Cardiovacular System

Normal processes

  • embryonic development, fetal maturation, and perinatal changes
  • organ structure and function
    • chambers, valves
    • cardiac cycle, mechanics, heart sounds, cardiac conduction
      • Cardiac cycle:
        Sounds: S4 (atrial contraction) S1 S2 (splitting upon inspiration) S3
        Valves (which side first): AV close (L) AP open (R) AP close (L) AV open (R)
        Murmurs start at: AV close = AV regurgitation, Septal AP open = Aortic stenosis (squirting) AP close = AP regurgitation AV open = AV stenosis (squirting)
        Jugular vein pulse: a (atrial contraction) c (tricuspid bulge) v (pressure drop when AV opens/begins to fill)
      • Mechanics:
        Phase: 4: before reaching threshold 0: depolarize 1: repolarize 2: contraction 3: repolarize
        Pacemaker channels open: Na+ (If) Ca2+ K+ (DRK)
        Ventricular channels open: K+ (IRK) Na+ K+ (ItoK) Ca2+ K+ (DRK)
      • Conduction:
        • SA → AV (delay separates atrial and ventricular contraction) → Bundle of His → Perkinje fibers
        • ECG:
          • PR interval = a measure of AV delay. AV block if > 0.2 sec (1 big square)
            • P wave = atrial depolarization. SA dead if none seen.
            • PR segment = AV delay.
          • QT interval = duration of ventricular systole ~ 0.4 sec (2 big squares)
            • QRS interval = ventricular depolarization. Normally < 0.1 sec (1/2 big square). Only SA, AV, and bundle of His produces normal looking QRS. Abnormal QRS = PVC, V Tach.
            • ST segment = ventricles depolarized ~ 0.1 sec (1 big square)
            • T wave = ventricular repolarization ~ 0.1 sec (1 big square)
        • ECG vectors:
          ECG Vectors
    • hemodynamics, including systemic, pulmonary, coronary, and blood volume
      • Venous return
        • Greater return if stiffer veins (sympathetic vasoconstriction).
      • Pulmonary
        • Does not hold back on flow (high compliance and low resistance, lack of constrictors from myogenic, metabolic, sympathetic regulation).
        • Demand driven homeostasis: divert blood where there's most oxygen (constrict hypoxic + injured areas).
        • Keep pressure to minimum to prevent filtration and edema.
        • Block in pulmonary backs up on right ventricle (right ventricle failure), deprives left ventricle (decrease stroke volume).
        • Block in left ventricle pushes back on pulmonary (pulmonary edema).
      • Heart
        • Stroke volume: how much the heart squeezes out. Preload and contractility helps stroke volume. Afterload works against it.
          • Preload: how much the ventricles fill (venous pressure) before contraction. Tachycardia = no time for ventricle refill = decreased preload.
          • Afterload: force heart must overcome when squeezing. Increased afterload means increased diastolic pressure, stiff arteries, aortic valve stenosis.
          • Contractility: how hard the heart contracts.
        • Cardiac output = mean arterial pressure / resistance
        • Systole: Systolic pressure increases with large stroke volume and stiff arteries.
        • Diastole: Diastolic pressure increases with vasoconstriction.
        • Heart rate: increased rate decreases time in diastole/ventricular filling.
      • Circulation
        • Resistance is greatest in arterioles and least in the vena cava.
        • Resistance increases with vasoconstriction.
      • Symptoms:
        • Old age: increased blood pressure (both systolic and diastolic), incrased pulse pressure.
    • circulation in specific vascular beds
  • cell/tissue structure and function
    • heart muscle, metabolism, oxygen consumption, biochemistry, and secretory function
    • endothelium and secretory function, vascular smooth muscle, microcirculation, and lymph flow (including mechanisms of atherosclerosis)
      • Endothelium: release NO (vasodilation), prostacyclin (anticlot).
      • Vascular smooth muscle: responds to intrinsic (myogenic, metabolic, autacoids) and extrinsic (sympathetic, parasympathetic, hormonal) regulation.
        • Myogenic = flow homeostasis = constrict when pressure is high, dilate when pressure is low. Present in arteries except for pulmonary.
        • Metabolic = metabolic products as vasodilators
          • flow homeostasis: fast flow washes away vasodilators → vasoconstriction → decreased flow
          • demand driven: high metabolism → vasodilation
        • Autacoids = autacrines and paracrines.
          • Vasodilators: histamine, NO, prostacyclin
          • Vasoconstrictors: Thromboxane, endothelin
    • neural and hormonal regulation of the heart, blood vessels, and blood volume, including responses to change in posture, exercise, and tissue metabolism
      • Homeostasis driven
        • Arterial baroreflex: maintain homeostasis by modifying sympathetic and parasympathetic (vagus) system.
          • baroreceptors in left and right carotid sinuses and in aortic arch. They fire in response to stretch during systole.
          • baroreceptors resets: takes chronic high/low blood pressure as the norm. Consequences: works only to stabilize short-term changes in blood pressure. Eg. standing up after prolonged bed-rest causes drop in blood pressure and syncope.
        • Venous baroreflex: homeostasis by modifying ADH, renin release (and to lesser extent sympathetic and vagal system).
          • receptors in vein-atria junction (mostly right). They fire in response to atrial stretch during diastole.
        • Renin-Angiotensin: increases blood pressure.
          • Renin is released by the kidney. Catalyzes angiotensinogen → angiotensin I.
          • ACE (angiotensin converting enzyme) catalyzes angiotensin I → angiotensin II.
        • Cerebral ischemic reflex: raises blood pressure (sympathetic) during severe hypotension. Symptoms: unconscious patient with tachycardia maintaining low to normal bp.
      • Demand driven
        • Arterial chemoreflex: metabolic demand (low O2, high CO2, high H, low pH) causes sympathetic stimulation, increased respiratory rate.
          • sensors in ventral medulla, carotid body, aortic body.
        • Cushing reflex: try to get blood flowing in the brain when strong intracranial pressure is squeezing on the brain vessels. Symptoms: hypertension (sympathetic, both sys- and diastolic) + bradycardia (vagal drive, mechanism unknown).
        • Pain, fear, anger increases sympathetic drive.
      • Vasoconstrictors = NE, angiotensin, vasopressin = increase intracellular Ca2+ (Ca 2+ channels open + SR release)
      • Vasodilators = Histamine, Bradykinin, Nitroglycerin, EPI, NE = decrease intracellular Ca2+ (Ca 2+ channels close + SR sequestration)
  • repair, regeneration, and changes associated with stage of life

Abnormal processes

  • infectious, inflammatory, and immunologic disorders
  • traumatic and mechanical disorders
  • neoplastic disorders
  • metabolic and regulatory disorders (including dysrhythmias, systolic and diastolic dysfunction, low- and high-output heart failure, cor pulmonale, systemic hypertension, ischemic heart disease, myocardial infarction, systemic hypotension and shock, and dyslipidemias)
    • Atrial arrhythmias
      • Sinus bradycardia = everything normal, just that SA is firing slow (< 60/min, over 5 big squares per beat).
      • Sinus tachycardia = everything normal, just that SA is firing fast (> 100/min, less than 3 big squares per beat).
      • Premature atrial contraction (PAC) = everything normal except for an occasional premature beat.
      • Atrial bigeminy = every other beat is premature.
      • Paroxysmal supraventricular tachycardia (PSVT) = tachycardia without P waves.
      • Atrial flutter/fibrillation = oscillations/vibrations of the baseline with normal QRS waves.
    • Ventricular arrhythmias
      • Premature ventricular contraction (PVC) = everything normal except an occasional ugly QRS.
      • Ventricular tachycardia = tachycardia with ugly QRS.
      • Ventricular fibrillation = no QRS.
    • AV Blocks
      • 1st degree: PR interval over 0.2 sec (1 big square)
      • 2nd degree: Dropped beats: some P waves dont make it (not followed by QRS)
        • Mobitz type I (Wenckebach): progressively increasing PR interval leads to dropped beat.
        • Mobitz type II: dropped beats without changes in PR interval.
      • 3rd degree: none of the P waves make it → AV takes over → slow, regular beats.
  • vascular disorders
  • systemic diseases affecting the cardiovascular system
  • congenital and genetic disorders of the heart and central vessels
  • idiopathic disorders
  • drug-induced adverse effects on the cardiovascular system
  • degenerative disorders

Principles of therapeutics

  • mechanisms of action, use, and adverse effects of drugs for treatment of disorders of the cardiovascular system
    • coronary and peripheral vasodilators
    • antiarrhythmic drugs
    • antihypertensive drugs
    • measures used to combat hypotension and shock
    • drugs affecting cholesterol and lipid metabolism
    • drugs affecting blood coagulation, thrombolytic agents, and antiplatelet agents
    • inotropic agents and treatment of heart failure
    • immunosuppressive, antimicrobial, antineoplastic, and antiparasitic drugs
    • drugs to treat peripheral arterial disease
    • other pharmacotherapy
  • other therapeutic modalities

Gender, ethnic, and behavioral considerations affecting disease treatment and prevention, including psychosocial, cultural, occupational, and environmental

  • emotional and behavioral factors
  • influence on person, family, and society
  • occupational and other environmental risk factors
  • gender and ethnic factors