Cardiovascular System Final Edition PDF Notes

ANATOMY, PHYSIOLOGY & PATHOLOGY NOTES OF THE CARDIOVASCULAR SYSTEM FINAL EDITION PRE-SUMMARIZED FOR THE TIME-POOR READY-TO-STUDY MEDICAL, PRE-MED, HIGH-YIELD NOTES USMLE OR PA STUDENT...

ANATOMY, PHYSIOLOGY & PATHOLOGY NOTES OF THE CARDIOVASCULAR SYSTEM FINAL EDITION PRE-SUMMARIZED FOR THE TIME-POOR READY-TO-STUDY MEDICAL, PRE-MED, HIGH-YIELD NOTES USMLE OR PA STUDENT 201 PAGES  A Message From Our Team Studying medicine or any health-related degree can be stressful; believe us, we know from experience! The human body is an incredibly complex organism, and finding a way to streamline your learning is crucial to succeeding in your exams and future profession. Our goal from the outset has been to create the greatest educational resource for the next generation of medical students, and to make them as affordable as possible. In this fourth and final edition of our notes we have made a number of text corrections, formatting updates, and figure updates which we feel will enhance your study experience. We have also endeavoured to use only open- source images and/or provide attribution where possible. 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Likewise, if you haven’t yet got our Bundle Deal, (which includes ALL of our subjects at an 80% discount), then NOW is the time! To upgrade, simply visit this link for instructions: https://www.medstudentnotes.com/pages/bundle-upgrade-process. Table Of Contents: What’s included: Ready-to-study anatomy, physiology and pathology notes of the cardiovascular system presented in succinct, intuitive and richly illustrated downloadable PDF documents. Once downloaded, you may choose to either print and bind them, or make annotations digitally on your iPad or tablet PC. Anatomy & Physiology Notes: ANATOMY OF THE HEART ELECTROPHYSIOLOGY OF THE HEART ELECTROCARDIOGRAM (ECG) PHYSIOLOGY MECHANICAL EVENTS OF THE CARDIAC CYCLE CARDIO-DYNAMICS HAEMODYNAMICS / HEMODYNAMICS BLOOD PRESSURE PHYSIOLOGY ANATOMY & PHYSIOLOGY OF BLOOD VESSELS PHYSIOLOGY OF HYPERTENSION PHYSIOLOGY OF SHOCK PHYSIOLOGY OF MYOCARDIAL ISCHAEMIA / ISCHEMIA THE EFFECTS OF AGEING ON THE HEART Pathology Notes: CONGENITAL HEART DEFECTS ANEURYSMS & DISSECTIONS ARRHYTHMIAS DRUG CLASSES FOR TREATING ARRHYTHMIAS DYSLIPIDAEMIA ATHEROSCLEROSIS ISCHAEMIC HEART DISEASE ACUTE CARDIOGENIC PULMONARY OEDEMA HEART FAILURE CARDIOMYOPATHIES (“HEART MUSCLE DISEASES”) PATHOLOGY OF HYPERTENSION PATHOLOGY OF SHOCK DVT & PE CARCINOID HEART DISEASE INFECTIVE ENDOCARDITIS NON-INFECTIVE ENDOCARDITIS (NBTE - Non Bacterial Thrombotic Endocarditis) LYMPHANGITIS MYOCARDITIS – VIRAL & TOXIC PERICARDITIS PERICARDIAL EFFUSION CARDIAC TAMPONADE ACUTE ARTERIAL OCCLUSION (“CRITICAL LIMB ISCHAEMIA”) PERIPHERAL VASCULAR DISEASE VARICOSE VEINS CHRONIC SKIN ULCERS TUMOURS OF VESSELS IMPORTANT VASCULITIDES RHEUMATIC FEVER & RHEUMATIC HEART DISEASE VALVULAR HEART DISEASE & MURMURS CARDIOVASCULAR DISEASE & OBESITY; NUTRITION & PHYSICAL EXERCISE ANATOMY OF THE HEART  HEART ANATOMY: Anatomical Location of the Heart: Snugly enclosed within the middle mediastinum (medial cavity of thorax). Contains: o Heart o Pericardium o Great Vessels o Trachea o Esophagus Middle Mediastinum – located in the inferior mediastinum (lower than the sternal angle) Extends obliquely from 2nd rib → 5th intercostal space. Anterior to Vertebrae Posterior to Sternum Flanked by 2 lungs Rests on the diaphragm 2/3 of its mass lies to the LHS of the midsternal line. Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). The Pericardium: (Coverings of the Heart) A double-walled sac contains a film of lubricating serous fluid 2 Layers of Pericardium: o Fibrous Pericardium: § Tough, dense connective tissue § Protects the heart § Anchors it to surrounding structures § Prevents overfilling of the heart – if fluid builds up in the pericardial cavity, it can inhibit effective pumping. (Cardiac Tamponade) o Serous Pericardium: (one continuous sheet with ‘2 layers’) § Parietal Layer – Lines the internal surface of the fibrous pericardium § Visceral Layer – (aka Epicardium) Lines the external heart surface Layers of the Heart Wall: Epicardium: o Visceral layer of serous pericardium Myocardium: o Muscle of the heart o The layer that ‘contracts’ Endocardium: o Lines the chambers of the heart (Endothelial Cells) o Prevents clotting of blood within the heart o Forms a barrier between the O2 hungry myocardium and the blood. (blood is supplied via the coronary system) Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2) Fibrous Skeleton of the Heart: The network of connective tissue fibers (collagen & elastin) within the myocardium Anchors the cardiac muscle fibers + valves + great vessels. Reinforces the myocardium Provides Electrical Isolation 2 Parts: o Septums: § Flat sheets separating atriums, ventricles & left and right sides of the heart. § Electrically isolates the left & right sides of the heart (conn. Tissue = non-conductive) Important for cardiac cycle § (interatrial septum/atrioventricular septum/interventricular septum) o Rings: § Rings around great vessel entrances & valves § stop stretching under pressure Source: unable to attribute. Chambers & Associated Great Vessels: 2 Atria (superior): [Atrium = Entryway] o Thin-walled Receiving Chambers o On the superior aspect of heart (above the ventricles). o Each have a small, protruding appendage called Auricles – increase atrial volume. o Separated by Atrial Septum (Site of Foetal Shunt Foramen Ovale) o Right Atrium: § Ridged internal anterior wall – due to muscle bundles called Pectinate Muscles. § Blood enters via 3 veins: Superior Vena Cava Inferior Vena Cava Coronary Sinus (collects blood draining from the myocardium) o Left Atrium: § Blood enters via: The 4 pulmonary veins (O2 blood) 2 Ventricles (inferior): [Vent = Underside] o Thick, muscular Discharging Chambers o The ‘pumps’ of the heart o Trabeculae Carneae [crossbars of flesh] line the internal walls o Papillary Muscles play a role in valve function. o Right Ventricle: § Most of heart’s Anterior Surface § Thinner – responsible for the Pulmonary Circulation – Via Pulmonary Trunk o Left Ventricle: § Most of the heart’s Postero-Inferior Surface § Thicker – it is responsible for the Systemic Circulation – Via Aorta CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Landmarks of the Heart: Coronary Sulcus (Atrioventricular Groove): o Encircles the junction between the Atria & Ventricles like a ‘Crown’ (Corona). o Cradles the Coronary Arteries (R&L), Coronary Sinus, & Great Cardiac Vein Anterior Interventricular Sulcus: o Cradles the Anterior Interventricular Artery (Left Anterior Descending Artery) o Separates the right & left Ventricles anteriorly o Continues as the posterior Interventricular Sulcus. Posterior Interventricular Sulcus: o Cradles the Posterior Descending Artery o Continuation of the Anterior Interventricular Sulcus o Separates the right & left Ventricles posteriorly CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Pathway of Blood Through the Heart: The right side of the heart pumps blood through the pulmonary circuit (to the lungs and back to the left side of the heart). o Blood flowing through the pulmonary circuit gains oxygen and loses carbon dioxide, indicated by the colour change from blue to red. The left side of the heart pumps blood via the systemic circuit to all body tissues and back to the right side of the heart. o Blood flowing through the systemic circuit loses oxygen and picks up carbon dioxide (red to blue colour change) CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Coronary Circulation: The myocardium’s own blood supply The shortest circulation in the body Arteries lie in epicardium – prevents the contractions inhibiting bloodflow There is a lot of variation among different people. Arterial Supply: o Encircle the heart in the coronary sulcus o Aorta → Left & Right coronary arteries § Left Coronary Artery → 2 Branches: 1- Anterior InterVentricular Artery (aka. Left Anterior Descending Artery...or LAD). o Follows the Anterior InterVentricular Sulcus o Supplies Apex, Anterior LV, Anterior 2/3 of IV-Septum. 2- Circumflex Artery o Follows the Coronary Sulcus (aka. AtrioVentricular Groove) o Supplies the Left Atrium + Lateral LV § Right Coronary Artery → 2 (‘T-junction) Branches: 1- Marginal Artery: o Serves the Myocardium Lateral RHS of Heart 2- Posterior Interventricular Artery: o Supplies posterior ventricular walls o Anastomoses with the Anterior Interventricular Artery (LAD) Blausen.com staff (2014). Blausen Medical Communications, Inc. Venous Drainage: o Venous blood – collected by the Cardiac Veins: § Great Cardiac Vein (in Anterior InterVentricular Sulcus) § Middle Cardiac Vein (in Posterior InterVentricular Sulcus) § Small Cardiac Vein (along Right inferior Margin) o - Which empties into the Right Atrium. Heart Valves: Ensure unidirectional flow of blood through the heart. 2x AtrioVentricular (AV) (Cuspid) Valves: o Location: § At the 2 Atrial-Ventricular junctions o Function: § Prevent backflow into the Atria during Contraction of Ventricles o Chordae tendinae (tendinous cords) “heart strings” - Attached to each valve flap. § Anchor the cusps to the Papillary Muscles protruding from ventricular walls. Papillary muscles contract before the ventricle to tension the chordae tendinae. Prevent inversion of valves under ventricular contraction. o Tricuspid Valve (Right ): § 3 flexible ‘cusps’ (flaps of endocardium + Conn. Tissue) o Mitral Valve (Left): § (resembles the 2-sided bishop’s mitre [hat]) 2x SemiLunar (SL) Valves: o Located at the bases of both large arteries issuing from the Ventricles. o Each consists of 3 pocket-like cusps resembling a crescent moon (semilunar = half moon) o Open under Ventricular Pressure o Pulmonary Valve: § Between Right Ventricle & Pulmonary Trunk o Aortic Valve: § Between Left Ventricle & Aorta Valve Positions During Ventricular Contraction CNX OpenStax, CC BY 4.0 , via Wikimedia Commons  Valve Positions During Ventricular Relaxation CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Valve Sounds: o 1- “Lubb”: § Sound of AV Valve Closure § (M1 = Mitral Component) § (T1 = Tricuspid Component) o 2- “Dupp”: § Sound of Semilunar Valve Closure § (A2 = Aortic Component) § (P2 = Pulmonary Component) Where to Listen: Adaptation of File:Precordial Leads 2.svg (by Jmarchn) and Rib_Cage (Jeroen Hut) ELECTROPHYSIOLOGY OF THE HEART:  ELECTROPHYSIOLOGY OF THE HEART The Heartbeat: - Heart is a Muscle & Requires: o O2 o Nutrients, & o Action Potentials; to function. - However, these neural signals don’t come from the brain; o Rather, the heart has its own conduction systems. § These systems allow it to contract autonomously o Hence why a transplanted heart still operates (if provided with O2 & nutrients) - Cardiac Activity is Coordinated: o To be effective, the Atria & Ventricles must contract in a coordinated manner. o This activity is coordinated by the Heart’s Conduction Systems...... - The Entire Heart is Electrically Connected...By: o Gap Junctions: § Allows action potentials to move from cell to cell o Intercalated Discs: § Support synchronised contraction of cardiac tissue CNX OpenStax, CC BY 4.0 , via Wikimedia Commons The Heart’s Conduction Systems: - SA Node →AV Node →Bundle Of His →R & L Bundle Branches →Purkinji Fibres → Myocyte Contraction CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Conductile Cardiac Cell Physiology (SA/AV Node Cells): - Action Potentials: Slow ‘Pacemaker’ Type - Have UNSTABLE Resting Membrane Potentials → Spontaneous Electrical Activity: o Spontaneously Depolarises to Threshold § This gradual depolarisation is called a ‘Prepotential’. § Due to Leaky Na+ Membrane Ion Channels § Therefore – Firing Frequency Depends on Na+ Movement o Depolarisation: § Once Threshold is reached, Ca2+ channels open § → Influx of Ca+ § → Causes an action potential. o Repolarisation: § Once peak MP is reached, Ca+ channels close, K+ channels open § → K+ Efflux makes MP more –ve § → Causes repolarisation o (Na+ brings to threshold, but Ca+ is responsible for Depolarisation.) - With a Hierarchy of control over the heart. o Hierarchy based on natural intrinsic rate. (fastest node (SA node) takes control) CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Contractile Cardiac Cell Physiology (Purkinje Fibres & Myocytes): - Action Potentials: Fast ‘Non-Pacemaker’ Type - Have STABLE Resting Membrane Potentials. o Resting Membrane Potential (MP): § Na+ & Ca+ channels are closed. § Any +ve change to MP causes Fast Na+ channels to open → +ve feedback → Threshold o Depolarisation: § If MP reaches threshold, all Fast Na+ channels open; § → Massive influx of Na+ into cell § → Membrane depolarises o Plateau: § Fast Na+ channels inactivate. § → The small downward deflection is due to Efflux of K+ ions § → Action potential causes membrane Voltage-Gated Ca+ channels to open This triggers further Ca+ release by the Sarcoplasmic Reticulum into the Sarcoplasm. (“Ca induced Ca Release”) o This increased myoplasmic Ca+ causes muscular contraction. Plateau is sustained by influx of Ca+, balanced by efflux of K+ ions o Repolarization: § Influxing Ca+ channels close…..The effluxing K+ channels remain open; → Result is a net outward flow of +ve charge. → Downward Deflection → As the MP falls, more K+ channels open, accelerating depolarization. → Membrane Repolarizes & most of the K+ channels close. o What Happens to the Excess Ions?? § Excess Na+ in the cell from depolarization is removed by the Na/K-ATPase. § Deficit of K+ in the cell from repolarization is replaced by the Na/K-ATPase. § Excess Ca+ from the Plateau Phase is eliminated by a Na/Ca Exchanger. NOTE: There is a considerable delay between Myocardial Contraction & the Action Potential. CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Refractory Periods: - In Cardiac Muscle, the Absolute Refractory Period continues until muscle relaxation; o Therefore summation isn’t possible → tetany cannot occur (critical in heart) o Ie: The depolarised cell won’t respond to a 2nd stimulus until contraction is finished. - Absolute Refractory Period: o Approx 200ms o Duration: from peak → plateau → halfway-repolarised. - Relative Refractory Period: o Na+ channels are closed – but can still respond to a stronger-than-normal stimulus. o Approx 50ms o Duration: Last half of repolarisation The SinoAtrial (SA) Node: - = The “PaceMaker” of the Heart: Unregulated Rate: 90-100bpm......however; o Parasympathetic NS lowers heart rate → Keeps Normal Resting HR at 70bpm o Sympathetic NS raises heart rate. - Location: o Posterior Wall of the Right Atrium near the opening of the Superior Vena Cava - Nature of Action Potentials: o Continually Depolarizing 90-100bpm o Takes 50ms for Action-Potential to reach the AV Node. - Role in Conduction Network: o Sets the pace for the heart as a whole. - Portion of Myocardium Served: o Contracts the Right & Left Atrium The AtrioVentricular (AV) Node: - 2nd in Command: Slower than the SA Node: 40-60bpm - Location: o Inferior portion of the InterAtrial Septum; Directly above the TriCsupid Valve. - Nature of Action Potentials: o Continually Depolarizing – but slower than the SA Node. (40-60bpm) - Role in Conduction Network: o To delay the impulse from the SinoAtrial Node → Bundle Branches; o Delay allows the Atria to empty their contents before Ventricular Contraction o Delay: Approx. 100ms - Portion of Myocardium Served: o Conducts the SA Node Impulses to the Purkinje Fibres (which supply the Ventricular Walls) Image licensed under Creative Commons license; Madhero88 The Bundle Branches (Bundles of His): - 3rd in Command: Slower than AV & SA Nodes: 20-40bpm - Location: o Fork of branches – Superior Portion of InterVentricular Septum - Nature of Action Potentials: o Continually Depolarising – Slower than AV & SA Nodes (20-40bpm) - Role in Conduction Network: o Serves as the only connection between the 2 Atria & 2 Ventricles. o The 2 Atria & 2 Ventricles are isolated by the fibrous skeleton and lack of gap junctions. - Portion of the Myocardium Served: o Transmits impulses from the AV Node to the R & L Bundle Branches, § Then along the InterVentricular Septum → Apex of the Heart. The Purkinje Fibres: - Specialised Myocytes with very few myofibrils → don’t contract during impulse transmission. - Location: o The Inner Ventricular Walls of the Heart – just below the Endocardium o Begin at the heart apex, then turn superiorly into the Ventricular Walls. - Nature of Action Potentials: o Conductile; but...Resembles those of Ventricular Myocardial Fibers; § However the Depolarisation is more pronounced & Plateau is longer. § Long Refractory period o Capable of Spontaneous Depolarisation – 15bpm - Role in Conduction Network: o Carry the contraction impulse from the L & R Bundle Branches to the Myocardium of the Ventricles; o Causes Ventricles to Contract. - Portion of Myocardium Served: o R & L Ventricles. CardioNetworks: De-Conduction_ap.png Effects of the Autonomic Nervous System (ANS): - Although the heart can operate on its own, It normally communicates with the brain via the A.N.S. - Parasympathetic NS: o Innervates SA & AV Nodes → Slows Heart Rate o Direct Stimulation → Releases AcetylCholine → Muscarinic receptors in SA/AV Nodes → § Causes increased K+ permeability (Efflux) → Hyperpolarises the cell → Cell takes longer to reach threshold → Lower Heart Rate - Sympathetic NS: o Innervates the SA & AV Nodes & Ventricular Muscle. § → Raises Heart Rate § → Increases Force of Contraction § → Dilates Arteries o Indirect Stimulation → Sympathetic Nerve Fibres Release NorAdrenaline (NorEpinephrine) @ their cardiac synapses → Binds to Beta 1 Receptors on Nodes & Muscles → § Initiates a Cyclic AMP Pathway → Increases Na+ + Ca+ Permeability in Nodal Tissue & Increases Ca+ Permeability(Membrane & SR) in Muscle Tissue. o Effects on Nodal Tissue: § ++Permeability to Na+ → more influx of Na+ → Membrane ‘drifts’ quicker to threshold → Increased Heart Rate § ++Permeability to Ca+ → more influx of Ca+ → Membrane Depolarisation is quicker → Increased Heart Rate o Effects on Contractile Tissue: § ++ Membrane Permeability to Ca+ → More influx of Ca+ → § ++Sarcoplasmic Reticulum Permeability to Ca+ →Efflux of Ca+ into cytoplasm→ Increases available Ca+ for contraction → Contractile Force Increases CNX OpenStax, CC BY 4.0 , via Wikimedia Commons ELECTROCARDIOGRAM (ECG) PHYSIOLOGY:  ELECTROCARDIOGRAM (ECG) PHYSIOLOGY: What Is An ECG? - A Recording of all Action Potentials by Nodal & Contractile Cells in the heart at a given time. o NOTE: It IS NOT a single action potential. o NOTE: A “Lead” refers to a combination of electrodes that form an imaginary line in the body, along which the electrical signals are measured. § Ie: A 12 ‘lead’ ECG usually only uses 10 electrodes. - Measured by VoltMetres → record electrical potential across 2 points: o 3x Bipolar Leads: Measure Voltages between the Arms...OR...Between an Arm & a LEg: § I = LA (+) RA (-) § II = LL (+) RA (-) § III = LL (+) LA (-) o 9x Unipolar Leads: § Look at the heart in a ‘3D’ Image. o (A “Lead” refers to a combination of electrodes that form an imaginary line in the body, along which the electrical signals are measured. Ie: A 12 ‘lead’ ECG usually only uses 10 electrodes.) - Graphic Output: o X-axis = Time o Y-axis = Amplitude (voltage) – Proportional to number & size of cells. - Understanding Waveforms: o When a Depolarisation Wavefront moves toward a positive electrode, a Positive deflection results in the corresponding lead. o When a Depolarisation Wavefront moves away from a positive electrode, a Negative deflection results in the corresponding lead. o When a Depolarisation Wavefront moves perpendicular to a positive electrode, it first creates a positive deflection, then a negative deflection. Based on ECG Vector.jpg by MoodyGroove How Each Wave & Segment Is Formed: P – Wave: - Depolarization of the Atria - Presence of this waves indicates the SA Node is working PR-Segment: - Reflects the delay between SA Node & AV Node. - Atrial Contraction is occurring at this time. Q – Wave: - Interventricular Septum Depolarization - Wave direction (see blue arrow) is perpendicular to the Main Electrical Axis → results in a ‘Biphasic’ trace. o Only the –ve deflection is seen due to signal cancellation by Atrial Repolarization. o Sometimes this wave isn’t seen at all R – Wave: - Ventricular Depolarization - Wave Direction (blue arrow) is the same as the Main Electrical Axis → Positive Deflection. - R-Wave Amplitude is large due to sheer numbers of depolarizing myocytes. S – Wave: - Depolarisation of the Myocytes at the last of the Purkinje Fibres. - Wave Direction (black arrow) opposes the Main Electrical Axis → Negative Deflection - This wave is not always seen. ST – Segment: - Ventricular Contraction is occurring at this time. o Due to the lag between excitation & contraction. T – Wave: - Ventricular Repolarisation - Positive deflection despite being a Repolarisation wave – because Repol. Waves travel in the opposite direction to Depol Waves. Relating ECG Waves To Events In The Cardiac Cycle: - Contractions of the Heart ALWAYS Lag Behind Impulses Seen on the ECG. - Fluids move from High Pressure → Low Pressure - Heart Valves Ensure a UniDirectional flow of blood. - Coordinated Contraction Timing – Critical for Correct Flow of Blood. CNX OpenStax, CC BY 4.0 , via Wikimedia Commons Wikimedia Commons: Wiggers Diagram.svg The Heart’s Electrical Axis: o Refers to the general direction of the heart's depolarisation wavefront (or 'mean electrical vector') in the frontal plane. o It is usually oriented in a 'Right Shoulder to Left Leg' direction. o Determining The Electrical Axis From an ECG Trace: o 3 Methods: o Quadrant Method (the one you’re concerned with) o Peak Height Measurement Method o The Degree Method o The Quadrant Method: Source: unable to attribute. o Normal Axis. QRS positive in I and aVF (0 90 degrees). Normal axis is actually 30 to 105 degrees. o Left Axis Deviation (LAD). QRS positive in I and negative in aVF, 30 to 90 degrees o Right Axis Deviation (RAD). QRS negative in I and positive in aVF, +105 to +180 degrees o Extreme RAD. QRS negative in I and negative in aVF, +180 to +270 or 90 to 180 degrees Algorithm For Looking At ECGs: - Check Pt ID - Check Voltage & timing o 25mm/sec o 1large square = 0.2s (1/5sec) o 1small square = 0.04s - What is the rate? o 300/number of large squares between QRS Complexes § Tachycardia >100bpm § Bradycardia