhibitors: ACE inhibitors (e.g., captopril, enalapril, lisinopril), ARBs, and ARNI (sacubitril/valsartan).
• Mineralocorticoid receptor antagonists (MRAs): spironolactone, eplerenone.
• Beta-blockers (BB): reduce sympathetic drive and improve remodeling.
• SGLT2 inhibitors: reduce preload and afterload, lower sympathetic activity, slow HF progression.
• Diuretics (loop diuretics like furosemide) for congestion relief.

Therapeutic focus differs by HF phenotype: HFrEF has strong recommendations for ARNI/ACE/ARB, BB, MRA, SGLT2; HFpEF therapy centers on symptom control (diuretics) and selective evidence-based agents.

🩺 Myocardial infarction (MI) and ischemia

MI results from reduced coronary blood flow due to plaque rupture and thrombus. STEMI implies complete occlusion; NSTEMI implies partial occlusion. Rapid reperfusion is critical.

🦵 Peripheral arterial disease (PAD)

Atherosclerosis in lower extremities causes claudication and impaired walking. PAD shares risk factors with coronary disease.

✅ Key takeaways

• The heart and vascular system maintain perfusion via coordinated cardiac output, vessel tone, and blood volume.
• BP is regulated acutely by neural/hormonal mechanisms and chronically by renal control of volume.
• Hypertension drives atherosclerosis and end-organ damage; early management reduces risk.
• Heart failure is categorized by EF and treated with a combination of RAAS blockade, beta-blockade, diuretics, SGLT2 inhibitors, and device/surgical options as indicated.

Use these notes to guide deeper study of physiology, pathophysiology, diagnostic criteria, and evidence-based therapies.