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Repost from ONLINE MEDICAL LIBRARY
KEPPRA
CVS
PART 1: ANATOMY OF CARDIOVASCULAR SYSTEM
1️⃣ HEART – Structural Anatomy
Location
Middle mediastinum
Between lungs
Apex at left 5th intercostal space
Coverings
Pericardium (fibrous + serous)
2️⃣ Layers of Heart Wall
Endocardium (inner)
Myocardium (muscular layer)
Epicardium (outer)
Myocardium thickness:
Left ventricle > Right ventricle (because systemic circulation requires more force)
3️⃣ Chambers and Flow Sequence
Venous blood →
Right Atrium → Tricuspid Valve → Right Ventricle → Pulmonary Valve → Lungs →
Left Atrium → Mitral Valve → Left Ventricle → Aortic Valve → Aorta → Body
4️⃣ Conducting System of Heart
Sequence
SA node → AV node → Bundle of His → Right & Left bundle branches → Purkinje fibers
SA node = natural pacemaker (60–100/min)
AV node delay allows ventricular filling
PART 2: PHYSIOLOGY (FUNCTIONAL CONCEPTS)
1️⃣ Cardiac Cycle
Duration ≈ 0.8 sec
Phases:
Atrial systole
Ventricular systole
Diastole
2️⃣ Stroke Volume (SV)
Amount pumped per beat ≈ 70 mL
3️⃣ Cardiac Output (CO)
CO = SV × HR
= 70 × 70 ≈ 5 L/min
Regulation:
↑ Sympathetic → ↑ HR + ↑ contractility → ↑ CO
↑ Vagal tone → ↓ HR → ↓ CO
4️⃣ Blood Pressure
BP = CO × Peripheral Resistance
Normal: 120/80 mmHg
Determinants:
Cardiac output
Total peripheral resistance
Blood volume
Elasticity of vessels
PART 3: REGULATION OF BLOOD PRESSURE
1️⃣ Neural Regulation (Short term)
Baroreceptors:
Carotid sinus
Aortic arch
If BP ↑ → Baroreceptor firing ↑ → ↓ sympathetic → BP falls
2️⃣ Renal Regulation (Long term)
Kidney controls:
Sodium balance
Water balance
RAAS system
3️⃣ RAAS SYSTEM
↓ BP → Kidney releases renin →
Renin converts Angiotensinogen → Angiotensin I →
ACE converts → Angiotensin II →
Angiotensin II:
Potent vasoconstrictor
↑ Aldosterone
↑ Sodium retention
↑ BP
PART 4: PATHOPHYSIOLOGY OF MAJOR DISORDERS
1️⃣ HYPERTENSION
Definition: Persistent BP > 140/90 mmHg (exam value)
Types:
Primary (90–95%)
↑ RAAS activity
Sympathetic overactivity
2️⃣ CONGESTIVE HEART FAILURE (CHF)
Definition: Heart unable to pump adequate blood.
Pathophysiology: ↓ CO → Kidney senses low perfusion → RAAS activated → Fluid retention → Edema
Compensatory:
Ventricular hypertrophy
Sympathetic stimulation
3️⃣ ANGINA PECTORIS
Cause: Imbalance between oxygen supply and demand.
Types:
Stable
Unstable
Variant (Prinzmetal)
4️⃣ ARRHYTHMIA
Abnormal impulse:
Formation problem
Conduction problem
Causes:
Ischemia
Electrolyte imbalance
Drug toxicity (e.g., digoxin)
PART 5: PHARMACOLOGY
1️⃣ ANTIHYPERTENSIVE DRUGS
Classification:
A. Diuretics
Thiazides (Hydrochlorothiazide)
Loop (Furosemide)
K⁺ sparing (Spironolactone)
Mechanism: ↓ Blood volume → ↓ CO → ↓ BP
B. Sympatholytics
1. Beta blockers
Propranolol
Atenolol
Metoprolol
Mechanism: ↓ HR + ↓ Renin release
2. Alpha blockers
Prazosin
Mechanism: Vasodilation
3. Central acting
Clonidine
Methyldopa
Mechanism: ↓ Sympathetic outflow
C. RAAS Inhibitors
ACE inhibitors:
Enalapril
Ramipril
ARBs:
Losartan
Telmisartan
Direct renin inhibitor:
Aliskiren
D. Calcium Channel Blockers
Amlodipine
Verapamil
Diltiazem
Mechanism: ↓ Ca²⁺ entry → Vasodilation → ↓ BP
2️⃣ DRUGS FOR CHF
Diuretics
ACE inhibitors
Beta blockers
Aldosterone antagonists
Digoxin
Vasodilators
SGLT2 inhibitors
3️⃣ ANTIANGINAL DRUGS
Nitrates → Venodilation → ↓ Preload
Beta blockers → ↓ Oxygen demand
CCB → Vasodilation
Ranolazine
Ivabradine
4️⃣ ANTIARRHYTHMICS
Class I – Na⁺ channel blockers
Class II – Beta blockers
Class III – K⁺ channel blockers
Class IV – Ca²⁺ channel blockers
Others:
Adenosine
Digoxin
Magnesium sulfate
5️⃣ DIURETICS (Nephron Based)
PCT – Acetazolamide
Loop of Henle – Furosemide
DCT – Thiazides
Collecting duct – Spironolactone
Repost from N/a
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