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Semester 3 > AP300 (Ch 20) > Flashcards

AP300 (Ch 20) Flashcards

1
Q

ch 20

A

..

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2
Q

how many times heart beats each day

A

100000

35 million beats in a year and about 2.5 billion times in an average lifetime

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3
Q

how much blood pump each day

A

14,000 L

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4
Q

average mass of heart

A

250g female

300g male

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5
Q

roughly same size as

A

closed fist

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6
Q

cardiology

A

scientific study of heart and diseases

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7
Q

where does heart rest

A

thoracic cavity

directly behind sternum

in mediastinum

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8
Q

about mediastinum

A

mass of CT

cushions/protects heart

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8
Q

where mediastinum, from where to where

A

sternum to vertebral column

first rib to diaphragm

& between lungs

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9
Q

parts of mediastinum (physically divided)

A

anterior, middle, posterior mediastinum

superior, inferior mediastinum

inferior mediastinum consists of anterior/middle/posterior “

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10
Q

what landmark divides superior/inferior mediastinum

A

angle of louis (manubrial angle)

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11
Q

position of heart

A

2/3 on left of midline

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12
Q

apex of heart, formed by

A

tip of left ventricle

rests on diaphragm

points anterior, inferior, lateral (left)

@ 5th intercostal space

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13
Q

the base of heart

A

formed by atria

mostly left atrium

points, posterior, superior, lateral (RIGHT)

@ 3rd costal cartilage

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14
Q

heart sides – anterior surface

A

anterior surface
(deep to sternum, ribs)

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15
Q

inferior surface of heart

A

inferior surface
(BETWEEN APEX and RIGHT BORDER)

RESTS ON DIAPHRAGM

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16
Q

right border

A

Faces the right lung

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17
Q

left border

A

AKA pulmonary border

Faces LEFT LUNG

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18
Q

pericardium

A

Membrane that surrounds and protects the heart

Maintains the position of the heart within the mediastinum but also allows movement

a. fibrous pericardium
b. serous pericardium
(parietal serous pericardium
visceral serous pericardium )

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19
Q

fibrous pericardium

A

superficial, tough, strong, inelastic, dense irregular connective tissue

Anchor the heart in the mediastinum

Prevents overstretching of the heart

Provides protection

ATTACHES TO PARIETAL PERICARDIUM (serous)

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20
Q

serous pericardium

A

deep, thinner, delicate layer

parietal – outer layer
—> fused to the fibrous pericardium

visceral – inner layer
aka epicardium
—> One of the layers of the heart wall and adheres to the surface of the heart

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21
Q

Pericardial Cavity

A

the space between the parietal & visceral layers of the serous pericardium

pericardial fluid

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22
Q

pericardial fluid

A

viscous fluid that helps reduce friction between the layers during heart contractions

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23
Q

serous pericardium analogy

A

waterballoon

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24
Q

where does fibrous pericardium also attach

A

tunica adventitia of great vessels

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25
Q

pericarditis

A

inflammation of the pericardium

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26
Q

cardiac tamponade

A

excess accumulation of pericardial fluid

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27
Q

tamponade

A

“closure or blockage (as of a wound or body cavity) by or as if by a tampon, especially to stop bleeding”

“It’s from tampon, a stoppage/plug/etc. With -ade added to make it a new noun.”

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28
Q

layers of heart

A

a. Epicardium

b. Myocardium

c. Endocardium

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29
Q

epicaridium

A

External layer

Aka visceral layer of the serous pericardium

Gives the heart it’s smooth, slippery texture

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30
Q

myocardium

A

middle layer that makes up 95% of the heart

cardiac muscle tissue; striated & involuntary

Responsible for the hearts pumping action

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31
Q

endocardium

A

innermost layer

Thin layer of endothelium overlying a thin layer of connective tissue

Provides a smooth lining for the chambers of the heart and covers the heart valves

Continuous with the endothelial lining of the blood vessels attached to the heart

Minimizes friction of blood as it passes through the heart

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32
Q

heart chambers

A

there are 4 chambers altogether
2 atria – superior receiving chambers
2 ventricles – inferior pumping chambers

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33
Q

atria

A

the 2 superior chambers (right & left)

has auricles – “little ears”

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34
Q

where auricles

A

atriaw

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35
Q

which part

A

located on the anterior surface of each atrium, wrinkled pouch-like structure

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36
Q

what do

A

helps increase the capacity/volume of the heart

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37
Q

septu,m, septa

A

fibrous connective tissue that separates chambers

ventricles = interventricular septum

atrium = interatrial septum

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38
Q

sulci

A

small grooves on cardiac surface that hold blood vessels & fat

Mark the external boundary between two chambers of the heart

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39
Q

coronary sulcus

A

i. coronary sulcus - encircles the heart and separates the atrium from the ventricles

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40
Q

anterior interventricular sulcus

A

separates the 2 ventricles on the anterior side

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41
Q

posterior interventricular sulcus

A

separates the 2 ventricles on the posterior side

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42
Q

where blood go /come from each chamber

A

..

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43
Q

RA

A

Right atrium receives blood from systemic circuit

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44
Q

RV

A

Right ventricle pumps blood into pulmonary circuit

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45
Q

LA

A

Left atrium receives blood from pulmonary circuit

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46
Q

LV

A

Left ventricle pumps blood into systemic circuit

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47
Q

RA and right border of heart

A

Forms the right border of the heart

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48
Q

where receive de-O2 blood from?

A

superior vena cava

inferior vena cava

coronary sinus

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49
Q

anterior wall of RA

A

Rough due to pectinate muscles

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50
Q

pectinate muscles of RA

A

Muscular ridge that extend into the auricle

contribute to forceful atrial contractions.

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51
Q

valve between RA and RV

A

Blood passes from RA to RV through the Right atrioventricular valve (AV valve)

aka tricuspid valve

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52
Q

LA, vs base of heart

A

Forms most of the base of the heart

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53
Q

where receive blood (LA)

A

Receives oxygenated blood from the lungs through 4 pulmonary veins

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54
Q

LA anteiror wall

A

Smooth

“Embryologically, the left atrium is also derived from the sinus venosus and a primitive auricle. Similar to the RA, the sinus venosus provides a smooth back wall to the atrium, but, unlike the RA, almost the entire atrial wall is baldly smooth.”

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55
Q

LA auricle

A

Rough due to pectinate muscles

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56
Q

blood from LA to LV via

A

Blood passes from the LA to the LV through the bi-cuspid (mitral) valve

aka Left AV- valve

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57
Q

fossa ovalis

A

Oval depression in the interatrial septum

Remnant of the foramen ovale, an opening in the interatrial septum of the fetal heart

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58
Q

foramen ovale (of heart)

A

some blood skips pulmonary circuit

goes RA to LA

–> babies lungs don’t oxygenate blood

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59
Q

ligamentum arteriosum

A

remnant of ductus arteriosus in the fetal heart

Connects pulmonary trunk with aorta

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60
Q

ductus arteriosus

A

connect pulmonary trunk (artery) to aorta

some blood skips pulmonary circuit

–> babies lungs don’t oxygenate blood

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61
Q

RV, anterior surface

A

Forms most of the anterior surface of the heart

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62
Q

RV, receives from

A

Receives de-oxygenated blood from the right atrium

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63
Q

trabeculae carnae

A

Series of ridges formed by raised bundles of cardiac muscle fibers

Some help with cardiac conduction system, other are mechanical

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64
Q

chordae tendinae

A

Tendon-like cords

attach to the cusps of the tricuspid valve and to cone-shaped trabecular carneae called papillary muscles

help stabilize and strengthen the cusps and preventing them from everting during forceful ventricle contraction

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65
Q

trabeculae carneae etymology

A

Word origin: Latin columnae (column) + carneae (flesh) Synonyms: trabeculae carneae. fleshy beams.

“small beam”

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66
Q

trabeculae carnae, papillary muscles

A

Each ventricle features large cone-shaped trabeculae carneae known as papillary muscles

(these are a specific type of trabeculae carneae)

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67
Q

pulmonary (semilunar) valve

A

Blood passes from the RV to the Pulmonary trunk via the pulmonary valve (aka Pulmonary semilunar valve)

pulmonary trunk in turn becomes the right and left pulmonary arteries

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68
Q

LV, apex of heart

A

Forms the apex of the heart

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69
Q

largest, strongest

A

The largest & strongest of the 4 chambers

Its myocardium is the thickest and therefore generates the most amount of force during contraction

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70
Q

why strongest

A

The left ventricle is the strongest because it has to pump blood out to the entire body.

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71
Q

trabeculae carneae, chordae tendinae

A

also has
Trabecular carneae and Chordae tendinae

anchor down the mitral (BICUSPID, left AV) valve to papillary muscles

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72
Q

where go from LV

A

Blood passes from the LV to the ascending aorta through the aortic valve (aka aortic semilunar valve)

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73
Q

where coronary arteries branch from

A

Coronary arteries branch from the ascending aorta to feed the heart muscle

Blood from ascending aorta to the arch of the aorta and thoracic and abdominal aorta then throughout the body

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74
Q

fibrous skeleton of heart

A

4 dense CT rings that surround the valves of the heart

fuse with one another and merge with the interventricular septum

Prevent overstretching of valves

Point of insertion for bundles of cardiac muscle fibers

Acts as an electrical insulator between atria and ventricles (CONTRACT INDEPENDENTLY)

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75
Q

electrical insulator

A

fibrous skeleton/septa

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76
Q

overstretching valves?

A

Prevent overstretching of valves (CT rings of fibrous skeleton

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77
Q

cardiac mjscles insertion

A

fibrous skeleton/setpa/CT rings

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78
Q

cardiac pathologies

A

..

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79
Q

myocarditis

A

inflammation of the muscles of the heart

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80
Q

myocarditis why

A

Usually due to viral infections, rheumatic fever, or chemical or pharmacological agents (drugs)

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81
Q

endocarditis

A

inflammation of the endocardium usually due to bacterial infections and typically involved the heart valves

dangerous, can be fatal

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82
Q

pericarditis

A

inflammation of the pericardium usually due to viral infections

m/c is acute pericarditis that begins suddenly

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83
Q

(ACUTE?) pericarditis mistaken for

A

Can be mistaken for a heart attack due to left shoulder and arm pain as a result of irritation to the pericardium

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84
Q

pericardial friction rub

A

Can have pericardial friction rub

“A pericardial friction rub, also pericardial rub, is an audible medical sign used in the diagnosis of pericarditis. Upon auscultation, this sign is an extra heart sound of to-and-fro character, typically with three components, two systolic and one diastolic.”

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85
Q
A
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86
Q

chronic pericarditis

A

Gradually and long lasting

Build up of pericardial fluid – leads to cardiac tamponade

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87
Q

chronic pericarditis risk factors

A

May be caused by cancer, TB

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88
Q

heart valves

A

All 4 valves ensure the one-way flow of blood (note trabeculae carneae and chordae tendinae)

Valves open and close in response to pressure changes as the heart contracts and relaxes

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89
Q

AV valves

A

Allow only one-way blood flow from atrium into ventricle

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90
Q

semilunar valves

A

at exit from each ventricle; allow only one-way blood flow from ventricle out into
aorta or pulmonary trunk

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91
Q

AV valve structure

A

Each has three (tricuspid) or two (mitral/bicuspid) cusps

Cusps attach to tendon-like connective tissue bands = chordae tendineae

Chordae tendineae anchored to thickened cone-shaped papillary muscles

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92
Q

AV valves when open?

A

When pressure is higher in atria than ventricle, AV valves open

rounded ends of the cusps project into the ventricle

Ventricles relaxed
Papillary muscles relaxed, chordae tendineae slack

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93
Q

is ventricles relaxed when atria contract?

A

Yes

including papillary muscles / chordae tendinae

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94
Q

when AV valves closed?

A

When pressure is higher in ventricle than atria, AV valves close

Cusps up

Ventricles Contracted

Pressure of blood in ventricles drives the cusps upwards

Papillary muscles contract, chordae tendineae tight

—> (Prevents everting of valves)

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95
Q

semilunar valves (pulmonary/aortic)

A

Composed of 3 crescent moon-shaped cusps

Each cusp is attached to the arterial wall by its convex outer margin

The free border of each cusp project into the lumen of the artery

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96
Q

when semilunar valves open

A

Ventricles contract

Pressure builds up within the ventricles

Valves open when pressure in the ventricles exceeds the pressure in the arteries

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97
Q

why doesn’t blood go back into atria when pressure in ventricles exceed atria/arteries?

A

because chordae tendinae & papillary muscles (special trabeculae carnae) contract the cusps of the tricuspid/bicuspid valves to prevent these valves from EVERTING

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98
Q

when semilunar valves closed?

A

Ventricles relax

pressure gradient changes again

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99
Q

stenosis

A

A narrowing of a heart valve opening, artery, or other structure (?) that restricts blood flow

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100
Q

stenosis risk factors, causes

A

Congenital heart defect

Aortic valve calcification

Rheumatic fever

High blood pressure

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101
Q

rheumatic fever, stenosis

A

The most common cause of mitral stenosis is rheumatic fever — a complication of strep throat.

This infection can scar the mitral valve, causing it to thicken with scar tissue and narrow

While rheumatic fever is now rare in the United States, it is still common in developing countries.

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102
Q

aortic valve calcification, stenosis

A

related to the presence of cardiovascular risk factors such as male sex, arterial hypertension, diabetes mellitus, dyslipidemia, and smoking, sharing many similarities with the process that regulates atherosclerosis

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103
Q

dyslipidemia

A

Dyslipidemia refers to abnormal levels of lipids in the bloodstream, which poses a significant risk factor for cardiovascular (CV) diseases.

Dysregulation in these lipid levels, whether due to genetic predispositions or lifestyle factors, can lead to atherosclerosis and other CV complications.

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104
Q

symptoms of stenosis

A

An irregular heart sound (heart murmur), palpitations

Chest pain (angina) or tightness with activity

SOB, faintness, dizziness, fatigue

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105
Q

irregular heartbeat stenosis?

A

recall that heart beating sound is blood opening valves, and valves making contact with structures (E.g. Aorta)

with stenotic valves (narrowing that restricts blood blow) that sound may be weaker (?) or with different pattern from usual (?)

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106
Q

angina (?), stenosis

A

a type of chest pain caused by reduced blood flow to the heart. Angina is a symptom of coronary artery disease.

reduced opening (narrowing) of valves = reduced blood flow to heart

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107
Q

valve insufficiency or incompetance

A

Failure of a valve to close completely

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108
Q

valve insufficiency can be caused by

A

Mitral Valve Prolapse (eversion) –> I.e. papillary muscles and chordae tendinae not functioning appropriately

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109
Q

valve insufficiency, mitral valve prolapse

A

backflow of blood from LV to LA

MOST COMMON VALVE DISORDER

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110
Q

what percentage of population affected by mitral valve prolapse?

A

m/c valvular disorder, affects 30% of the population

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111
Q

symptoms of valve insufficiency (E.g. Mitral valve prolapse)

A

A racing or irregular heartbeat (arrhythmia)

Dizziness or lightheadedness

shortness of breath, fatigue

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112
Q

rheumatic fever..

A

Infectious disease that can damage or destroy heart valves

Acute systemic inflammatory disease

Usually occurs after a streptococcal infection of the throat

AB’s attack connective tissue of joints, valves and other organs

Most often damage is to the mitral and aortic valves

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113
Q

rheumatic fever in North America (?)

A

Worldwide, incidence ranges from 8 to 51/100,000 (1), with lowest rates (< 10/100,000) in North America and Western Europe

Rheumatic fever is rare in Canada, the United States, and Europe. But it was fairly common until the 1950s. Widespread use of antibiotics to treat strep throat has greatly lowered the number of new cases of rheumatic fever.

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114
Q

pulmonary and systemic circulation

A

Systemic circulation
the system that brings blood to/from the rest of the body

Pulmonary circulation
the system that brings blood to/from the lungs

coronary circuit (?)

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115
Q

arteries

A

Arteries (carry blood away from the heart)

Also called efferent vessels

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116
Q

arterioles

A

Arterioles

small arteries, very little BP (pulse)

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117
Q

capillaries

A

exchange substances between blood and tissues

Interconnect smallest arteries and smallest veins

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118
Q

venules

A

small veins, low pressure, NO pulse

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119
Q

veins

A

Veins (carry blood to the heart)

Also called afferent vessels
Very low pressure, no pulse

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120
Q

aorta

A

largest artery, highest amount of BP, oxygenated blood

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121
Q

4 parts of aorta

A

Ascending Aorta
Aortic Arch
*Descending Thoracic Aorta
*Descending Abdominal Aorta

*sometimes/generally referred together as the descending aorta

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122
Q

systemic arteries

A

branches or extensions of the aorta

noticeable pulse & BP

major systemic arteries:
Carotid
Vertebral
iliac
Femoral
radial
ulnar

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123
Q

systemic capillaries

A

smallest of the blood vessels, NO pulse, NO BP

site where O2 & CO2 exchange

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124
Q

major veins

A

Inferior Vena Cava (from lower body)

Superior Vena Cava (from upper body, head, brain)

Pulmonary veins (from lungs ,*oxygenated)

coronary sinus (?)

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125
Q

pulmonary circuit

A

Right Atrium
Right Ventricle
Pulmonary Arteries
Pulmonary Arterioles
Pulmonary Capillaries
Pulmonary Venules
Pulmonary Veins
Left Atrium
Left Ventricle

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126
Q

systemic circuit

A

Left Atrium
Left Ventricle
Systemic Arteries (via Aorta)
Systemic Arterioles
Systemic Capillaries
Systemic Venules
Systemic Veins
Right Atrium
Right Ventricle

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127
Q

coronary circuit

A

Continuously supplies cardiac muscle (myocardium)
with oxygen/nutrients

Left and right coronary arteries
arise from ascending aorta;
fill when ventricles are
relaxed (diastole)

Myocardial blood
flow may increase
to 9 times the resting
level during maximal
exertion

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128
Q

why do coronary arteries fill when ventricle relaxed?

A

POSSIBLE THEORY:

pressure inside LV exceeds pressure of Aorta

causesaortic semilunar valve to open and fills aorta with blood

valve stays open until pressure gradient switches back

when pressure gradient switches back Left ventricle (ventricles in general) relaxes

at that point pressure inside aorta rises and causes blood to flow from area of higher pressure to area of lower pressure (Which includes coronary arteries

(Left and right coronary arteries from ascending aorta)

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129
Q

left coronary artery

A

Passes inferior to the left auricle and divides into:

A) anterior interventricular branch

B) circumflex branch

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130
Q

A) anterior interventricular branch

(aka. LAD – left anterior descending)

A

Passes in the anterior interventricular sulcus
supplies blood to both ventricles

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131
Q

B) circumflex branch

A

lies in coronary sulcus

supplies blood to left atrium & ventricles

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132
Q

RIGHT coronary artery

A

Supplies small branches to the right atrium and continues inferiorly to the right auricle and divides into:

A) posterior interventricular branch

B) marginal branch

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133
Q

circumflex define

A

bending around something else; curved.

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134
Q

A) posterior interventricular branch

(Posterior descending artery)

A

follows the posterior interventricular sulcus

supplies blood to both ventricles

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135
Q

B) Marginal branch

A

lies in the coronary sulcus

supplies blood to the right ventricle

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136
Q

coronary sinus

A

Deoxygenated blood from the myocardium drains into this large vascular sinus located in the coronary sulcus on the posterior surface of the heart

Empties directly into the right atrium

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137
Q

where cornary sinus

A

coronary sulcus on the posterior surface of the heart

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138
Q

coronary sinus receives blood from

A

Great Cardiac Vein
Middle Cardiac Vein
Small Cardiac Vein
Anterior cardiac Vein

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139
Q

great cardiac vein

A

Lies in the anterior interventricular sulcus
(with left anterior descending)

Drains the areas of the heart supplied by they left coronary artery (LV,RV,LA)

–> circumflex and LAD branch

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140
Q

Middle Cardiac Vein

A

Lies in the posterior interventricular sulcus

Drains the areas of the heart supplied by the posterior interventricular branch of the RCA (LV,RV)

(posterior descending artery)

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141
Q

Small Cardiac Vein

A

Lies in coronary sulcus

Drains RA and RV

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142
Q

Anterior Cardiac Vein

A

Drains RV and opens directly into RA (??)

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143
Q

myocardial ischemia

A

ischemia is the lack of blood supply due to partial obstruction of a vessel

causes hypoxia or anoxia

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144
Q

myocardial ischemia e..g

A

angina pectoris

myocardial infarction (MI, heart attack)

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145
Q

angina pectoris

A

Inadequate blood supply to the heart

mild to severe, crushing chest pain associated with myocardial ischemia

usually this pain pattern is referred to the neck, chin, left arm down to elbow

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146
Q

myocardial infarction

A

complete obstruction of coronary artery resulting in death of cells & tissue (infarction)

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147
Q

MI signs

A

chest pain or discomfort

uncomfortable, squeezing pressure over the chest

radiating pain to the jaw and over neck region

pain in epigastric region

nausea or vomiting

sweating

dizziness

shortness of breath

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148
Q

MI in women

A

Chest pain in only 30%

Unusual fatigue or weakness

Sleep Disturbances

Indigestion

shortness of breath

Anxiety

Cold sweats

Discomfort/pain between shoulder blades

Dizziness

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149
Q

silent heart attack

A

You may not even know you’ve had a silent heart attack until weeks or months after it happens. It’s best to know what’s normal for your body and get help when something doesn’t feel right. Knowing the subtle signs of a silent heart attack can help you identify one.

Studies differ, but some suggest that silent heart attacks are more common in women than in men. Women and their physicians may also be more likely to chalk up symptoms of a silent heart attack to stress or anxiety and dismiss them.

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150
Q

coronary angioplasty

A

a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.

Angioplasty and Stent Placement for the Heart

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151
Q

coronary artery bypass grafting

A

CABG

vein graft sewn to bypass blockage

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152
Q

cardiac muscle tissue

A

..

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153
Q

cardiac vs skeletal ituse

A

..

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154
Q

length

A

Shorter in length (card

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155
Q

transvers seciton

A

Less circular in transverse sections

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156
Q

branching

A

Exhibit branching

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157
Q

cardiac nucleus

A

One centrally located nucleus (usually)

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158
Q

cardiac conection

A

Specialized intercellular connections

Intercalated discs = branching interconnections between cells

159
Q

mitochondria

A

Larger and more numerous Mitochondria (cadiac)

160
Q

tv tubules

A

transverse tubules are wider and less abundant

161
Q

SR

A

Smaller sarcoplasmic reticulum

162
Q

straitions

A

hows striations
alternating bands of light and dark
Same striations as skeletal muscle
Same arrangement of actin and myosin
Same bands, zones, Z discs

163
Q

volun invol

A

considered involuntary
no conscious willful control

164
Q

intecalated cdiskc

A

Intercalated discs
Connect neighboring cardiac muscle fibers

165
Q

contain

A

i. desmosomes

ii. gap junctions

166
Q

desmsomes

A

tight cell to cell junctions for lots of stability
hold the fibers together

167
Q

gap juucnto

A

tubular shaped cell to cell junctions that allow for transmission of substances and/or signals between adjacent cells

allow muscle action potentials to conduct from one muscle fiber to its neighbor allowing the cardiac muscles to contract in coordinated fashion

168
Q

cardiac conduciotn

A

Autorhythmicity = cardiac muscle’s ability to contract at its own pace independent of neural or hormonal stimulation

169
Q

autorhymtmicity

A

Autorhythmicity = cardiac muscle’s ability to contract at its own pace independent of neural or hormonal stimulation

170
Q

specialized cardiac fibres,

A

autorhythmic fibres

These specialized cardiac muscle fibers, called autorhythmic fibers, are self-excitable

can generate their own action potentials even without nerve attachments.

171
Q

what percent of cardiac muscle fibreso are self exciatble

A

Only about 1% of the cardiac muscle fibers are autorhythmic fibers

172
Q

conducting system

(PACEMAKER/conducting cells)

A

Conducting system = network of specialized cardiac muscle cells (pacemaker and conducting cells) that initiate/distribute a stimulus to contract

173
Q

components of conducting system

A

A) Sinoatrial node (SA node)

B) Internodal pathways

C) Atrioventricular node (AV node)

D) AV bundle and bundle branches

E) Purkinje fibers

174
Q

pacemaker (cells)

A

concentration of cells that “set the rhythm” for contraction through electrical excitation

Under normal functioning conditions, the SA node is the pacemaker

175
Q

what part of conducting systme is pacemaker?

A

SA NODE

(under normal conitions)

176
Q

1) SA node

A

Natural pacemaker: sets the fundamental rhythm

Nerve impulses from the ANS and blood borne hormones (epinephrine) modify the timing and strength of each heart beat

177
Q

what modifies timing and strength of each heart beat

A

nerve singals from ANS (vagus nerve?)

hormones (e.g. epinephrine)

178
Q

SA node, AP

A

Each heartbeat begins
with action potential
generated here

In posterior wall of
right atrium, near
superior vena cava

Impulse is initiated here
and spreads through adjacent cells

Average 60–100 bpm

179
Q

where is SA node

A

In posterior wall of
right atrium, near
superior vena cava

180
Q

graded potential of heartbeat?

A

“Pacemaker potential” (?)

181
Q

2) internodal pathways

A

Formed by
conducting cells

Distribute signal
through both atria

182
Q

3) AV node

A

At junction between
atria and ventricles

Relays signals from
atria to ventricles

Has pacemaker cells
that can take over
pacing if SA node fails

AV pacing is slower—40 to 60 bpm

183
Q

where is AV node

A

junction between
atria and ventricles

184
Q

where does AV node send/transmit signals

A

Relays signals from
atria to ventricles

185
Q

which part of conducting system can take over if SINOATRIAL node malfunctions?

A

AV node

186
Q

what is AV pace

A

40 to 60 bpm

187
Q

what is SA pace

A

60-100 bpm

188
Q

4) AV bundle

A

Conducting cells
transmit signal from
AV node down through interventricular septum

Usually only
electrical connection
between atria/
ventricles

189
Q

which structure does AV budnle run along

A

transmit signal from
AV node down through interventricular septum

IV SEPTUM

190
Q

5) AV bundle branches

A

Right and left
branches

Left bundle branch
larger

Conducting cells
transmit signal to
apex of heart, then
spreading out in
ventricular walls

191
Q

6) purkinje fibres

A

Radiate upward
through ventricular
walls

Propagate action
potentials as fast as
myelinated neurons

Stimulate ventricular
myocardium and trigger contraction

192
Q

what is diameter of purkinje fibre cells

A

large

193
Q

which structure’s speed do they match?

A

neurons with mylenated axons

194
Q

which part of mycardium do purkinje cells stimulate

A

Stimulate ventricular
myocardium and trigger contraction

195
Q

pathology

artificial pacemakers

A

If the SA node becomes damaged or diseased an artificial pacemaker may be inserted

196
Q

which structure’s function does artificial pacemaker replace

A

SA node

197
Q

artificial pacemaker about

A

Runs on a battery w/ leads into the right atrium, this simulates the firing of the SA node which in turn propagates a signal down the normal conduction system.

198
Q

what is a feature of new artificial pacemakers

A

New - activity adjusted pacemakers

Automatically speed up during exercises

199
Q

skeletal muscle vs cardiac muscle contraction

A

..

200
Q

AP

A

Brief action potential
(skeletal)

Long action potential
(cardiac)

201
Q

Ca2+ speed

A

(SKELETAL)
Contraction ends when sarcoplasmic reticulum reclaims Ca2+

(CARDIAC)
Ca2+ enters cells over prolonged period
–>Long contraction
(~250 msec)

202
Q

refractory period

A

(SKELETAL)
Short refractory period ends before peak tension develops

(CARDIAC)
Refractory period continues into relaxation

203
Q

wave summation / tetany

A

(SKELETAL)
Twitches can summate; tetanus can occur

(CARDIAC)
No tetanic contractions occur (otherwise heart couldn’t pump blood)

204
Q

important note about AP, contraction, and refractory period

A

by the time cardiac muscle relative refractory period ends, heart muscle is close to fully relaxed

by the time absolute refractory period ends, heart muscle is partially relaxed

FOR SKELETAL MUSCLE, RELATIVE REFRACTORY PERIOD ENDS BEFORE MUSCLE FIBRE EVEN REACHES MAXIMUM TENSION

ABSOLUTE REFRACTORY FOR SKELETAL MUSCLE ENDS ALMOST BEFORE MUSCLE FIBRE EVEN BEGINS CONTRACTING (?)

205
Q

repolarization of membrane potential in cardiac muscle

A

in skeletal muscle, repolarization occurs @ end of ABSOLUTE REFRATORY PERIOD

in cardiac muscle, full repolarization occurs @ end of relative refractory period

partial repolarization in cardiac muscle occurs @ end of absolute refractory period

206
Q

3 stages of cardiac muscle AP

A

Rapid depolarization

Plateau

Repolarization

207
Q

1) rapid depolarization

A

similar to that in skeletal muscle

At threshold, voltage-gated fast sodium channels open

Massive, rapid Na+ influx

Channels
open quickly
and very
briefly

208
Q

2) Plateau

A

from -90 RMP, to +30 after rapid depolarization

leading into PLATEAU is quick dip from +30 to 0mV (where it stays for plateau period)

209
Q

why stay @ 0mV for plateau phase

A

Fast sodium channels close as potential nears +30 mV, Cell actively pumps Na+ out

K+ channels outflow into interstitial fluid

Voltage-gated slow calcium channels open— Ca2+ influx

Opening of slow Ca2+ channels in sarcolemma increasing Ca2+ in cytosol and triggering a contraction (calcium induced calcium release)
****

So, because Ca2+ positive charge offset Na+ leaving cell (?)

210
Q

note subtances that alter flow of Ca2+ through slow Ca2+ channels

–> how do they influence strength of heart contractions??

A

Substances that alter the movement of Ca2+ through slow Ca2+ channels influence the strength of heart contractions (contractility)

E.g.
Epinephrine: increases Ca2+ = increases contraction force

211
Q

3) repolarizaiton

A

Slow calcium channels close

Slow potassium channels remain open; K+ rushes out; causes rapid repolarization and restores resting potential

212
Q

cardiac muscle ATP produciton

A

Produces little ATP by anaerobic cellular respiration
(same as all cells, relatively, but more so here)

Relies on aerobic cellular respiration in its numerous mitochondria

213
Q

what do cardiac muscle fibres use for energy during aerobic repsiration?

A

AT REST:
Oxidation of fatty acids (60%) and glucose (35%)

214
Q

what do they use during exercise?

A

Use lactic acid

215
Q

heart also uses

A

creatine phosphate

216
Q

note creatine phosphate vs creatine kinase

what does creatine kinase do?

A

Creatine Kinase is the enzyme that catalyzes transfer of a phosphate group from CP to ADP to make ATP

217
Q

what is the creatine kinase test?

A

normally is contained in the muscle tissue but will be released in any cardiomyopathy

CK is the 1st enzyme in blood they test for in heart attacks.

218
Q

ECG

A

a recording of the electrical currents generated by action potentials propagating through the heart.

219
Q

what does ECG determine

A

1) If the conduction pathway is abnormal (i.e.. arrhythmias)

2) If the heart is enlarged (?)

3) If certain regions of the heart are damaged (i.e.. MI)

4) Causes of chest pain

220
Q

how ECG show enlarged heart?

A

An electrocardiogram (ECG) can show if the heart is beating too fast or too slow. A health care provider can look at signal patterns for signs of a thickened heart muscle (hypertrophy).

221
Q

ECG, MI

A

The most frequently used electrocardiographic criterion for identifying acute myocardial infarction is ST segment elevation in two or more anatomically contiguous leads.

222
Q

12 LEAD ECG

A

10 electrodes placed in specific positions

By comparing electrodes, 12 different trackings are produced (12 leads)

223
Q

12 leads ?

A

6 limb leads

6 precordial (chest) leads

224
Q

precordial

A

in front of the heart; involving the precordium.

from English precordium ((anatomy) The region of the body over the heart and thorax.)

225
Q

6 limb leads

A

I, II, III, aVR, aVL, aVF

Measure vertical vectors or electrical conduction

226
Q

6 precordial leads

A

V1-V6
Measure horizontal vectors of electrical conduction

227
Q

note movement of ELECTRIC VECTOR towards/away positive pole, and corresponding positive/negative inflection on ECG

A

Movement towards positive pole gives positive inflection on ECG

Movement away from positive pole gives negative inflection on ECG

228
Q

random facts, leads

A

The electrical axis of the heart is most similar to lead II

Therefore, lead II is often used as reference for basic ECG

229
Q

ECG,

P, QRS, T

A

P wave

QRS complex

T wave

230
Q

P wave =

A

ATRIAL DEPOLARIZATION

231
Q

QRS complex =

A

VENTRICULAR DEPOLARIZATION

ATRIAL repolarization occurs @ same time as Ventricular depolarization (so it’s hidden under QRS complex)

232
Q

T wave =

A

ventricular repolarization

233
Q

more about P wave

A

P wave = atrial depolarization

Atria begin contracting ~25 msec after P wave starts

234
Q

more about QRS complex

A

QRS complex = ventricular depolarization

Larger wave due to larger ventricle muscle mass

Ventricles begin contracting shortly after R wave peak

Atrial repolarization also occurs now but is masked by QRS

235
Q

why QRS complex wave larger?

A

Larger wave due to larger ventricle muscle mass

236
Q

when do ventricles begin contracting?

A

begin contracting shortly after R wave peak

237
Q

INTERVALS/SEGMENTS

A

P-Q interval
(sometimes called P-R interval)

Q–T interval

S–T segment

238
Q

PQ interval (or PR interval)

A

Period from start of atrial depolarization to start of ventricular depolarization

239
Q

what does a PQ interval greater than 200ms indiciate?

A

> 200 msec may mean damage to conducting pathways or AV node

Possibly from scar tissue d/t previous MI

240
Q

QT interval

A

beginning of the QRS complex to the end of the T-wave.

This represents the time from start of ventricular depolarization to the end of ventricular repolarization.

241
Q

QT interval is from

A

from BEGINNING of ventricular depolarization

to END of ventricular repolarization

242
Q

what causes lengthened QT interval?

A

May be lengthened by

electrolyte disturbances,

medications,

conduction problems (conduction system/NODES/pacemaker cells),

coronary ischemia,

myocardial damage

243
Q

ST segment

A

end of the QRS complex to the beginning of the T-wave. This represents the interval between ventricular depolarization and repolarization

244
Q

ST segment is from

A

from END of DEPOLARIZATION

to BEGINNING of REPOLARIZATION

(interval where there is neither depolarization, nor repolarization – PLATEAU phase)

245
Q

note ST segment vs PLATEAU phase

A

The ST segment corresponds to the plateau phase of the ventricular transmembrane action potential.

(NEITHER depolarization, nor repolarization)

–> actually technically, it is depolarized, and in a continuous state of “

246
Q

why elevated ST segment (length?)

A

Can see and elevated ST segment in acute MI

247
Q

ECGs and arrythmias

A

ECGs valuable for detecting/and diagnosing arrhythmias

248
Q

cardiac arrhythmias

A

abnormal patterns of cardiac electrical activity

249
Q

what percentage of healthy people experience a few abnormal heartbeats each day?

A

About 5% of healthy people experience a few abnormal heartbeats each day

Not a clinical problem unless pumping efficiency is reduced

250
Q

ECG and average heartrate

A

Average heart rate is between 60 - 100 bpm

Tachycardia = fast heart rate (>100 bpm)

Bradycardia = slow heart rate (<60 bpm)

251
Q

note bradycardia not necessarily pathological

A

some athletes can have lower than 60bpm resting heartbeat

252
Q

PREMATURE ATRIAL CONTRACTIONS (PACs)

A

Often occur in healthy people

Normal atrial rhythm momentarily interrupted by “surprise” atrial contraction
I.e.
SOONER THAN EXPECTED

Increased incidences caused by stress, caffeine, various drugs that increase permeability of the SA pacemakers

Normal ventricular contraction follows the atrial beat

253
Q

Paroxysmal atrial tachycardia (PAT)

A

Premature atrial contraction triggers flurry of atrial activity

Ventricles keep pace

Heart rate jumps to about 180 bpm

254
Q

ATRIAL FIBRILLATION

A

Impulses move over atrial surface at up to 500 bpm

Atria quiver—not organized contraction

Ventricular rate cannot follow, may remain fairly normal

Atria nonfunctional, but ventricles still fill passively

Person may not realize there is an arrhythmia

255
Q

arrhythmias affecting ATRIA

A

Premature atrial contractions (PACs)

Paroxysmal atrial tachycardia (PAT)

Atrial fibrillation

256
Q

arrythmias affecting VENTRICLES

A

Premature ventricular contractions (PVCs)

Ventricular tachycardia

Ventricular fibrillation

257
Q

Premature ventricular contractions (PVCs)

A

Purkinje cell or ventricular myocardial cell depolarizes; triggers premature contraction

Cell responsible called an ectopic pacemaker (pacemaker other than the SA node)

Single PVCs common, not dangerous

Frequency increased by epinephrine, stimulatory drugs, or ionic changes that depolarize cardiac
muscle cells

258
Q

Ectopic pacemaker cells

A

An ectopic pacemaker, also known as ectopic focus or ectopic foci, is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart.

It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat.

259
Q

ectopic define

A

in an abnormal place or position.

ektopos: out of place

ectopia: present of tissue, cells, etc. in an abnormal place

260
Q

ectopia

A

a situation in which an organ or body part is in the wrong position, either from birth or because of an injury

261
Q

ventricular tachycardia

A

Also known as VT or V-tach

Defined as four or more PVCs without intervening normal beats

Multiple PVCs and V-tach may indicate serious cardiac problems

262
Q

Ventricular fibrillation

A

Also known as VF or V-fib

Responsible for condition known as cardiac arrest

Rapidly fatal because ventricles quiver, but cannot pump any blood

263
Q

note ECGs and exercise stress test

A

Exercise Stress test

Continuous ambulatory electrocardiographs

Holter monitor

264
Q

Holter monitor

A

A Holter monitor is a small, wearable device that records the heart’s rhythm, usually for 1 to 2 days.

It’s used to spot irregular heartbeats, also called arrhythmias.

A Holter monitor test may be done if a traditional electrocardiogram (ECG or EKG) doesn’t provide enough details about the heart’s condition.

265
Q

INTRO TO CARDIAC CYCLE

A

Two phases:

Contraction (systole)—blood leaves the chamber

Relaxation (diastole)—chamber refills

266
Q

contraction sequence (Atria contract)

A

Atria contract together first (atrial systole)

Push blood into the ventricles

Ventricles are relaxed (diastole) and filling

267
Q

contraction sequence (Ventricles contract)

A

Ventricles contract together next (ventricular systole)

Push blood into the pulmonary and systemic circuits

Atria are relaxed (diastole) and filling

268
Q

how long does cardiac cycle last?

A

Typical cardiac cycle lasts 800 msec (0.8 secs)

60s / 0.8 = 75 (BPM)

269
Q

cardiac cycle

A

..

270
Q

what is cardiac cycle

A

period between start of one heartbeat and the next (a complete round of systole and diastole)

271
Q

2 phases of cariac cycle

A

Contraction (systole)—blood leaves the chamber

Relaxation (diastole)—chamber refills

272
Q

sequence of contractions

A

Atria contract together first (atrial systole)

Ventricles contract together next (ventricular systole)

Typical cardiac cycle lasts 800 msec (0.8 secs)

273
Q

atria push…

ventricles are…

A

Push blood into the ventricles

Ventricles are relaxed (diastole) and filling

274
Q

ventricles push…

atria are…

A

Push blood into the pulmonary and systemic circuits

Atria are relaxed (diastole) and filling

275
Q

assuming 800msec cardiac cycle

A

heart rate 75 bpm

276
Q

phases for 75bpm

A

1)
Cardiac cycle begins—all four chambers are
relaxed (diastole; ventricles are passively refilling)

2)
​Atrial systole (100 msec)—atria contract; finish filling ventricles

3)
​Atrial diastole (270 msec)—continues until start of next cardiac cycle (through ventricular systole)

4)
Ventricular systole—first phase. Contracting ventricles push AV valves closed but not enough pressure to open semilunar valves
(= isovolumetric
contraction—no
volume change)

5)
​Ventricular systole—second phase. Increasing pressure opens semilunar valves; blood leaves ventricle (= ventricular ejection)

6)
​Ventricular diastole—early. Ventricles relax
and their pressure drops; blood in aorta and
pulmonary trunk backflows, closes semilunar valves

7)
​Isovolumetric relaxation. All valves closed; no volume change; blood passively filling atria

8)
​Ventricular diastole—late. All chambers relaxed; AV valves open; ventricles fill passively to ~70%

277
Q

note about atrial systole

A

SA node fires, causing both atria to contract (atrial systole)

Increases pressure within atrium, pressure remains low in ventricles

Blood is ejected thru AV valve (tricuspid & mitral) from atrium to ventricles

Contributes 25mL to an already 105mL in each ventricle = total of 130mL in the ventricles at the end of atrial systole/ventricle diastole

Called the end diastolic volume (EDV)

278
Q

what causes atria to contract?

A

SA nodes

279
Q

what does atrial contracting add to ventricles

A

25mL to 105mL that was already in ventricles

105 from passively filling

280
Q

what is amount in ventricles called AFTER atria contract?

A

END DIASTOLIC VOLUME

“diastolic” referring to the end of diastole for the ventricles, before they contract

I.e.
after atria finish contracting, then immediately ventricles are @ end of diastole
I.e.
ventricular systole begins exactly when atrial systole ends

281
Q

when does first 105mL fill?

A

during period when both atria and ventricles are in diastole (second phase of ventricular diastole)
—> (about half the entire Cardiac Cycle)

(filling passively)

282
Q

about ventricular systole

A

During ventricular systole the atria are relaxed (atrial diastole)

(atrial diastole begins precisely when ventricular systole begins)

283
Q

what is a significant feature of the EARLY VENTRICULAR CONTRACTION

A

BOTH SEMILUNAR AND AV valves are CLOSED

I.e.
Isovolumetric contraction

(Iso- “same” – volume)
I.e.
volume of ventricle doesn’t change during early ventricular contraction

UNTIL the pressure in the chamber is enough to EXCEED the pressure in the pulmonary trunk & Aorta (pressure of the semilunar valves).

After this pressure is reached, the valves open and blood enters the pulmonary/systemic circuit.

284
Q

WHAT IS THE pressure required to open the semilunar valves

A

LV pressure > 80mmHg (continue to rise to 120mmHg)

RV pressure > 20mmHg (continue to rise to 25-30mmHg)

285
Q

how long does ventricle ejection last?

A

I.e. how long ventricular systole last (?)

250-270msec (?)

notes say 250msec

diagram shows 270msec for ventricle systole

286
Q

WHAT IS THE VOLUME at the END of ventricular systole

A

END SYSTOLIC VOLUME

287
Q

In our example of 130mL End diastolic volume, how much of that blood can be expected to be ejected via ventricular systole?

A

about 70mL

end systolic volume would be 60mL in this example

288
Q

what portion of the cardiac cycle are BOTH atria+ventricles RELAXED

A

about 1/2 cardiac cycle

400msec in example of 800msec cycle

289
Q

what portion of cardiac cycle are ventricles relaxed

A

about 500msec / 800

290
Q

what portion of cycle are atria relaxed

A

about 700msec / 800

291
Q

more about ventricular diastole

A

Ventricle pressure decreases and blood in the aorta and pulmonary trunk flows back toward the low pressure ventricles = closing the semilunar valves

Aortic valves close at 100mmHg

292
Q

why aorta valves close at 100mmHg, when they initially opened at 80mmHg

A

because as blood from LV flows into aorta, pressure increases from 80 –> 120 (in this example)

???
therefore, when LV pressure decreases to 100, there is not enough pressure to continue flowing into aorta, and backflow closes aortic semilunar valve

Why?
both pressure simultaneously decrease to 100mmHg, until decrease in LV exceeds decrease in aorta @ 100mmHg, and backflow closes SL valve (?)

293
Q

when do ventricles begin filling again?

A

Ventricle pressure drops below atrial pressure and the AV valves open and ventricle filling begins

(PASSIVE FOR MAJORITY OF FILLING)

recall:
passively filling for about 400msec / 800
(entire heart diastole) –NOT QUITE –> they fill during SECOND phase of Ventricular DIASTOLE, not the entire duration

= 105 / 130 mL
last 25mL via atrial systole

294
Q

note again, pressure changes in aorta

A

Increase in pressure with opening of aortic valve

Drop in pressure with closing of aortic valve (because blood moves along aorta and away from the initial segment, causing pressure to decrease gradually

295
Q

NOTE DICROTIC NOTCH

A

even though pressure gradually decreases with aortic semilunar valve closing,

there is a short pressure rise in aorta as ELASTIC WALLS RECOIL

phenomenon known as DICROTIC NOTCH in pressure tracing

296
Q

dicrotic

A

(dúo, “two”) +‎ κρότος (krótos, “beat”)

297
Q

cardiac cycle and heart sounds

A

Auscultation – the process of listening to sounds in the body (heart, GI, lungs)

performed with a stethoscope

298
Q

heart sounds

A

The sounds of the heartbeat come from blood turbulence created by closing valves

S1 ( “lubb”)—when AV valves close; marks start of ventricular contraction

S2 (“dupp”)—when semilunar valves close

S3 - —very faint; rarely heard in adults
blood flowing into ventricles

S4—almost always pathologic (?)

299
Q

heart murmers

A

abnormal sounds (whooshing or swishing) that is heard before, between or after normal heart sounds.

They may also mask normal heart sounds

Tends to be common in children due to developing cardiac structures, but abnormal in adults

2-4 years old
Innocent or functional heart murmurs
vs.
Congenital heart murmurs

300
Q

what age innocent/functional heart murmers

A

2-4 years old

301
Q

what can heart murmers do to normal heart sounds

A

They may mask normal heart sounds

302
Q

when can heart murmers be heard relative to normal heart sounds

A

heard before, between or after normal heart sounds

303
Q

what can the noise of heart murmers resemble

A

abnormal sounds (whooshing or swishing)

304
Q

what about heart murmers in adults

A

Not always indicative of heart problems (innocent)

May indicate valve disorder
E.g.
Stenosis or valvular insufficiency

305
Q

cardiac output

A

the amount/volume of blood that is ejected from the left ventricle each minute

Measured in mL/min

306
Q

how to calculate Cardiac outpute

A

Cardiac Output = HR × SV

heart rate stroke volume

307
Q

HR SV

A

Heart rate (HR) = # contractions/minute (beats per minute)

Stroke volume = volume of blood pumped out of ventricle per contraction

308
Q

how is CO changed

A

By changing either or both HR and SV, cardiac output is precisely controlled to meet changing needs of tissues.

309
Q

IMPORTANT NOTE ABOUT SV

A

Right ventricle SV = left ventricle SV

Stroke volume depends on the relationship between end-diastolic volume and end-systolic volume

310
Q

calculate stroke volume

A

SV = EDV – ESV

311
Q

assuming SV 70mL and HR 75bpm, what is CO

A

70*75
= a bit over 5000mL

I.e. entire volume of blood is pumped through entire circuit(s) in 1 minute

312
Q

how increase CO

A

any factor icnreasing SV or HR

313
Q

CARDIAC RESERVE

A

the difference between the maximum CO & CO at rest

314
Q

average person cardiac RESERVE

A

Average person has a CR of 4 to 5 times resting value

315
Q

certain athletes cardiac reserve

A

Athletes have reserves up 7-8 times their resting Cardiac Output (CO)

316
Q

what about cardiac reserve of people with heart disease (esp severe)

A

almost no reserves

= limited ADLs

317
Q

regulation of heart rate

which TWO factors?

A

Important in short-term control of CO and BP

Most important regulators of heart rate are:

1) the ANS

2) hormones released by the adrenal medulla

note that ANS signals to adrenal medulla, so it’s really just the ANS that regulates HR

318
Q

resting heart rate facts

A

Varies with age, general health, physical conditioning

Normal range is 60–100 bpm

Bradycardia
Heart rate slower than normal (<60 bpm)

Tachycardia
Heart rate faster than normal (>100 bpm)

*note that certain athletes may have lower than 60bpm but still normal

319
Q

note about SA node and heart rate regulation

A

Pacemaker potential in SA node cells occurs 80–100 times/min

Establishes heart rate

SA node brings AV nodal cells to threshold before they reach it on their own, thus SA node paces the heart

320
Q

SA node pacemaker potential rate

A

80–100 times/min

321
Q

autonomic regulation of heart rate is @

A

@
cardiovascular center of the medulla oblongata
(anterior to cerebellum)

322
Q

where does (cardiovascular centre of) medulla oblongata get signal from

A

input from sensory receptors and higher brain centers

323
Q

higher brain centres =

A

limbic system, cerebral cortex

324
Q

what does CV centre of medulla oblongata do with signal from higher brain centres and sensory receptors?

A

directs the divisions of the ANS to increase or decrease frequency of nerve impulses

325
Q

what 3 sensory receptors give feedback to CV centre @ medulla?

A

A)
baroreceptors – pressure changes (aorta, carotid aa)

B)
chemoreceptors – chemical changes in blood

C)
proprioceptors – sensory from the limbs & extremities

326
Q

note baroreceptor of carotid

A

when pressing on carotid, can change BP, activate sensory feedback of baroceptor

–> change heartbeat (?) or change BP (?)

327
Q

recall two divisions of ANS

A

sympathetic, parasympathetic

328
Q

CV centres of medulla

–> two parts

A

Cardioinhibitory center

Cardioacceleratory center

329
Q

Cardioinhibitory center

A

Controls parasympathetic neurons; slows heart rate

Parasympathetic supply to heart via vagus nerve (X); synapse in cardiac plexus

Postganglionic fibers to SA/AV nodes, atrial musculature

330
Q

which nerve gives parasympathetic signals to HEART?

where does it send those signals?

A

vagus nerve (CN X)

to Cardiac Plexus

331
Q

where do the nerves ultimately synapse?

A

(???)

Postganglionic fibers to SA/AV nodes, ultimately atrial musculature

332
Q

2) Cardioacceleratory center

A

Controls sympathetic neurons; increases heart rate

Sympathetic innervation to heart via postganglionic fibers in cardiac nerves; innervate nodes, conducting system (nodes/branches/bundles), atrial and ventricular myocardium

333
Q

how do sympathetic signals travel?

via which structure(s)?

A

sympathetics travel thru CARDIAC ACCELERATORY NERVES in the thoracic region of the spinal cord

334
Q

what NT is released via sympathetic signal of CARDIAC ACCELERATORY NERVES?

A

Releases norepinephrine:

—> Speeds the rate of spontaneous depolarization

—> Enhances calcium entry – increasing contractility

335
Q

what other variable is altered via norepinephrine release?

A

Enhances calcium entry – increasing contractility

336
Q

how do parasympathetic signals travel?

via which structure(s)?

A

parasympathetics travel thru the right and left Vagus Nerve (CN X)

337
Q

what NT is released via parasympathetic signal of VAGUS NERVES?

A

Release acetylcholine:

—> Decreases rate of spontaneous depolarization

338
Q

more about sympathetic influence

A

Sympathetic stimulation increases heart rate

(norepinephrine can also increase BP)

Binding of norepinephrine to beta-1 receptors opens ion channels:

—> Increases rate of depolarization

—> Decreases repolarization

339
Q

key thing to note:

“Binding of norepinephrine to beta-1 receptors opens ion channels” (increase depolarization)

But what else does norepinephrine do to beta receptors?

A

NOTE BETA BLOCKERS mechanism:
(sympathetic response also affect BP)

Beta blockers are medicines that lower blood pressure. They also may be called beta-adrenergic blocking agents.

The medicines block the effects of the hormone epinephrine, also known as adrenaline.

Beta blockers cause the heart to beat more slowly and with less force. This lowers blood pressure.

340
Q

more about parasympathetic influence

A

Parasympathetic stimulation decreases heart rate

ACh from parasympathetic neurons:
A) Opens K+ channels in plasma membrane

B) Hyperpolarizes membrane (K+ outflow?)

C) Slows rate of spontaneous depolarization

D) Lengthens repolarization

341
Q

note chemical factors affecting HR

A

Electrolyte Imbalances:

Ca2+: elevated interstitial levels ↑ strength of contraction and speeds heart rate

K+: elevated blood levels will decrease/block AP, thus decreases ↓ muscle contraction and HR

342
Q

other chemical factors affecting HR

A

Hormones:
(REMEMBER SAME SUBSTANCE CAN BE CONSIDERED EITHER NT OR HORMONE DEPENDING ON HOW IT IS RELEASED. RELEASE FROM GLAND = HORMONE, FROM NEURON = NT)

Hormones:
epinephrine & norepinephrine will ↑ HR and contractility

—> (From adrenal medulla)

343
Q

other hormones affecting HR

A

Thyroid hormones:

Increase cardiac contraction and increase HR

344
Q

other miscellaneous factors affecting HR

A

Age
Gender
Physical fitness
Body temperature

345
Q

REGULATION OF STROKE VOLUME (SV)

A

recall that there is always 40-50% of blood volume that remains in the ventricles after full ventricular systole (approx 60 mls)

346
Q

which 3 factors regulate SV

A

Preload

Contractility

Afterload

347
Q

1) Preload

A

The degree of stretch on the heart before it contracts, proportional to the END DIASTOLIC VOLUME

348
Q

note Frank-Starling Law

A

akin to a rubber band, the more you stretch it, the more force it will snap back with.

Thus, the more blood enters the ventricles, the higher the volume, the more stretch or load on the muscle tissues the greater the contraction.

(NOTE THAT TOO MUCH STRESS CAN STILL DECREASE CONTRACTILITY, just like with Skeletal muscle)

349
Q

which two factors determine End Diastolic Volume?

A

The duration of ventricle diastole

Venous return
(passively filling ventricles)

350
Q

2) CONTRACTILITY

A

the strength of contraction of muscle tissue/fibers

351
Q

which substances affect contractility

A

positive inotropic agents increase contraction

negative inotropic agents decrease contraction

352
Q

inotropic define

A

“modifying the force or speed of contraction of muscles.”

From Ancient Greek ἴς (ís, “sinew, tendon; strength, force”) +‎ -tropic (“affecting, changing”)

353
Q

positive inotropic agents E.g.

A

sympathetic nervous system (CARDIAC ACCELERATORY NERVES),

digitalis (drug),

epinephrine (from adrenal medulla?),

anything that increases Ca2+ inflow (?)

354
Q

negative inotropic agents E.g.

A

parasympathetics (E.g. via Vagus Nerves),

anoxia,

drugs,

anything that blocks or inhibits Ca2+ inflow (calcium channel blockers)

355
Q

3) AFTERLOAD

A

the pressure that must be overcome before the semilunar valves (aortic & pulmonary) can open.

356
Q

what happens to SV if afterload INCREASES

A

Factors that increase the afterload will decrease the SV

357
Q

what can increase AFTERLOAD?

A

increase BP (hypertension) in systemic arteries

ex. via Atherosclerosis, Weight gain (??)

358
Q

so to increase SV, what happens to 3 variables

A

increased PRELOAD

increased CONTRACTILITY

decreased AFTERLOAD

ultimately?
increased SV –> increased CO

359
Q

Congestive Heart Failure (CHF)

A

A loss of pumping efficiency by the heart

360
Q

cause?

A

CAD,

congenital defects,

high BP,

MI,

valve disorders

361
Q

what happens during CHF

(A positive feedback loop)

A

Pumping becomes less effective

—> increase in EDV (preload)

—> heart becomes overstretched

—> contract less forcefully

362
Q

during CHF, which side usually fails before the other?

A

Left Ventricle more common, leads to pulmonary edema

Right Ventricle, leads to peripheral edema

363
Q

CARDIAC PATHOLOGIES

A

..

364
Q

arrythmias

A

Abnormal rhythm of the heart as a result of a defect in the conduction system of the heart

Leads to asynchronous contractions & therefore abnormal blood pumping

365
Q

arrythmias refects in

A

conduction system

366
Q

recall conduction system

A

nodes, branches, bundles, fibres, etc

367
Q

primary feature of arrythmias (dysrhythmias)

A

leads to asynchronous contractions & therefore abnormal blood pumping

368
Q

symptoms..

A

chest pain, shortness of breath, lightheadedness, dizziness, fainting

369
Q

potential risk factors for arryhtmias

A

stress, caffeine, alcohol, cocaine, nicotine, CAD, MI, HTN (many)

HTN = hypertension (?)

370
Q

E.g. arrythmia

A

Bradycardia (below 50beats/min) (60?)

Tachycardia (above 100beat/min)

Fibrillation (rapid, uncoordinated heartbeats)

371
Q

coronary artery disease (CAD)

A

Results from the effects of the accumulation of atherosclerotic plaques in coronary arteries, which leads to a reduction in blood flow to the myocardium

372
Q

primary cause

A

accumulation of atherosclerotic plaques in coronary arteries

373
Q

risk factors, CAD

A

Smoking, high BP, DM, high cholesterol, obesity, sedentary lifestyle, family Hx

Males > females, > after 70 years of age

374
Q

signs symtpoms, CAD

A

dependent on severity (chest pain, dyspnea, etc.)

can have complications:
angina pectoris
MI

375
Q

leading cause of death

A

Cardiovascular disease is the leading cause of death

376
Q

athersclerotic plaques

arteriosclerosis vs atherosclerosis

A

athero - meaning gruel or paste and sclerosis meaning hardness

Arteriosclerosis: Thickening of artery walls and loss of elasticity

Atherosclerosis
One form of arteriosclerosis

377
Q

about atherosclerosis

A

Progressive disease characterized by the formation of lesions called atherosclerotic plaques in the walls of large and medium sized arteries

These plaques are cholesterol or fatty acid molecules that accumulate too much, too fast, too often

378
Q

Congenital heart defects, E.g.

A

Coarctation of the aorta

Patent ductus arteriosus

Septal defect (patent foramen ovale)

Tetralogy of Fallot

379
Q

Coarctation of the aorta

A

A segment of the aorta is narrowed

Resulting in reduced oxygenated blood flow

Sx: Depend on severity
Pale, sweating, dyspnea

Tx: catheterization and low BP medications

380
Q

Patent Ductus Arteriosus

A

The ductus arteriosus remains open rather than closing shortly after birth

Aortic blood flows into the lower pressure pulmonary trunk

Tx depends on severity, some are never recognized

381
Q

patent define

A

MEDICINE
(of a vessel, duct, or aperture) open and unobstructed; failing to close.

382
Q

Septal Defect

(E.g.? patent foramen ovale)

A

Atrial:
The fetal foramen ovale fails to close (patent foramen ovale)

Ventricular:
Incomplete development of the septum

Oxygenated and deoxygenated blood mix

383
Q

Tetralogy of Fallot

A

Combination of 4 defects:

1) Ventricular septal defect

2) Aorta that emerges from both ventricles (overriding aorta)

3) Pulmonary valve stenosis

4) Right ventricular hypertrophy

(note that if pulmonary SL valve is stenosed, RV requires more force to push blood into pulmonary circuit –> i.e. RV hypertrophy)

384
Q

tetralogy define

A

MEDICINE
a set of four related symptoms or abnormalities frequently occurring together.

385
Q

tetralogy of fallot can result in

A

Results in a decreased blood flow to lungs and a mixing of oxygenated and deoxygenated blood

can lead to cyanosis, “blue baby”

386
Q

overriding aorta

A

“An overriding aorta is a congenital heart defect where the aorta is positioned directly over a ventricular septal defect, instead of over the left ventricle”

I.e. septal defect is directly related to overriding aorta

387
Q

cardiac arrest

A

A clinical term meaning cessation of an effective heartbeat

Can be spontaneous (SCA) or due to trauma (TCA)

Causes:
Arrhythmia

Coronary artery disease

Cardiomyopathy or CHF

Penetrating wound or blunt trauma (commotio cordis)

388
Q

commotio cordis

A

Penetrating wound or blunt trauma

sudden arrhythmic death caused by a low/mild chest wall impact

About 59% of people who experience it survive. You’re most likely to survive if you receive CPR right away.

389
Q

commotio cordis – how common?

A

With commotio cordis (Latin for “agitation of the heart”), the impulse from the object disrupts the normal heart rhythm and leads to sudden cardiac arrest. How common is commotio cordis? Cases of commotio cordis are extremely rare. There are fewer than 30 cases each year.

“struck in the chest at a specific time in the heart rhythm cycle”

390
Q

Paroxysmal tachycardia

A

A period of rapid heartbeats that begins and ends suddenly

391
Q

Cardiomegaly (Heart enlargement)

A

SSx: dyspnea, arrhythmia, edema

Causes: MI, valve disease, cardiomyopathy, hypertension, anemia, etc.

392
Q

Cor Pulmonale (CP)

A

A term referring to right-sided heart failure from disorders that bring about HTN into the pulmonary circulation

Causes: Left-sided heart failure, COPD, cystic fibrosis, and more

393
Q

development of heart

A

The heart is the first functional organ

One of the first systems to form in an embryo

(heart and brain)

Begins its development from mesoderm on day 18/19 following fertilization

Develops from a group of mesodermal cells called the cardiogenic area

Most development occurs between weeks 5 and 9

394
Q

CPR

A

a rescue technique in which an unconscious, pulseless person is assisted in maintaining heart rate (cardio) and breathing (pulmonary)

CPR keeps oxygenated blood circulating until the heart can be restarted

395
Q

what to do when in doubt (CPR) ?

A

When in doubt – chest compressions, chest compressions, chest compressions

2007 Japanese study found that in lay-person rescue, chest compressions alone are equally as effective as traditional CPR with ventilation

Place the heel of your hand on the centre of the person’s chest, then place the palm of your other hand on top and press down by 5 to 6cm (2 to 2.5 inches) at a steady rate of100 to 120 compressions a minute.

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Semester 3 (32 decks)

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