Medical Textbook Library - Full Catalogue

Anatomy (8 books)

• Color Atlas of Ultrasound Anatomy, 3e
• Color Atlas of Human Anatomy Vol 1, 2, 3 (Thieme)
• General Anatomy and Musculoskeletal System (THIEME Atlas)
• Gray's Anatomy for Students
• Imaging Anatomy - Bones, Joints, Vessels and Nerves
• Netter's Atlas of Human Anatomy

Anesthesiology (3 books)

• Barash, Cullen & Stoelting's Clinical Anesthesia, 9e
• Miller's Anesthesia, 10e (2 Vol Set)
• Morgan & Mikhail's Clinical Anesthesiology, 7e

Biochemistry (3 books)

• Basic Medical Biochemistry - A Clinical Approach, 6e
• Biochemistry - Lippincott Illustrated Reviews, 8e
• Harper's Illustrated Biochemistry, 32e

Cardiology (3 books)

• Braunwald's Heart Disease, 2 Vol Set
• Fuster and Hurst's The Heart, 15e
• Textbook of Clinical Echocardiography

Community Medicine (1 book)

• Park's Textbook of Preventive and Social Medicine

Dermatology (4 books)

• Andrews' Diseases of the Skin (Clinical Atlas + Clinical Dermatology)
• Dermatology, 2-Volume Set, 5e
• Fitzpatrick's Dermatology, 2 Vol

Embryology (2 books)

• Langman's Medical Embryology
• The Developing Human - Clinically Oriented Embryology

Emergency Medicine (3 books)

• ROSEN's Emergency Medicine, 9e
• Roberts and Hedges' Clinical Procedures in Emergency
• Tintinalli's Emergency Medicine, 9e

ENT / Otolaryngology (6 books)

• Cummings Otolaryngology Head and Neck Surgery
• K.J. Lee's Essential Otolaryngology
• Scott-Brown's Otorhinolaryngology Head & Neck Surgery (3 vols)
• Shambaugh Surgery of the Ear

Family Medicine (3 books)

• Pfenninger and Fowler's Procedures for Primary Care, 3e
• Swanson's Family Medicine Review
• Textbook of Family Medicine, 9e

Forensic Medicine (6 books)

• Brogdon's Forensic Radiology
• DiMaio's Forensic Pathology, 3e
• Forensic Anthropology - A Comprehensive Introduction, 2e
• P.C. Dikshit Textbook of Forensic Medicine and Toxicology
• Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
• The Essentials of Forensic Medicine and Toxicology, 36e (2026)

Gastroenterology (3 books)

• Clinical Gastrointestinal Endoscopy, 3e
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease
• Yamada's Textbook of Gastroenterology, 3 Vol, 7e

Gastrointestinal Surgery (1 book)

• Maingot's Abdominal Operations

General Surgery (8 books)

• Bailey and Love's Short Practice of Surgery, 28e
• Campbell's Operative Orthopaedics (listed under surgery)
• Current Surgical Therapy, 14e
• Fischer's Mastery of Surgery, 8e
• Mulholland and Greenfield's Surgery, 7e
• Pye's Surgical Handicraft, 22e
• S. Das - A Manual on Clinical Surgery, 13e

Genetics (2 books)

• Emery's Elements of Medical Genetics and Genomics
• Thompson & Thompson Genetics and Genomics in Medicine, 9e

Histology (2 books)

• Histology - A Text and Atlas (Pawlina), 9e
• Junqueira's Basic Histology - Text and Atlas, 17e

Immunology (3 books)

• Cellular and Molecular Immunology (Abbas)
• Janeway's Immunobiology, 10e
• Roitt's Essential Immunology

Internal Medicine (7 books)

• Firestein & Kelley's Textbook of Rheumatology, 2 Vol Set
• Frameworks for Internal Medicine
• Goldman-Cecil Medicine, 2 Vol Set (International Edition)
• Harrison's Principles of Internal Medicine, 22e (2025)
• Rheumatology, 2-Volume Set (2022, Elsevier)
• Symptom to Diagnosis - An Evidence Based Guide, 4e
• The Washington Manual of Medical Therapeutics

Laboratory Medicine (3 books)

• Henry's Clinical Diagnosis and Management by Laboratory Methods
• Quick Compendium of Clinical Pathology, 5e
• Tietz Textbook of Laboratory Medicine, 7e

Microbiology (3 books)

• Jawetz, Melnick & Adelberg's Medical Microbiology, 28e
• Medical Microbiology, 9e
• Sherris & Ryan's Medical Microbiology, 8e

Nephrology (3 books)

• Brenner and Rector's The Kidney, 2 Vol Set
• Comprehensive Clinical Nephrology, 7e
• National Kidney Foundation Primer on Kidney Diseases, 8e

Neurology (4 books)

• Adams and Victor's Principles of Neurology, 12e
• Bradley and Daroff's Neurology in Clinical Practice
• Localization in Clinical Neurology, 8e
• Plum and Posner's Diagnosis and Treatment of Stupor and Coma

Neuroscience (3 books)

• Eric Kandel - Principles of Neural Science, 6e
• Neuroanatomy through Clinical Cases, 3e
• Neuroscience: Exploring the Brain, 5e

Obstetrics & Gynecology (2 books)

• Berek & Novak's Gynecology
• Creasy & Resnik's Maternal-Fetal Medicine - Principles and Practice

Ophthalmology (2 books)

• Kanski's Clinical Ophthalmology, 10e
• The Wills Eye Manual, 7e

Orthopedics (3 books)

• Campbell's Operative Orthopaedics, 15e (2026)
• Miller's Review of Orthopaedics, 9e
• Rockwood and Green's Fractures in Adults, 10e (2025)

Pathology (2 books)

• Robbins & Kumar Basic Pathology (Robbins Pathology)
• Robbins, Cotran & Kumar Pathologic Basis of Disease

Pediatrics (2 books)

• Red Book 2021 - Report of the Committee on Infectious Diseases
• The Harriet Lane Handbook, 23e (Johns Hopkins)

Pharmacology (3 books)

• Goodman & Gilman's The Pharmacological Basis of Therapeutics
• Katzung's Basic and Clinical Pharmacology, 16e
• Lippincott Illustrated Reviews: Pharmacology

Physiology (4 books)

• Costanzo Physiology, 7e
• Ganong's Review of Medical Physiology, 26e
• Guyton and Hall Textbook of Medical Physiology
• Medical Physiology (Boron & Boulpaep)

Psychiatry (6 books)

• Kaplan & Sadock's Comprehensive Textbook of Psychiatry
• Kaplan and Sadock's Synopsis of Psychiatry
• Stahl's Essential Psychopharmacology
• The Clozapine Handbook
• The Maudsley Deprescribing Guidelines
• The Maudsley Prescribing Guidelines in Psychiatry, 15e

Pulmonology (2 books)

• Fishman's Pulmonary Diseases and Disorders, 2 Vol Set
• Murray & Nadel's Textbook of Respiratory Medicine, 2 Vol

Radiology (1 book)

• Grainger & Allison's Diagnostic Radiology

Urology (3 books)

• Campbell Walsh Wein Urology, 3 Vol Set

• Answer any cardiology question by searching Braunwald's and other cardiology textbooks in this library - just ask your clinical question and I'll pull the relevant content for you.
• Look up specific topics - heart failure, coronary artery disease, arrhythmias, valvular disease, cardiomyopathies, ECG interpretation, etc.
• Summarize sections on any cardiovascular topic you're studying or working on.

• Purchase at Elsevier's official store or Amazon
• Access through your institution's library (most medical schools subscribe to ClinicalKey or similar platforms)
• Borrow through your hospital or university library

Pathophysiology of Heart Failure

1. Definition and Basic Concept

• HFrEF (Heart Failure with Reduced Ejection Fraction): EF <45%; systolic dysfunction dominates. Typical of acute MI.
• HFpEF (Heart Failure with Preserved Ejection Fraction): EF normal or near-normal; diastolic dysfunction (impaired relaxation/filling) dominates. Typical of hypertrophy and stiff myocardium.

2. Initial Triggers - Increased Cardiac Work

• Robbins, Cotran & Kumar Pathologic Basis of Disease

3. Cardiac Hypertrophy - The Initial Compensatory Response

• New sarcomeres added in parallel to existing ones
• Increases cross-sectional area of myocytes
• Increases wall thickness (thick, non-dilated ventricle)
• Seen in: hypertension, aortic stenosis

• New sarcomeres added in series with existing ones
• Leads primarily to ventricular dilation
• Wall thickness may be normal, increased, or decreased
• Seen in: aortic/mitral regurgitation, dilated cardiomyopathy

• Enlarged or multiple nuclei (increased DNA ploidy without cell division)
• Expression of immediate-early genes (FOS, JUN, MYC, EGR1) driving altered protein synthesis
• Re-expression of fetal gene programs - fetal myosin isoforms, natriuretic peptides, collagen
• Increased mitochondrial numbers
• Critically: capillary density does not increase proportionally - creating relative ischemia

4. The Four Major Compensatory Mechanisms

A. Sympathetic Nervous System Activation

• Baroreceptors sense falling blood pressure and reduce their firing
• Vasomotor center receives reduced inhibitory input; sympathetic outflow increases, parasympathetic decreases
• Effects: tachycardia (chronotropy), increased contractility (inotropy), vasoconstriction (increased preload and afterload)
• Short term: maintains perfusion
• Long term: increases cardiac workload, promotes toxic catecholamine exposure to myocytes, contributes to arrhythmia and cell death

B. RAAS Activation (Renin-Angiotensin-Aldosterone System)

• Reduced renal perfusion triggers renin release
• Sympathetic activity further stimulates renin release
• Angiotensin II and aldosterone formation follows
• Effects: peripheral vasoconstriction (increased afterload), sodium and water retention (increased preload)
• If the failing heart cannot handle the extra volume returned, venous pressure rises, causing pulmonary and peripheral edema
• High angiotensin II and aldosterone also directly promote myocardial fibrosis, remodeling, and inflammation - maladaptive long-term

C. Natriuretic Peptides (the counter-regulatory response)

• Increased preload (wall stretch) triggers release of ANP (atrial) and BNP (B-type)
• Counter-regulatory effects: vasodilation, natriuresis, inhibition of renin and aldosterone, reduction of myocardial fibrosis
• This is the only one of the four compensatory mechanisms that is beneficial
• In chronic HF, resistance to natriuretic peptides develops, blunting this protective effect
• BNP is clinically used as a biomarker of HF severity

D. Myocardial Hypertrophy (Frank-Starling Mechanism)

• Stretching of myocardial fibers initially increases force of contraction (Frank-Starling law)
• Excessive fiber elongation eventually results in weaker contractions and reduced ejection
• The thickened, stiffened wall in diastolic dysfunction impairs relaxation and ventricular filling

5. The Vicious Cycle of Progression

Reduced cardiac output → neurohormonal activation (NE, Angiotensin II, endothelin) → vasoconstriction → increased afterload → further reduction in ejection fraction and cardiac output → more neurohormonal activation...

6. Calcium Dysregulation at the Cellular Level

• Chronic neurohormonal stimulation impairs calcium homeostasis
• Abnormal calcium cycling leads to reduced contractile force and arrhythmias
• Agents that increase intracellular calcium (or sensitize the contractile machinery to calcium) increase contractility - the basis for inotropic drugs
• Lippincott Illustrated Reviews: Pharmacology

7. Structural Consequences: Left vs. Right Heart Failure

• Passive congestion backs blood into the pulmonary circulation
• Results in pulmonary edema, dyspnea, orthopnea
• Reduced forward flow causes organ hypoperfusion

• Systemic venous congestion
• Peripheral edema, hepatomegaly, ascites, jugular venous distension

8. Physiologic vs. Pathologic Hypertrophy

• Accompanied by proportional increase in capillary density (unlike pathologic hypertrophy)
• Associated with decreased resting heart rate and blood pressure
• Volume-load pattern with beneficial remodeling
• Static exercise (weightlifting) produces mild pressure hypertrophy with less benefit
• Robbins, Cotran & Kumar Pathologic Basis of Disease

Summary Diagram (Conceptual)

Initial Injury / Overload
        ↓
Myocyte hypertrophy + Fetal gene re-expression
        ↓
↓ Cardiac output
        ↓
Baroreceptors activated → ↑ SNS + ↑ RAAS
        ↓
↑ HR, ↑ Contractility, ↑ Vasoconstriction, Na+/H₂O retention
        ↓
↑ Preload + Afterload → More cardiac work
        ↓
Fibrosis, myocyte loss, calcium dysregulation
        ↓
Further ↓ EF → Pulmonary/peripheral congestion → End-stage HF

• Robbins, Cotran & Kumar - Pathologic Basis of Disease
• Katzung's Basic and Clinical Pharmacology, 16e
• Lippincott Illustrated Reviews: Pharmacology

MCQs: Pathophysiology of Heart Failure

• A) Sarcomeres added in series, increasing ventricular length
• B) Sarcomeres added in parallel, increasing wall thickness
• C) Sarcomere loss with compensatory fibrosis
• D) Sarcomeres added both in series and parallel equally

• A) Concentric hypertrophy due to pressure overload
• B) Sarcomere addition in series due to volume overload
• C) Myocyte apoptosis with fibrous replacement
• D) Decreased sarcomere synthesis with cellular atrophy

• A) Sympathetic nervous system activation
• B) RAAS activation
• C) Natriuretic peptide release
• D) Myocardial hypertrophy

• A) Increased parasympathetic outflow causing bradycardia
• B) Decreased sympathetic outflow reducing afterload
• C) Increased sympathetic outflow and decreased parasympathetic outflow
• D) No change in autonomic tone

• A) Adult beta-myosin heavy chain and elastin
• B) Fetal myosin isoforms, natriuretic peptides, and collagen
• C) Troponin I and connexin-43
• D) Alpha-myosin heavy chain and titin

• A) Systolic dysfunction due to myocyte loss
• B) Diastolic dysfunction due to impaired ventricular relaxation and filling
• C) High-output failure due to increased metabolic demand
• D) Right-to-left shunting causing reduced preload

• A) Bradykinin
• B) Nitric oxide
• C) Endothelin
• D) Prostacyclin

• A) ↓CO → ↓Renal perfusion → ↑Renin → ↑Ang II → ↑Aldosterone → Na+/H₂O retention → ↑Venous pressure → edema
• B) ↑CO → ↑Renal perfusion → ↓Renin → Natriuresis → ↓Preload → edema
• C) ↓CO → ↑ANP → ↑Aldosterone → Na+ retention → edema
• D) ↑SNS → ↑Parasympathetic → Vasodilation → Fluid leak → edema

• A) Capillaries proliferate faster than myocytes; results in hyperemia
• B) Capillary density does not increase proportionally; results in relative ischemia of hypertrophied myocytes
• C) Capillaries are destroyed by inflammatory cells; results in infarction
• D) Capillaries increase proportionally; no significant consequence

• A) Released by renal cells in response to hypoxia; used to assess renal function
• B) Released by ventricular myocytes in response to increased wall stretch; used as a biomarker of HF severity
• C) Released by the adrenal medulla in response to SNS activation; used to assess sympathetic tone
• D) Released by endothelium in response to shear stress; used to detect atherosclerosis

• A) Aerobic exercise causes concentric hypertrophy with reduced ejection fraction
• B) Aerobic exercise produces hypertrophy with proportional capillary proliferation and reduced resting heart rate
• C) Aerobic exercise re-expresses fetal gene programs identical to pressure overload
• D) Aerobic exercise causes sarcomere loss and replacement fibrosis

• A) Direct spread of infection from the left to right ventricle
• B) Left-sided failure causes pulmonary hypertension, increasing right ventricular afterload, eventually causing right-sided failure
• C) RAAS activation selectively increases right ventricular preload
• D) Natriuretic peptide resistance causes isolated right ventricular dilation

• A) They increase heart rate and contractility, boosting cardiac output directly
• B) They interrupt the maladaptive neurohormonal cycle that drives progressive cardiac remodeling and dysfunction
• C) They increase natriuretic peptide synthesis in ventricular myocytes
• D) They promote concentric hypertrophy, protecting against eccentric dilation

• A) Viral infection of cardiomyocyte nuclei
• B) Increased DNA ploidy from DNA replication without cell division
• C) Mitotic spindle failure causing binucleation
• D) Apoptosis with nuclear fragmentation

• A) Ejection fraction is typically severely reduced
• B) Cardiac output is elevated but still insufficient for the body's demands
• C) RAAS activation is the primary driver of symptoms
• D) Positive inotropic drugs are the treatment of choice