Bms 6633 Cardio & Resp Test 1 Easy Stuff

Front 1

Back 1

Blood islands: develop into horseshoe shaped endothelial tube (primitive heart)

Primary heart field develops into pericardial cavity

Front 2

Back 2

Top = splanchnic mesoderm layer (where blood islands form)

Bottom = primary heart field blood islands

blue = ectoderm
Orange = mesoderm
yellow = endoderm

Front 3

Back 3

Myocardium = from endocardial mesoderm

Cardiac jelly = acellular matrix around myocardium

Epicardium = derived from coelomic wall mesoderm (migrates into place)

Front 4

Back 4

Truncus arteriosus = ascending aorta, pulmonary trunk

Bulbus cordis = Smooth portion of R ventricle, conus arteriosus, aortic sinuses

Primitive ventricle = trabeculae carneae

Primitive atrium = pectinate muscles (trabeculated muscles)

Sinus venosus = coronary sinus, smooth muscle in R atrium

Inflow from bottom, outflow from top

Front 5

Back 5

Umbilical veins = from chorion = round ligament of liver

Vitelline veins = from yolk sac = portal system

Cardinal veins = caval system

Front 6

Back 6

Notochord cells move from hindbrain to arches 3, 4, 6 to help with this development

Front 7

Tetralogy of Fallot

Back 7

1: stenosis of pulmonary trunk
2: hypertrophied right ventricle
3: overriding aorta
4: ventricular septal defect

DiGeorge syndrome, environmental, genetic

Front 8

Back 8

Persistent truncus arteriosus (no division between pulmonary trunk and aorta)

Front 9

Back 9

D-transposition

RV pumps to aorta, LV pumps to pulmonary

No aorticopulmonary septum twist

Front 10

Back 10

L-transposition, functional "corrected transposition"

Viewed as a twist of great vesicles or twist of ventricles

Front 11

Back 11

Double outlet right ventricle (interventricular septum defect)

Front 12

Back 12

Front 13

Transesophageal echocardiogram TEE

Back 13

Common atrium (cors triloculare biventricular)

no primary / secondary septum development

Front 14

Back 14

Atrioventricular canal fuses week 5, if no fusion then persistent common AV canal

Front 15

Back 15

endocardial cushions of atrioventricular valve become AV valves

Front 16

Back 16

Ebstein's anomaly

Defective tricuspid valve, creates atrialized right ventricle and a small functional right ventricle.

Front 17

Back 17

Tricuspid Atresia

right AV canal seals, no valve develops

Front 18

Back 18

interventricular septum

Derives from crescentic fold (until week 7), composed of muscular and membranous part

Front 19

Back 19

venticular septal defect

Front 20

Back 20

Cor triloculare biatriatum

resorption of myocardial tissue during formation of interventricular septum

Front 21

Node Development

Back 21

1: primitive atrium = temp pacemaker, then sinus venosus takes over

2: SA develops week 5 and part of sinus venosus (part of R atrium)

3: AV node develops from cells in wall of sinus venosus

Front 22

Aortic arch artery 1,3,4,6

Back 22

1: Portion of maxillary sinus
3: Common and internal carotid arteries
4: Right subclavian artery, part of aortic arch
6: ductus arteriosus, proximal pulmonary arteries

Front 23

Intersegmental arteries

Back 23

intercostal arteries, lumbar arteries, common iliac arteries, portions of vertebral, sublcavian, lateral sacral arteries

Front 24

umbilical arteries
Umbilical Vein

Back 24

medial umbilical ligaments
round ligament of the liver

Front 25

Vitelline Arteries

Back 25

Celiac trunk, superior mesenteric artery, inferior mesenteric artery

Front 26

Vitelline veins

Back 26

hepatic portal system, hepatic veins, intrahepatic segment of inferior vena cava

Front 27

Anterior cardinal veins

Back 27

superior vena cava, brachiocephalic veins, internal jugular veins

Front 28

Subcardinal veins

Back 28

Lower inferior vena cava, renal / suprarenal veins, gonadal veins

Front 29

Supracardinal veins

Back 29

azygous system of veins, inferior vena cava between kidney / liver

Front 30

Back 30

develops as outpocket of gut tube

Front 31

Back 31

Lower respiratory develops at week 4, starts as median laryngotracheal groove in caudoventral wall at primitive pharynx

deepens into ventricular diverticulum, enlarging into lung bud

Front 32

Back 32

Front 33

Back 33

Tracheoesophageal fistula

Front 34

Back 34

2 bronchial buds grow into pericardioperitoneal cavity, becomes pleural cavities

Front 35

Lung Bud Development

Back 35

week 5 = each bronchial bud enlarges to primordium of primary bronchus, dividing into secondary and then tertiary bronchi by week 7. Week 24 is 14 divisions, creating respiratory bronchioles. 7 more divisions remaining.

Surrounding mesenchyme creates cartilage, smooth muscle, connective tissue, capillaries

Front 36

Pleurae

Back 36

Lungs: pleura derived from splanchnic mesenchyme

Thoracic wall: parietal pleura derived from somatic mesoderm

Front 37

Back 37

Front 38

Heart Location

Back 38

Within mediastinum

Oblique from 2nd rib to 5th intercostal space

Front 39

Back 39

Fibrous pericardium: protection, anchor to diaphragm / great vessels, prevent overfilling

Serous pericardium: parietal layer junction with fibrous pericardium, visceral layer = epicardium, pericardial cavity in between (serous fluid)

Front 40

Back 40

directly under pulmonary trunk / aorta

Front 41

Cardiac Tamponade

Back 41

tear in myocardium / epicardium, outflow of blood into pericardial cavity leading to heart failure from pressure

Front 42

Pericardiocentesis

Back 42

Used to treat cardiac tamponade, insert needle into pericardial cavity

Front 43

Pericarditis

Back 43

may appear as extra liquid on epicardium, or fibrous appearance

Front 44

Sternocostal surface of heart

Back 44

R atrium & R ventricle

Front 45

Diaphragm surface of heart

Back 45

posterior & inferior wall of L ventricle

Front 46

Back 46

Coronary sulcus: contains coronary sinus

Anterior interventricular sulcus: anterior interventricular branch of L coronary artery and great cardiac vein

Posterior interventricular sulcus: posterior interventricular artery and middle cardiac vein

Front 47

Fibrous heart skeleton

Back 47

Collagen (type 1) & elastin

Strengthens pulmonary / aortic trunks

Stabilizes, reinforces, provides elasticity

Front 48

Site of auscultation

Back 48

Auscultate at fifth intercostal space, sternal border. Contributes to S1

Cusps = leaflets

Front 49

Site of auscultation

Back 49

Auscultate at 5th intercostal space, medial to left midclavicular line. Contributes to S1

Bicuspid = mitral. Cusps = leaflets

Front 50

AV function

Back 50

papillary muscles contract and pull chordae tendinae during ventricular contraction in order to keep valve closed and prevent prolapse (as depicted) / regurgitation of blood

function based off of pressure

Front 51

Pulmonary & Aortic Semilunar Valve auscultation sites

Back 51

Pulmonary: L 2nd intercostal space

Aortic: R 2nd intercostal space

Both contribute to S2, possible split due to late pulmonary valve closure from decreased thoracic pressure during breath (longer for pulmonary trunk pressure to exceed R ventricle pressure)

Front 52

Semilunar valve function

Back 52

Valves function based off of gravity acting on blood rather than pressure

Front 53

Back 53

Front 54

Back 54

Front 55

Back 55

Front 56

Back 56

Left coronary artery can trifurcate instead of bifurcate, into anterior interventricular branch, circumflex branch, as well as the variation of a "Ramus Branch" in between

Front 57

Back 57

Conus branch normally extends off of the right coronary artery, however a variant can extend directly off of aorta and is referred to as the third coronary artery

Front 58

Back 58

Coronary artery bypass surgery

Great Saphenous vein or internal thoracic vein can be used as candidate vessels.

Front 59

Back 59

anterior cardiac veins unique because drain directly into right atrium rather than cardiac sinus,

Front 60

Back 60

Coronary Sinus empties through the Thebsian valve into the right atrium.

Front 61

Venae Cordis Minimae

Back 61

smallest cardiac veins which empty myocardium, most abundant in right atrium, least abundant in left ventricle

Front 62

L sinus venosus horn vs R sinus venosus horn

Back 62

L sinus venosus becomes coronary sinus

R sinus venosus becomes sinus venarum (smooth portion of R atrium)

Front 63

Back 63

Front 64

Back 64

Thoracic duct empties into venus angle

Front 65

Back 65

Front 66

Back 66

Front 67

Cardiocytes

Back 67

Identified by intercalated discs made with adhesions

Front 68

Back 68

Front 69

Back 69

Front 70

Back 70

Front 71

Back 71

external maxillary artery = facial artery

Maxillary artery 1st part: Middle meningeal, inferior alveolar

2nd: buccinator

3rd sphenopalantine

Front 72

Back 72

Forms portion of circle of willis

Front 73

Back 73

Anterior kiesselbach area = majority of epistaxis

posterior from ethmoidal arteries or sphenopalatine arteries may result in a more serious epistaxis

Front 74

Back 74

Front 75

Back 75

vertebral artery runs up through transverse froamen of cervical spine into skull

Front 76

Back 76

Pericardiacophrenic artery stems from internal thoracic artery

Front 77

Visceral branches of thoracic aorta

Back 77

Front 78

Back 78

Front 79

Back 79

superior mesenteric artery can actually obstruct duodenum because it lies directly over it

can also compress left renal vein

Front 80

Back 80

Front 81

Back 81

internal iliac supplies, bladder, walls of pelvis, genitalia

Front 82

Back 82

Front 83

Back 83

Front 84

Back 84

Front 85

Back 85

Front 86

Long QT syndrome genetic concepts

Back 86

Inheritable

Locus heterogeneity (single phenotype could be caused by many different loci mutations). Panethnic

Incomplete penetrance

Variable expressivity

genetic susceptibility to meds

Front 87

Long QT syndrome phenotype

Back 87

Long QT interval: >470 male, >480 female, normal ≤ 400

T wave abnormalities: tachyarrhythmias, torsades de pointe (ventricular tachycardia)

Syncope, sudden death

Front 88

KCNQ1 protein

Back 88

Interacts with KCNE proteins to form potassium channels

Found in inner ear, kidney, lung, GI, heart

Mutations cause Romano-Ward syndrome

Some mutations linked with SIDS

Front 89

Romano-Ward Syndrome (elongated QT syndrome)

Back 89

most common form, autosomal dominant (incomplete penetrance, variable expressivity)

point mutations, insertions, deletions in KCNQ1 (>140 known)

potassium channels work at reduced efficiency, prolong the amount of time for repolarization. Also lower threshold for depolarization.

Front 90

KCNH2 protein

Back 90

interacts with KCNE2 to form potassium channel

mutations also cause Romano-Ward syndrome

Front 91

Jervell & Lange-Nielsen syndrome (long QT syndrome)

Back 91

Less common, autosomal recessive

Result of a mutation creating short nonfunctional KCNQ1 protein, potassium channels do not function

More severe than Romano-Ward syndrome

Front 92

Long QT syndrome prognosis

Back 92

syncope from arrhythmias = common symptom, 30-50% never show syncope however.

Cardiac episodes frequent in preteens-20s, risk decreases with age.

30% are within normal range, stress EKG needed to identify elongated QT

very dangerous to prescribe QT elongating drugs

Front 93

Congenital Heart defect genetic concepts

Back 93

Multifactorial inheritance (many contributing genes and environment)

Single gene or chromosome defect (usually associated with other defects)

Somatic mosaicism (problem may occur during embryogenesis, not all cells will be affected)

Empiric risks (population risk given rather than personalized risk)

Carter effect (if one sex is less susceptible and you have a sibling of that sex with the disease, then you are at a higher risk)

Front 94

Syndromic congenital heart disease

Back 94

Uncommon and due to single gene defects, therefore associated with other defects in development

Noonan, Alagille, Holt-Oram, Simpson-Goabi-Behmel (don't memorize probably)

recurrence risk is the same from one population tothe next

Front 95

Isolated Congenital Heart Defects

Back 95

More common, many forms with different empiric risks

Flow lesions, defects in cell migration or death, abnormal extracellular matrix, defects in targeted growth

Multifactorial inheritance, low penetrance, likely environmental factors, polygenic

recurrence risk is different from one population to the next

two hit hypothesis may also apply

somatic mosaicism has been observed in some forms

22q11 = tetralogy of fallot

Front 96

Multifactorial inheritance concepts

Back 96

higher risk if more family members affected

higher risk if severe expression in family member

higher risk if family member is of less commonly affected sex (Carter effect)

risk decreases for more distant relatives

additive risk

Front 97

Cardiac defects in

Trisomy 13 (patau)

Trisomy 18 (edward)

Trisomy 21 (down)

Back 97

13 = right sided heart rather than left, atrial septal defect, patent ductus arteriosus, ventricular septal defect

18 = atrial septal defect, patent ductus arteriosus, ventricular septal defect

21 = atrioventricular septal defect, atrial septal defect, patent ductus arteriosus, ventricular septal defect

Front 98

Back 98

Front 99

Chest Radiograph

Back 99

common, cheap, fast

Good for pulmonary / bony structures

Bad for heart / soft tissue

Front 100

Chest radiograph direction

Back 100

PA = posterior to anterior (normal)
AP = anterior to posterior (sick, bedridden patients)

Anything further from film is magnified, so you would prefer to have the heart closer to the film (PA)

Front 101

Back 101

Front 102

Back 102

Pleural calcification (asbestos)

Front 103

Back 103

Pneumothorax (collection of air between visceral and parietal pleura)

Displaces the heart, compressing blood supply and causing cardiac arrest

May result from trauma or central line placement (subclavian vein near pleura)

Air hides shadows, appears blacker than usual

Front 104

Back 104

Pleural effusion

Liquid collects first in the costophrenic angles due to gravity, may traverse upwards due to surface tension. Appears white, loses sharp angles at bottom of lung.

Ultrasound good for localizing spot for chest tube due to the presence of liquid rather than air (always insert above rib, never below)

Front 105

Sections of the mediastinum

Back 105

Superior: thymus, superior VC & brachiocephalic veins, aortic arch / branches, trachea, esophagus, vagus & phrenic nerves, thoracic duct

Anterior: thymic remnants, areolar tissue, lymph nodes.

Middle: heart, ascending aorta, lower half of superior VC with azygos vein, bifurcation of trachea & two bronchi, pulmonary artery, R&L pulmonary veins, phrenic nerve, lymph nodes, pericardiacophrenic vessels.

Posterior: Descending aorta, esophagus, thoracic duct, azygos veins, vagus nerve

Front 106

Back 106

hilum, made up of pulmonary artery, bronchus, pulmonary vein, lymph nodes

may become enlarged due to enlarged lymph nodes (picture above: hilar adenopathy)

Front 107

Back 107

Right bronchus is wider and shorter than left

Endotracheal tube should be 5cm above carina, can find carina by drawing 45 degree line from aorta. If it falls into a bronchus (more often the right due to size) it will collapse the opposite lung.

Front 108

Back 108

Right lung (three lobes)

Left long has only one pulmonary fissure (major) and is two lobed

Front 109

Back 109

Secondary pulmonary lobule, smallest lung unit surrounded by connective tissue septum.

1-2cm, 5-15 pulmonary acini containing alveoli.

Center is supplied by terminal bronchiole with centrilobular artery

Interlobular septum supplied by pulmonary veins and lymphatics

Front 110

Back 110

Interstitial process (such as pneumonia, tuberculosis, silicosis)

Lines referred to as Kerley Lines

Front 111

Back 111

Pulmonary edema

Presents as bilateral alveolar infiltrate, appears as batwing

Front 112

Back 112

Cardiothoracic ratio

ratio should be less than 50% (remember should be done on a PA chest)

Front 113

Back 113

MRA: magnetic resonance angiography, no need for catheter with contrast

Front 114

Back 114

aortic aneurysm of the ascending aorta

Front 115

Back 115

aortic dissection

Front 116

Central line placement

Back 116

tip of catheter ends at superior vena cava, must make sure the catheter doesn't track up one of the jugular veins

Front 117

Back 117

Coronary CTA (computer tomography angiography)

Used to search for occlusions or other vascular problems

Front 118

Back 118

Pericardial effusion

cannot tell on chest radiography (middle) if due to chamber enlargement or pericardial effusion. Easier to see on ultrasound (left) or CT (right)

Front 119

Back 119

intravascular ultrasound. Left = normal, right = occluded from plaque buildup

Front 120

Back 120

Ventilation perfusion scan (V/Q)

ventilation imaged with xenon

perfusion with technetium labelled albumin. White spots = defects in perfusion

Front 121

Back 121

myocardial perfusion imaging, darker areas = ischemic due to not taking up radioactive tracer

good to do under stress to identify ischemic areas

Front 122

Body fluid compartments

Back 122

80% circulating fluid in interstitium

20% in plasma

Front 123

Flow equation

Back 123

Front 124

Resistance equation

Back 124

L = tube length

n = fluid viscosity

r = internal radius of tube

Front 125

Flow equation with full resistance equation

Back 125

Front 126

Back 126

peripheral vascular resistance

Rt = RA+ Ra + Rc + Rv + RV

Front 127

Total peripheral resistance

Back 127

Organs are arranged in parallel (except GI and liver in series)

1/TPR = 1 / Rorgan + 1 /Rorgan.....+ 1/Rorgan

Removing one source of parallel resistance will increase resistance

Front 128

Cardiac output

Back 128

CO = Stroke volume X heart rate

Average = 5L /min

Blood volume = 5.5 - 6L

Front 129

Back 129

Pacemaker cells, slow response

Funny channels open, sodium moves in, potassium out
T calcium channels open, calcium moves in
L calcium channels open, rapid depolarization
Potassium channels open, potassium moves out, repolarization

Front 130

Back 130

Contractile cell action potential (ventricular action potential, fast response)

0 = sodium channels open, sodium moves in rapid depolarization
1 = sodium channels close, sodium movement slows
2 = potassium inward channels open, calcium L channels open. Calcium moves in causing plateau against potassium moving out
3 = potassium delayed channels open, calcium L channels close. Potassium moves out, repolarizing
4 = potassium channels open, sodium and calcium closed.

Front 131

Autonomic influences on heart

Back 131

Sympathetic = B1 norepinephrine = increased heart rate, supplied to SA node, AV node, ventricular myocardium (contractility). Increases open state of calcium channels, faster spontaneous depolarization

Parasympathetic = M2 acetylcholine = decreased heart rate, supplied to SA and AV node from vagus nerve. More open K+ and more closed Ca+, decreased rate of spontaneous depolarization / hyperpolarizes.

Blood vessels: alpha 1 norepinephrine = contraction, beta 2 dilates some. Both sympathetic

Front 132

Cardiovascular transport equation

Back 132

Convective transport

X = transport rate, Q = flow rate, [X] = concentration

Front 133

Fick principle (utilization rate)

Back 133

Xtc = transcapillary efflux rate

Q = blood flow

[X]a, v = arterial / venouc concentration

Front 134

Filtration vs reabsorption

Back 134

filtration = net fluid movement out of capillary

reabsorption = fluid movement into capillary

Front 135

Starling forces / equation

Back 135

NDF > 0 = filtration

NDF < 0 = reabsorption

edema occurs if constant filtration (either increased capillary hydrostatic pressure, or decreased capillary osmotic pressure)

Front 136

Cardiac cycle

Back 136

Atrial contraction, isovolumetric contraction, rapid ventricular ejection, slow ventricular ejection, isovolumetric relaxation, rapid passive filling, slow passive ventricular filling

Front 137

Back 137

Front 138

Stroke volume

Ejection fraction

Back 138

SV = End diastolic volume - end systolic volume

Ejection fraction = Stroke volume / end diastolic volume

Front 139

S1

S2

S3

S4

Back 139

S1= closure of mitral / tricuspid valves (isovolumetric contraction)

S2 = closure of semilunar valves (isovolumetric relaxation)

S3 = occurs during rapid filling of ventricle if ventricle is very compliant

S4 = occurs with atrial contraction against stiff ventricle (concentric hypertrophy, or myocardial infarction)

Front 140

Venous pulse

Back 140

Varies with right side of heart and respiratory cycle. Read at end of expiration when intrapleural pressure is close to 0

a = right atria contraction
c = tricuspid valve bulging due to isovolumetric contraction
x = atrial relaxation
v = filling of atrium during ventricular contraction
y = rapid filling of right ventricle upon opening of tricuspid valve

Front 141

Back 141

First = atrial fibrillation, no full contraction so pressure never builds up except during ventricular systole

Second = tricuspid valve insufficiency causing backflow of blood during systole increasing venous pressure

Third = stenotic tricuspid valve, atrial pressure is increased against the stiff valve

Front 142

Back 142

Front 143

Back 143

a = ventricular filling

b = isovolumetric contraction

c = ventricular ejection

d = isovolumetric relaxation

Front 144

Back 144

Aortic valve stenosis (left ventricle must create more pressure against a stiff valve). Pressure gradient above aortic pressure

Crescendo-decrescendo murmur heard loudest over 2nd intercostal space at sternal border

Front 145

Back 145

Mitral valve stenosis, left atrial pressure higher than 15, blood builds up against stiff mitral valve and not as much is pushed through. Pressure gradient is higher than left ventricular pressure during diastole.

S1 may be louder due to closure of stiff valve, S2 is followed by snap opening of mitral valve followed by rumbling deep murmur. Best heard over apex

Front 146

Back 146

Aortic Valve regurgitation. No pressure gradient, however pressure is still high. Blood leaks back and increases EDV, larger fall off of aortic pressure during diastole.

Murmur begins with diastole and is described as a decrescendo.

Front 147

Back 147

Mitral regurgitation. No pressure gradient but heightened left atrial pressure. Mitral valve leaks allowing blood back into left atrium, extra blood increases EDV which increases SV. More complete emptying of the heart decreases ESV also increasing SV.

Murmur is heard during systole, is holosystolic (high frequency plateau, no crescendo-decrescendo)

Front 148

Back 148

Because of reduced conductance through myocardium, contraction follows action potential by roughly 250msec

Front 149

EKG box values

Back 149

Horizontal: 1 large = .2sec
1 small = .04 sec

Vertical: 1 large = .5mV
one small = .1mV

Front 150

Back 150

segment = connect two waves

interval = contain at least 1 wave

Front 151

P wave

Back 151

Left half of wave = right atria (first to depolarize)

Right half of wave = left atria

Front 152

PR Segment

Back 152

Caused by AV node, creating a pause

Front 153

QRS

Back 153

Ventricular depolarization, septal fascicle depolarizes septum first, then anterior and posterior fascicles depolarize the rest of the ventricle

Q = first downward deflection before any up
R = first upward deflection
S = first downward deflection after any up

Front 154

T wave

Back 154

ventricular repolarization (atrial repolarization is hidden by QRS)

Front 155

EKG lead

Back 155

Positive deflection = depolarization towards positive electrode or repolarization away from positive electrode

Negative deflection = depolarization away from positive electrode, or repolarization toward positive electrode.

Result = QRS and T wave usually same deflection because repolarization starts where depolarization stopped

Biphasic wave = depolarization perpendicular to electrode

Front 156

Limb leads

Back 156

3 standard and 3 augmented leads

All measure in frontal (coronal) plane

I = Right to left arm
II = R arm to left leg
III = L arm to right leg
AVL = All to left arm
AVR = All to right arm
AVF = All to feet

Front 157

Precordial leads

Back 157

6 leads placed, measure in the transverse plane (horizontal)

Front 158

Back 158

Front 159

Back 159

Standard for 1mV set at beginning of each EKG, usually 10mm. Sometimes 1/2 standard for very high deflections.

Speed of paper can also vary

Front 160

Back 160

HR = 300 / # large boxes

Or 300, 150, 100, 75, 60, 50

Front 161

Rhythm

Back 161

Rate between 60-100 (bradycardia or tachycardia if beyond)

Every P wave followed by QRS (if no P wave then QRS didn't originate from SA node)

P wave upright in leads I & II. Inverted in aVR

Front 162

Axis

L axis deviation? I, II, aVF

R axis deviation? I, II, aVF

Back 162

Determining the ventricular axis (vector of the electric conductance)

QRS should be positive in I & II

L axis deviation will be positive in I but negative in II, negative aVF

R axis deviation will be positive in II but negative in I, positive aVF

Front 163

Intervals (PR, QRS, QT)

Back 163

PR interval = .12 - .20 sec, 3-5 little boxes

QRS = less than .10 sec, or less than 2.5 little boxes

QT interval less than half of R-R interval

Front 164

Morphology

Back 164

Amplitude and duration of waves

Front 165

P wave morphology

Back 165

should be upright in II, biphasic in V1

Front 166

P wave

Back 166

Right atrial enlargement, left atrial enlargement

(Taller, wider)

In R atria enlargement, L atria still needs to contract and is normal so duration is the same but R atria has more myocytes so increased voltage.

In L atria enlargement right atria has already contracted and L atria takes longer to contract, so the P wave is elongated

Front 167

QRS morphology

Back 167

less than .1 seconds, variable amplitude

conduction disturbance = wider than normal
ventricular hypertrophy = taller than normal

Q wave = normally from septal fascicle

V1/2 = negative, V3/4 = biphasic, V5/6 = positive
If 1/2 are positive, could be R ventricular hypertrophy

Front 168

ST morphology

Back 168

flat and at isoelectric point

Used for diagnosing: ischemia (depression), infarction (regional elevation), pericarditis (diffuse elevation)

Front 169

T wave morphology

Back 169

Ventricular repolarization, should be same direction as QRS complex

Diagnostic: ischemia (peaked & inverted), hyperkalemia (peaked)

Front 170

Mean arterial pressure short term regulation

Back 170

detected by baroreceptors, integrated in brainstem, controlled by autonomic NS, effecting heart & blood vessels

Front 171

Baroreceptors

Back 171

Have a baseline frequency of action potentials, increased pressure increases frequency, decreased pressure decreases frequency

Front 172

Medulla oblongata role in pressure

Back 172

Medulla oblongata = cardiovascular control center, uses arterial baroreceptors, low pressure baroreceptors, chemoreceptors, proprioceptors, and higher brain centers to control output via ANS.

Low pressure receptors located in large veins and in right atrium

Parasympathetic: SA and AV node

Sympathetic: SA & AV node, ventricular myocardium, arterioles, veins (increased tone)

Front 173

Afferent nerves for baroreceptor information

Back 173

Carotid sinus baroreceptors: cranial nerve 9 (glossopharyngeal)

Aortic Arch baroreceptors: cranial nerve 10 (vagus)

Front 174

Long term blood pressure regulation

Back 174

Happens via blood volume using renin angiotensin aldosterone system (RAAS)

Juxtaglomerular cells around afferent arterioles in the kidney sense decreased blood pressure, decreasing NaCl levels, or b1 receptor activation (sympathetic). They secrete renin in response to these stimuli, converted to angiotensin 1 by angiotensinogen (from liver). Converted to angiotensinogen 2 by ACE in pulmonary capillaries. Angiotensin 2 stimulates aldosterone release.

Front 175

Angiotensinogen effects

Back 175

vasoconstriction of arterioles

aldosterone secretion, increased sodium reabsorption in late distal tubules & collecting ducts

Anti-diuretic hormone secretion, increasing water reabsorption in late distal tubules / collecting duct

Thirst stimulation in hypothalamus

Front 176

Thoracic / abdominal changes in pressure during respiration

Back 176

Front 177

Back 177

This is why highest arterial pressure = femoral arteries while standing up, due to gravity.

Front 178

Reaction to exercise

Back 178

skeletal muscle blood flow x10, heart x3, brain unchanged, kidney 1/4th, skin x4, splanchnic organs 1/2

vasodilation of skeletal arterioles due to adenosine, potassium, lactate

PO2 and PCO2 are unchanged in arterial system due to increased ventilation, venous system PO2 is decreased and PCO2 is increased

pH may decrease due to lactic acid

MAP increased

Blood flow large increase, TPR large decrease (dilation of skeletal muscle arterioles)

Pulmonary circulation = flow increase, vascular resistance large decreases, increased blood volume, increased perfused capillaries

Front 179

Effect of physical conditioning

Back 179

Increased arteriole number, decreasing resistance during exercise

Increased capillary density

Increased oxidative enzymes in mitochondria