CARDIOVASCULAR SYSTEM

HEART AND MEDIASTINUM

Dr. JESUS J. GRACILLA

-MD
MEDIASTINUM - middle portion of the thoracic cavity; space between the lungs SUPERIOR
mediastinum CONTENTS INFO
DIVISIONS: PLANES:
Thoracic plane/ Transverse thoracic plane/ Transthoracic plane/
Plane of Ludwig -> divides the mediastinum into superior and inferior
mediastinum
Glandular Thymus gland Central/ primary lymphoid organ.

SUPERIOR mediastinum INFERIOR mediastinum Venous R & L Brachiocephalic Union of internal jugular +
veins subclavian veins behind the sternal
ends of the clavicles near the
sternoclavicular joints
Boundarie Superior: Thoracic inlet Superior: ​Transverse thoracic plane left length is IIx (2x) as long as the
s Inferior: Transverse thoracic Inferior: ​Dome of the diaphragm right
plane Anterior: ​Body of sternum Superior vena cava
Anterior: Manubrium Posterior: ​T5 - T12 Union of R + L brachiocephalic veins
Posterior: T1 - T4 Laterally: ​Mediastinal pleura Start @ 1st costal cartilage
Laterally: Mediastinal pleura Open to R atrium @ 3rd costal
cartilage

Divisions Divided into 5 PLANES Divided into 3 COMPARTMENTS:

(anterior to posterior): 1. Anterior Arterial-nervous Aortic arch Left recurrent Laryngeal nerve hooks
1. Glandular 2. Middle Learn your ABCs beneath the Ligamentum arteriosum
2. Venous 3. Posterior ➔ Ligamentum arteriosum: remnant
3. Arterial nervous of the fetal ductus arteriosus
4. Visceral Aortic arch
5. Lymphatic Brachiocephalic veins (L & R)
Carotid arteries (L, R) Right recurrent Laryngeal nerve hooks
Subclavian veins (L,R) beneath the Right subclavian artery
INFERIOR
mediastinum BOUNDARIES CONTENTS
COMPARTMENTS: Vagus nerve *COMPARE: Passes posterior to the
​brachiocephalic vein​and the​root of
the lungs
Anterior Superior: ​Transverse thoracic plane ● Lower portion of the thymus in CHILDREN
Inferior:​Dome of the diaphragm (thymus = greatest size @ 2 yrs old, shrinks Phrenic nerve Sole motor supply to the diaphragm
Anterior: ​Body of sternum after puberty) ) *COMPARE: Passes anterior to root
Posterior: ​Pericardium enclosing the heart of the lungs
Lateral: ​Mediastinal pleura
When injured/irritated:
● Hiccup reflex - sudden diaphragm
Middle Superior: ​Transverse thoracic plane ● Longest contraction
Inferior:​Dome of the diaphragm ● Most of the organs/vessels/nerves etc. -> ● Kehr’s sign - referred pain to the
Anterior:​Anterior margin of the pericardium Heart, Pericardium, Ascending aorta, SVC tip of the shoulder blade;
Posterior:​Posterior border of the pericardium (lower ½), Azygos vein (terminal), Phrenic symptom of ruptured spleen
Lateral:​Mediastinal pleura nerve, Tracheal bifurcation, R & L bronchi

Posterior Superior​: Transverse thoracic plane ● Descending thoracic aorta Visceral Trachea Start @ C6 (larynx)
Inferior​: Dome of the diaphragm ● Azygos Vein - attaches IVC + SVC; right 16-20 C-shaped rings of hyaline
 HEART HEART VALVES
BASIC STRUCTURES AV valve: R 2nd ICS Tricuspid valve: almost vertical; L 5th ICS
Pulmonary valve: horizontal; L 2nd ICS Mitral valve: L 5th ICS midclavicular line
● Pericardium - double layer that encloses the heart
a) Epicardium - thin external layer (mesothelium)
b) Myocardium - thick Middle layer
CONDUCTING SYSTEM - responsible for the initiation & conduction of cardiac
c) Endocardium - thin internal layer (Endothelium) impulse; damage causes cardiac arrhythmias (irregular ♥ beat)
● Apex - located @ L 5th intercostal space; maximal pulsation of the heart; heartbeat
● Base - posterior; composed of 2 atria: ⅔ L atrium: ⅓ R atrium Sinoatrial Node/ SA ● Pacemaker
● 4 Fibrous skeleton - keeps the AV and SL valves patent/ open and unobstructed; electrical node ● Generates impulses @ 70/min
● Triggers contraction of both atria
insulator; attachment for the myocardium & cusps and leaflets of the valves
● Located in the floor of the sulcus terminalis near its junction
with the SVC
CHAMBERS
Add’t info: Check arrows for blood circulation
Right right auricle; musculi pectinati; crista terminalis; sulcus terminalis; sinoatrial Atrioventricular Bundle ● Conducts impulse to the ventricle by the AV bundle
atrium node (​pacemaker​); sinus venarum cavarum; opening of the SVC; opening of (Bundle of His) ● Generates impulses @ 60/min
the IVC; opening of the coronary sinus; right AV orifice; interatrial septum; ● Most common cause of defective conduction: atherosclerosis
fossa ovalis; annulus ovalis

R & L Branches of ● R: Passes down to the right side of the interventricular

Left most of the base of the ♥; 4 pulmonary veins (2 superior & 2 inferior) Bundle of His septum and them becomes subendocardial on the right side of
atrium the septum
entering its posterior wall
● L: Descends on the L side of the ventricular septum, divides
into purkinje fibers which are distributed to the septum and L
Right largest part of the anterior surface of the heart; conus arteriosus ventricle
Ventricle (infundibulum); trabeculae carnae; tricuspid valve; right AV orifice; chordae
tendinae; papillary muscles; septomarginal trabeculae; interventricular
septum; pulmonary valve Subendocardial ● The terminal branches of the R & L branches of the bundles
Purkinje Fibers of His and spread subendocardialy over the septum and the
rest of the ventricular wall
Left ●apex of the ♥; mitral valve; aortic valve; aortic sinus
ventricle
ABNORMALITIES
INNERVATION- innervated by sympathetic and parasympathetic fibers of the autonomic nervous system via the superficial ● Mediastinum: if WIDENED: Acute aortic rupture/dissection; Neck infection spreads to
and deep cardiac plexuses ANTERIOR; Tumors tend to project on the right dead space on the SUPERIOR

● Arterial Supply (*PIA = posterior interventricular artery) ● Trachea: carina becomes distorted and flattened by the spread of bronchogenic carcinoma
○ R dominance: 90% of people; PIA from RCA
○ L dominance: PIA from LCA ●Heart: AORTIC KNUCKLE: aneurysm, lung consolidation; AORTO-PULMONARY WINDOW:
enlarged lymph nodes; RIGHT PARATRACHEAL STRIPE: paratracheal mass, enlarged lymph
● Venous Drainage: Coronary sinus - Main vein of the ♥ node; CARDIOTHORACIC RATIO (CTR): Cardiac Size​: distance between most lateral points
○ Tributaries: of the ♥. Thoracic Width​: distance between the widest points of the rib cage. >>> CTR ratio
■ Great, middle, & small cardiac vein possible explanation: enlarged RV, LV, pectus excavatum; JUGULAR VEIN DISTENTION:
■ Left posterior vein CHF, pulmonary HTN, SVC obstruction; cardiac tamponade (compression of the heart, 2 most
Remember: circumflex artery is from LCA ■ Left marginal vein common features: dyspnea & tachypnea)
BIOPHYSICS OF CIRCULATION
Dr. VICTOR MENDOZA

-SR
 CARDIOVASCULAR SYSTEM AND FLOW THRU
FACTORS AFFECTING BLOOD FLOW RIGID TUBES TYPES OF FLOW

Pressure difference → rate of flow Similarities Differences LAMINAR (orderly, silent) TURBULENT (noise)
Longer tube → resistance
(flow is INVERSELY proportional to the tube length)
Radius → resistance Blood is fluid Blood vessel are distensible, Concentric layers Move irregularly in axial,
dynamic radial, and circumferential
Viscosity → resistance
direction
CALIBER greatest impact on the resistance
Blood vessels are arranged in Blood is NOT a Newtonian fluid
parallel and series Parabolic velocity, zero Vortices develop
PARALLEL velocity in layers adjacent
SERIES
Compliance = ΔV / Δ P to the wall, MAXIMUM
velocity @ center

ZERO -Container is full, walls are rigid

-Pressure already high Flow: Axial direction parallel MORE pressure is required
-NO additional volume can be to the axis for flow to occur
accommodated
REYNOLDS NUMBER
Tendency to develop a turbulent flow
INFINITE -Certain volume → No dimensions
expansion/stretching of the walls
Reynolds number > 3000 → turbulent flow develops
-Very little change in pressure
-Walls are very distensible Factors:
- Velocity
Segment 1 (least resistance); Amount of flow through the entire - Density
Segment 3 (most resistance) system = SAME with the parent -
FINITE -More volume → pressure Radius
Amount of flow through each tube -
increases (there is also expansion Viscosity
segments = SAME TOTAL resistance = less than the
resistance of any single tube of the wall)
-Any change in volume → change VISCOSITY
in pressure Viscosity of blood is dependent upon:
- Hematocrit
VELOCITY
- Velocity → viscosity
● Veins more compliant > arteries - Blood vessel size
● 60% of the total blood volume is contained within the venous - Plasma protein content
Bio segments
component of the circulation - Temperature → viscosity
arranged in series ●
Capillaries VEINS = capacitance blood vessels - <200um tube → viscosity d/t fluidization of
Arteries in series with
(biggest of all RBC and streamline flow (FAHRAEUS-
arterioles is in turn
LINDQVIST EFFECT)
with capillaries and the segments)
Intravascular pressure > external compressing pressure → blood - Cellular elements such as RBCs tend to
so forth → large cross-
flow aggregate in the central axial core
sectional area Intravascular pressure < external pressure → blood vessels may - Near the walls, blood vessels tend to be less
Blood vessels → SLOWEST collapsed cellular (more plasma)
branch off arranged
Blood pressure @ which blood vessel closes completely → blood - Blood vessel branches off → blood flow towards
in parallel
flow is stopped = CRITICAL CLOSING PRESSURE the branches → less cellular (more plasma)
ELECTROPHYSIOLOGY OF THE
HEART/ECG

Dr. VICTOR MENDOZA

-SR
 TRANSMEMBRANE POTENTIAL IN
RESTING MEMBRANE POTENTIAL (RMP) SA NODE FAST AND SLOW ACTION POTENTIALS

FAST SLOW = SA & AV node; AV

3 principal currents: junction
1. Inward calcium Initial fast, inward current is small or absent
!!!
RMP of current (Brown)
cardiac 2.Hyperpolarization- Phase 0: Rapid onset Slower initial depolarization phase
induced inward current depolarization
cell = -
(Red)
90mV
Cardiac 3. Outward potassium
Concentration gradient favors potassium out current (Blue) Phase 1: Initial repolarization Lower amplitude overshoot
cell MORE
of the cell (rapid reversal of the overshoot
permeable
Counterbalanced by the electrostatic force potential)
to
→ inward movement of the ion → potassium
Establishing a resting equilibrium potential
Phase 2: LONG Plateau phase Shorter and less stable plateau
phase

Phase 3: Rapid Repolarization Repolarization to a lower unstable,

GOLDMAN-HODGKIN-KATZ EQUATION slowly depolarizing resting
potential → DIASTOLIC
Calculation of the combined effects of various ions and ● SA node generates impulses at greatest frequency → main or DEPOLARIZATION/
normal pacemaker of the heart Phase 4: RMP PACEMAKER POTENTIAL
the transmembrane potential
● Active depolarization in any one area → depolarize immediately
adjacent areas of the membrane
● Discharge frequency of pacemakers cells depend on:
1. Rate of depolarization during phase 4
2. Maximal negativity during phase 4 0 = Fast Na+ channels open → 1 = fast Na+ channels close and the
REFRACTORY PERIOD 3. Threshold potential cell begins to repolarize → 2= K+ channels close and the Ca2+
channels open (plateau) → 3 = exit of K+ ions (end of plateau) → 4 =
C to A = increased rate of slow diastolic RMP
depolarization → threshold potential is
attained earlier, HR increases DIASTOLIC DEPOLARIZATION d/t:
A to B = rise in the threshold potential → 1. Progressive in the membrane’s permeability to K+
delays the onset of phase 0 → HR reduced
2. Slight in the permeability of Na+
A to D = maximal negative potential is
3. in the permeability of the membrane to Ca2+
increased → more time is required to
reach threshold potential
CONDUCTION VELOCITY
Speed of propagation of AP

EFFECTIVE refractory period = once fast response has been Catecholamines → frequency or rate of depolarization Factors:
initiated, the depolarized cell is NO LONGER EXCITABLE until the Acetylcholine → the rate of depolarization 1. Diameter
cell partially repolarizes Calcium channel blocker → rate of depolarization Diameter (AV node) → SLOWER
RELATIVE refractory period = AP may be triggered only when the Sympathetic stimulation → rate of depolarization Diameter (Purkinje fiber) → FASTER
stimulus is STRONGER than the stimulus that could elicit a Parasympathetic stimulation → rate of depolarization 2. Intensity of the local depolarizing current
response during phase 4 Rapid depolarization favors rapid conduction
3. Capacitive or resistive properties of the cell membrane
 ACTION POTENTIALS IN DIFFERENT AREAS OF
ELECTROCARDIOGRAM (ECG) THE HEART MEAN ELECTRICAL (QRS) AXIS

✅ graphic representation of the electrical forces produced by the P wave Atrial ✅ orientation of the wave of depolarization during the
heart depolarization most intense phase of ventricular depolarization, R
✅ non-invasive measure of the sum of all electrical activity of the wave reaches its peak
heart QRS complex Ventricular ✅ INDICATOR whether or not ventricular depolarization
❌ not showing an action potential depolarization is proceeding over normal pathways
❌ tells us nothing about contractility or performance
LARGER cardiac muscle strip → amplitude T wave Ventricular
MECHANISM OF ECG repolarization Computation
Depolarized end (right) of the muscle 1. Establish the isoelectric line = PR segment
strip 2. Above the isoelectric line =
PR interval Total AV
Left to right direction of the wave of conduction 3. Below the isoelectric line =
depolarization 4. Measure the amplitude of the deflection above the
Wave of depolarization → going to isoelectric line = R wave
the pole → UPWARD deflection QT interval Ventricular
systole 5. Measure the amplitude of the deflection below the
isoelectric line = Q wave (Lead I) / S wave (Lead III)
Depolarized end (left) of the muscle
QRS complex Rapid
strip
depolarization NORMAL ECG TRACING
Right to left direction of the wave of
(phase 0)
depolarization
Wave of depolarization → going to - P wave, QRS complexes, T wave, and all leads are present
away from the pole → ST segment Plateau phase - Lead I, II, III represent standard limb leads
DOWNWARD deflection (phase 2) - Lead I (bipolar leads)
Both P wave and T wave are upright
QRS complex is upright
T wave Repolarization - aVR, aVL, aVF represents augmented limb leads
Biphasic deflection (phase 3) - aVR
From the left side to the midpoint Both P wave and T wave are negative
→ UPWARD QRS complex is mainly downwards
From midpoint to the right side → - Chest leads (unipolar leads)
DOWNWARD - QRS Complexes
Normal speed is 25 mm/s
R wave is amplitude from V1 to V6
EINTHOVEN TRIANGLE CONCEPT S wave is amplitude from V1 to V6
Lead II = Lead I + Lead III Horizontal axis= time - Rhythm is REGULAR, coming from SA node
The human torso: The heart: 1 BIG square along the - Estimate of HR is around 80s; Mean electrical axis is around
- a sphere ❌ - at the center of the horizontal axis = 0.2s +20
- of infinite size ❌ torso (NOT exactly 1 SMALL square = 0.04s
- of homogenous conducting true)
ability ✅ - is considerably Vertical axis = magnitude of
smaller ✅ the potential
Lead 1 = Positive electrode (Left arm); Negative electrode (Right arm)
Lead 2 = Positive electrode (Left leg); Negative electrode (Right arm)
1 mV = 10 mm
Lead 3 = Positive electrode (Left leg); Negative electrode (Left arm)
 WAVE OF DEPOLARIZATION

Atrial Septal depolarization Apical and early ventricular Late ventricular Repolarization
depolarization depolarization depolarization

Lead I Moves from R → L Going to L → R Going downwards towards the Moving towards the left and T waves, upright deflection
and downwards (Initial Q a downward left upwards
(P wave upright) deflection) (R wave a passive deflection) (More R wave an upward
deflection)

aVF Going inferiorly Moving downwards Going downwards Moving upwards T waves, upright deflection
(P wave upright) (Initial R wave without the Q) (R wave a passive deflection) (Negative deflection, S wave)

P WAVE QRS T WAVE

Lead I = Upright COMPLEX Lead I = Upright
aVF = Upright Lead I = Positive aVR = Inverted
aVR = Inverted aVR = Negative
MECHANICAL ACTIVITY + REGULATION
OF THE HEART

Dr. VICTOR MENDOZA

-WR
 PRESSURE VOLUME DIAGRAM FRANK STARLING LAW
STROKE VOLUME- amt of blood
ejected to great vessels
(CARDIAC PERFORMANCE)

norepinephrine
END DIASTOLIC VOLUME
(PRELOAD)

venous return → contract → blood to aorta

EJECTION FRACTION: amount of ventricular volume

ejected to great arteries (55%)

P in great arteries → P in ventricles → open semilunar → eject blood

CONCEPT OF PRELOAD CONCEPT OF AFTERLOAD
INC RESTING LENGTH Afterload Shortening & cardiac performance
INC VELOCITY OF SHORTENING Muscle strip
ENHANCE HEART
PERFORMANCE

Cardiac
performance

Afterload Stroke volume & cardiac performance

(+) Inotropic Agent Heart

(-) NaK ATPase

X Na in cell

X Na-Ca exchange

Ca in cell → contraction Measures of afterload

 EXCITATION-CONTRACTION COUPLING ISOMETRIC CONTRACTIONS
ELECTRICAL ACT → MECHANICAL ACT CARDIAC
END OF ONE HEARTBEAT CYCLE OF NEXT HEARTBEAT
TO THE BEGINNING
(Action Potential → Contraction)

(2) L-type calcium channels not enough DIASTOLE = heart muscle RELAXES AND REFILLS with blood
Optimal (Lmax) SYSTOLE = heart muscle CONTRACTS AND PUMPS blood
(1) Action potential (7) to
extracellular fluid
INC CONTRACTION → INC P → WILL RELEASE BLOOD
“ISO” = NO change in volume
(6) (+) Na-Ca HIGH P
exchange (3 Na
in, 1 Ca out) INFLOW PHASE - inlet valve is open; outlet valve is closed
Contraction & tension | shortening ATRIAL SYSTOLE - AP > VP | Blood from
muscle length = tension A→V
(3) calcium release channels (5) + Ca-ATPase *LMAX = length of muscle with max amt of tension
(/ crossbridge)
ISOVOLUMETRIC CONTRACTION PHASE - both valves closed
MECHANISMS: → NO blood flow; VP > AP; DEpolarization of ventricle
● Extent of overlap of thick & thin filaments
● Sensitivity of myofilaments to calcium (most impt!)
(4) extracellular Ca → heart ● Calcium release
OUTFLOW PHASE - outlet valve is open; inlet valve is closed
contraction!
VENTRICULAR EJECTION - VP > P of
ISOTONIC CONTRACTIONS great arteries
ISOTONIC AFTERLOADED
Action potential → to transverse tubules → to longitudinal sarcoplasmic
tubules → release of calcium → (+) calcium-induced calcium release →
ISOVOLUMETRIC RELAXATION PHASE - both valves closed →
open ryanodine receptor channels → calcium interact with troponin C → NO blood flow; AP > VP; REpolarization of ventricle
(+) cross-bridge formation WIGGERS
RAPID VENTRICULAR FILlING - AP > VP | blood from A → V

FACTORS AFFECTING CONTRACTION DIAGRAM

Rest → Contract → shorten → stops

1. PRELOAD & AFTERLOAD
● Freeload (resting length) = cardiac performance
● Afterload = cardiac performance Muscle length = Constant Tension
Muscle length = Contractile potential
1. POSITIVE INOTROPIC EFFECT *Once contractile potential / tension = load → shortening
● NOREPINEPHRINE - neurotransmitter of SNS →
stimulates Ca → isometric tension → contractility
ISOTONIC CONTRACTION SET-UP
● Only one end is fixed
1. NEGATIVE INOTROPIC EFFECT
● Reaches particular resting length d/t weight added
● Isometric tension→ contractility
● (+) stimulation → muscle contracts & shortens
AFTERLOAD CONTRACTION SET-UP
1. FREQUENCY OF CONTRACTION
● Strip is stretched @ particular length d/t + 1g
Frequency Tension
Inc Action Potential
● + 2g weight → stretch the muscle since it is resting
RISE on the table
DROP
(STEADY STATE)
● Continue to shorten until it reaches a length that is
capable of producing an active tension (3g)
BOWDITCH STAIRCASE (FORCE TRAPPE EFFECT)
PERIPHERAL CIRCULATION
Dr. VICTOR MENDOZA

-MD
Peripheral vascular system - everything except the ; system of BVs; blood distribution regulated BLOOD PRESSURE
by ARTERIOLES bec the walls are more muscular

BLOOD VESSELS SYSTOLIC (SBP) DIASTOLIC (DBP)

ARTERY VEIN CAPILLARY

*not innervated by
Definition Highest pressure which occurs when the blood is Point of minimal pressure in the arterial system
sympathetic nervous system
ejected from the heart into the aorta which coincides with the end of diastole

Blood flow -> body body -> Fluid exchange Ventricles PUSH blood out Ventricles get FILLED

Blood AWAY Blood VAVALIK

Normal 120 mmHg 80 mmHg

Blood carried O2 rich CO2 rich Mixed

Trends Higher CO -> Higher SBP Higher SBP -> Higher DBP
Higher SV -> Higher SBP Longer duration of outflow -> Higher DBP
Higher TPR -> Higher SBP Slower outflow rate -> Higher DBP
Wall Thick, elastic Thin, non-elastic Thin Higher rate of ejection -> Higher SBP Lesser compliance -> normal or Lower DBP
Lesser compliance -> Higher SBP

Lumen Narrow/ small Wide/ large Narrow/small ● Pulse Pressure (PP) = (SBP - DBP) dependent on compliance
● MAP = DBP + ⅓ PP sum of the diastolic blood pressure and 1⁄3 of the pulse pressure
● MAP= TPR x CO product of the cardiac output and the total peripheral resistance
Valve Absent Present (blood Absent
● MAP is also determined by getting the area under the curve
cannot backflow)

Blood pressure High Low Low

SMOOTH MUSCLES

Compliance Low High

● VASCULAR TONE - general contractile state of a vessel or vascular region
● INTRINSIC TONE - arterioles remain in a state of partial constriction even when all external influences on them have
been removed
● BASAL TONE - smooth muscle cells inherently and actively resist being stretched
COMPLIANCE ○ Local metabolic influences
■ vasoDILATOR: Nitric oxide, hypothermia, Histamine, K+, Mg2+, CO2, H+, acetate, citrate
● distensibility/elasticity of vessels ■ vasoCONSTRICTOR: Endothelin, Ca2+
● total quantity of blood that can be stored in a given portion of the circulation for each mm Hg ○ Neural influences
pressure rise ■ vasoDILATOR: sympathetic
● The stiffer the aorta, the less compliant Young – HIGH compliance ■ vasoCONSTRICTOR: parasympathetic
Elderly – LESS compliance ○ Hormonal influences
■ vasoDILATOR: adenosine
● Hypertension - ​single largest contributor to CV disease -> risk of atherosclerosis -> cause stroke, ■ vasoCONSTRICTOR: NE, Epi,Vasopressin, Ang II
HF, CAD, Kidney disease
 the rate at which blood returns to
VENOUS RETURN the thorax from the peripheral COMPLIANCE
vascular beds

FACTORS AFFECTING VENOUS RETURN SYSTOLIC (SBP) DIASTOLIC (DBP)

●Capacity of the venous system

●Muscle pump Definition Highest pressure which occurs when the blood is Point of minimal pressure in the arterial system
●Respiratory pump ejected from the heart into the aorta which coincides with the end of diastole
●Vis a tergo - pressure from the left side of the heart, pushing blood from behind towards the right
side of the heart
●Vis a fronte - during ventricular contraction, atrium gets expanded and this creates a negative
pressure in the right atrium
●Action of the pericardium Normal 120 mmHg 80 mmHg

SYSTEMIC ARTERIAL PRESSURE Trends Higher CO -> Higher SBP Higher SBP -> Higher DBP
Higher SV -> Higher SBP Slower outflow rate -> Higher DBP
Higher TPR -> Higher SBP Longer duration of outflow -> Higher DBP
●Arterial baroreceptor - Sensory receptor found in abundance in the walls of aorta and carotid Higher rate of ejection -> Higher SBP
arteries; Both ​MAP and ​PP affect the baroreceptor firing Lesser compliance -> Higher SBP
■ Carotid​- connected to CN IX
■ Aortic​– connected to CN X ● Pulse Pressure (PP) = (SBP - DBP) dependent on compliance
●Components of reflex pathway​: ● MAP = DBP + ⅓ PP 1/3 of the pulse pressure is added to the diastolic pressure to get a clinical estimate of the mean
■ sensory receptors arterial pressure
■ afferent pathways ● MAP= TPR x CO product of the cardiac output and the total peripheral resistance
■ integrating centers in the CNS ● MAP is also determined by getting the area under the curve
■ efferent pathways
■ effector organs
●HIGH BP -> stimulate parasympathetic nervous system
●LOW BP -> stimulate sympathetic nervous system

● VASCULAR TONE - general contractile state of a vessel or vascular region

● INTRINSIC TONE - arterioles remain in a state of partial constriction even when all external influences on them have
been removed
● BASAL TONE - smooth muscle cells inherently and actively resist being stretched
○ Local metabolic influences
■ vasoDILATOR: Nitric oxide, Histamine, K+, Mg2+, CO2, H+, acetate, citrate
●vasoCONSTRICTOR: Endothelin, Ca2+
○ Neural influences
■ vasoDILATOR: sympathetic
■ vasoCONSTRICTOR: parasympathetic
○ Hormonal influences
●vasoDILATOR
■ vasoCONSTRICTOR: NE, Epi,Vasopressin, Ang II
MICROCIRCULATION
Dr. VICTOR MENDOZA

-ZC
 Capillaries: Transcapillary Exchange Processes:
● Exchange of gases and other substances ● Diffusion
● Overall permeability is affected by ● Filtration
endothelium and basement membrane
● Change shape with pressure reduction
Precapillary region:
● Small blood vessels
● With single amount of muscle coat
● Controls blood flow distribution and area
of capillary bed
● Thoroughfare channels or arteriovenous
anastomosis allow complete bypass of
the capillary bed
● Thoroughfare or preferential channels
(mesentery): lower resistance
Comprised of: arteriovenous connections and lateral
sphincters
● Smallest arterioles
● ● Arcade arterials
Metarterioles
● Precapillary sphincters ● Postcapillary venules
● Capillaries ● Collecting venules
● Venules
● Arteriovenous anastomosis Vasomotion:
● Contraction & relaxation of precapillary
Functional components: sphincters & metarterioles (>/=30 secs)
● Resistance vessels ● Resting skeletal muscle: 15 secs
● Exchange vessels ● Affected by: beta adrenergic stimulation,
● Shunt vessels vasoactive substances
● Capacitance vessels ● O2 metabolism: decreased O2 tension
enhances local perfusion and vice versa
Types of blood flow: ● Tissue O2 tension → capillary density
● Nutritional Flow: nutrients and gases ● These factors & intercapillary distance
● Non-nutritional or Shunt Flow: AV gradient for O2 diffusion
● Control mechanism: regulation of flow in
anastomoses, body temperature
capillary density or surface area
Diffusion: Factors affecting filtration rate Lymphatic system
● Guiding force → concentration gradient ● Returns excess tissue fluid and protein to
● Filtration Coefficient (K)
● Small molecular weight substances: intravascular compartment
● Capillary Hydrostatic Pressure (Pc) ● Fenestrations
› CO2 and O2 (lipid soluble): diffuse freely
› H2O and H2O-soluble: pores or splits ● Interstitial Fluid Hydrostatic Pressure ● Collagenous anchoring filaments
● Rate of blood flow primary determinant of (Pi) ● Pinocytosis
transport ● Plasma Colloid Osmotic Pressure (𝛑c) ● Smooth muscle valves prevent retrograde
● Large molecules (sucrose) limited by pore flow
● Interstitial Fluid Colloid Osmotic
size ● Blood capillary > interstitial space > lymphatic
Pressure (𝛑i) capillary > collecting duct > lymphatic vessels
● Diffusion rates: inversely related to
molecular size ● filtration
Net Starling rate:
Equation (Starling Forces) > lymph nodes > ducts (RLD / TD) > great
● Differences between the forces veins (subclavian vein)
Factors affecting diffusion: tending to move fluid outward
Functions of lymphatic circulation:
● Intercapillary distance (capillary hydrostatic pressure)
● Returns protein, water, and electrolytes
● Blood flow and oncotic pressure in the
(capillary filtrate) from tissue spaces to blood
● Concentration gradient for the solute interstitial space
● Absorption of fats (GIT)
● Inward movement: hydrostatic
● Capillary permeability ● Removes RBCs (hemorrhage)
pressure and oncotic pressure
● Capillary surface area ● Filters foreign particles and bacteria
(phagocytic cells)
Factors enhancing diffusion:
● Diffusion distance Increase in lymph flow::
● Surface area
● Time available for exchange ● Increase in capillary pressure
● Increase in capillary surface area
Filtration: ● Increase in capillary permeability
● Fluid movement from difference in hydrostatic ● Increase in functional activity
or osmotic pressure across a membrane ● Massage and tissue movement
● Plasma Protein (albumin, globulin) ● Hypertonic Solutions
› High concentration in blood compartments
› Low in interstitial
› Colloid osmotic pressure or oncotic
pressure
› 75% of total oncotic pressure of plasma
result from albumin
SPECIAL CIRCULATION
Dr. MITZI T ASERON

-JE
 SKELETAL MUSCLE CIRCULATION

FACTORS THAT ALTER O2 EXTRACTION

● Blood flow (constant) + Tissue (cool) → ↑venous O2 → ↓O2 extraction → ↓blood flow
● Blood flow (constant) + Tissue (warm) → ↓venous O2 → ↑O2 extraction → ↑blood flow

FACTORS THAT ALTER BLOOD SUPPLY

● Vasoconstriction: ↓O2 req’t → ↑vascular resistance → ↑sympathetic activity → ↓blood flow

● Vasodilation: ↑O2 req’t → ↓vascular resistance → ↓sympathetic activity → ↑blood flow

CIRCULATORY ADJUSTMENTS

● At REST, sympathetic (resting tone) dominates.

● During EXERCISE,
○ ↑ in O2 extraction (70-75%) ○ ↑ SNS activity: vasoconstriction in most tissues
→ Arterial O2 (20%), Venous O2 (5%), AV diff. (15%) → blood shunted towards tissue needing it most + ↑ heart rate, contractile force and sweating
○ ↑ blood flow to tissues ○ Local release of vasodilator metabolites: d/t ↑ temperature and local acidosis
■ 80% CO = 30L/min ■ Nitric oxide → ↑ blood flow

CUTANEOUS CIRCULATION

REFLEX CONTROL VASCULAR RESPONSE TO STIMULATION

● Lower core temperature: low temp (hypothalamus) → vasoconstriction → piloerection → ↑ thermogenesis

● Higher core temperature: high temp (hypothalamus) → vasodilation → sweating → ↓ thermogenesis
● Cutaneous vasculature: promote heat loss > prevent heat loss
○ Heat: 30x ↑blood flow
○ Cold: 10x ↓blood flow
● Hunting response: alternate constriction and dilation d/t prolonged exposure
→ protective against ischemia
 CORONARY CIRCULATION

BLOOD SUPPLY FACTORS AFFECTING OXYGEN DEMAND (CHISEE)

Venous supply:
Arterial supply: ● Cardiac work ● Systolic pressure (wall tension)
Coronary sinus (major)
R and L coronary arteries ● Heart rate ● Extent of shortening
Coronary veins, Anterior luminal vessels
● Inotropic state ● Energy sources
and Thebesian vessels (minor)

DETERMINANTS OF CORONARY BLOOD FLOW

SYSTOLIC COMPRESSION NEUROGENIC TONE

PERFUSION PRESSURE
↑ perfusion pressure → ↑ blood flow

MYOCARDIAL O2 REQUIREMENT
(Result: ↑ blood flow)
○ Extravascular compression (systole) → ↓ in L coronary blood flow
○ ↑ cardiac work → ↑ O2 requirement
○ Removal of compression (diastole) → ↑ in L coronary blood flow
○ Reactive hyperemia: O2 deprivation
○ Systole (R ventricle): maximal flow because extravascular pressure do not exceed
○ Autoregulation: ↑ in O2 demand
aortic pressure
○ Metabolic metabolites (O2, Lactate,
Histamine, Prostaglandin, Adenine
REMEMBER:
nucleotide, Adenosine) → NO production
Systole = maximal flow in R ventricle
Diastole = maximal flow in L ventricle
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