Cabs Unit 3 Cardio Questions

Front 1

2300mg

Back 1

What is the recommended amount of Na intake/day per the AHA?

Front 2

4,700 mg of K+/day

Back 2

Institute of Medicine Recommendation of potassium (K)

Front 3

0.4

Back 3

Industrialized or Societies w/ Primary HTN have a potassium/sodium ratio of:

Front 4

Distribute blood to the cells of the body, remove cellular waste and permit intercellular communication and regulation via hormones, cytokines and components of immunity

Back 4

The purpose of the cardiovascular system is to

Front 5

Low pressure, Into the pulmonary circulation

Back 5

The right side of the heart is a -high or low- pressure system that pumps blood where?

Front 6

High pressure, into the systemic circulation

Back 6

The left side of the heart is a -high or low- pressure system that pumps blood where?

Front 7

When blood pressure drops too low, as in circulatory shock, tissues are inadequately perfused, and ischemia and infarction may result.

Back 7

What happens in circulatory shock?

Front 8

Alterations in the diameter of blood vessels

Back 8

What determines the amount and direction of blood flow, and thus the degree to which a tissue is perfused with blood?

Front 9

autonomic nervous and endocrine systems

Back 9

The coordination of the changing activity of the heart and blood vessels is largely controlled by:

Front 10

To generate an arterial blood pressure that is sufficient to perfuse organs

Back 10

The primary function of the heart is

Front 11

A measure of the heart’s function

Back 11

What is cardiac output a measurement of?

Front 12

The normal volume/ min at rest in an adult is from 5-6 L/ minute.

Back 12

What is the normal cardiac ouput at rest per minute?

Front 13

Heart rate and stroke volume

Back 13

Cardiac output is dependent on two factors:

Front 14

Stroke volume is the amount of blood pumped by either right or left ventricle per heartbeat.

Back 14

What does stroke volume represent?

Front 15

Stroke volume is defined as the difference between the volume of blood within the ventricle at the end of the relaxation/filling phase (i.e diastole, therefore this volume of blood is referred to as “end diastolic volume or EDV”) and the volume of blood remaining at the end of the contraction/ejection phase (i.e. systole, therefore this volume of blood is referred to as “end systolic volume or ESV”.)

Back 15

How is stroke volume defined?

Front 16

EDV – ESV

Back 16

SV=

Front 17

1) preload; 2) afterload; and 3) inotropy

Back 17

Stroke volume is determined by three qualities of the cardiac muscle:

Front 18

The tension required to stretch the cardiac muscle. Preload is the force generated within the ventricular muscle wall prior to ventricular contraction. This force is created by the inflowing blood which stretches the cardiac muscle fibers (sarcomeres)

Back 18

What is preload?

Front 19

1) end diastolic volume (sometimes equated with end diastolic pressure), and 2) compliance

Back 19

Two factors affect preload:

Front 20

1) venous blood pressure (which is influenced by venous blood volume and venous compliance); 2) ventricular compliance (ischemia, infarction and hypertrophy decrease compliance); 3) heart rate; 4) atrial contractility; 5) inflow resistance, and 6) outflow resistance.

Back 20

The factors that affect the end diastolic volume are:

Front 21

TRUE

Back 21

End diastolic volume alters preload- True or False

Front 22

Venous return

Back 22

Preload is equated with what other concept?

Front 23

SAME

Back 23

The heart pumps out the -less, same or more- volume of blood that it receives

Front 24

Frank Starling relationship

Back 24

The ability of the heart to maintain an equilibrium of the blood received=blood pumped is an intrinsic quality of the cardiac muscle that is described by

Front 25

Increases preload

Back 25

Increasing venous return does what to preload?

Front 26

Increases stroke volume

Back 26

Increasing preload does what to stroke volume?

Front 27

Reduces preload by dilating vessels and having more blood be stored in the veins than returned to the heart. Decreased amount of blood fills the rt ventricle, thus reduced preload.

Back 27

How do nitrates affect preload?

Front 28

Afterload is the force that the heart must pump against, i.e. the pressure in the aorta

Back 28

What is afterload?

Front 29

Wall stress

Back 29

A more complete definition of afterload defines it in terms of

Front 30

Wall stress = (systolic pressure X systolic radius) / (2*wall thickness)

Back 30

In terms of the left ventricle, afterload can be described by the formula:

Front 31

With an increase in ventricular pressure during systole from such events as aortic stenosis, hypertension, increased total peripheral resistance, and hypertrophic cardiomyopathy

Back 31

Wall stress increases when…

Front 32

Calcium channel blockers and ACE inhibitors produce vasodilation

Back 32

Name two examples that reduce the aortic pressures and afterload in patients with hypertension

Front 33

Increases

Back 33

Wall stress also -increases or decreases- with a widening of the radius of the ventricle during systole.

Front 34

Increased

Back 34

A dilated ventricle has -increased or decreased- wall stress

Front 35

Wall stress is inversely related to ventricular wall thickness.

Back 35

How is wall stress related to ventricular wall thickness?

Front 36

Initially, the ventricle responds to the higher pressure by becoming thicker (hypertrophy), thereby reducing wall stress and afterload

Back 36

How does the ventricle change over time in response to high afterload?

Front 37

Hypertrophy leads to subendocardial ischemia, myocardial atrophy, fibrosis, and eventually heart failure

Back 37

What is the problem with having a hypertrophied left ventricle?

Front 38

Higher levels of O2- higher risk of ischemia

Back 38

Does hypertrophy require -more or less- oxygen to function?

Front 39

1) the sympathetic nervous system, 2) the renin-angiotensin-aldosterone system (RAAS), and 3) atrial natriuretic peptide

Back 39

Heart failure produces a compensatory activation of neurohumoral responses such as

Front 40

Beneficial in some respects because it increases preload (increases stroke volume), heart rate and contractile force which increases cardiac output.

Back 40

How does activation of the sympathetic nervous system affect the cardiac cycle? - PROS

Front 41

Also detrimental because it increases afterload (via arterial vasoconstriction) which increases the workload of the heart. It is also detrimental because activation of the sympathetic ns causes the myocardium to be exposed to excess epinephrine and norepinephrine which may increase cell death (apoptosis), and desensitize B-adrenergic receptors (which decreases contractility).

Back 41

How does activation of the sympathetic nervous system affect the cardiac cycle? - CONS

Front 42

ventricular remodeling

Back 42

Growth of the cardiac muscle is also known as:

Front 43

1) Growth of parallel sarcomeres increases the thickness of the ventricular wall- a concentric hypertrophy, 2) Growth of sarcomeres in a serial fashion increases the length of the myocyte and creates an eccentric hypertrophy

Back 43

The growth of the cardiac myocytes occurs in two patterns:

Front 44

Pressure overload, as in aortic stenosis or essential hypertension

Back 44

What can cause concentric hypertophy?

Front 45

This occurs in response to a volume overload, which develops in aortic regurgitation or the later stages of failure

Back 45

What can cause eccentric hypertrophy?

Front 46

BNP is an especially important diagnostic serum marker for the presence of heart failure

Back 46

What is BNP used for?

Front 47

produces a larger and stiffer heart

Back 47

What does ventricular modeling produce?

Front 48

There is also a change in the manner in which the myocardium handles calcium. There is slowing of calcium delivery to the contractile proteins, and slowing of calcium reuptake by the sarcoplasmic reticulum. This reduces the contractile force of the myocardium.

Back 48

What happens with calcium during ventricular remodeling?

Front 49

Transudation of plasma fluid into the lungs, thus creating pulmonary edema and pleural effusion

Back 49

Elevated pulmonary pressures cause what time of pleural effusions?

Front 50

Symptoms include SOB, exertional dyspnea, orthopnea, and paroxysmal dyspnea (PND).

Back 50

Symptoms of CHF include:

Front 51

PND occurs because of decreased adrenergic effects at night, and increased venous return in a recumbent position

Back 51

How does PND (paroxysmal dyspnea) occur?

Front 52

Elevated systemic venous pressures create higher hydrostatic venous pressures that are particularly noticeable in the gravity dependent extremities

Back 52

What causes pitting edema of the ankles?

Front 53

Backwards

Back 53

Elevated ventricular pressures in heart failure typically result in 'forward' or 'backward' failure?

Front 54

end systolic volume

Back 54

What does afterload alter?

Front 55

Velocity of shortening of the cardiac muscle decreases…why? Since there is a finite time for the ejection of blood from the ventricle due to the electrical events that regulate systole, a slower and shorter contraction will eject less blood.

Back 55

What happens as the afterload increases?

Front 56

Forward failure

Back 56

The decrease in cardiac output typically causes a "backwards failure" or “forward failure”?

Front 57

Symptoms are as a result from hypoxia include fatigue (decreased oxygen supply to tissue), and confusion (decreased oxygen supply to the brain).

Back 57

Symptoms from forward failure include:

Front 58

FALSE- They are intrinsic disorders of the myocardium,i.e. they are not secondary to MI, HTN, or a valvular disorder

Back 58

Cardiomyopathies are secondary to MI, HTN, or a valvular disorder- True or False

Front 59

1) dilated cardiomyopathy; 2) restrictive cardiomyopathy; and 3) hypertrophic cardiomyopathy

Back 59

Name the 3 cardiomyopathies

Front 60

idiopathic hypertrophic subaortic stenosis. In hypertrophic cardiomyopathy, the heart is thick and hypertrophic with diastolic dysfunction.

Back 60

What is hypertrophic cardiomyopathy?

Front 61

In dilated cardiomyopathy the heart is flabby and hypocontracting with systolic dysfunction

Back 61

What happens to the heart with dilated cardiomyopathy?

Front 62

Angina is common in the hypertrophic type.

Back 62

Angina is common in which of the 3 cardiomyopathies?

Front 63

Inotropy is the intrinsic contractility of the cardiac muscle, independent of muscle fiber length

Back 63

What is inotrophy?

Front 64

It is dependent on the calcium ion concentration within the cardiac myocyte. (It was once thought that higher calcium levels created more actin-myosin cross-bridges, but now it is thought that they simply create a more efficient actin-myosin cross-bridge interaction by enhancing the sensitivity of troponin-C for calcium

Back 64

What is inotrophy dependent upon?

Front 65

Increased

Back 65

Inotropy is referred to as positive when it is

Front 66

A positive inotropic agent will increase the force of contraction of the cardiac muscle without increasing the stretch of the myocardium. It will aslo increase the ejection fraction of the heart via an increase in the stroke volume

Back 66

A positive inotropic agent will affect force of contraction how?

Front 67

The percentage of the end diastolic volume that is ejected into either the pulmonary trunk or aorta.

Back 67

Ejection fraction is defined as

Front 68

SV / EDV x 100%

Back 68

Ejection Fraction =

Front 69

Ventricular function

Back 69

Ejection fraction and stroke volume are measures of

Front 70

The catecholamines: epinephrine and norepinephrine. The cardiac glycosides such as digitalis and digoxin are positive inotropes used in the treatment of New York Heart Association Stage III and IV heart failure to enhance cardiac output. Beta-adrenergic agonists such as dopamine, dobutamine, epinephrine and isoproterenol are positive inotropes

Back 70

Examples of positive inotropes:

Front 71

The cardiac glycosides inhibit the sodium potassium pump which leads to an increase in intracellular calcium.

Back 71

How do cardiac glycosides work?

Front 72

Negative

Back 72

Heart failure is associated with- positive or negative- inotropy

Front 73

ischemia, arrhythmia, valvular disease, or cardiomyopathy.

Back 73

Heart failure often results from:

Front 74

1) blood flow; 2) blood pressure; and 3) total peripheral resistance

Back 74

When describing the functions of the vascular system the relevant concepts are:

Front 75

High to low

Back 75

In order for blood to flow there must be a pressure gradient from

Front 76

95-100mm Hg

Back 76

The high pressure is the mean arterial pressure which is between

Front 77

0-2mm Hg

Back 77

The low pressure is the central venous pressure that is found in the thoracic vena cavae, but most commonly measured in the right atrium between

Front 78

This pressure difference is due to the cardiac pump, and the differing resistances and compliances of the systemic arterial and venous systems.

Back 78

What accounts for the pressure difference between the high pressure (aorta) and low pressure (venous return)?

Front 79

The arterial system

Back 79

Which system is a low compliance, low resistance system, with a high resistance stenosis point?

Front 80

Venous system

Back 80

Which system is a high compliance, low resistance system?

Front 81

Compliance refers to the change in the volume of a vessel per change in a given pressure applied to the vessel

Back 81

What does compliance refer to?

Front 82

As a person ages, the percentage of elastin decreases and the aorta becomes less compliant

Back 82

Why do systolic pressures in the elderly tend to be higher?

Front 83

Isolated hypertension

Back 83

When the systolic pressure is elevated above 140 mm Hg, and the diastolic pressure is normal, this is referred to as

Front 84

TRUE

Back 84

An elevated systolic pressure in the elderly is the most significant predictor of heart disease- True or False?

Front 85

A change in pressure and the frictional resistance to flow.

Back 85

Blood flow is determined by

Front 86

The difference between the systolic and diastolic pressure.

Back 86

The pulse pressure is

Front 87

1) vessel compliance; and 2) stroke volume

Back 87

Pulse pressure is influenced by two factors:

Front 88

Inversely

Back 88

Total peripheral resistance is-directly or inversely- related to the radius of the blood vessel?

Front 89

Systemic vascular resistance (SVR) or total peripheral resistance (TPR)

Back 89

Resistance refers to the entire systemic circulation, so it is often referred to as

Front 90

Resistance is inversely related to the fourth power of the radius, and it is the radius of the blood vessel that has the largest effect on resistance

Back 90

How does resistance relate to the radius of the blood vessel?

Front 91

Increases

Back 91

In polycythemia, there is an excess of RBCs which- increases or decreases- the viscosity of the blood?

Front 92

increased viscosity of the blood actually hinders blood flow and the delivery of oxygen.

Back 92

How does polyceythemia affect blood flow and perfusion to tissues?

Front 93

Central venous pressure

Back 93

What determines the filling pressure of the right ventricle and ultimately, ventricular stroke volume?

Front 94

venous compliance and venous blood volume...More specifically, cardiac output, sympathetic tone, gravity, skeletal muscle activity, and respiratory activity all affect central venous pressure via venous return.

Back 94

The factors that regulate CVP (central venous pressure) are?

Front 95

a decrease in cardiac output (which increases right heart blood volume); an increase in total blood volume; activation of the renin-angiotensin aldosterone system (RAAS); sympathetic vascular tone (decreases venous compliance); arterial dilation (occurs with local metabolite effects during exercise); skeletal muscle contraction in the lower extremities; and inspiration (decreases thoracic pressures, and creates an abdominal to thoracic pressure gradient for venous return)

Back 95

Factors that increase central venous pressure include:

Front 96

A fast acting, short term nervous system baroreceptor reflex; and a slower acting, long term endocrine and renal system (renin angiotensin aldosterone system , RAAS, in conjunction with arginine vasopressin and atrial natriuretic peptide).

Back 96

There are two principal mechanisms to maintain homeostasis within the cardiovascular system:

Front 97

Changes in body position, for example from a supine to standing posture in order to maintain perfusion to the brain and heart

Back 97

The baroreceptor mechanism responds to

Front 98

RAAS

Back 98

Long term decreases in blood pressure due to prolonged standing, loss of blood volume via dehydration or hemorrhage, or cardiac failure trigger what response system?

Front 99

Juxtaglomerular cells (kidney) in response to an increase in sympathetic activity, decreased glomerular filtration, or a decrease in glomerular blood pressure as occurs with renal artery stenosis

Back 99

Renin is released from where?

Front 100

An increased synthesis of angiotensin II, aldosterone, and arginine vasopressin

Back 100

The end result of renin release is

Front 101

The net effect is to increase renal sodium and water retention which increase blood volume, and produce systemic vasoconstriction which increases resistance.

Back 101

What is the net affect of the RAAS system?

Front 102

A counter-regulatory hormone to RAAS, is atrial natriuretic peptide (ANP). It is released from the right atrium in response to an increased blood volume (sensed as an increased stretch of the right atrium). ANP’s effects are opposite to angiotensin II.

Back 102

What is ANP?

Front 103

It causes a natriuresis and diuresis, thus decreasing blood volume and blood pressur

Back 103

What is the function of ANP?

Front 104

Systemic vascular resistance, venous compliance, blood volume, and cardiac function.

Back 104

The neurohumoral mechanisms that regulate blood pressure act via changes in

Front 105

The mediastinum is the space located between the right and left pleural cavities, and posterior to the sternum.

Back 105

What is the mediastinum?

Front 106

The mediastinum is divided into a superior and inferior mediastinum. The inferior mediastinum is divided into an anterior, middle, and posterior mediastinum.

Back 106

what are the divisions of the mediastinum?

Front 107

Divides the superior from the inferior mediastinum, passes through the sternal angle and T4/T5 vertebral interspace and serves as a guide to the location of the arch of the aorta and the bifurcation of the trachea.

Back 107

What is the importance of the transthoracic plane?

Front 108

arch of the aorta, and the roots of its major branches (brachiocephalic trunk, left common carotid artery, left subclavian artery); brachiocephalic veins, superior vena cava, vagus and phrenic nerves, trachea, esophagus, thoracic duct, and thymus gland.

Back 108

The superior mediastinum contains the following structures:

Front 109

Begins the level of the sternal angle and passes up and back and to the left.

Back 109

The arch of the aorta begins where and travels where:

Front 110

The R and L vagus nerves pass posterior to the root of the lung, whereas the phrenic nerves pass anterior to the root of the lung.

Back 110

Where do the vagus and phrenic nerves travel in relation to the lungs?

Front 111

Pericardium, heart, ascending aorta, pulmonary trunk, superior vena cava, inferior vena cava, and bronchi at the root of the lungs.

Back 111

The middle mediastinum contains the following structures:

Front 112

Descending thoracic aorta; thoracic duct; azygos and hemiazygos veins; esophagus, thoracic sympathetic trunk, and posterior mediastinal lymph nodes.

Back 112

The posterior mediastinum contains the following structures:

Front 113

The arrangement of the structures is described as a “duck between 2 geese”, i.e. the thoracic duct lies between the azygos vein on the right, and the esophagus on the left.

Back 113

How are the structures of the posterior mediastinum decribed in accordance with anatomical position?

Front 114

The azygos vein drains the back, thoracoabdominal walls, and mediastinal viscera.

Back 114

What does the azygos vein drain?

Front 115

It serves as a collateral pathway for venous drainage from the inferior vena cava to the superior vena cava into which it drains after arching over the R root of the lung.

Back 115

What is the purpose of the azygos vein?

Front 116

The thoracic duct drains lymph from the left thorax, left upper extremity, left head and neck, and the entire abdominal and pelvic cavities, and lower extremities. (Simply stated, it receives lymph from the entire body below the diaphragm, and the left side of the body above the diaphragm.)

Back 116

What is the purpose of the thoracic duct?

Front 117

The bronchial arteries which supply the lower trachea and bronchial tree; the posterior intercostal arteries that the supply the intercostal muscles, vertebral column and spinal cord, deep back muscles, and the skin overlying the intercostal spaces; and the superior phrenic arteries which supply the diaphragm.

Back 117

The branches of the descending thoracic aorta include

Front 118

As it descends in the thoracic cavity, the descending thoracic aorta begins on the left and anterior to the trachea, and then moves midline and posteriorly to lie against the vertebral column

Back 118

How does the descending aorta travel in the thorax?

Front 119

Via the aortic hiatus at T 12

Back 119

The thoracic aorta passes through the diaphragm where?

Front 120

Via the esophageal hiatus at the T 10 vertebral level

Back 120

The esophagus passes through the diaphragm where?

Front 121

Once the thoracic aorta passes through the diaphragm into the abdominal cavity it is known as the abdominal aorta.

Back 121

What distinguishes the thoracic from abdominal aorta?

Front 122

Behind the sternum and 3rd –5th ribs on the left of the thorax. The heart is pyramidal in shape with an apex that points anteriorly to the left

Back 122

The heart is situated where in the thoracic cavity?

Front 123

Anterior or sternocostal surface formed by the right ventricle; inferior or diaphragmatic surface formed mostly by the left ventricle; and the left or pulmonary surface formed mostly by the left ventricle.

Back 123

What are the 3 surfaces of the heart?

Front 124

located in the left fifth intercostal space approximately 8 cm from the midsternal line

Back 124

Where is the apex located?

Front 125

The base of the heart is located in the third intercostal space

Back 125

Where is the base of the heart located?

Front 126

The right border of the heart is formed by the right atrium between the superior and inferior vena cavae

Back 126

What forms the right border of the heart?

Front 127

The inferior border of the heart is formed mostly by the right ventricle, and a bit of the left ventricle

Back 127

What forms the inferior border of the heart?

Front 128

The left border of the heart is formed by mostly the left ventricle.

Back 128

What forms the left border of the heart?

Front 129

The superior border of the heart is formed by the left and right atria.

Back 129

What forms the superior border of the heart?

Front 130

The primary difference is in the thickness of the muscular wall of the ventricles, with the left being 2-3 times thicker than the right.

Back 130

What is the primary difference (anatomically) between the left and right ventricles of the heart?

Front 131

Left ventricle (100mm Hg) vs right ventricle (15mm Hg)

Back 131

Which ventricle pumps against a higher pressure?

Front 132

The right atrium receives venous blood from the systemic circulation via the superior (SVC) and inferior vena cavae (IVC), and from the heart itself via the coronary sinus.

Back 132

How does the right atrium receive blood supply?

Front 133

Landmarks within the right atrium are the fossa ovalis, a depression in the interatrial wall that is a remnant of the fetal foramen ovale

Back 133

What is the fossa ovalis and where is it located?

Front 134

Right atrium; the sinus venarum which is a smooth thin walled posterior region which receives venous blood and therefore contains openings from the superior and inferior vena cavas, and the coronary sinus

Back 134

What is the sinus venarum and where is it located?

Front 135

The pectinate muscle is a muscular anterior region of both atria

Back 135

What is pectinate muscle and where is it located?

Front 136

Right atria, The sulcus terminalis is an external demarcation point between the sinus venarum and the pectinate muscle

Back 136

What is the sulcus terminalis and where is it located?

Front 137

Right atria, it is an internal demarcation point between these pectinate muscle and the sulcus terminalis

Back 137

What is the crista terminalis and where is it located?

Front 138

The coronary sinus is located between the openings of the IVC and the atrioventricular orifice.

Back 138

The coronary sinus is located where?

Front 139

The sinuatrial node (SA node) is located just deep to the epicardium at the junction of the SVC and the right atrium (at the superior end of the sulcus terminalis).

Back 139

Where is the SA node located?

Front 140

The atrioventricular node (AV node) is located in the posteroinferior region of the interatrial septum near the opening of the coronary sinus.

Back 140

Where is the AV node located?

Front 141

Primordial atrium during embryonic development; later in life functions to serve as extra capacity for blood

Back 141

What is an auricle?

Front 142

Tricuspid

Back 142

What is the rt AV valve?

Front 143

The 3 cusps are the anterior, posterior and septal.

Back 143

What are the cusps of the tricuspid valve?

Front 144

Chordae tendinae attach to the cusps and connect to papillary muscles on the ventricular wall.

Back 144

What attaches to the cusps of the AV valves?

Front 145

Before (slightly)

Back 145

The papillary muscle contracts slightly - before or after- ventricular contraction?

Front 146

The chordae tendinae prevent the valves from prolapsing and inverting during the elevated pressures of ventricular contraction, thus preventing regurgitation of blood into the right atrium.

Back 146

What is the function of the chordae tenindae?

Front 147

The septomarginal trabecula (also known as the “moderator band”) connects the interventricular septum to the anterior papillary muscle.

Back 147

What is the function of the septomarginal trabecula?

Front 148

At the end of the conus arteriosus. It is at the level of the left 3rd costal cartilage

Back 148

Where is the pulmonary semilunar valve located?

Front 149

The semilunar valves prevent regurgitation of blood into the ventricles

Back 149

What is the function of the semilunar valves?

Front 150

The membranous portion of the interventricular septum is the most common site for ventricular septal defects (VSD).

Back 150

Where is the most common site for VSD (ventricular septal defects)?

Front 151

VSD

Back 151

What is the most common congenital heart disease?

Front 152

Large VSDs cause a left to right shunt of blood resulting in pulmonary hypertension, and right ventricular hypertrophy.

Back 152

What does VSD cause?

Front 153

The lungs via the 4 pulmonary veins which are valveless.

Back 153

The left atrium receives oxygenated blood from

Front 154

It is called the mitral valve because the shape of the valve resembles a Catholic bishop’s miter (hat).

Back 154

Where did the name mitral valve come from?

Front 155

The mitral valve is located posterior to the sternum at the level of the 4th costal cartilage.

Back 155

Where is the mitral valve located?

Front 156

Mitral valve

Back 156

What is the most frequently diseased valve?

Front 157

The aortic semilunar valve is located posterior to the left side of the sternum at the level of the 3rd intercostal space.

Back 157

Where is the aortic valve located?

Front 158

The openings of the right and left coronary arteries are located within the right and left aortic sinuses which are dilations of the aortic wall just superior to the semilunar valves

Back 158

Where are the locations of the left and right coronary arteries?

Front 159

During diastole

Back 159

When is max flow to the coronary arteries?

Front 160

Ascending aorta

Back 160

The right and left coronary arteries are branches from

Front 161

In the coronary sulcus

Back 161

The rt coronary artery travels where:

Front 162

Right atrium, most of the right ventricle, the diaphragmatic surface of the left ventricle, and the posterior 1/3 of the interventricular septum. It also supplies the SA node 60% of the time, and the AV node 80% of the time. In 67% of people it also gives rise to the posterior interventricular artery

Back 162

What does the rt coronary artery supply:

Front 163

Whether the left or rt coronary artery supplies the posterior interventricular artery -aka PDA- (most of the time- 67%- it is the rt coronary so there is rt dominance)

Back 163

What determines 'heart dominance'?

Front 164

1) SA nodal branch near its origin; 2) AV nodal branch (posterior); 3) right marginal branch (along the right border of the heart) also known as the acute marginal segment; 4) posterior interventricular artery (posterior descending artery, PDA); and 5) posterolateral branches to the diaphragmatic surface of the heart beyond the PDA .

Back 164

Major branches of the right coronary artery are:

Front 165

The posterior 1/3 of the interventricular septum, and gives rise to the AV nodal branch

Back 165

What does the PDA supply?

Front 166

It divides into the anterior interventricular artery which is also known as the left anterior descending artery (LAD), and the circumflex artery.

Back 166

What are the divisions of the left coronary artery?

Front 167

The LAD travels in the anterior interventricular groove to the apex.

Back 167

Where does the left coronary artery travel?

Front 168

Both ventricles and the interventricular septum (via septal branches), and gives rise to the lateral diagonal branches to the anterior surface of the heart. The circumflex artery supplies the posterior surface of the left ventricle and gives rise to the obtuse marginal arteries (1st to 3rd) which supply the lateral wall of the left ventricle. Also, the left atrium, most of the left ventricle, part of the right ventricle, and 2/3 of the interventricular septum. It also supplies the SA node via the SA nodal artery (a branch of the circumflex artery) 40% of the time, and gives rise to the posterior interventricular artery 10% of the time.

Back 168

What does the left coronary artery supply?

Front 169

a thin anterior and thick posterior fascicle

Back 169

The left bundle branch further divides into

Front 170

Bundle branch block

Back 170

Blocks in the conduction within the right and left bundle branches are called

Front 171

The pericardium is the fibroserous covering of the heart. It consists of a fibrous pericardium (outermost layer) that is attached to the central tendon of the diaphragm and is fused with the outer layer (tunica adventitia) of the great vessels of the heart. The parietal serous layer of the pericardium is fused with the fibrous pericardium. The visceral serous layer of the pericardium is called the epicardium, and is the external layer of the heart wall.

Back 171

What is the pericardium?

Front 172

epicardium, myocardium (cardiac muscle), and endocardium (an epithelial layer that lines the chambers of the heart).

Back 172

The heart wall consists of 3 layers:

Front 173

The referred pain pattern associated with cardiac muscle ischemia and injury is based upon visceral sensory innervation via sympathetic neurons from T1-T5. Left sided arm, chest and neck pain is due to a common spinal cord origin for these sympathetic neurons, the medial cutaneous nerve of the arm (T1-T3), the dermatome of T1, and the lateral cutaneous branches of the 2nd and 3rd intercostals nerves.

Back 173

How does referred pain with cardiac events occur?

Front 174

umbilical veins to ductus venosus (bypass the liver from the left portal vein to the IVC), to the IVC. Within the heart the blood enters the right atrium, and the IVC valve directs much of the blood through the foramen ovale into the left atrium, thus bypassing the immature lungs. The blood is then ejected out of the left ventricle into the aorta and returns via the umbilical arteries to the placenta. Most of blood that enters the right ventricle and pulmonary artery (originating from the SVC and being relatively less oxygenated) also bypasses the lungs via the ductus arteriosus that connects the left pulmonary artery with the arch of the aorta.

Back 174

What is the pattern of fetal circulation?

Front 175

After birth, the alveoli in the lung open, and the pressure gradient in the pulmonary circulation switches from a high pressure to a low pressure system. The foramen ovale closes and becomes the fossa ovalis. The ductus arteriosum closes and becomes the ligamentum arteriosum.

Back 175

What happens to fetal circulation after birth?

Front 176

Functional closure of the ductus arteriosum is triggered by prostaglandins and occurs within a few days, whereas anatomic closure occurs in the 3rd postnatal month.

Back 176

What triggers closure of the ductus arteriosum?

Front 177

The ductus venosus closes within 2-3 months and becomes the ligamentum venosum within the liver

Back 177

When does the ductus venous close after birth?

Front 178

The lumen of the umbilical veins remain patent even in an adult, and are called the ligamentum teres within the falciform ligament of the abdominal cavity. The umbilical arteries become the medial umbilical ligaments.

Back 178

What happens with the lumen of the umbilical veins after birth?

Front 179

Dilation

Back 179

What affect does lactate, increased CO2 and low pH have on blood vessel diameter?

Front 180

Aspiring produces irreversible inhibition of platelet aggregation, NSAIDS produce reversible

Back 180

How does aspirinand NSAIDS affect prostaglandins?

Front 181

In the heart and lungs- produces vasoconstriction, in skeletal muscle- produces vasodilation

Back 181

How does hypoxia affect blood vessel diameter?

Front 182

16 fold increase

Back 182

Decreasing the radius by 1/2 has what affect on resistance?

Front 183

Erythropoeitin

Back 183

In COPD, the kidneys secrete what hormone to stimulate RBC production in response to hypoxia?

Front 184

Afterload has increased, then venous return decreases ultimately too

Back 184

If you increase total peripheral resistance, why does CO decrease?

Front 185

Diastolic

Back 185

If you are under the age of 50, what is the better indicator for CAD- diastolic or systolic?

Front 186

All 3

Back 186

B/w the ages of 50-60, what is the best indicator(s) for CAD? - Diastolic, systolic or pulse pressure

Front 187

Systolic

Back 187

If older than age 60, what is the best indicatory for CAD? Diastolic or systolic?

Front 188

Framingham

Back 188

What was the important study done to determine risk factors for CAD?

Front 189

Higher velocity in the aorta than all capillaries together, the narrower a more single vessel is, the more rapid the flow

Back 189

How does velocity vary from the aorta to the capillaries?

Front 190

Increased velocity (more narrow vessels), decreased viscosity (anemia). Decreased Nitric oxide is produced

Back 190

What causes turbulent blood flow?

Front 191

Albumin (proteins)

Back 191

What creates osmotic pressure?

Front 192

Increases, you've lost fluid,

Back 192

Osmotic pressure -increases or decreases- at the venule end?

Front 193

B1 receptors increase HR, conduction velocity and contractility

Back 193

What are the B1 sympathetic affects on the heart and blood vessels?

Front 194

Vascular smooth muscle (skin, renal and splanchic) constriction, also constriction of the skeletal vascular smooth muscle

Back 194

What are the alpha 1 receptors sympathetic affects on the heart and blood vessels?

Front 195

Dilation of the vascular smooth muscle (skeletal muscle)- i.e. think pulmonary. Sympathetic affects are to dilate the airways

Back 195

What are the B2 receptor sympathetic affects on the heart and blood vessels?

Front 196

Decrease HR, velocity, contractility, dilate vascular smooth muslce (all)

Back 196

What are the muscarinic parasympathetic affects on the heart and blood vessels?

Front 197

Causes kidney to increase reabsorption of water, opens pores in which water flows out of lumen back into the blood. Also with severe blood volume loss, can create vasoconstriction (not under normal circumstances)- why it is also called AVP, VASOconstriction

Back 197

What does ADH do?

Front 198

Increase of bradykinin stimulates the cough

Back 198

Why does ACE cause cough?

Front 199

Na reabsorbtion, get rid of potassium. Aldosterone binds everyday to stimulate the reabsorption of sodium and excretion of potassium…Evoluationarily- did NOT grow up in a sodium rich environment but rather a potassium rich environment (based off veggies and fish/meats). Now everything has TONS of sodium. This was done to avoid hyperkalemia (BAD).

Back 199

What is the kidney’s normal system?

Front 200

Distal tubule

Back 200

Where do thiazide diuretics work?

Front 201

Thick ascending limb at the loop of henle

Back 201

Where do loop diuretics work?

Front 202

Collecting tubule

Back 202

Where do K+ sparing diuretics work?

Front 203

Deficiency of vitamin B1 (thiamine)- typical with alcoholics

Back 203

Which patients are at greatest risk for Beriberi?

Front 204

Isovolumic releaxation

Back 204

Diastole begins with

Front 205

Rapid filling and diastasis - both are PASSIVE- followed by atrial contraction- ACTIVE filling

Back 205

Filling of the ventricles consists of 2 stages-

Front 206

AGING

Back 206

What tends to cause aortic stenosis?

Front 207

Blood is less viscous and flows more turbulently

Back 207

What happens in blood flow for patients who have anemia?

Front 208

Changes in pressure- not the valves/muscles themselves

Back 208

What causes the valves to open?