Physiology Flashcards

Question

Why is conduction through the AV node so slow?

Answer 1

Allows atria to fully contract and empty before ventricles contract

Answer 2

The AV node exhibits decremental conduction wherein multiple repeated stimulation results in slower transmission of the action potential. Fast stimulation prevents Ca++ channels from being reset Prevents A fib from resulting in V fib

Answer 3

Apex to base Epicardium to endocardium AP legnth (endocardium has longer APs)

Answer 4

refractory periods (inactivation Na+ Ca++ channels to the activation of K+ channels)

Answer 5

Bipolar limb leads: Lead 1 LA⇒RA Lead 2 RA⇒LL Lead 3 LA⇒LL Unipolar limb leads: aVR WCT⇒RA aVL WCT⇒LA aVF WCT⇒LL Unipolar Percordial Limb leads: V1 V2 V3 V4 V5 V6

Answer 6

Atrial depolarization + deflection of lead I and aVF

Answer 7

Ventricular depolarization

Answer 8

Ventricular repolarization

Answer 9

AV conduction Prolonged=conduction failure at AV node Shortened=ventricular preexcitation (WPW syndrome)

Answer 10

Ventricular excitation Should be 2.5 small blocks or narrower Widened=slow conduction in the Purkinje fibers or ventricular muscle

Answer 11

Ventricular AP duration long or short QT interval means increased risk for arrhythmia

Answer 12

AP duration corrected for heart rate. Bazett's correction: QTc= QT/(HR^0.5)

Answer 13

Reflects the plateau phase of the ventricular AP should be at the same height as the TP segment. If significant injury is present S-T will be elevated or depressed.

Answer 14

**X axis**: 1 small box = 40 msec (0.04 sec) 1 large box = 200 msec (0.2 sec) **Y axis:** 1 small = 0.1 mV

Answer 15

HR = 300/N on a 10 second ECG Acquire 1 target QRS wave on a solid line, subsequent QRS on dar line gives HR in given intervals: 1 box = 300 2 boxes = 150 3 boxes = **100** 4 boxes = 75 5 boxes = **60** 6 boxes = 50

Answer 16

**Tachycardia:** HR \> 100 **Bradycardia:** HR \< 60

Answer 17

- HR = 60-100 - One P wave (and only one) per QRS - PR interval normal - Upright P wavves in I, II, aVf

Answer 18

Anything that is **not** normal sinus rhythm

Answer 19

Breathing Physical fitness etc.

Answer 20

Look at: **Rate** **Rhythm** **Intervals** **Axis** **Morphology**

Answer 21

* *P-wave**: 0.06 - 0.1sec (1. 5-2.5 small boxes) **PR**: 0.12 - 0.2sec (3-5 small boxes) * *QRS**: 0.06 - 0.1sec (1. 5-2.5 small boxes) **QT**: 0.4 sec (10 small boxes)

Answer 22

-30º to +90º

Answer 23

- If QRS is (+) in Lead I and (+) in Lead II ==\> Normal Axis - If (+) in Lead I and (-) in Lead II ==\> Left Axis Deviation - If (-) in Lead I and (+) in Lead II ==\> Right Axis Deviation

Answer 24

Identify the isoelectric lead and axis will be +/- 90º

Answer 25

- Incorrect lead placement - Heart irregularly positioned to right instead of left - Enlarged right ventricle

Answer 26

- Do the PQRST waves look normal? - P waves should be upright in Leads II, III, and aVf - QRS should be normal width - ST segments should be same level as PR - T waves should not be peaked or flattened

Answer 27

- PR interval \< 120ms - Normal P vector - Presence of delta wave - QRS duration \> 100ms

Answer 28

- \> Found in 1-2% of normals and often goes away with age or can be fixed surgically - Is disqualifying for pilots

Answer 29

Closing of AV valves - slow, low pitched vibration

Answer 30

Closure of aortic and pulmonary valves - rapid, high frequency "snap"

Answer 31

Rapid ventricular filling, sometimes heard

Answer 32

Atrial contraction Infrequently heard

Answer 33

Semilunar valves are Aortic and Pulmonary valves - Do not have cordae tendineae - Prevent backflow during Systole - Close and open passively and close due to back pressure - More rigid due to working with more pressure - Strong, yet, pliable base - smaller than Atrioventricular valves

Answer 34

- Left ventricle is large, thick, and muscular and produces 120 mmHg pressure during systole Diastolic pressure is 6 mmHg - Right antrium has a systolic pressure of 4 mmHg Diastolic pressure is 2 mmHg - Right ventricle is systolic of 25 mmHg Diastolic pressure is 2 mmHg - Left atrium is systolic pressure of

Answer 35

They are beginning isovolumetric contraction. Pulmonary and Aortic, as well as tricuspid and mitral, valves are closed, while ventricles initiate contraction.

Answer 36

They're open and blood is entering the pulmonary artery and aorta.

Answer 37

About 1.5 They fill the ventricles with amount of blood resulting in the end diastolic volume

Answer 38

Channels in gap junctions that ellectrically couple cardiac myocytes, allowing for conduction of the action potential and subsequent cell depolarization/contraction.

Answer 39

They hold cells together and transmit mechanical force from cell-to-cell - they are called "molecular rivets"

Answer 40

large invaginations in sarcolemma rich with voltage-gated Ca²⁺ channels (dihydropyridine receptors) - Action potential depolarization propogates down the T-tubule activating channels, allowing Ca²⁺ into the cell, initiating contraction - much less prominent in skeletal muscle

Answer 41

storage organelle for Ca²⁺which complexes with the T-tubule - influx of Ca²⁺ from T-tubule dihydropyridine receptors triggers the ryanodine receptor on the surface of the SR, inducing calcium induced calcium release (CICR) - this calcium binds to Troponin-C, which allows tropomyosin to roll away and expose actin-myosin binding sites, allowing for contraction

Answer 42

Myofibers contain many myocytes, which contain many sarcomeres - sarcomeres are the contracting unit of the myocyte

Answer 43

the site where the T tubule, Ca channel, and SR meet - SR wraps around sarcomeres and invaginating T tubules allow for SR and Ca channels to be closer together

Answer 44

- Action potential plateau opens L-type Ca channel - Ca influx triggers release of Ca from SR (CICR) - Ca binding to TnC allows for cross-bridge formation - ATP req'd for power stroke and new cross-bridge - Diastolic relaxation requires reduced [Ca²⁺]

Answer 45

**SERCA** (sarco/endoplasmic reticulum Ca²⁺-ATPase) pumps Ca back into the SR (uses ATP) **Na/Ca²⁺ exchanger channels** allow calcium to be released to the extracellular space

Answer 46

1. Preload 2. Afterload 3. Contractility 4. Heart Rate and Rhythm

Answer 47

The tension in the myocardial wall prior to contraction - End Diastolic Volume (EDV) stretches the myocytes and sets the sarcomere length - volume difficult to measure clinically: pressure serves as surrogate

Answer 48

T = (P)(R)/2\*(H) T = tension P = Pressure R = Radius of Chamber H= Thickness of Wall Used to calculate tension of myocardial wall prior to contraction for **Preload**

Answer 49

The tension in the chamber wall **during** contraction - also calculated by the Law of La Place - clinical surrogate measure is the peak pressure in that chamber (i.e. LV systolic pressure) - during systole, chamber radius falls, so afterload decreases during ejection --\> heart is doing less work as systole progresses

Answer 50

Increasing preload **increases** the velocity and extent of shortening if afterload is constant Increasing afterload **reduces** the velocity and extent of shortening for any given preload **Increased preload = increased systolic performace Increased afterload = decreased systolic performance**

Answer 51

Cardiac muslce increases strength of contraction through changing contractility - for any given preload and afterload, the contractile state determines: Velocity of muscle fiber shortening extent of shortening - Independent of preload and afterload

Answer 52

* **[Ca²⁺] available to cardiac myocytes** - In vivo, stimulation of ß-adrenergic receptors increases [Ca] and developed tension - this can also be achieved in vitro by increasing [Ca] of solution in which cell is contraction * **Number of crossbridges formed between actin and myosin** * **Rapidity with which the crossbridges are formed, broken, and reformed**

Answer 53

Stimulation of ß-adrenergic receptors activates G-coupled proteins that activate adenylyl cyclase, increasing conversion of ATP --\> cAMP - This allows for phosphorylation of V-gated Ca2+ channels (increasing rate of Ca entering cell) - Increased Ca2+ entry leads to Ca2+ release from SR and bindign to troponin C - Faster uptake by SR and extrusion by Na/Ca Exchanger allows for faster relaxation

Answer 54

Increased heart rate improves cardiac performace by at least two mechanisms: - Increased number of systolic episodes per minute means greater volume pumped per minute - Direct increase in contractiliyty due to increased [Ca²⁺] accumulation in the SR (small effect in absence of ß-adrenergic receptors)

Answer 55

Skeletal muscle can increase force through increasing frequency Only cardiac muscle can increase force through increasing contractility

Answer 56

Volume of blood that is pumped into the aorta per unit time (L/min) (Normal resting = 5L/min) CO = (HR)(Stroke Volume)

Answer 57

volume of blood pumped into the aorta during one cardiac cycle CO = HR(EDV - ESV) EDV = End Diastolic Vol. ESV = End Systolic Vol. | (Normal = 60-100mL/beat)

Answer 58

``` Cardiac Output (CO) adjusted for differences in Body Surface Area (BSA) (Normal values = 2.5-4.0 L/min/m²) ``` Cardiac Index = CO/BSA

Answer 59

Clinical Index of Contractility Fraction of EDV that is ejected during systole, expressed as percentage (Normal = 55-70%) Ejection Fraction = (EDV - ESV)/EDV = SV/EDV

Answer 60

Echocardiogram Cardiac Catheterization Cardiovascular MRI Cardiac CT Nuclear Medicine Scan

Answer 61

Because "contractility" is used interchangeablyl with ionotropic state, the **rate of rise of ventricular pressure during isovolumetric contraction (dP/dt)** is the index of contractility - Volume, radius, and wall thickness are constant during isovolumetric contraction, therefore, rate of rise of tension is directly proportional to dP/dt

Answer 62

Amount of energy that the heart converts to work during a single cardiac cycle (Normal = 45-75 mg-m/m²/Beat) Best depicted by the use of ventricular pressure-volume diagrams: area within pressure-volume loop

Answer 63

- **External Work** (99%): moves stroke volume from venous system to arterial circulation \> Pressure work: accommodates a greater developed tension \> Volume work: accommodates a greater stroke volume - **Kinetic Energy of Blood Flow** (1%): accelerates blood to velocity of ejection

Answer 64

Ratio of work output to toal chemical energy expenditure (Normal = 20-25%) - Most chemical energy is converted into heat rather tahn work output, and efficiency can decrease to 5-10% durign heart failure

Answer 65

- Heart derives most chemical energy from **oxidative metabolism** of fatty acids (to a lesser extent lactate and glucose), therefore, **oxygen consumption** provides a measure of the chemical energy liberated during cardiac work - **Wall Tension** is an indicator of amount of energy needed for contraction--Dilated ventricle with increased radius will have to overcome more tension than a normal ventricle and consume more O₂

Answer 66

* *Phase I**: Period of Filling - From L atrium to ventricle * *Phase II:** Period of Isovolumetric Contraction - When all valves are closed, before ventricular pressure exceeds taht in aorta * *Phase III:** Period of Ejection - When ventricular pressure exceeds that in aorta, aortic valve opens, and blood flows out of ventricle into aorta * *Phase IV:** Period of Isovolumetric Relaxation - Wehn aortic valve closes and ventricluar pressure returns to diastolic pressure levels

Answer 67

Decremental conduction causes a smaller, slower AP due to reduced Ca channel availability - AV nodal conduction slows with faster stimulation rate

Answer 68

Normal, intrinsic delay of AP propagation through the heart due to decremental conduction of the AV node is bypassed by an accessory pathway The accessory pathway depolarizes the adjacent ventricle sooner than it is supposed to and earlier than the other ventricle

Answer 69

Decremental conduction is able to reduce the speed of AP propagation through the ventricles A heart in atrial fibrillation \> 300bpm and working decremental conduction allows the AV node to slow ventricular contraction rate to 60-100bpm A lack of decremental conduction will lead to ventricular rates that are too high (WPW will be shown with a wide QRS, showing conduction is not thorugh the His-Purkinje system)

Answer 70

**"Supraventricular tachycardia"** - atrial (or nodal) tissue is essential in maintaining rhythm (annoying, but not usually life threatening) * *"Ventricular tachycardia"** - only vetnricular tissue essential in maintaining rhythm

Answer 71

**Reentry**: self-perpetuating waves of depolarization **Triggered activity**: secondary depolariation of a focus "triggered" by a preceding beat **Enhanced automaticity**: Spontaneous depolarization of a focus outside SA node

Answer 72

Requires 3 Conditions: - Presence of adjacent cardiac tissue with **different refractory periods** - Unidirectional conduction **block** - **Slow conduction** to allow refractory tissue to recover and allow conduction where it was previously blocked

Answer 73

- Can be initiated by a closely coupled premature atrial complex with blocks in the accessory pathway - contraction conducts through the AV - retrograde conduction via accessory pathway prematurely activates atrial contraction - Inverted P wave produced by retrograde conduction visible in ECG leads

Answer 74

**If QRS is narrow**, conduction to the ventricle uses the AV node-His Purkinje system and reentry must be **supraventricular** **If QRS is wide**, reentry circuit is located in ventricle

Answer 75

By shocking with 360 Joules * *- Electrical countershock depolarizes entire myocardium, blocking wavefront (reentry circuit will be reset)** - Sinus node should be first tissue to regain excitability, resulting in normal rhythm - May see pause due to "overdrive suppression" by arrhythmia - rapid stimulation causes activation of the NA/K-ATPase pump, hyperpolarizing SA node **- Premature stimluation can terminate reentry by inducing bi-directional block** (may accelerate tachy.) **- Drugs (**beta blockers, Ca channel blockers, etc**) which prolong AP duration or slow conduction velocity sometimes helpful in non-life threatening situations** **- Surgical destruction of pathway**

Answer 76

The impulse from the SA node is blocked before it enters the atrial muscle Due to the resultant standstill of the atria, ECG shows absence of a P wave Rate of ventricular QRS-T complex is slowed by not otherwise altered due to spontaneous AV node depolarization

Answer 77

Conditions that can either decrease the rate of impulse conduction in the bundle of His (AKA A-V bundle) or block the impulse from passing from the atria to the ventricles

Answer 78

**Ischemia of the AV node or AV bundle fibers:** Often delays or blocks conduction from atria to ventricles Coronary insufficiency can cause ischemia of AV node and bundle **Compression of AV bundle:** Scar tissue or calcified portions of the heart can depress or block conduction from atria to ventricles **Inflammation** **of AV node or AV bundle:** Can depress conductivity from A to V Inflammation results from different types of myocarditis (i.e. diphtheria or rheumatic fever) **Extreme stimulation of heart by vagus nerve:** In rare instances blocks impulse conduction through AV node. Can result from strong stim. of baroreceptors in people with carotid sinus syndrome

Answer 79

Slowing of heart rate (\< 60bpm) - may be caused by increased vagal tone, ischemia, or degenerative disease of conduction

Answer 80

**Prolonged P-R interval ( \> 200ms)** ECG shows only one P wave for each QRS Usually due to enhanced vagal tone causing slow conduction through the AV node Sometimes called a *first-degree incomplete heart block* because conduction is delayed, not actually blocked Not usually treated pharmacologically

Answer 81

**Conduction through AV bundle is slowed enought to increase PR interval to 0.25 - 0.45s** - **AP is somtimes strong enough to pass through bundle and sometimes not** More P waves than QRSs PR interval gets progressively longer before dropped QRS Usually due to increased vagal tone and disappears with exercise (benign form) **(AKA: Wenkebach)**

Answer 82

**Slowed conduction through AV bundle to increase PR interval, AP is sometimes strong enough to conduct through to ventricles and sometimes not** PR interval does not change prior to dropped QRS Note wide-complex QRS, suggesting diffuse disease in conduction system His-Purkinje system has become undependable (think frayed wire) and can progress unexpectedly to complete heart block

Answer 83

Also known as complete AV block **When condition causing poor conduction in AV node or bundle becomes severe, complete block of impulse from atria to ventricles occurs** - Atria is no longer connected to ventricles Atrial depolarization rate faster than ventricluar (more P waves than QRS) PR interval changes constantly without altering ventricular rhythm Can become asystole without warning

Answer 84

* *Anatomic** - reentry occurs around fixed, non-conducting structure * *ECG monotonous** (i. e. atrial flutter, atrioventricular reciprocating tachy, V tachy around dead tissue from previous MI) * *Functional** - reentry occufrs around area which is temporarily non-conductiong but may move * *ECG chaotic** (i. e. atrial fibrillation, ventricular fib)

Answer 85

- Arises from ectopic focus in ventricles - Early QRS not preceded by P wave - Will have unusual QRS shape: Odd vector Prolonged QRS duration - Will have a compensatory pause

Answer 86

Q = k(r^4)(P)/L Q = flow k = π/(8n) n = viscosity P = change in pressure L = length

Answer 87

a) Q is proportional to r^4 b) Q is proportaional to 1/L

Answer 88

- Flow is laminar - Flow is through smooth cylindrical rigid tubes - Flow is steady and constant - viscosity of the fluid is constant

Answer 89

When fluid flows at a steady rate through along, smooth cylindrical tube, it flows in streamlines It is laminar flow when each layer of blood remains the same distance form the vessel wall and the central most portion of fluid stays in the center of the vessel Results in a parabolic velocity profile

Answer 90

Turbulent flow can result from an obstruction during laminar flow the fluid, instead of flowing in streamlines, flows in all directions in the vessel and continually mixes

Answer 91

- Branching of vessels - Arterial plaques (disrupt smooth arterial walls, cause bruits) - Valves in the heart (aortic and mitral)

Answer 92

Due to Poiseuille's law: Increased viscosity --\> Increased resistance --\> Decreased flow Also, if blood is too viscous, it won't perfuse organs as well and can lead to a lack of O₂ availability Increased viscosity can be due to increased hematocrit and proteins in blood (or decreased water)

Answer 93

Series: R_total = R₁ + R₂ + R₃... Parallel: 1/R_total = 1/R₁ + 1/R₂ + 1/R₃...

Answer 94

Mean pressure is 1/T multiplied by the integral from T₁-T₂ of Pdt ==\> Mean pressure = DPr + (Pulse Pressure)/3 DPr = diastolic pressure Pulse Pressure = SPr - DPr SPr = systolic pressure

Answer 95

Part of the vascular system comprised of small arterioles, capillaries and small venules

Answer 96

to regulate blood flow and nutrient exchange between blood and tissue

Answer 97

**arterioles** control blood flow and they are able constrict **precapillary sphincters** to control microflows

Answer 98

There is no one-way flow Blood flows according to open and closed precapillary sphincters

Answer 99

_Forces favoring **Fluid loss**:_ * *Pc** = capillary hydrostatic pressure * *π_if** = Interstitial fluid colloid osmotic pressure Forces favoring **Reabsorbtion**: * *P_if** = Interstitial fliud hydrostatic pressure * *π_c** = capillary colloid osmotic pressure

Answer 100

Net fluid movement = Forces favoring fluid loss - Forces favoring reabsorbtion F = (P_c + π_if) - (P_if + π_c) F \> 0: Forces fluid out of vessel F \< 0: Forces fluid into vessel

Answer 101

Pressure on capillaries (by skeletal muscle) moves fluid through the lymph system Valves throughout the vessels prevent back flow of lymph Pores vessel walls make the system good for picking up large, cellular debris Pores also have valves that are opened by pressure to move lymph into the lymph system - these valves are anchored to the ECM by anchoring filaments

Answer 102

- Remove unabsorbed interstitial fluid - Remove interstitial protein - Remove cellular debris - Minimize interstitial fluid presssure to **prevent** **edema**

Answer 103

- Increased capillary permeability - Decrease in plasma colloid osmotic pressure - Elevated capillary pressure - Lymphatic obstruction

Answer 104

**- Thickness of vessel wall** Increased thickness = decreased diffusion **- Available surface area** Decreased SA = decreased diffusion **- Particle size** Increased particle size = slower equilibration **- Solubility of particle** Increased solubility = faster equilibration **- Charge of particle** Charged particle = decreased diffustion (membranes in vivo are lipid)

Answer 105

- Postural changes - Local changes (exercise) - Hemorrhage - Return from space - Sexual activity

Answer 106

Reflex initiated by stretch receptors located at specific points in the walls of several large systemic arteries - A rise in arterial pressure stretches baroreceptors and casues them to transmit signals into the CNS - "Feedback" signals are then sent through the autonomic nervous system to the circulation to reduce arterial pressure

Answer 107

1. Wall of the internal carotid arteries slightly above the carotid bifurcation (area known as carotid sinus) 2. Wall of the aortic arch

Answer 108

As blood pressure rises, baroreceptors initiate sinus nerve stimulation, resulting in the lowering of blood pressure. - receptors respond rapidly to changes in arterial pressure - Rate of impulse firing increases in fracion of a second during each systole and decreases during diastole - Receptors also respond much more to rapidly changing pressure than to stationary pressure

Answer 109

1. **Vasodilation** of veins and arterioles throughout peripheral circ. sys. 2. **Decreased HR and Strength of Contraction** ==\> Causes arterial pressure to decrease (Conversely, low pressure has opposite effect)