Cardiovascular anatomy, physiology

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Cardiovascular anatomy, physiology
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2013-03-26 14:32:14
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Cardiovascular anatomy and physiology
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    • Coronary artery anatomy
    • Right coronary artery (RCA):
    • -SA and AV nodes are usually supplied by RCA
    • Acute marginal artery: supplies right ventricle

    • →Posterior descending/interventricular artery (PD): supplies posterior 1/3 of interventricular septum and posterior walls of ventricles
    • -Right dominant circulation: 85%; PD arises from RCA

    • Left main coronary artery (LCA):
    • →Left circumflex coronary artery (LCX): supplies the lateral and posterior walls of left ventricle
    •      →LCX → left marginal artery
    •      →Left dominant circulation: 8% (PD artery arises from LCX
    • → Left anterior descending artery (LAD): supplies anterior 2/3 of interventricular septum, anterior papillary muscle, and anterior surface of LV
  1. Posterior descending 
    right-, left-, co-dominant circulation
    • Right-dominant circulation: 85% = PD arises from RCA
    • Left-dominant circulation: 8% = PD arises from LCX
    • Codominant circulation: 7% = PD arises from both LCX and RCA
  2. Most commonly occluded artery
    LAD
  3. Coronary arteries fill during ______.
    • Diastole
    • Pathological tachycardia (Wolff-Parkinson-White syndrome; >250bpm) is problematic due to decreased filling time
    • Diastolic refilling time sets the limit for maximam useful heart rate
  4. What is the most posterior part of the heart?
    • The most posterior part of the heart is the left atrium
    • → enlargement: dysphagia (due to compression of the esophagus); hoarseness (due to compression of the left recurrent laryngeal nerve)
  5. Transesophageal echocardiography (TEE)
    • TEE is useful for diagnosing:
    • -left atrial enlargemnet
    • -aortic dissection
    • -thoracic aortic aneurysm
    • -vegetation on valves
  6. Cardiac output
    simple equation, fick principle
    • CO = stroke volume (SV) × heart rate (SV)
  7. Mean arterial pressure
    • MAP = 2/3 Diastolic pressure + 1/3 Systolic pressure
  8. Pulse pressure
    • Pulse pressure = systolic pressure - diastolic pressure
    • Pulse pressure is proportional to stroke volume
  9. Stroke volume
  10. Exercise and CO
    • Early stages of exercise: CO is maintained by ↑ HR and ↑ SV
    • Late stages of exercise: CO is maintained by ↑ HR only (SV plateaus)
  11. Cardiac output variables
    • **SV CAP
    • -Stroke Volume affected by Contractility
    • -Afterload
    • -Preload

    • Stroke volume increase with:
    • - ↑ preload

    • - ↓ afterload
    • - ↑ contractility

    • Contractility (and SV) increase with:
    • -Catecholamines (↑ activity of Ca2+ pump in sarcoplasmic reticulum)
    • -↑ intracellular Ca2+
    • -↓ extracellular Na+ (↓ activity of Na+/Ca2+ exchanger)
    • -Digitalis (blocks Na+/K+ pump → ↑ intracellular Na+ → ↓ Na+/Ca2+ exchanger activity → ↑ intracellular Ca2+)

    • Contractility (and SV) decrease with:
    • 1-blockade (↓ cAMP)
    • -Heart failure (systolic dysfunction)
    • -Acidosis
    • -Hypoxia/hypercapnea (↓ PO2/↑ PCO2)
    • -Non-dihydropyridine Ca2+ channel blockers
  12. Stroke volume
    • ↑SV in:
    • -Anxiety
    • -exercise
    • -pregnancy

    A failing heart has ↓ SV
  13. Myocardial O2 demand is increased by:
    • ↑ afterload (proportional to arterial pressure)
    • ↑ contractility
    • ↑ heart rate
    • ↑ heart size (↑ wall tension)
  14. Preload vs afterload
    • Preload = ventricular EDV
    • Afterload = mean arterial pressure (proportional to peripheral resistance)
    • *VEnodilators (e.g., nitroglycerin) ↓ prEload
    • *VAsodilators (e.g.e, hydrAlazine) ↓ Afterload (arterial)

    • Preload ↑ with:
    • -Exercise (slightly)

    • - ↑ blood volume (e.g., overtransfusion)
    • - Excitement (↑ sympathetic activity)
  15. Starling curve
    • Force of contraction is proportional to end-diastolic length of cardiac muscle fiber (preload)
    • ↑ contractility with sympathetic stimulation, catecholamines, digoxin
    • ↓ contractility with loss of myocardium (MI), β-blockers, calcium channel blockers
  16. Ejection fraction (EF)
    • EF is an index of ventricular contractility
    • EF is normally ≥ 55%
    • EF is decreased in systolic heart failure
  17. Resistance, pressure, flow
    R, ΔP, Q
    • ΔP = Q × R
    • (similar to Ohm's law: ΔV= I × R)
    • Pressure gradient drives flow from high pressure to low pressure

    • Resistance = driving pressure/ flow
    • -Directly proportional to the viscosity of the fluid and length of the vessel
    • -Inversely proportional to the radius to the 4th power
  18. Total Resistance
    • Total resistance of vessels in series = R1 + R2 + R3...
    • Total resistance of vessels in parallel = 1/R1 + 1/R2 + 1/R3...
    • Arterioles account for most of total peripheral resistance → regulate capillary flow
  19. Viscosity of blood
    Viscosity (μ) depends mostly on hematocrit

    • Viscosity ↑ in:
    • -Polycythemia
    • -Hyperproteinemic states (e.g., multiple myeloma)
    • -Hereditary spherocytosis

    • Viscosity ↓ in:
    • - anemia
  20. Cardiac and vascular function curves
    • Operating point of normal heart
    • Cardiac output - venous return
  21. Cardiac function curve
    Exercise, AV shunt (↓TPR)
    • + inotropy
    • ↑ blood volume (venous return)
  22. Cardiac function curve
    Hemorrhage before compensation can occur (↑TPR)
  23. Cardiac and vascular function
    Heart failure, narcotic overdose
    • Venous return is "normal"
    • decreased inotropic state
  24. Cardiac cycle
    Pressure-volume curve; phases (LV)
    • 1. Isovolumetric contraction: period between mitral valve closure and aortic valve opening; period of highest O2 consumption
    • 2. Systolic ejection: period between aortic valve opening and lcosing
    • 3. Isovolumetric relaxation: period between aortic valve closing and mitral valve opening
    • 4. Rapid filing: period just after mitral valve opening
    • 5. Reduced filling: period just before mitral valve closure
  25. Cardiac cycle:
    ↑ contractility, ↑ SV, ↑ EF, ↓ ESV
  26. Cardiac cycle:
    ↑ afterload, ↑ aortic pressure, ↓ SV, ↑ ESV
  27. Cardiac cycle:
    ↑ Preload → ↑SV
  28. Wigger's diagram
  29. Heart sounds
    • S1: mitral and tricuspid valve closure; loudest at mitral area
    • S2: aortic and pulmonary valve closure; loudest at left sternal border
    • S3: in early diastole during rapid ventricular filling phase
    • -Associated with ↑ filling pressures (e.g., mitral regurgitation, CHF)
    • -More common in dilated ventricles (but normal in children and pregnant women)
    • S4: "atrial kick" in late diastole
    • -High atrail pressure
    • -Associated with ventricular hypertrophy
    • -Left atrium push against stiff LV wall
  30. Jugular venous pulse (JVP)
    • a wave: atrial contraction
    • c wave: RV contraction (closed tricuspid valve bulging into atrium)
    • x descent: atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
    • v wave: ↑ right atrial pressure due to filling against closed tricuspid valve
    • y descent: blood flow from RA to RV
  31. Splitting
    • Normal splitting
    • Wide splitting
    • Fixed splitting
    • Paradoxical splitting
    • Normal splitting
    • Inspiration → drop in intrathoracic pressure → ↑ venous return to the RV → increased RV stroke volume → ↑ RV ejection time → delayed closure of pulmonic valve

    ↓ pulmonary impedance (↑ capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve
    • Wide splitting
    • Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block)
    • Delay in RV emptying causes delayed pulmonic sound (regardless of breath)
    • An exaggeration of normal splitting
    • Fixed splitting
    • Seen in ASD
    • ASD → left-to-right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
    • Paradoxical splitting
    • Seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block)
    • Normal order of valve closure is reserved so that P2 sound occurs before delayed A2 sound
    • On inspiration, P2 closes later and moves closer to A2, thereby "paradoxically" eliminating the split
  32. Auscultation of the heart
  33. Auscultation of the heart
    Aortic area
    • Systolic murmur:
    • -Aortic stenosis
    • -Flow murmur
    • -Aortic valve sclerosis
  34. Auscultation of the heart
    Pulmonic area
    • Systolic ejection murmur:
    • -Pulmonic stenosis
    • -Flow murmur (e.g., ASD, PDA)
  35. Auscultation of the heart
    Left sternal border
    • Diastolic murmur:
    • -Aortic regurgitation
    • -Pulmonic regurgitation

    • Systolic murmur:
    • -Hypertrophic cardiomyopathy
  36. Auscultation of the heart
    Tricuspid area
    • Pansystsolic murmur:
    • -Tricuspid regurgitation
    • -Ventricular septal defect

    • Diastolic murmur:
    • -Tricuspid stenosis
    • -Atrial septal defect
  37. Auscultation of the heart
    Mitral area
    • Systolic murmur:
    • -Mitral regurgitation

    • Diastolic murmur:
    • -Mitral stenosis
  38. Bedside maneuvers: effect on heart sounds/murmurs
    • Inspiration: ↑ intensity of right heart sounds
    • Expiration: ↑ intensity of left heart sounds
    • Hand grip (↑ systemic vascular resistance): 
    • -↑ intensity of MR, AR, VSD, MVP mumurs
    • -↓ intensity of AS, hypertrophic cardiomyopathy murmurs
    • Valsalva (↓ venous return): 
    • -↓ intensity of most murmurs
    • -↑ intensity of MVP, hypertrophic cardiomyopathy murmurs
    • Rapid squatting (↑ venous return, ↑ preload, ↑ afterload with prolonged squatting):
    • -↓ intensity of MVP, hypertrophic cardiomyopathy murmurs
  39. Systolic heart sounds
    • aortic/pulmonic stenosis
    • mitral/tricuspid regurgitation
    • ventricular septal defect
  40. Diastolic heart sounds
    aortic/pulmonic regurgitation, mitral/tricuspid stenosis
  41. Ventricular action potential
    • Cardiac myoccytes, bundle of His, Purkinje fibers
    • Phase 0: rapid upstroke
    • Phase 1: initial repolarization
    • Phase 2: plateau
    • Phase 3: rapid repolarization
    • Phase 4: resting potential
  42. Cardiac myocytes
    currents

    • Phase 0: voltage gated Na+ channels open
    • Phase 1: inactivation of voltage-gated Na+ channels; voltage-gated K+ channels begin to open
    • Phase 2: Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux; Ca2+ influx triggers Ca2+ released from SR and myocyte contracts
    • Phase 3: massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage gated Ca2+ channels
    • Phase 4: high K+ permeability through K+ channels
  43. Cardiac muscle
    compared to skeletal muscle
    • Cardiac AP has plateau, due to Ca2+ influx and K+ efflux
    • Myocyte contraction occurs due to Ca2+-induced Ca2+ release from the sarcoplasmic reticulum
    • Cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to Ifchannels ("funny current" channels responsible for a slow, mixed Na+/K+ inward current)
    • Cardiac myocytes are electrically coupled to each other by gap junctions
  44. Pacemaker action potentials
    • Occurs in the SA and AV nodes
    • Phase 0: upstroke is due to voltage gated Ca2+ channels
    • -Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting voltage of these cells
    • -slow conduction velocity; used by AV node to prolong transmission from atria to ventricles
    • Phase 2: plateau is absent
    • Phase 3: inactivation of the Ca2+ channels and ↑ activation of K+ channels → ↑ K+ efflux
    • Phase 4: slow diastolic depolarization
    • -membrane potential spontaneously depolarizes as Na+ conductance ↑ (If different from INa)
    • -Automaticity of SA and AV nodes
    • -Slope of phase 4 in SA node determines HR
    • -ACh/adenosine ↓ the rate of diastolic depolarization and ↓ HR
    • -Catecholamines ↑ depolarization and ↑ HR
    • Sympathetic stimulation ↑ the chance that If channels are open and thus ↑ HR
  45. Speed of conduction
    Purkinje > atria > ventricles > AV node
  46. Pacemakers
    • SA node → atria → AV node → common bundle → bundle branches → Purkinje fibers → ventricles
    • SA node "pacemaker" inherent dominace with slow phase of upstroke
    • AV node: 100-msec delay; allows time for ventricular filling
  47. Conduction system
  48. Atrial natriuretic peptide
    • ANP is released from atrial myocytes in response to ↑ blood volume and atrial pressure
    • Causes generalized vascular relaxation
    • ↓ Na+ reabsorption at the medullary collecting tubule
    • Constricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated)
    • Promotes diuresis and contributes to "escape from aldosterone" mechanism
  49. Baroreceptors and chemoreceptors
    • Receptors:
    • -Aortic arch: transmits via vagus nerve to solitary nucleus of medulla (responds only to ↑BP)
    • -Carotid sinus: transmits via glossopharyngeal nerve to solitary nucleus of medulla (reponds to ↓ and ↑ in BP)
  50. Baroreceptors
    • Hypotension → ↓ arterial pressure → ↓ stretch → ↓ afferent baroreceptor firing → ↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation → vasoconstriction, ↑ HR, ↑ contractility, ↑ BP
    • -Important in the response to severe hemorrhage

    Carotid massage: ↑ pressure on carotid artery → ↑ stretch → ↑ afferent baroreceptor firing → ↓ HR

    • Cushing reaction: triad of hypertension, bradycardia, respiratory depression
    • -↑ intracranial pressure constricts arterioles → cerebral ischemia and reflex sympathetic increase in perfusion pressure (hypertension) → ↑ stretch → reflex baroreceptor induced-bradycardia
  51. Chemoreceptors
    • Peripheral: carotid and aortic bodies
    • -Stimulated by ↓ PO2 (<60mmHg), ↑ PCO2, and ↓ pH of blood

    • Central
    • -Stimulated by changes in pH and PCO2 of brain interstitial fluid; which in turn are influenced by arterial CO2
    • -Do NOT directly respond to PO2
  52. Pressures in the heart
    • Right Atrium: <5
    • Right Ventricle: 25/5
    • Pulmonary Artery: 25/10
    • PCWP: <12 (good approximation of left atrial pressure)
    • **In mitral stenosis, PCWP > LV diastolic pressure
    • Left atrium: <12
    • Left ventricle: 130/10
    • Aorta: 130/90
  53. Circulation through organs
    • Lung: organ with largest blood flow (100% CO)
    • Liver: largest share of systemic CO
    • Kidney: highest blood flow per gram of tissue
    • Heart: largest arteriovenous O2 difference because O2 extraction is~80%
    • -↑O2 demand is met by ↑ coronary blood flow, not by ↑ extraction of O2
  54. Autoregulation
    • Heart: local metabolites (vasodilatory) - CO2, adenosine, NO
    • Brain: local metabolites (vasodilatory) - CO2 (pH)
    • Kidneys: Myogenic and tubuloglomerular feedback
    • Lungs: Hypoxia causes vasoconstriction (**Unique; other organs: hypoxia → vasodilation)
    • Skeletal muscle: Local metabolites - lactate, adenosine, K+
    • Skin: sympathetic stimulation most important mechanism; temperature control
  55. Capillary fluid exchange
    • Governed by the starling equation
    • Pc = capillary pressure
    • Pi - interstitial fluid pressure
    • πc = plasma colloid osmotic pressure (pulls fluid into capillary)
    • πi = interstitial fluid colloid osmotic pressure (pulls fluid out of capillary)
    • Kf = filtration constant (capillary permiability)
  56. Edema
    • Excess fluid outflow into interstitium
    • commonly caused by:
    • -↑ capillary pressure (heart failure)
    • -↓ plasma proteins (nephrotic syndrome, liver failure)
    • -↑ capillary permeability (toxins, infections, burns)
    • -↑ interstitial fluid colloid osmotic pressure (lymphatic blockage

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