Physiology Flashcards

Question

What are the 2 curves of the pressure-volume loop?

Answer 1

1. EDPVR = End- diastolic pressure volume relation Indicates the pressure volume relationship during cardiac filling 2. ESPVR = End-systolic pressure-volume relation Indicates the pressure-volume relationship at END SYSTOLE (at aortic valve closure)

Answer 2

When you ↑ demand of the heart, the heart will follow the demande and the end systemic volume will be the same. In other words, it will work harder to acheive the demand. With all other factors equal, stroke volume increases as cardiac filling increases, until a plateau effect or heart failure.

Answer 3

1. Ventricular Preload Amount of blood in the heart at the end of the filling period (i.e. end diastolic volume) 2. Ventricular Afterload The pressure against which the heart contracts during ejection (proportional to mean arterial pressure) 3. Ventricular Contractility Inherent strength of the heart’s contraction during systole

Answer 4

* An increased end-diastolic volume * An unchanged end-systolic volume * An increased stroke volume On the contrary, a decrease in the preload results in: * A decrease in the end-diastolic volume * An unchanged end-systolic volume * A reduced stroke volume

Answer 5

* An unchanged end-diastolic volume * An increased end-systolic volume * A decreased stroke volume On the contrary, a decrease in the afterload results in: * An unchanged end-diastolic volume * A decreased end-systolic volume * An increased stroke volume

Answer 6

* An unchanged end-diastolic volume * A reduced end-systolic volume * An increased stroke volume On the contrary, a decrease in the contractility results in: * An unchanged end-diastolic volume * An increased end-systolic volume * A decreased stroke volume

Answer 7

A **positive chronotropic** effect is one in which the **HEART RATE is INCREASED** (and inversely) A **positive inotropic effect** is one in which the **CONTRACTILITY is INCREASED** (and inversely)

Answer 8

**1. Fick's principle** **CO = _VO2_** **Ca – Cv** CO = Cardiac output VO2 = Oxygen consumption Ca – Cv = Arterial oxygen concentration – Venous oxygen concentration **2. Thermodilution Method** Saline of a known temperature is injected rapidly through a catheter side port into the right side of the heart, at a specific distance from the distal tip of the catheter. The cardiac output is proportional to the rate of the temperature change and is automatically calculated by the equipment

Answer 9

Minimum: diastolic pressure Maximum: systolic pressure Pulse pressure = systolic-diastolic (height of the pulse) Mean arterial pressure MAP = diastolic + 1/3 pulse = should be around 100 mmHg

Answer 10

False : every reflex has a different speed of operation and strength of reflex. They operate over different ranges of BP (ex, tel reflexe va s'en meler quand on atteint tel threshold de BP) and different gains.

Answer 11

In the carotid sinus. Every heartbeat causes stretching in the walls of that sinus.

Answer 12

Afferent:if BP increases, baroreceptors will feel it and sense it to the brain, which is going to process it. Efferent: it is the motor part of the reflex. They will send an order to the organ to react to that input.

Answer 13

1. Increase HR 2. Increase ventricular contractility 3. Increase vasoconstriction (increase sympathetic output to almost all vessels in the body. Squeezing down veins = greater pressure in veins). 4. Increasing arteriolar constriction (since it's a resistance vessel. Increasing TPR means that BP will go up).

Answer 14

Anything that increases the heart rate

Answer 15

Reflex preventing us from labile hypertension. However, the MAP is unchanged in this situation - which means that something else is controlling the MAP .

Answer 16

Loss of Butter reflex.

Answer 17

Renin will transform Angiotensinogen into Angiotensin 1. Angiotensin 1 goes to the lungs. ACE enzyme will convert it into Angiotensin 2. First action: Angiotensin 2 will circulate in the body, and has effect on constriction of arterioles -increasing of BP. Second action: angiotensin 2 goes to the brain & release of ADH (vasopressin) will induce constriction. Will also induce more production of anti-diuretic hormone.

Answer 18

Less renal Na+ and H20 secretion More plasma volume More blood volume More venous pressure More venous return More end-diastolic volume More stroke volume More Cradiac Output INCREASE IN BP WOUHOU

Answer 19

Angiotensin 2 creates an increase in quantity of aldosterone --\> goes to the kidneys --\> decrease the amount of sodium excretion --\> same physiology than 2nd action with ADH secretion.

Answer 20

1. Aldosterone-receptor antagonists (blood volume falls --\> BP falls) 2. At-II-receptor blockers (blocks the receptor on adrenal, arterioles, brain: stopped the action of Angiostensin 2, BP falls) 3. ACE inhibitors: amount of angiotensin 2 drops, BP drops. 4. Renin Inhibitors: Inhibit the action of renin on angiotensinogen, so less amount of angiotensin 1, so less angiotensin 2, so BP drops.

Answer 21

When considering the renal output in an intact kidney (inside a body), the slope is a lot steeper: a tiny increase in arterial blood pressure is going to change by a LOT the renal output - BP falls.

Answer 22

Anti-diuretics

Answer 23

Heart rate Ventricular contractility Vessel diameter Adrenal hormones

Answer 24

The SINUS NODE and it is innervated by both para and sympathetic systems.

Answer 25

ACh on muscarinic receptor

Answer 26

NE on B1-adrenergic receptor

Answer 27

Para: slows it down Sympa: speeds it up

Answer 28

On the ventricular muscles. Only sympathetic system. B1-adrenergic receptors. First major effect: speeding up heart rate Second major effect: increase force of contraction

Answer 29

1. To set appropriate flow for each organ 2. To maintain Mean blood pressure

Answer 30

ANS Hormones in the bloodstream Endothelium (the innermost layer can have effects). Waste products (they surround the vessel and can act on the SM).

Answer 31

Capillaries --\> no smooth muscle

Answer 32

Maintaining the constancy of our internal environement - whether it is for temperature, O2 concentration, pH, ionic composition, osmolarity

Answer 33

Peripheral venous compartment (large & diverse) Central venous compartment (small, intrathoracic, vena cava + RA)

Answer 34

Peripheral venous compartment, 3650ml.

Answer 35

Peripheral venous comparment.

Answer 36

Arterioles

Answer 37

4.5L. The vessels are inflated - an extra 1L of blood creates a pressure on the vessels. 140 ml of blood = 1 mm Hg. So this volume creates a 7 mmHg internal pressure : the mean systemic filling pressure. Pressure we would have in the absence of flow.

Answer 38

1. Circulating blood volume 2. State of the peripheral venous vessel tone (compliance)

Answer 39

It increases the pressure throughout the system. Has almost no effect if arterioles do because there is almost no blood (compared to veins). Also, capillaries & arteries do not actively change their volume.

Answer 40

Volume enclosed by the right atriumand the great veins in the thorax.

Answer 41

Venous return goes in, cardiac output goes out. They are normally equal - otherwise it means there is an accumulation of blood in Central venous compoartment or peripheral vasculature. \*There are however some small temporary differences.

Answer 42

Blood flow from the peripheral venous compartment to the central venous comparment.

Answer 43

Mean systemic filling pressure

Answer 44

VN = (Mean systemic filling pressure - Right atrial Pressure) / Venous resistance

Answer 45

1. When there is no flow, MSFP = CVP. In other words, no flow so the pressures are the same. 2. If the inlet pressure (peripheral) remains at 7 mmHg, decreasing RAP (outlet) will increase DeltaP (P inlet - P outlet) --\> increase the venous return. So, **venous return increases as RAP decreases.** **3.** if RAP is below the intrathoracic pressure, the thin-walled veins of the thorax are compressed and collapse,limiting venous return. Flat part means that **at this point, lowering the RAP won't increase venous return.**

Answer 46

An increase in PVP

Answer 47

1. Changing blood volume - Less blood if blood loss, loss of body fluis by vomiting, sweating, vomiting --\> **reducing PVP** **-**Transfusion, fluid retention by kidney, transcapillary fluid reabsorption --\> **increasing PVP** 2. Changing venous tone Usually done by increasing/decreasing the activity of the sympathetic: **pvp increases when activity of sympathetic increases.** Also could be tone by increasing in force compressing the veinson the outside (ex, exercise or elastic socks)

Answer 48

Up: increased blood volume or venous tone (PVP increased) Down: blood less or less venous tone (PVP decreased)

Answer 49

No - only change the slope. Higher slope = decreased resistance, increase in venous return Reduced slope = increased resistance, decrease in venous return

Answer 50

Cardiac output and venous return.

Answer 51

Afterload, contractility, HR

Answer 52

THe right atrial pressure and the cardiac output

Answer 53

False. They are constantly changing to meet needs of the body.

Answer 54

Measure the internal jugular veins pressure, by measuring the # higher than the angle of Louis.

Answer 55

Depressed cardiac function curve (shift to the right) or right-shifter venous function curve

Answer 56

Shift to the left of the venous curve OS elevated cardiac function curve (to the left)

Answer 57

We would do that if we have good reasons to think that it is different from RA pressure. It is done with a specialized flow-directied venous catheter, with a small inflatable balloon.Goes through IVC,RA, RV, PA & then in the pulmonary smaller arteries (in the lungs). Balloon is deflated, cannula is advanced until it wedges into a capillary/terminal branch. Recorded at this junction and estimates the left atrial pressure.

Answer 58

Flow = _C_out - C_in_ x A DDM * Diffusion is proportional to **surface area** and inversely proportional to **thickness** * Diffusion is proportional to **partial pressure difference** (gradient) * Diffusion is proportional to the solubility of the gas in the tissue, but inversely proportional to the of **molecular weight** (diffusion constant)

Answer 59

5L (normal total volume) 450 ml (1 unit), 70 ml (stroke volume)

Answer 60

∆P = Flow x (R1+R2)

Answer 61

Flow = ∆P x 1/R₁+ 2/R₂

Answer 62

* Hydrostatic pressure = mass x acceleration gravity. * 1 mm Hg = 14 mm H₂O = 0.13 Pa.

Answer 63

* Perfusion pressure (∆P) = P_arterial– P _venous P_a\>\> P_v(100 mmHg vs 5 mmHg). * No perfusion pressure = no flow. P_a- P_v= flow.

Answer 64

Bradycardia in trained athletes or tachycardia during exercise

Answer 65

* Ectopic complexes: beat originating in a site other than the sinus node. They can be premature, ex: premature atrial ectopic complexes PAC (different P wave) and PVC (no P wave). * Ectopic tachycardias: may be paroxysmal (start and stop abruptly, usually by initiating or terminating factor) or nonsustained or sustained

Answer 66

**1. Early afterdepolarizations (EADs)** Caused by excessive action potential (AP) prolongation, which allows Ca²⁺ channels to recover and depolarize the cell, induced by drugs that block K+ channels and favoured byslow HR, long Q-T interval on ECG, To treat it, you stop drugs that block K+ channels and normalize HR **2. Delayed afterdepolarizations (DADs)** Caused by spontaneous diastolic Ca²⁺release, favoured by excess cellular Ca²⁺load

Answer 67

1. Ca²⁺ enters through Ca²⁺ channel during phase 2 of the AP 2. Ca²⁺entry triggers release of more Ca²⁺ through RyR2 3. Increased free intracellular Ca²⁺ causes contraction (EM coupling) 4. Cytosolic Ca²⁺removal (essential for relaxation) occurs by 2 mechanisms: - Uptake into SR by Ca²⁺ uptake pump - Na⁺, Ca²⁺ exchange across cell membrane

Answer 68

To have re-entry, you need 2 paths that go in the same place. One has a short refractory period and the other one has a long one. A premature impulse can find one pathway refractory when the other can conduct because the impulse conducts in the forward (antegrade) direction in the shorter RP path and then retrograde in the long RP. When is goes back to the proximal end of the refractory pathway, it starts again if the conditions are right: if the re-entry time in the circuit is greater than the longest RP.

Answer 69

Pathological bradyarrhythmias cause syncope when clinically significant. 1. Sick sinus syndrome 2. Atrioventricular (AV) Block 1. First-degree AV block 2. Second-degree AV block 1. Mobitz Type 1 2. Mobitz Type 2 1. Third-degree block **Bradyarrhythmias treatment** * Acute: atropine and isoproterenol or temporary transvenous pacemaker * Chronic: permanent pacemaker

Answer 70

Sinus node intermittently fails to fire, typically causes syncope, not sudden death, occur in elderly.

Answer 71

1. First-degree AV block: very common, slowing of atrial-ventricular conduction (long PR interval \> 0.2), no blocked beats 2. Second-degree AV block: some beats fail to conduct; divided into 2 subtypes 1. Mobitz Type 1: progressive PR lengthening on a beat-to-beat basis, until conduction to the ventricles fails (“blocked” P-wave), in the AV, rarely progress in 3^rd degree AV block 2. Mobitz Type 2: blocked P waves occur without gradual PR lengthening, long QRS because the His-Purkinje system is affected, progress in third degree block 1. Third-degree block: also called complete AV block; no sinus impulses get to ventricles but escape rhythms maintain cardiac activity when peacemaking from above fails, almost always requires pacemaker

Answer 72

Is an AV node re-entry and is common in healthy people. Normally, the stimulus comes from the SA node and is regulated by it. The re-entry causes tachycardia because there is more frequent stimulus coming from the re-entry loop.

Answer 73

**Stop AV node re-entry** 1. Block Ca²⁺channels mediating AV node conduction (CALCIUM CHANNEL BLOCKERS) 2. Hyperpolarize AV node cells by enhancing K+ current so that their action potentials are further away from threshold (ADENOSINE) **Prevent AV node re-entry** 1. Block Ca²⁺channels mediating AV node conduction (oral Ca²⁺channel blocker). 2. Suppress adrenergic enhancement of Ca²⁺current (beta blockers)- not as effective. 3. Suppress premature complexes that initiate tachycardias-not as effective. 4. Eliminate anatomical basis by burning one AV nodal pathway. **Other uses of AV-node depressing drugs** Reduce ventricular response rate to atrial arrhythmias because consequences of arrhythmia depend on ventricular rate

Answer 74

Is defined by the Atria firing too fast (400-600 bpm). AF increases risk of stroke due to embolism of clot from static blood pool in fibrillating LA appendage: most common cause of stroke in the elderly (\> AGE). **Treatment: restore sinus rhythm** 1. Drugs that increase atrial RP, terminating re-entry (effective for recent AF) 2. D.C. electrical shock, terminates re-entry by simultaneously depolarizing tissue (\>95% effective) **Treatment: maintain sinus rhythm** Challenge because AF tend to reoccur, the choice of treatment is decided by the patient. 1. Can use drugs that increase atrial RP. 2. A variety of ablation approaches, targeting atrial zones that are critical in initiating and/or maintaining AF.

Answer 75

**We use the** **C** _{chronic heart failure (1)}**H** _{hypertension (1)} **A** _{age > 75 (1)}**D** _{diabetes (1)}**S** _{Prior Stroke/TIA/Thromboembolism(}**₂₎** **1:** 1.5%/yr **3:** 6%/yr **6:** 8%/yr

Answer 76

Is defined by a rapid and regular atria firing (240-300 bpm). Need large drug effects (e.g. by up to 200 ms prolongation of RP) before benefit and a bit of exercise may be enough to get abrupt acceleration. Therefore, rate control generally more difficult for atrial flutter versus atrial fibrillation. **Treatment** 1. Rate control more difficult 2. Ablation often simpler, more successful since only 1 macroreentrant circuit 3. IMPORTANT: Anticoagulation indications are the same for atrial flutter as atrial fibrillation

Answer 77

Is defined by a rapid rhythm arising from a region in the ventricles, most typically 150-180 bpm. Can be caused by: * Enhanced automaticity (acute MI, responds to drugs that block Na⁺ channels) * DADs (cardiac hypertrophy, responds to blockers of Na⁺channels in phase 0 activation) * EADs (LQT Syndrome, responds to treating underlying condition, ↑ HR and correction serum K⁺) * Re-entry (post MI, responds to drugs that increase refractory period by increasing APD) **Principles of management** * When mechanistic diagnosis is possible (e.g. congenital syndromes, acquired LQTS, post-MI scar reentry), mechanism-based therapy is possible and appropriate. * Direct-current cardioversion should be used to terminate VT when severe hemodynamic compromise is life-threatening

Answer 78

Is defined by chaotic ventricular rhythm, no effective cardiac pumping. It is Lethal within minutes in the absence of cardiac massage by thoracic compression (requires emergency DC cardioversion). **Treatment** Individuals resuscitated from VF generally require implantation of a defibrillator to prevent recurrence; drug therapy not reliable enough.

Answer 79

* CPVT: usually responds to beta-blocker * Long QT syndrome: usually responds to beta-blocker but some recurrences, which requires implantable cardioverter/defibrillator

Answer 80

The **height** of the internal jugular venous column (termed the “jugular venous pressure” or JVP) is an accurate representation of the **RA pressure.**

Answer 81

Two major **upward** components: * *a* wave RA contraction * *v* wave RA filling Two **descents**: * *x* descent (x and x’) RA relaxation and enlargemen * *c* wave tricuspid valve closure * *y* descent atrium empties in ventricle

Answer 82

* right ventricular hypertrophy * tricuspid stenosis

Answer 83

Tricuspid regurgitation (during systole blood is pushed into the right atrium from the right ventricle)

Answer 84

Constrictive pericarditis

Answer 85

BEN NON. If the patient is in atrial fibrilation, there is no contraction of atria !!!

Answer 86

1. Flow across a partial obstruction (e.g., aortic stenosis) 2. Increased flow through normal structures (e.g., aortic systolic murmur associated with a high-output state, such as anemia) 3. Ejection into a dilated chamber (e.g., aortic systolic murmur associated with aneurysmal dilatation of the aorta) 4. Regurgitant flow across an incompetent valve (e.g., mitral regurgitation) 5. Abnormal shunting of blood from one vascular chamber to a lower-pressure chamber (e.g. ventricular septal defect [VSD])

Answer 87

1. S₁ = Closure of the AV valves (mitral and tricuspid) Can hear it louder at the of the heart with the diaphragm part of the stetoscope 2. S₂ = Closure of the semilunar valves (aortic and pulmonic) Vary with the respiratory cycle: A₂ and P₂ are normally fused as one sound during expiration. They become audibly separated during inspiration, a situation termed “physiologic splitting”.

Answer 88

1. **Ejection clicks** Indicate the presence of congenital aortic or pulmonic valve stenosis or dilatation of the pulmonary artery or aorta. 2. **Non-ejection clicks** Occurring in mid-systole are usually the result of systolic prolapse of the mitral or tricuspid valves. They are loudest over the mitral or tricuspid auscultatory regions.

Answer 89

1. Opening snap (OS) 2. Third heart sound (S₃) – Ventricular gallop 3. Fourth heart sound (S₄) – Atrial gallop 4. Pericardial knock

Answer 90

Sharp pitch extra diastolic sounds. Corresponds to mitral or tricuspid opening, caused by valvular stenosis (can’t be heart normally)

Answer 91

Extra sound heard in early diastole when there is **exaggerated early diastolic filling** (can sometimes be normal or with heart failure because of high right ventricle pressure) It is a dull, **low-pitched** sound best heard with the bell of the stethoscope at the cardiac apex

Answer 92

Extra sound in late diastole heard when there is atrial contraction into a **stiff, non-compliant ventricle** (abnormal) Is a **low-pitched** sound best heard with the bell of the stethoscope at the cardiac apex

Answer 93

When a patient has an S₃ and an S₄(ça va pas ben son affaire)

Answer 94

A murmur is the sound generated by turbulent blood flow.

Answer 95

Timing Systole or diastole, or is continuous (begins in systole and continues into diastole). Intensity The intensity of the murmur is typically quantified by a grading system (I - VI) Pitch High-pitch (high pressure gradient) and low-pitch (less of a pressure gradient heard with bell) Shape Crescendo, decrescendo, crescendo-decrescendo, uniform Location Aortic, Tricuspid, Pulmonary or Mitrsl Radiation From their primary locations, murmurs are often heard to radiate to other areas of the chest depending on the direction of the turbulent flow. Response to maneuvers Valsalva, squatting, handgrip, leg raise

Answer 96

1. Systolic ejection murmurs 2. Pansystolic (holosystolic) murmurs 3. Late systolic murmurs

Answer 97

Typical of aortic or pulmonic valve stenosis, crescendo-decrescendo murmur Begins a short time after S₁and terminates before or at S₂ * EX: Innocent systolic murmur: Increased systolic flow across normal aortic and pulmonic valves or flow through a ventricular septal defect

Answer 98

Caused by regurgitation of blood across an incompetent mitral or tricuspid valve 1. **Mitral**: uniform sound, no gab between S₁and murmur, heard best at the apex, is high pitched and “blowing” in quality 2. **Tricuspid**: intensity increases with inspiration, radiates to the right sternum but heard in left sternum 3. **Ventricular Septal Defect**: associated with a thrill, the smaller the VSD, the higher the murmur

Answer 99

Late systole and continue S₂ Ex: mitral valve prolapse

Answer 100

1. Early decrescendo murmurs 2. Mid-to-late rumbling murmurs

Answer 101

Decressendo from S₂, high pitch (diaphragm) * Regurgitant flow through **aortic** (best heard when leaning foward) * Regurgitant flow through **pulmonic valve** (increases with inspiration, pulmonary area)

Answer 102

Decressendo with a little increase at the end, low pitch, left side apex of heart. Result from either turbulent flow across a stenotic mitral or tricuspid valve or less commonly from abnormally increased flow across a normal mitral or tricuspid valve. If resulting from stenosis, the murmur begins after S₂ and is preceded by an opening snap

Answer 103

Since the intramural arteries run within the myocardium, they are **squeezed during ventricular systole**. Thus, the blood flow is greater during diastole in the left ventricle, since the intramural pressure is very high during systole. Clinical importance: during tachycardia, the diastole time decreases and that can compromise the coronary circulation. In a healthy heart, this effect is counterbalanced by the increased blood flow provoked by the increased metabolic demands. EX: ventricular fibrillation is fatal because of that.

Answer 104

1. Metabolic: local reduction of pO2 and the local accumulation of waste products of metabolism will act to produce arteriolar vasodilation followed by vasoconstriction to go back to normal (Bayliss reflex/effect). 2. Myogenic: smooth muscle of arteries will contract (myogenic reflex) when Ca²⁺ ↑

Answer 105

NO os induced by ACh through a receptor in the endothelial cells that will release NO, which will diffuse in the adjacent muscle cell and cause vasodilation. NO is also atheroprotective (iprotects against the development of atherosclerosis)

Answer 106

1. ACh will bind to a receptor in the endothelial cells that will release NO, which will diffuse in the adjacent muscle cell and vasodilate it. 2. When ACh binds to a smooth muscle receptor, this causes vasoconstriction. In healthy people, the endothelial effect (NO release) greater, resulting in a total **vasodilation**.

Answer 107

* age * family history * smocking * diabetes * obesity * hypercholesteremia * hypertension Adverse results are partly reversible when risk factors are removed.

Answer 108

* HR (↑ --\> ↑) * Wall stress (↑ --\> ↑ --\> heart failure) * Contractility (↑ --\> ↑)

Answer 109

* While total blood flow to the brain remains more or less fixed, the flow to a particular region of the brain depends on the level of activity in that region (local metabolic control). This is the physiologic basis underlying functional magnetic resonance imagining scans (fMRI). * Central Ischaemic Reflex: massive sympathetic activation that vasoconstricts the rest of the body. Th ecentral ischemic reflex is called the Cushing reflex when it is elicited by increased intracranial pressure. * Endothelial cells of the brain play an important role in the blood-brain barrier and use a lot of energy.

Answer 110

* Low pressure * Unlike systemic arterioles, pulmonary arterioles constrict in response to a fall in pO2 (or rise in pCO2). This hypoxic vasoconstriction diverts blood away from underventilated areas of the lung and towards well-ventilated areas, thus matching ventilation to perfusion ratio (V/Q ratio) and maximizing the O2 content of the blood exiting the pulmonary capillaries.

Answer 111

* Low arterio-venous difference * Portal system (2 capillary beds in series) * Flow regulated by myotonic and metabolic autoregulation. * Sympathetic activation will reduce flow to kidneys (explains the necessity of measuring urinary output in patients with shock to guard against the development of ischaemic renal damage)

Answer 112

* Low-pressure perfusion system * Elevation of the central venous pressure can cause a rise in the pressure both in the hepatic vein (causing hepatic congestion) and in the sinusoids (causing extravasation of fluid into the peritoneal cavity.

Answer 113

The blood flow to resting skeletal muscle on a unit weight basis is low, since the metabolic requirement of resting muscle is low. The **myogenic** tone is thus much larger than the neurogenic tone.

Answer 114

* Cold: ↓ vascularisation (vasoconstriction) * Heat: ↑ evaporation (sweating), constant **radiation**, **conduction** and **convection**

Answer 115

Does not change. Sistolic falls a bit, diastolic rises a bit.

Answer 116

Baroreflex

Answer 117

All decrease

Answer 118

Increase in TPR (BFs fall in forearm, renal, splanchnic) Increase in contractility of the heart (helps to preserve stroke volume) Venoconstriction (Increase VP, VR, SV, CO,BP)

Answer 119

Increase the central blood volume, increase venous pressure, increase MSFP

Answer 120

Muscle pump helps loose less fluid in interstitial space (because capillary beds can leak if pressure is too high in the legs --\> so muscle pump helps sending blood back up)

Answer 121

Arteria = filtration Veinss = absoroption

Answer 122

Infection of lymph nodes by a parasitic worm.

Answer 123

HR goes up, stroke voulme goes a little bit up (up to a certain point, because at one poitn it decreases), and CO increase to supply muscles.

Answer 124

It triples --\> so the O2 consumption is 9x, since it depends on the blood flow (here, the CO has tripled) and the a-v difference.

Answer 125

HUGE increase in skeletal muscles Skin Heart

Answer 126

1. Adrenal medulla secreting NE in blood (a-receptor for constriction) 2. Sympathetic activation (a-receptor for constriction) 3. Adrenal medulla secretes epinephrine in bloo (a-receptor for constriction but Breceptor for dilatation)

Answer 127

False, it is lower.

Answer 128

True (in particular resting SV and max SV). This is due to training-induced ventricular hypertrophy.

Answer 129

1. Exercise: venous valves in arms/legs & pumping blood back to the heart, increasing CO. 2. Orthostasis: make lose less fluid in interstitial space 3. Orthostasis: calf muscles contract, sending blood back to the heart.

Answer 130

MS causes a marke reduction in VO2 max, max CO and max SV. It reduces the ability to exercise.

Answer 131

Because of a larger CO.

Answer 132

Because of a higher SV - NOT because of a higher Heart rate.

Physiology Flashcards

(165 cards)