Cardiovascular System Flashcards

Question

EKG Intervals

Answer 1

* **P-P interval** used to determine heart rate & rhythm * **PR interval** used to estimate how long it takes for AP to get through the AV node (and His/Purkinje system) * PR prolongation indicative of abnormality in conduction pathway * **QRS widening** suggests that ventricle depolarization is slower than normal * Found in cases of impaired conduction through the bundle of His = **bundle branch block**

Answer 2

The summation of the directions of electrical activity. Certain cardiac abnormalities may alter the path of current flow through the heart changing the direction of the electrical axis.

Answer 3

Coordinate system allowing interpretation of the signals from various EKG leads in terms of the MEA. When MEA is _aligned_ with a lead the signal recorded will be _maximally positive_. When MEA is _perpendicular_ to a lead there is _no deflection recorded_ in that lead = **isoelectric lead**. Various leads can be used to determine the MAE. Because the left ventricle is larger than the right ventricle, a normal MAE is between **-30° (aVL) and +90° (aVF)**.

Answer 4

Pathophysiological conditions can alter the position of the MEA. RVH means right side of the heart makes a greater contribution to total current flow causing QRS complex in lead 1 to be smaller than normal ⇒ **right axis deviation**. (MAE beyond +100°) LVH causes MEA to move more towards the left and aV_F ⇒ **left axis deviation**. (MEA more negative than -30°)

Answer 5

Decreased AV nodal conduction causes PR prolongation. **First-degree heart block**: Increased PR-interval but every P-wave is followed by a QRS-complex. **Second-degree heart block**: Worsening PR prolongation causes some P-waves to occur without subsequent QRS-complex. **Third-degree heart block**: AV nodal conduction completely blocked causing atria and ventricles to depolarize independently of each other. Ventricular contraction driven by a latent pacemaker.

Answer 6

Pathologies can cause the atrial rate to exceed that needed to attain proper propagation through the AV node (250-350 bpm). **Atrial Flutter:** Not every P-wave is followed by a QRS-complex. **Atrial Fibrillation:** Atrial contraction driven by a number of local currents instead of the SA node resulting in uncoordinated atrial firing. No P waves are detected.

Answer 7

Ectopic pacemaker sites in the ventricle or re-entry circuits caused by abnormal propagation causes ventricular rate to exceed atrial rate. **Ventricular Tachycardia:** HR 100-200 bpm **Ventricular Flutter:** HR \> 200 bpm Both V-tach and V-flutter can lead to **ventricular fibrillation** where the electrical activity & pumping is completely uncoordinated.

Answer 8

The heart is activated by a spontaneous AP in the ventricular cells leading to an abnormal QRS complex.

Answer 9

* Ventricular repolarization is very sensitive to myocardial perfusion. * Decreased perfusion can lead to alterations in the ST wave. * ST elevations are only observed for first few days after myocardial infarct meaning they are indicators of recent injury.

Answer 10

Represents mild to moderate deprivation of blood flow primarily affecting the subendocardial layers of the myocardium. Causes region to have a higher than normal resting potential due to lack of Ox Phos, ATP, and Na⁺/K⁺-ATPase activity. Interpreted by the lead as a wave of depolarization causing a higher than normal baseline. ST segment appears depressed.

Answer 11

Associated with severe transmural deprivation of blood flow in subepicardial as well as subendocardial layers. Causes entire ventricular wall to have a higher than normal resting potential. Perceived by the lead as a wave of depolarization going away from it resulting in a lower than normal baseline. ST segment appears elevated.

Answer 12

Period when the ventricle is contracting Heart spends ~ 1/3 of its time in systole.

Answer 13

Remainder of the cardiac cycle. Includes relaxation and filling.

Answer 14

**Ventricular Filling** * Blood enters left atrium from pulmonary vein (~ 10-15 mmHg) * Left ventricle relaxed & expanding * Ventricular pressure \< atrial pressure * _Mitral valve opens_ * Blood from left atrium ⇒ left ventricle **Atrial Contraction** * Atrial contraction (a-wave) follows P-wave of EKG * Forces additional blood into left ventricle increasing ventricular pressure by additional 10-12 mmHg * If atrium contracts against a stiffened ventricle, such as with LVH, an _S4 (atrial gallop)_ occurs in late diastole **Ventricular Contraction** * Ventricular contraction follows QRS complex on EKG * At systole onset, mitral valve open so atrial pressure increases * As blood flows back into atrium the mitral valve closes = _S1 heart sound_ * Mitral valve bulges causing slight increase in atrial pressure = c-wave * Ventricular contraction continues with both aortic & mitral valves closed = no change in volume ⇒ i_sovolumetric contraction_ * When ventricular pressure \> aortic pressure (~80 mmHg) the _aortic valve opens_ * Blood from ventricle to aorta ⇒ _rapid ejection_ * Aortic & ventricular pressures continue to rise **Ventricular Relaxation** * [Ca²⁺] decreases ⇒ ventricular relaxation begins ⇒ pressure starts to drop * Blood continues to enter aorta at slower rate ⇒ _reduced ejection_ * When ventricular pressure \< aortic pressure the aortic valve closes = _S2 heart sound_ * S2 can be split into A2 and P2 if pulmonic valve closes after aortic valve * More pronounced with deep inspiration * Ventricle relaxation continues with closed mitral & aortic valves ⇒ _isovolumetric relaxation_ * Blood enters left atrium from pulmonary vein with closed mitral valve ⇒ atrial pressure increases * When atrial pressure \> ventricular pressure the _mitral valve opens_ * As ventricle fills atrial pressure drops producing "v-wave" * _S3 (ventricular gallop)_ may be heard during ventricular filling * Normal in children due to supple ventricle * Abnormal & indicative of dilated cardiomyopathy in adults Right-side follows a similar cycle but requires less pressure.

Answer 15

* Aortic pressure oscillates between ~ 80 mmHg to ~ 130 mmHg normally * Due to aortic compliance * Provides a constant pressure gradient allowing continuous blood flow in systemic circulation

Answer 16

**Segment a:** * Mitral valve opens & blood enters ventricle. * Slight pressure drop initially due to continued ventricular relaxation. * Ventricle continues to fill with minimal change in pressure due to ventricular compliance. * Volume after filling = _end diastolic volume (EDV)_ **Segment b:** * Ventricular contraction begins causing increased pressure and mitral valve closes. * _Isovolumetric contraction_ occurs. **Segment c:** * When ventricular pressure \> aortic pressure, aortic valve opens. * Blood enters aorta as contraction continues = _rapid ejection phase_ * Ventricular relaxation begins but blood still being ejected = _reduced ejection phase_ * When ventricular pressure \< aortic pressure, aortic valve closes * Ventricular volume after contraction = _end systolic volume (ESV)_ **Segment d:** * _Isovolumetric relaxation_ occurs. * When ventricular pressure \< atrial pressure, mitral valve opens.

Answer 17

**End Diastolic Pressure-Volume Relationship** **(EDPVR)** * represents passive filling of the ventricle * indicative of the passive length-tension curve of the ventricle **End Systolic Pressure-Volume Relationship** **(ESPVR)** * represents the maximum pressure that can be developed for any given ventricular volume. * indicative of the active length-tension curve of the ventricle **Stroke Volume** SV = EDV - ESV **Ejection Fraction** EF = SV / EDV **Work** done by the heart is proportional to the area of the loop.

Answer 18

* The load aka blood volume present before contraction has started * Represents ventricular stretching prior to contraction * Set by the extent of filling * Provided by the venous return * Higher CVP = larger preload * Increasing end-diastolic volume (EDV) * produces little change in passively-developed pressure (end-diastolic pressure) * has a significant effect on the actively-developed pressure during systole * Due to Lo

Answer 19

Within physiological limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction.

Answer 20

Resting length = end-systolic volume The optimal length is greater than the resting length. Maximal force is generated at the point where the ventricles have filled.

Answer 21

* Increasing preload _increases end diastolic volum_e but has no effect on aortic pressure * Causes widening of the pressure-volume loop to the right * Results in _increased SV and EF_ * Leads to _increased CO_

Answer 22

* Increasing preload is used as a compensatory mechanism for heart failure in order to maintain cardiac output. * Chronic excessive preloading leads to increased ventricular volumes causing greater ventricular wall stress. * Wall stress is a major determinant of myocardial O₂ demand leading to ischemia and subsequent infarction. * Wall thickness increased in order to counter-act wall stress leading to cardiac hypertrophy. * Makes ventricular filling more difficult.

Answer 23

**σ = _P x r_** **2h** σ = wall stress P = pressure r = chamber radius h = wall thickness

Answer 24

* The amount of force (aka pressure) that must be generated by the ventricle in order to move blood out of the heart and into the aorta. * Defined as the wall stress (σ) present at peak systolic pressure. * In the absence of aortic stenosis, afterload is very close to aortic pressure (P_Ao) * Aortic pressure often used as a measurement of afterload.

Answer 25

If afterload is increased: * Can be a result of hypertension * Heart must generate greater pressures to open the aortic valve * Aortic valve will also close at a higher pressure * Decreases fiber shortening velocity * Slowing reduces the amount of blood ejected in a contraction **decreasing stroke volume & ejection fraction** * More blood remains at the end of systole **increasing ESV** * Venous return added to remaining volume causing a concurrent **slight** **increase in EDV** * **Results in overall decreased cardiac output** * HR increased in order to compensate * Leads to increased O₂ demand

Answer 26

* Left ventricular emptying is impaired due to narrowing of the aortic valve * Generates a murmur which can be heard between S₁ and S₂ * High aortic valve resistance = increased afterload * Requires higher pressures to be generated by ventricular contraction * In mild cases, sufficient CO can be generated. * In severe cases: * reduction in SV leads to drop in arterial pressure * compensatory increase in EDV limited by ventricular hypertrophy associated with chronic afterload increase * Can lead to a large increase in end-diastolic pressure associated with reduced end-diastolic volumes

Answer 27

Represents the whole heart equivalent of the length-tension curve for isolated fibers. Measure of cardiac function. Pre-contraction length ≈ ventricular end-diastolic volume Depends on the end-diastolic pressure.

Answer 28

The ability to modulate the degree of force generation in cardiac muscle contraction. Controlled by the ANS. **Increasing inotropy ⇒ increases ventricular emptying ⇒ decreases ESV & EDV ⇒ increases SV & EF ⇒ increases CO** Slight decrease in EDV b/c venous return is being added to a smaller ESV. _Increasing inotropy:_ Shifts the Starling curve upwards and to the left. ESPVR curve is shifted left and becomes steeper. Expands pressure-volume loop curve to the left

Answer 29

The distance that blood moves in a given time. Units of cm/sec.

Answer 30

The volume of blood moved in a given time. Unit of L/min.

Answer 31

**Q = *v* x A** Q = blood flow *v* = velocity A = cross-sectional area

Answer 32

Since the circulatory system is closed, the amount of blood moving through each class of vessel must be constant. Q_a = Q_b = Q_c

Answer 33

Describes fluid flow through a rigid pipe. Applies more to arteries than veins due to venous compliance.

Answer 34

**Flow increases with increasing pressure.** **Q œ Δ P** * Pressure gradient between aorta and vena cava drives flow through system * Short-term increases in pressure effective in increasing blood flow * Prolonged HTN bad

Answer 35

**Small changes in vessel diameter can have significant effects on flow.** **Q œ r⁴** * Resistance arterioles change vessel diameter to alter blood flow to specific tissues.

Answer 36

Lipoprotein plaques cause decreased vessel radius. Leads to decreased blood flow (Q). ΔP has to increase to compensate ⇒ hypertension

Answer 37

**Flow decreases as vessel length increases.** Q œ 1/L * Increased resistance to flow due to friction between blood and vessel wall * No physiological role as length is constant

Answer 38

As viscosity increases, resistance to flow increases. Plasma is 20% more viscous than water due to proteins. As # of RBC's (hematocrit) increases, viscosity increases.

Answer 39

1. Altitude * Increases hematocrit (% RBC) to compensate for reduced oxygen availability * Increases viscosity 2. Polycythemia vera * Pathological overproduction of RBC * Increases hematocrit and viscosity 3. Severe Dehydration * Loss of plasma volume without decrease in RBC * Increases viscosity 4. Sick-cell anemia * Decreased pliability of RBC * Increases apparent viscosity

Answer 40

**R = 8Ln/πr⁴** Series: R_Total = R₁ + R₂ + R₃ Parallel: 1 / R_Total = 1/R₁ + 1/R₂ + 1/R₃

Answer 41

The sum of all the vascular resistances that lie between the aorta and the vena cava. **TPR = (MAP - CVP) / CO** Typically 15-18 HRU (Hybrid Resistance Units or mmHg/L/min)

Answer 42

PP = SBP - DBP Increases as contractility or inotropy increases.

Answer 43

MAP = DBP + PP/3 Because heart only spends 1/3 of the cardiac cycle in systole.

Answer 44

Clinical state in which tissue blood flow is inadequate for tissue requirement or oxygen utilization is impaired. Most shock states are associated with an increase in TPR in an attempt to increase blood pressure. Exception is distributive (septic) shock which is associated with a large drop in TPR.

Answer 45

1. Laminar vs turbulent flow 2. Viscosity of blood changes with velocity 3. Compliance of blood vessels

Answer 46

* Streamline Flow * Fluid experiences drag caused by friction between fluid and walls of the tube * Velocity center \> velocity edge * Follows Poisuille's law * Turbulent Flow * Flow patterns unstable and disorganized * Can occur when blood forced through a constriction * Velocity must increase to maintain flow * No longer follows Poiseuille's Law * Greater pressure gradient required to maintain flow

Answer 47

Dimensionless number used to analyze flow through tubes. Ratio of inertial forces (disrupt laminar flow) to viscous forces ( stabilizes laminar flow). **N_R \> 2,000 = turbulent flow**

Answer 48

Sound associated with partial occlusion of the brachial artery with a pressure cuff that reflects blood spurting at high velocity through the constriction. Used to approximate systolic and diastolic blood pressures clinically.

Answer 49

Slow moving blood shows greater apparent viscosity due to interactions of proteins and cells. As velocity increases, cell-cell & cell-protein interactions are disrupted and viscosity decreases.

Answer 50

Compliance = ΔV / ΔP Arteries have low compliance so follows Poiseuille's law more closely. Veins have high compliance (capacitance vessels) so do not follow Poiseuille's law.

Answer 51

System of vessels with diameter less than 100 µm. 1. Arterioles: 5 - 100 µm * Resistance vessels * High content of smooth muscle 2. Metarterioles * Provides bypass around capillary bed * Less muscular 3. Capillaries: 4 - 8 µm * Facilitates exchange of nutrients, waste products, and gases * Precapillary sphincter = on/off switch 4. Post-capillary venules ⇒ Venules * Thin walled * Highly compliant * No smooth muscle

Answer 52

Ateriovenous Anastomosis * Highly muscular * Provides a path for blood to flow directly from arterial to venous system without entering the capillaries * Mainly a mechanism for retaining heat

Answer 53

1. **Simple Diffusion** * Lipid soluble substances * Gases * Travels down concentration gradient 2. **Bulk Flow** * Water, electrolytes, small molecules * Diffusion through narrow passageways between adjacent endothelial cells * Size/complexity of pores varies by tissue * CNS with very tight junctions * Liver, GI, kidney with wide gaps * Driven by pressure difference 3. **Pinocytosis** * Macromolecules * Travel via vesicles 4. **Facilitated diffusion or active transport** * Ions or small molecules

Answer 54

1. **Continuous** * most common * intercellular junctions between endothelial cells 2. **Fenestrated capillaries** * Perforated * Most often found surrounding epithelia 3. **Sinusoidal (discontinuous)** * Large gaps between cells * Found in liver

Answer 55

1. **Capillary Hydrostatic Pressure (P_C)** * ~ 35 mmHg at the arterial end of capillary * ~15 mmHg at the venous end of capillary * Facilitates blood flow through capillary bed * Forces out water and salts into interstitium 2. **Capillary Osmotic Pressure (π_C)** * ~25 mmHg * Caused by proteins/salts within the blood * Albumin, globulins, fibrinogen * Main driving force to retain & recover fluid from interstitium * Capillary beds filter \< 1% of fluid so fluid loss does not considerably change π_C 3. **Tissue Hydrostatic Pressure (P_i)** * Considered zero * May actually be sub-atmospheric due to "sucking" action of lymphatics 4. **Tissue Osmotic Pressure (π_i)** * Normally a very small amount of protein leaks out causing ~ 1-2 mmHg * Considered 0 because most returned via lymphatics

Answer 56

Relationship between the forces affecting capillary fluid flow and net fluid movement. In healthy person, **P_{C (outward)}** and **π_{C (inward)}** are the main driving forces. * Q = flow * k = capillary membrane filtration constant * tissue-specific * accounts for surface area variations * acknowledges differences in vascular permeability

Answer 57

* **Net plasma** **osmotic pressure of ~ 25 mmHg** * Plasma oncotic (~27 mmHg) * Tissue oncotic (~ 2 mmHg) * Drives fluid from _interstitium ⇒ blood_ * Stable from one side of the capillary to the other * **Arteriole side:** * Hydrostatic pressure ~ 35 mmHg * Hydrostatic \> osmotic pressure * Water & solutes driven out of capillary * **Venule side:** * Hydrostatic pressure drops to ~ 15 mmHg * Osmotic \> Hydrostatic pressure * Fluid reabsorbed by capillary

Answer 58

* Lymphatic vessels are open at one end * Undergo rhythmic contractions that suck fluid in * Returns interstitial fluid into blood circulation

Answer 59

* Blood enters glomerular apparatus at high pressures ~ 45 mmHg * Large amounts of fluid filtered out into renal tubule * Mechanisms to later recover components as needed * Remainder leaves as urine

Answer 60

* Blood enters pulmonary capillaries at ~ 15 mmHg * Hydrostatic pressure \< oncotic pressure * Pulmonary capillaries absorb fluid along their entire surface * Prevents us from drowning in pulmonary secretions * Fluid impedes gas exchange

Answer 61

* Heart failure = decreased CO * Unable to clear venous return * Venous congestion increases pressure in venous system which is transmitted to capillaries * Reduces capillary ability to reabsorb fluid * Hydrostatic pressure does not fall below osmotic * Net result of increased fluid being filtered into interstitium * When lymphatic capacity exceeded edema occurs

Answer 62

* Plasma proteins catabolized * Kwashiorkor-type malnutrition * Lowers plasma oncotic pressure * More fluid filtered out into interstitium * Less fluid reabsorbed * Fluid builds up mainly around midsection ⇒ ascites

Answer 63

* _Decreased plasma protein concentration_ * Lowers plasma osmotic pressure * _Arteriolar dilation_ * Increases blood flow into capillaries * P_C greater ⇒ more fluid leaves * _Venous obstruction_ * Blood cannot flow through venous system * Backs up upstream * Results in increased P_C * More fluid leaks out * _Histamine_ * Increases capillary permeability * Increases K from Starling's law

Answer 64

Independent of CNS. Depends on the state of the tissue. Control at the level of precapillary sphincters, metarterioles, and small arteries. 1. **Metabolic control** * More metabolism = more ATP demand = increased O₂ demand * Metabolites causing vasodilation of precapillary sphincters: * adenosine * lactate * H⁺ * CO₂ (from TCA cycle) * K⁺ 2. **Myogenic Response** * Intrinsic mechanism of smooth muscle blood vessels * Increased intravascular pressure leads to constriction * Decreased intravascular pressure leads to relaxation

Answer 65

Mainly through the ANS and involves CNS. Control at the level of precapillary sphincters, metarterioles, and small arteries. * **Humoral Factors:** * Leads to vasoconstriction or vasodilation * **Neural:** * Sympathetic NS * Norepinephrine ⇒ constrict resistant arterioles. * There is no intrinsic PNS input. * Exogenous Ach can lead to vessel relaxation.

Answer 66

* Coronary arteries begin at the root of the aorta via two **ostia** * **Left coronary artery** * splits into the **circumflex** and **left anterior descending** arteries * **Right coronary artery** * Heart possesses many **collateral circulations** which are normally held closed * Contains a dense capillary network

Answer 67

* **Left-side** * During isovolumetric contraction, compression of the coronary arteries restricts blood flow to the left heart * During diastole, myocardium relaxes and blood flow resumes * **Right-side** * Not as muscular * Minimal difference in flow between systole and diastole * Blood flow relatively constant * Coronary arteries enter from epicardium and go to endocardium * Endocardium last to receive blood * Compression of contraction also greatest in the endocardium * Because of this endocardium most at risk for ischemia/infarction * Heart extracts 75-80% of the oxygen from the blood * Only way to meet increased oxygen demand is by increasing blood flow

Answer 68

**RPP = HR x Systolic BP** * Surrogate measure of myocardial O₂ demand. * Measured as myocardial O₂ consumption (MVO₂). * Blood flow to the heart depends upon the work performed. * Factors that increase HR or SBP causes heart to work harder: * SNS activation * HTN * Increased blood volume

Answer 69

* Almost no CNS effect on blood flow * Blood flow primarily determined by **local control**: * Build up of _metabolites_ cause vasodilation * Adenosine (ATP breakdown product) * Lactate (sign of anaerobic respiration) * H⁺ * K⁺ (due to decreased [ATP] leading to decreased Na⁺/K⁺-ATPase activity) * **Autoregulation (aka myogenic response)** * Over a range of pressures, heart will ensure that it has proper blood flow by adjusting vessel resistance as pressure changes * When ΔP drops, decrease R via vasodilation to maintain Q. * When local control has maximized O₂ supply to the heart the only treatment left is to decrease O₂ demand * Heart very intolerant of anaerobic respiration * If blood flow is inadequate, hypoxia can lead to myocardial infarction or angina pectoris

Answer 70

* Oriented both in series and parallel * Organs of the GI system organized in _parallel_ including a blood supply to the liver via hepatic artery * Blood from GI organs enters the liver in _series_ via portal vein * Receives ~25% of cardiac output at rest * Serves as a reservoir of blood * Can increase markedly after a meal

Answer 71

Regulated by both local and central mechanisms: 1. **Local control:** minor mechanism * Controlled by metabolites 2. **Central control:** major mechanism * Enteric NS has as many neurons as the CNS combined * SNS activation decreases blood flow to the splanchnic circulation

Answer 72

* Structure of the **counter-current exchange system** sets up a gradient for O₂ flow * allows the venule to steal oxygen away from the ascending arteriole * Normally there is enough oxygen to nourish the villi afterwards * In low flow conditions (such as CHF) * SNS activation results in decreased total blood flow to the intestines * Can lead to anoxic injury of the villi * Villi slough off resulting in decreased SA for absorption * Leads to malnutrition (seen with end-stage CHF)

Answer 73

* Subcutanous fat provides an effective insulating barrier * Prevents heat loss to the environment in cold conditions * But also retards loss of heat in warm environments * Small vessels penetrate the fat and expand into numerous capillary hairpin loops immediately below the epidermis * Capillary loops connect to an extensive venous plexus * Allows heat exchange between the body's core and external environment * High surface area of capillaries * Slow blood velocity * Large temperature gradient between blood and external environment * AV anastomosis allows blood to bypass capillary network thus conserving heat in times of cold

Answer 74

Under central control by SNS only: * Core temperature decreases: * SNS releases **norepinephrine** * Leads to **vasoconstriction** * Increases core temperature * Core temperature increases slightly: * SNS **norepi** **release** **inhibited** * Leads to vasodilation by means of reduced vasoconstriction ⇒ **passive vasodilation** * Large increase in core temp: * SNS releases **Ach****** * Ach causes release of **bradykinin** and **nitric oxide** (NO) * Leads to **active vasodilation** * Allows greater heat loss

Answer 75

* Receives very little blood flow at rest with ~ 25% capillaries open * Blood flow significantly increases during exercise/stress * Due to large portion of body mass, is a major site of peripheral vasoconstriction * Serves as a **secondary pump** * Contraction/relaxation moves blood one way through veins * Decreases venous pressure * Aids in capillary perfusion * Especially important during exercise * Can contribute _up to half_ of the pumping needed to support max blood flow during aerobic exercise

Answer 76

Exhibits both local and central control: * **Central control:** * SNS releases norepi * Normally causes vasoconstriction while at rest * Stimulates adrenal medulla to release epi during stress * Epi lead to vasodilation via β₂-adrenergic receptor * **Local control:** * Vasodilation caused by metabolites * Able to overpower SNS control during exercise or fight-or-flight * Exhibits **reactive hyperemia**: * Prolonged interruption of blood flow causes build-up of vasodilating metabolites * When flow resumed, there is a marked increase in flow due to vasodilation * Over time metabolites are removed and vascular resistance/blood flow return to basal levels

Answer 77

* #1 organ in blood flow hierarchy * Very limited capacity for anaerobic respiration * 20-30% decrease = lightheadedness * 40-50% decrease = syncope * Uses SNS to reduce blood flow to other organs when supply low to provide for cerebral flow * Brain extracts maximal O₂ from blood * High capacity for _autoregulation_ * Relatively immune to CNS input

Answer 78

* Continuous endothelial cells connected via tight junctions * Provides CNS protection from most blood-borne factors * Transport into cerebral circulation: * Trans-cellular route is the main mechanism for getting materials into and out of the capillaries * Lipid soluble substances (EtOH) and gases (O₂, CO₂) easily diffuses through * Glucose is an exception * Transported by GLUT1 * Pinocytosis rare

Answer 79

Main mechanism for cerebral blood flow control: Functions over wide range of pressures (60-130 mmHg). Autoregulatory curve shifts to the right under chronic HTN to protect CNS over new range. * Dependent mainly on **partial pressure of CO₂** and to a lesser extent O₂ * CO₂ is the most sensitive measure of metabolic demand * Slight increase in P_CO2 (sensed as changes in H⁺ levels) causes a large increase in cerebral flow * Does not respond to decreases in P_O2 until ~ 50 mmHg (last ditch effort)

Answer 80

* Brain lies in closed cranium * Skull prevents increases in volume * Brain essentially incompressible * Changes in cerebral blood tend to be regional * Matched by opposite changes in a different part of the brain * Elevated ICP can result from bleeding, edema, or tumor * Changes in ICP can have huge effects on cerebral perfusion * Decreases perfusion pressure = decreased blood flow * Causes veins to collapse

Answer 81

**CPP = MAP - ICP** Pressure gradient that drives blood flow in the CNS.

Answer 82

Receives ~20% cardiac output. Highest by size of any organ. * **Afferent arterioles** feeds the glomerulus at high pressures * **Glomerular capillaries** are the site of filtration within Bowman's capsule * **Efferent arterioles** leave the glomerulus branching into peritubular capillaries * **Peritubular capillaries** surround the renal tubules * involved in counter-current exchange * Then form venules → veins which leaves kidney

Answer 83

**Shows both autoregulation and sympathetic control.** * Autoregulation occurs at afferent arteriole * Major role during normal kidney function * Systemic control via RAAS system Variations in afferent and/or efferent arteriole resistance determines whether glomerular filtration or peritubular reabsorption is effected: **B:** Inc. R_afferent Dec. pressure in glomerular capillaries → Dec. filtration Dec. pressure in peritubular capillaries → Inc. Absorption **D:** Inc. R_eff_erent Inc. pressure in glomerular capillaries → Inc. filtration Dec. pressure in peritubular capillaries → Inc. absorption

Answer 84

* used to compensate for pressure changes associated with shifting activity patterns * involves autonomic reflex loops consisting of: * **Pressure sensors** (baroreceptors) * monitor arterial pressure * **Integrator** (cardiovascular center) * determines whether pressure too high or too low * **Effector pathways** (SNS) * Adjusts pressure as needed

Answer 85

Measures stretch of blood vessel walls: 1. **Carotid sinus** * Located at fork of carotid arteries * Glossopharyngeal nerve to CN IX * Provides info on cerebral blood flow * More sensitive 2. **Aortic baroreceptors** * Located at aortic arch * Vagus nerve relays signals via CN X * Provides info regarding blood flow in the entire CV system

Answer 86

* Located within the atria and pulmonary artery. * Important in reporting info about blood volume, venous return, CVP **A receptors** * In atrium: sense atrial wall tension during contraction * report on HR * In pulmonary artery: * controls circulating blood volume * indirectly affects BP * triggers release of hormones that change water secretion/reabsorption **B receptors** * sense atrial stretch during filling * fires after contraction * report on atrial volume

Answer 87

* Receptors respond to rate of pressure change as well as MAP * Baroreceptors stretch as transmural pressure increases * Results in more frequent AP * Rate & timing of AP's convey info

Answer 88

Located within the nucleus tractus solitarius (**NTS**) of the medulla oblongata. Two distinct regions control CV activity: 1. **Vasomotor Center** * Activates vasoconstrictor & positive chronotropic/inotropic response * Acts via SNS * Inhibited by NTS * High BP = off * Low BP = on 2. **Cardioinhibitory Center** * Activates vagal outputs to the heart * Decreases HR * Acts via PNS * Stimulated by NTS * High BP: on * Low BP: off

Answer 89

* **_Blood Vessels_** * Sympathetic control (norepi) * Used by vasomotor center * Arteries: vasoconstriction → inc TPR → inc BP * Veins: vasoconstriction → inc VR → inc PL → inc BP * Exception: skeletal muscle * **_SA/AV nodes_** * sympathetic (norepi) & parasympathetic (Ach) * SA: * SNS: inc I_f → inc rate of phase 4 depol → inc HR * PNS: inc I_KAch → dec rate of phase 4 depol → dec HR * AV: * SNS: inc ICa++→ inc phase 0 rate → inc conduction velocity * PNS: dec ICa++→ dec phase 0 rate → dec conduction velocity * **Myocardium** * sympathetic (norepi) * inc ICa++→ inc Ca⁺⁺ entry → inc CICR → inc intropy * inc velocity of H/P system due to inc. density of Na⁺ channels * inc conduction through ventricular myocardium * **_Adrenal medulla_** * sympathetic (norepi) * medulla releases epi and norepi into blood * whole body effects * Heart: epi acts like norepi * Vascular: epi acts on skeletal muscle beds → vasodilation * Lungs: bronchodilation * Eyes: increase vision

Answer 90

Receptor distribution, receptor density, and intraceullar signaling pathways allow for different effects from the same molecule.

Answer 91

1. Immediately after standing blood pools from the central compartment into the venous compartment * Dec VR → Dec PL → Dec CO 2. Decreased CO sensed by baroreceptor as drop in BP 3. Baroreceptor reflex initiated 4. Reduced firing rate of receptor causes: * Disinhibition of vasomotor center → activation of SNS → inc HR/SV/TPR * Decreased stimulation of cardioinhibitory center → decrease PNS → release of PNS "brake" on SA node 5. Net result of BP increase * peripheral vasoconstriction → inc TPR * increased HR * increased inotrophy

Answer 92

Prolonged exposure to elevated pressures causes range of pressure over which the baroreceptors respond to shift towards higher pressures.

Answer 93

Affects vascular smooth muscle contraction and relaxation. Affects BP and distribution of blood flow. Endocrine or paracrine action. Changes TPR. **Biogenic animes:** norepi/epi serotonin histamine **Peptides:** Angiotensin II Atrial natriuretic peptide (ANP) ADH/AVP Endothelins

Answer 94

Target organs outside the CV system. Mostly involves ways to modulate effective circulatory volume. **Includes:** epinephrine serotonin histamine Angiotensin II ANP ADH

Answer 95

* **_Epinephrine_** * Binds to alpha-1 receptors on vascular smooth muscle cells * Causes vasoconstriction * Binds to beta-2 receptors on skeletal muscle vessels * Causes vasodilation * **_Serotonin_** * Local mediator * Causes vasoconstriction * **_Histamine_** * Released by mast cells/basophils in response to tissue damage * Causes vasodilation

Answer 96

* **Angiotensin II** * potent vasoconstrictor * controlled by RAAS system * **Atrial natriuretic peptide (ANP)** * released by atrial myocytes in response to low pressure baroreceptor stretch * vasodilator * **ADH/AVP** * released from posterior pituitary * vasoconstrictor activity at high concentrations * affects water reabsorption by kidneys at low concentration * **Endothelins** * released by endothelial cells * Type A receptors: * on smooth muscle cells * leads to vasoconstriction * Type B receptors: * on endothelial cells

Answer 97

* High pressure baroreceptors located on **afferent arterioles** which enter the nephron * Senses changes in systemic blood volume * Effects granular cells ability to secrete renin * Decreased BP = increased renin release * Drop in BP also sensed by carotid baroreceptors which stimulates SNS & results in renin release

Answer 98

1. Juxtaglomerular apparatus senses drop in BP stimulating release of renin from granular cells. * Carotid sinus via SNS also stimulates release. 2. **Renin** cleaves **angiotensinogen** into **angiotensin I** * Ang I is a weak vasoconstrictor 3. Angiotensin I converted to **angiotensin II** by *angiotensin converting enzyme (ACE)* * ACE secreted by renal and pulmonary endothelial cells 4. **Ang II:** * very potent vasoconstrictor * regulates synthesis and secretion of aldosterone * Aldosterone increases Na⁺ reabsorption by kidney resulting in subsequent water retention * stimulates thirst (dipsogenic effect) * stimulates ADH release 5. The net effect is increased arterial pressure by increasing TPR & blood volume.

Answer 99

* **Circumventricular organ** contains osmoreceptors which sense plasma osmolarity. * Hyperosmolarity triggers depolarization and increase in frequency of AP * Stimulates secretion of ADH * **Atrial and pulmonary baroreceptors** active when BP normal or high. * Inhibits ADH secretion * Increases urination and volume loss * Drop in BP deactivates baroreceptors and results in ADH secretion (secondary mechanism) * Requires 10% volume loss * **ADH function:** * stimulates renal collecting ducts to insert AQP2 allowing increased water reabsorption * at higher concentrations has vasoconstrictor activity * both result in increased BP

Answer 100

* Atrial myocytes synthesize and store ANP. * Myocardial stretch sensed by the cardiopulmonary receptors as sign of increased venous return and high circulating blood volume. * ANP release stimulated. * ANP antigonizes effects of Ang II. * Inhibits aldosterone/ADH secretion * vasodilatory action * Net effect is to reduce BP

Answer 101

* Primarily released in response to increased plasma levels of Ang II or potassium. * Acts on distal tubules to retain water by reabsorbing Na⁺ back into blood stream

Answer 102

NO made from arginine. 1. **Bradykinin,** **Ach, shear stress,** and others factors stimulate *_constitutive endothelial NO synthase (ecNOS)_* * High blood velocity = high demand = high shear stress * Endothelium protects itself from damage by generating NO leading to vasodilation * Inc SA = dec velocity 2. **Endotoxins** and **cytokines** stimulate *_inducible NO synthase (iNOS)_* * Causes massive NO production leading to huge TPR drop, BP drop, and shock

Answer 103

1. NO activates guanylyl cyclase which makes cGMP 2. cGMP activates PKG (& other things) 3. PKG inhibits MLCK & activates SERCA Ca²⁺ pump → smooth muscle relaxation → vasodilation

Answer 104

* Nitroglycerin or amyl nitrate given which breaks down into NO. * NO dilates resistance vessels and decreases TPR & afterload. * Mainly acts as a venodilator which decreases preload. * Reduces stroke volume & CO leading to decreased myocardial oxygen demand. * Protects heart from further damage.

Answer 105

* Thinner & more compliant walls allow veins to accomodate ~ 70% of the blood volume in the body. * At maximal fill levels, collagen resistant to further filling. * SNS stimulation causes venoconstriction pushing blood into arterial circulation. * Does not follow Poisuille's law due to compliance

Answer 106

* Upon standing, CVP decreases as blood moves into the venous reservoir of the legs. * Causes a loss of preload and cardiac output. * Lowers SBP * HR increases in an attempt to restore CO. * TPR increases in an attempt to restore preload. * Increases DBP * Most changes reversed with movement which turns on accessory venous pumps.

Answer 107

1. **Skeletal muscle pump** * contraction squeezes veins increasing venous return 2. **SNS stimulation from cardiovascular center** * Venoconstriction due to SNS stimulation causes blood to shift from venous to arterial side * Minimal increase in venous pressure but allows for faster blood flow & increased preload * SNS increases HR and inotropy - sucks blood from venous compartment generating a negative pressure * Increases pressure gradient between capillaries and atrium 3. **Increase in blood volume** * Chronic changes associated with the kidney

Answer 108

* When the pump is turned off (CO = 0), arterial and venous pressures are equal = MCP/MSP/MSFP * Depends on _blood volume_ and _vessel compliance_ of the entire system * Does not equal MAP * As CO increases, blood pulled from venous system and pushed into arterial system. * Arterial pressure increases * Venous pressure decreases

Answer 109

1. _Cardiac function curves_ (Starling curve) - **A** * Describes the effect of CVP (i.e. preload, EDFP, EDV) on CO * Looks at the pump * _Can be altered by changing the inotropic state of the heart_ 2. _Vascular function curve_ - **B** * Describes the effects of CO on CVP * Looks at the plumbing * _Can be changed by altering blood volume or arteriolar tone_ These two curves combined describes a phsyiological state which explains both the pump and pipes = Guyton Curve.

Answer 110

Superimposed vascular and cardiac function curves. Equilibrium point where curves intersect defines the relationship between cardiac and vascular function. CV system functions at this equilibrium point until one or both curves shift.

Answer 111

Increased inotropy shifts the curve upwards. Ex. increased SNS stimulation Decreased inotropy shifts the curve downwards. Ex. CHF or MI

Answer 112

Curves shift according to the apparent amount of blood in the venous system. **Hypervolemia or increased venous tone:** Shifts the vascular function curve upwards. Results in increased MCP which is dependent on blood volume. Ex. venoconstriction **Hypovolemia or decreased venous tone:** Shifts the curve downwards. Decreases MCP. Ex. massive blood loss, severe dehydration, venodilation

Answer 113

* Changes in arteriolar tone has no effect on MCP because very little blood in the resistance arterioles. * Arteriolar dilation does change the slope of the vascular function curve. * Decreases in resistance = decreased afterload ⇒ makes it easier for the heart to eject a given SV for any given venous pressure. * For any given filling pressure: * decreasing afterload will slide the curve up. * increasing afterload will slide the curve down.

Answer 114

Establishes a new equilibrium point defined by the intersection of the new Starling curve with the old vascular function curve. **Increased inotropy shifts the Starling Curve upwards and to the left.** (A⇒E) CVP drops because blood is moving from veins to arteries at a faster rate. **Decreased inotropy shifts the Starling Curve down and to the right.** (A⇒D) CVP increases because blood is no longer cleared as efficiently from the venous compartment.

Answer 115

Changes in blood volume results in a parallel shift in the vascular function curve. Increased blood volume ⇒ increased MCP ⇒ increased preload ⇒ increased CO without changes in inotropy (A ⇒B) Decreased blood volume ⇒ decreased MCP ⇒ decreased preload ⇒ decreased CO without changes in inotropy (A⇒C)

Answer 116

Increased arteriolar resistance ⇒ increased TPR ⇒ increased afterload ⇒ decreased CO (A⇒B) Decreased arteriolar resistance ⇒ decreased TPR ⇒ decreased afterload ⇒ increased CO (A⇒C) As TPR increases the pressure drop between arterial and venous circulation grows. Increasing TPR results in a lower CVP for any given CO.

Answer 117

Heart failure results in decreased cardiac output. (A⇒D) **Short term:** SNS increases inotropy and moves Starling curve back up. (D⇒A) **Long term:** Increased blood volume via renal system shifts to a new vascular function curve. (D⇒F)

Answer 118

* Inspiration results in more negative pressure in the thorax: * Increases pressure gradient between atrium and capillaries ⇒ increases venous return to right heart. * Both chambers of right heart increase in volume due to increased outward transmural pressure. * Inhalation distends capillaries in the lung: * Reduces pulmonary pressure * Decreases blood flow to left ventricle. **Inhalation:** Increased PL & SV in right heart Decreased PL & SV in left heart **Exhalation:** Increased PL & SV in left heart Decreased PL & SV in right heart

Answer 119

Straining against a closed glottis. 1. Straining increases intrathoracic pressure. * Aorta compression * Increased aortic pressure * Baroreceptor senses this as an increase in BP * Vena cava compression * Decreased venous return * Baroreceptor reflex decreases SNS activity * Decreased HR * If straining prolonged, CVP increases enough to cause backward blood flow reducing CO. 2. Compression reduces VR * CO decreases * Aortic pressure drop activates baroreceptor reflex * SNS inhibition relieved * HR increases 3. Maneuver stopped and breathing resumes. * Aorta compression reduced * Transient drop in aortic pressure * Baroreceptor reflex causes a further increase in HR 4. Intrathoracic pressure returns to normal. * Vena cava compression relieved * VR suddenly increases to a heart under SNS stimulation * Causes a rapid increase in CO & aortic pressure * Baroreceptor reflex triggered * PNS output increases * HR decreases

Answer 120

Sustained contraction towards the voluntary force limit by muscles that are held at constant length. (Isometric) * **Contraction** causes compression of blood vessels within the muscles ⇒ _increases TPR_ * __DBP increases as a reflection of TPR * CV system responds by increasing BP in an attempt to overcome TPR and maintain blood flow. * Change in BP is proportional to the size of the muscle involved & intensity of the contraction. * SBP increases as a reflection of CO * BP spike made worse by the Valsalva maneuver typically associated with straining. * Increases aortic pressure * Decreases venous return * MAP shows significant increase * Upon **relaxation**, blood surges into oxygen-starved tissues. * High ΔP * Due to central SNS output * Low TPR * Muscles stopped squeezing * Local control due to build up of metabolites leads to vascular dilation * Rapid & significant drop in arterial pressure. * Poor cerebral circulation. * Risk of syncope

Answer 121

Rhythmic cycles of contraction and relaxation involving isotonic muscular activity. **1) Anticipatory Phase** * Manipulation of the cardiovascular center by the cerebral cortex results in an anticipatory increase in CV performance **2) Exercise** * _Local = skeletal muscle_ * Metabolites build up as muscles contract causing vasodilation. * Flow enhanced by: * pressure gradient across the capillary bed * recruitment of capillaries previously inactive * Pre-capillary sphincters regulated by local metabolite concentrations * Dilation of resistance vessels causes TPR to drop. * Allows for enhanced flow from aorta to systemic circulation * _Central: sympathetic NS_ * Muscular contraction activates sensory nerve fibers in skeletal muscle sending impulses to the cardiovascular center increasing SNS response. * Inc. HR * Inc. inotropy * Adrenal medullary release of epi/norepi * Skeletal muscle vasodilation * Flow to non-critical organs diverted * Venoconstriction to increase blood volume/VR/PL

Answer 122

Increased SNS output and withdrawal of PNS from SA node results in increased HR. High venous return due to skeletal muscle flow & venoconstriction makes up for the decreased time available for ventricular filling with elevated HR. Increase in HR actually required to accommodate the additional preload.

Answer 123

Sympathetic drive directly increases cardiac inotropy via neural inputs to the ventricular myocytes. SNS indirectly increases inotropy through adrenal medulla release of epi/norepi. Inc. HR results in an additive increase of residual [Ca²⁺] in myocytes increasing inotropy ⇒ _Bowditch staircase / treppe_ _phenomenon_.

Answer 124

* Skeletal muscle blood flow increases from 1.2 L/min at rest up to 25 L/min during exercise. * Coronary flow increasing. * Flow restricted to non-essential organs such as the splanchnic system, kidneys, and non-working muscle. * Skin blood supply transiently decreased but restored within minutes then increased x3-4 to dissipate heat. * During intense exercise blood flow to the skin decreases again in order to support CO.

Answer 125

* SNS stimulates venoconstriction causing: * blood mobilization * increases VR * decreased venous capacity * increases velocity of blood returning to heart * Skeletal muscle acts as an accessory pump * Provides as much as 50% during exercise * Deep inhalation generates greater negative pressures in thorax amplifying the pressure gradient * Aids in blood flow from the microcirculation to the thorax * Increases VR * Brings in more oxygen

Answer 126

**_Static Exercise_** * Sustained contraction leads to increased TPR. * Marked elevation in blood pressure occurs through increased cardiac output & inotropy. * Significant increase in MAP. * Minimal change to pulse pressure as both DBP & SBP increase. * Rapid drop in pressure occurs upon relaxation ⇒ near-syncope. **_Dynamic Exercise_** * Characterized by a pronounced increase in CO that results largely from an increase in HR. * Tendency for high HR to decrease SV offset by enhanced VR and increased inotropy. * SV increases up to 40% of resting. * Aortic pressure markedly increased to drive enhanced CO towards working muscles. * TPR falls due to peripheral vasodilation. * Leads to a pronounced widening of pulse pressure. * MAP changes to a small degree.

Answer 127

Repetitive static exercise has little CV benefit. * High SBP and MAP produced during isometric contraction presents a high afterload to the heart → hypertrophy results. * Ventricular wall thickens to counter effects of wall stress. * Fibrils laid down in parallel. * Decreases intraventricular volume. * EDV may actually be decreased by training. * Parallel hypertrophy pushes coronary capillaries apart and decreases efficiency of O₂ delivery.

Answer 128

Aerobic training has a number of CV benefits. * Wall thickening limited to the septum. * Ventricular walls increase in mass to accommodate increased workload but fibrils laid down in series so myocytes become elongated. * Enlarges the ventricular cavity which increases SV by as much as 50% * Pushes CO towards 35 L/min compared to 20-25 L/min * At rest, lower HR required to achieve basal CO of 5 L/min. * Wider range of HR achievable * Able to maintain CO with a smaller change in HR * Increased vasculature through angiogenesis * Occlusive events likely to have less drastic consequences for myocardium

Answer 129

VO_{2 max} = CO_max x (PO_{2 arterial} - PO₂_venous)_max The limit to exercise resides mainly in the CV system and the ability of muscles to extract O₂. Untrained individuals can increase VO_{2 max} by 8-15 fold. Atheletes can achieve a 20 fold increase due to: 1. Cardiac hypertrophy 2. Training modifies the body's ability to carry and use O₂

Answer 130

Increases the percentage of slow fibers in muscle thereby increasing O₂ usage. Increase in capillary density within muscles allows for extraction of greater amounts of O₂ from the blood. Increases overall muscle mass.

Answer 131

Endurance training raises blood volume by ~ 12%. Enhances preload and facilitates increased CO. Helps offset plasma volume loss through exercise-induced sweating.

Answer 132

Training increases HDL levels & reduces triglycerides. Decreases risk factors associated with coronary heart disease.

Answer 133

The body's ability to exercise declines by 8-10% for every 10 years. Impairs virtually every step in O₂ uptake, delivery, and usage. An active lifestyle can significantly offset and delay decline. * Lungs: * reduced capacity and surface area for gas exchange * loses elasticity * respiratory muscles slowed * O₂ dissociates from Hb less readily which restricts availability * Decrease in maximal HR * Body compensates by increasing SV through PL and EDV * Cardiac efficiency declines * Decrease in overall vascular compliance * Elastin → collagen * Decreased baroreceptor sensitivity * Loss of muscle mass

Answer 134

**_Exercise Stress Test_** * Treadmill test while on an EKG. * As exertion increases, CO must increase to meet demands. * Any impediment to coronary blood flow results in ventricular ischemia ⇒ ST depression. **_Pharmacological Stress Test_** Dobutamine (β-AR agonist) used to increase HR, inotropy, and BP. Can be done in conjunction with echocardiogram to evaluate for heart abnormalities.

Answer 135

* Modulates the visceral organs * Primarily involved in maintaining homeostasis * Parasympathetic vs sympathetic divisions * Each pathway consists of a presynaptic & postsynaptic neuron

Answer 136

* Craniosacral outflow * Long _preganglionic_ fibers * Release Ach which act at _nicotinic receptors_ * Short _postganglionic_ fibers * Release Ach which act at _muscarinic receptors_ * Actions terminated by acetylcholinesterases * Overall function of PNS is to conserve energy * Enhances digestion

Answer 137

* Short _preganglionic_ fibers originate from thoracic & upper lumbar spine * Synapse on paravertebral & prevertebral ganglia * Can synapse with many post-ganglionic fibers = stimultaneous activation of multiple organ systems * Release _Ach_ which acts at _nicotinic Ach receptors_ * Long _postganglionic_ fibers * Release _norepi_ acting at _alpha_ & _beta_ _adrenergic_ _receptors_ * Exception is _sweat glands_ where _Ach_ acts at _muscarinic_ receptors * Actions terminated by reuptake and degradative enzymes * Overall function is to mobilize body for activity * Operates at low basal levels to continuously modulate organ function

Answer 138

* Synthesized from choline and acetate by **choline acetyltransferase** * Release from vesicles triggered by Ca⁺⁺ * Inhibited by botulinum toxin * Acts at nicotinic or muscarinic receptors * Degraded by **acetylcholinesterase** * Defect in enzyme results in desensitization

Answer 139

* **Synthesis** * Tyrosine converted to DOPA by tyrosine hydroxylase * DOPA converted to dopamine by decarboxylase * Dopamine conerted to norepi by dopamine-beta-hydroxylase * In adrenal medulla, norepi converted to epi by PNMT * **Termination** * Reuptake primary mech for norepi * Degradative enzymes * Monoamine oxidase (MAO) * Catechol-O-methyltransferase

Answer 140

SNS → Norepi → **β₂ AdR**→ bronchodilation → enhanced air movement PNS → Ach → **M₂ AchR**→ bronchoconstriction → decreased air movement

Answer 141

**SNS → Norepi/Epi → β₁ AdR** SA node: + chronotropic effect → inc HR AV node: + dromotropic → inc conduction Myocytes: + inotropic → inc force of contraction **PNS → Ach → M₂ ChR** SA node: - chronotropic effect → dec HR AV node: - dromotropic → dec conduction Myocytes: no innervation

Answer 142

Failure to achieve 85% of age predicted maximal HR. Increases mortality rate.

Answer 143

**SNS:** * **α₁ AdR**: skin & viscera - vasoconstriction * norepi & epi * **β₂ AdR**: skeletal muscle - vasodilation * epi **PNS:** No vascular innervation. Exogenous muscarinic drugs will cause vasodilation

Answer 144

**_Pupil_** * _Dilator radial muscle_ * Controlled by SNS * α₁ receptors * Leads to dilation * _Constrictor circular muscle_ * Controlled by PNS * M₃ receptors * Light reflex triggers PNS * Leads to constriction **_Ciliary Muscle: controls lens_** * SNS through β₂ receptors * Causes relaxation * Far vision * PNS through M₃ receptors * Causes contraction * Near-vision (accomodation)

Answer 145

SNS releases norepi. Binds β₂ receptors. Causes increased glucose release.

Answer 146

SNS release of norepi/epi leads to coordinated response: 1. Vasoconstriction of visceral capillary beds 2. Vasodilation of skeletal muscle capillary beds 3. Increased HR, AV conduction, inotropy 4. Bronchodilation 5. GI tract & bladder relaxation 6. Pupillary dilation, far vision 7. Skin to sweat 8. Glycogenolysis/gluconeogenesis by liver for energy

Cardiovascular System Flashcards

(172 cards)