Cardiovascular

Question 1

Lidocaine class and MOA

Answer 1

1b: Na channel blocker (inactive state - depolarized), shortens action potential

Question 2

Procainamide class and MOA

Answer 2

1a: fast Na channel blocker, slows phase 0, prolongs action potential

Question 3

Atenolol class and MOA

Answer 3

Class II: beta1 blocker

Question 4

Propranolol class and MOA

Answer 4

Class II: beta 1 & 2 blocker

Question 5

Esmolol class and MOA

Answer 5

Class II: beta 1 blocker

Question 6

Sotalol class and MOA

Answer 6

Class III: potassium blocker

Also beta blocker

Question 7

Amiodarone class and MOA

Answer 7

Class III: potassium blocker

Also I, II, and IV

Question 8

What is the most common primary cardiac tumor in dogs?

Answer 8

hemangiosarcoma (69%)

Question 9

Aortic body tumors are most common in which breeds?

Answer 9

Boxer, Bostons, English bulldogs, and also German shepherd dogs

Question 10

Capillary endothelium can be damaged by (6)?

Answer 10

1. Endotoxin
2. cytokines (TNFa, IL-6)
3. Arachidonic acid metabolites
4. complement components (C3a, C5a)
5. Vasoactive peptides (bradykinin, histamine)
6. chemokines (macrophage inflammatory protein 1 alpha)

Question 11

What is the Gibbs-Donnan effect?

Answer 11

Describes the behavior of charged particles in solution separated by semipermeable membrane, which does not allow some particles to pass. For example, albumin is not permeable and its negative charge will attract cations like sodium.

Question 12

What contributes the most to COP? What else contributes?

Answer 12

Albumin 65-80% of COP. Also: globulins, fibrinogen, hemoglobin, RBCs

Question 13

Describe the activation of RAAS in detail.

Answer 13

Decreased renal blood flow & decreased Na deliver to distal portion of nephron–> renin release from macula densa–> angiotensinogen to angiotensin I–> angiotensin II (via ACE) in pulmonary vasculature

Question 14

Effects of angiotensin II via RAAS system?

Answer 14

Increased thirst, vasoconstriction, cardiac and vascular remodeling and fibrosis, renal sodium & water retention, myocardial apoptosis, production of aldosterone

Question 15

Effects of chronic sympathetic nervous system activation?

Answer 15

Adrenergic Rc downregulation, persistent tachycardia, increased myocardial oxygen demand, myocyte necrosis

Question 16

Two main hormones that induce natriuresis, diuresis, and vasodilation?

Answer 16

Atrial natriuretic peptide (ANP)
B-type natriuretic peptide (BNP)
Both are increased in in dogs and cats with heart disease, roughly in proportion to disease severity

Question 17

What is the function of ANP & BNP ?

Answer 17

To serve as a counter-regulatory system to RAAS and SNS, but ANP & BNP are overwhelmed in later stages of heart disease

Question 18

What is the function of endothelin I?

Answer 18

Potent vasoconstriction produced by vascular endothelial cells in response to sheer stress, angiotensin II, and other various cytokines; alters normal calcium cycling within muscle cells and is directly toxic to myocardiocytes

Question 19

Describe normal calcium ion handling

Answer 19

During systole calcium ions enter the myocardial cell; this triggers release of additional calcium ions from the main storage area of calcium (sarcoplasmic reticulum). Calcium stored in the SR flows through the ryanodine channel and binds to troponin C. Binding to troponin C causes SR contraction, then release of calcium from troponin C initiates relaxation cycle. Ca++ ions are then moved back into the SR

Question 20

What happens to cells that have abnormal intracellular Ca distribution?

Answer 20

Electrical abnormalities, apoptosis, necrosis

Question 21

What does the Frank-Starling mechanism state?

Answer 21

That an increase in the initial volume or pressure within a ventricle increases the strength of subsequent ventricular contractions. Up to a physiologic limit, preload and contractility are positively associated

Question 22

What happens to the Frank-Starling curve during increased adrenergic drive?

Answer 22

Up and leftward; causes further improvement in cardiac performance

Question 23

What happens to the Frank-Starling curve during disease?

Answer 23

Shifted down and to the right; contraction is less vigorous despite increased preload and fluid retention

Question 24

What happens to the Frank-Starling curve with administration of diuretics?

Answer 24

Shifted to the left

Question 25

What happens to the Frank-Starling curve with administration of arterial vasodilators?

Answer 25

Shifted upwards, decrease afterload, similar to positive inotropes

Question 26

What happens to the Frank-Starling curve with administration of venous vasodilators?

Answer 26

Shifted leftward, decreased preload, similar to diuretics

Question 27

What happens to the Frank-Starling curve with administration of positive inotropes?

Answer 27

Shifted upwards

Question 28

What happens to the Frank-Starling curve with administration of mixed vasodilators?

Answer 28

Upward & leftward adjustment

Question 29

Name and describe the 4 classes of heart failure

Answer 29

A- Healthy breeds at risk for developing heart disease (Maine Coons, dobermans >4 yrs)
B- Animals who are asymptomatic but have a murmur or arrhythmia, etc
B1= no signs of heart disease on echo or imaging
B2= signs of heart disease on echo or imaging
C- Animals with cardiac remodeling and current or historical signs of heart failure
D- Fulminant, severe CHF even at rest

Question 30

Name the pulmonary and systemic pressures at which congestion may occur?

Answer 30

Pulmonary- >25 mm Hg

Systemic- >20 mm Hg

Question 31

List management strategies in dogs with DCM and acute CHF

Answer 31

1. Minimize stress/ensure rest
2. Perform thoracocentesis PRN for pleural effusion
3. Provide O2 support
4. Administer furosemide 2-6 mg/kg IV then boluses
   Administer 2% topical nitroglycerin 1-2 inches q 8
5. Treat life threatening arrhythmias
6. Sodium nitroprusside 2 mcg/kg/min until mean ABP 70 mm Hg
7. Dobutamine 2.5-5 mcg/kg/min
8. Other positive inotropes PRN

Question 32

The PROTECT study found what regarding dobermans and DCM?

Answer 32

Administering pimobendan to dobermans with pre clinical DCM prolonged the time to onset of clinical signs and improved survival

Question 33

DCM in some cocker spaniels is associated with what?

Answer 33

Low plasma taurine levels; supplementation with taurine and L-carnitine appears to improve myocardial function

Question 34

List secondary canine myocardial disease categories and examples

Answer 34

1. Drugs/toxins (doxorubicin, catecholamines)
2. Canine X linked muscular dystrophy
3. Infiltrative (glycogen storage diseases)
4. Neoplasia
5. Ischemic
6. Metabolic (acromegaly, DM, hyperthyroidism, hypertension)
7. Nutritional (Taurine, L-carnitine, vitamin E)
8. Inflammatory (myocarditis)
9. Infectious (parvo, distemper, Lyme)

Question 35

It is recommended to treat when you see ______ number of VPCs per 24 hrs in:

• Dobermans
• Boxers

Answer 35

Dobermans: 50 VPC/24 hrs
Boxers: 100 VPC/24 hrs
In both: treat if couplets, triplets, R on T, clinical, etc

Question 36

Treatment for AV myopathy (atrial standstill)?

Answer 36

Pacemaker- this improves short term outcome but most dogs will die of progressive myocardial failure

Question 37

Poor px signs in dobermans with DCM?

Answer 37

Atrial fibrillation, bilateral CHF

Question 38

Name 6 causes of secondary hypertension

Answer 38

Kidney disease
Diabetes mellitus
Hyperadrenocorticism
Hyperthyroidism
Hepatic disease
Pheochromocytoma
Hyperaldosteronism
Polycythemia
Chronic anemia

Question 39

What is the mechanism of hypertension in patients with hyperadrenocorticism?

Answer 39

Glucocorticoids induce hepatic production of angiotensinogen, which results in an exaggerated response of the renin-angiotensin-aldosterone system

Question 40

What is the mechanism of hypertension in patients with hyperthyroidism?

Answer 40

Secondary to the increased cardiac output caused by the effect of thyroid hormone on cardiac muscle

Question 41

What are the four proposed mechanisms of hypertension in human patients with diabetes mellitus?

Answer 41

In type I, its thought to develop due to effects of diabetes on renal function

In type II, there are three mechanisms:

1. Hyperinsulinemia secondary to insulin resistance causes sodium and water retention and increased sympathetic activity.
2. Hypertrophy of vascular smooth muscle secondary to the mitogenic effects of insulin.
3. Elevations in insulin levels lead to increased levels of intracellular calcium which results in hyper-responsive vascular smooth muscle contraction and increased peripheral vascular resistance.

Question 42

What is the mechanism of hypertension in patients with anemia?

Answer 42

Anemia leads to chronically dilated capillary beds. With resolution of the anemia, overcompensation of capillary constriction occurs, which results in an increase in peripheral vascular resistance.

Question 43

What is hypertensive urgency and how should it be treated?

Answer 43

Marked elevation in blood pressure but the animal does not demonstrate clinical signs directly attributable to the elevation.

Blood pressure should be lowered in a gradual and controlled fashion by determining the underlying cause and starting treatment with an anti-hypertensive medication to lower the systolic blood pressure to 170 mm Hg or less, mean arterial pressure to 140 mm Hg or less, and/or diastolic pressure to 100 mm Hg or less.

Question 44

What is hypertensive emergency and how should it be treated?

Answer 44

When the patient has a marked elevation in blood pressure as well as clinical signs directly attributable to hypertension.

Initial goal is to reduce mean arterial blood pressure by no more than 25% (within minutes to 1 hour), then if the patient is stable, to reduce blood pressure to 160/100 within the next 2 to 6 hours

Medications that may be used include amlodipine, sodium nitroprusside, hydralazine, enalaprilat, or nicardipine.

Question 45

List possible sequela to infective endocarditis

Answer 45

CHF, IMPA, IMGN, thromboembolism, severe cardiac arrhythmias

Question 46

With IE, what is exposed by damaged endothelium which triggers coagulation?

Answer 46

Extra cellular matrix proteins, thromboplastin and tissue factor

Question 47

In IE, ___________ mediates the primary attachment of bacteria to the disrupted endothelium

Answer 47

Fibrinogen binding

Question 48

In IE what triggers endothelial cell internalization and local proinflammatory and procoagulant responses?

Answer 48

Fibronectin binding

Question 49

In IE inflammation induces endothelial cell expression of ________ that bind bacteria and fibronectin to the extra cellular matrix

Answer 49

Integrins

Question 50

In IE, how does fibrinogen promote the disease process?

Answer 50

Fibrinogen binding mediates the primary attachment of bacteria to the disrupted endothelium

Question 51

In IE what is fibronectins role in perpetuating the disease process?

Answer 51

Fibronectin binding triggers endothelial cell internalization and local proinflammatory and procoagulant responses.

Question 52

What are MSCRAMMS?

Answer 52

Microbial surface components recognizing adhesive matrix molecules- special receptors on bacteria which allow them to adhere to damaged valves

Question 53

How is acute heart failure with IE different from normal CHF?

Answer 53

Due to acute nature, typically no left sided heart enlargement, fulminant pulmonary edema with alveolar flooding

Question 54

What are 3 risk factors for thromboembolism in IE?

Answer 54

Mitral valve involvement, large mobile vegetative lesions more than 1-1.5 cm or increasing lesion size during antibiotic therapy

Question 55

With CNS thromboembolism in IE what is the most common location and what are the results?

Answer 55

Middle cerebral artery, brain ischemia and possible ischemic necrosis (if persistent)

Question 56

What is the pathognomonic lesion of IE on echo?

Answer 56

Hyperechoic, oscillating, irregular shaped mass adherent to, yet distinct from the endothelial cardiac surface

Question 57

What are the major Duke modified criteria to diagnose IE in dogs?

Answer 57

1. Positive echo - Vegetative lesion, erosive lesion, abscess2. New valvular insufficiency3. >mild AI in absence of SAS4. Positive blood cultures: >2. Or > 3 with common skin contaminant.

Question 58

Duke minor criteria to diagnose IE in dogs

Answer 58

1. Fever 2. Medium to large breed > 15 kgs3. SAS4. Thromboembolic disease5. IMPA or IMGN6. Positive blood culture not meeting major criteria 7. Bartonella serology >1:1024

Question 59

What constitutes a definitive diagnosis of IE?

Answer 59

Pathology of the valve, 2 major criteria or 1 major and 2 minor criteria

Question 60

What constitutes a possible diagnosis of IE?

Answer 60

1 major and 1 minor criteria or 3 minor criteria

Question 61

What constitutes an unlikely diagnosis of IE?

Answer 61

Other diagnosis made, signs resolved in <3 days with tx

Question 62

What are the most likely bacteria to cause IE?

Answer 62

Staphylococcus (aureus, intermedius, coagulase positive and negative), Strep (canis, bovis, and beta hemolytic) and e.coli

Question 63

List 7 less likely but possible causes of IE

Answer 63

Enterococcus, enterobacter, erysipelothrix rhusiopathiae, pasteurella, proteus, pseudomonas, corynebacterium

Question 64

Where on the action potential does lidocaine work?

Answer 64

Depresses phase 0 in abnormal tissue (no effect in normal tissue), little effect on sinus rate, AV conduction, or action potential duration and refractoriness

Question 65

List possible sequela to infective endocarditis

Answer 65

CHF, IMPA, IMGN, thromboembolism, severe cardiac arrhythmias

Question 66

With IE, what is exposed by damaged endothelium which triggers coagulation?

Answer 66

Extra cellular matrix proteins, thromboplastin and tissue factor

Question 67

In IE, ___________ mediates the primary attachment of bacteria to the disrupted endothelium

Answer 67

Fibrinogen binding

Question 68

In IE what triggers endothelial cell internalization and local proinflammatory and procoagulant responses?

Answer 68

Fibronectin binding

Question 69

In IE inflammation induces endothelial cell expression of ________ that bind bacteria and fibronectin to the extra cellular matrix

Answer 69

Integrins

Question 70

In IE, how does fibrinogen promote the disease process?

Answer 70

Fibrinogen binding mediates the primary attachment of bacteria to the disrupted endothelium

Question 71

In IE what is fibronectins role in perpetuating the disease process?

Answer 71

Fibronectin binding triggers endothelial cell internalization and local proinflammatory and procoagulant responses.

Question 72

What are MSCRAMMS?

Answer 72

Microbial surface components recognizing adhesive matrix molecules- special receptors on bacteria which allow them to adhere to damaged valves

Question 73

How is acute heart failure with IE different from normal CHF?

Answer 73

Due to acute nature, typically no left sided heart enlargement, fulminant pulmonary edema with alveolar flooding

Question 74

What are 3 risk factors for thromboembolism in IE?

Answer 74

Mitral valve involvement, large mobile vegetative lesions more than 1-1.5 cm or increasing lesion size during antibiotic therapy

Question 75

With CNS thromboembolism in IE what is the most common location and what are the results?

Answer 75

Middle cerebral artery, brain ischemia and possible ischemic necrosis (if persistent)

Question 76

What is the pathognomonic lesion of IE on echo?

Answer 76

Hyperechoic, oscillating, irregular shaped mass adherent to, yet distinct from the endothelial cardiac surface

Question 77

What are the major Duke modified criteria to diagnose IE in dogs?

Answer 77

1. Positive echo - Vegetative lesion, erosive lesion, abscess2. New valvular insufficiency3. >mild AI in absence of SAS4. Positive blood cultures: >2. Or > 3 with common skin contaminant.

Question 78

Duke minor criteria to diagnose IE in dogs

Answer 78

1. Fever 2. Medium to large breed > 15 kgs3. SAS4. Thromboembolic disease5. IMPA or IMGN6. Positive blood culture not meeting major criteria 7. Bartonella serology >1:1024

Question 79

What constitutes a definitive diagnosis of IE?

Answer 79

Pathology of the valve, 2 major criteria or 1 major and 2 minor criteria

Question 80

What constitutes a possible diagnosis of IE?

Answer 80

1 major and 1 minor criteria or 3 minor criteria

Question 81

What constitutes an unlikely diagnosis of IE?

Answer 81

Other diagnosis made, resolved in

Question 82

What are the most likely bacteria to cause IE?

Answer 82

Staphylococcus (aureus, intermedius, coagulase positive and negative), Strep (canis, bovis, and beta hemolytic) and e.coli

Question 83

List 7 less likely but possible causes of IE

Answer 83

Enterococcus, enterobacter, erysipelothrix rhusiopathiae, pasteurella, proteus, pseudomonas, corynebacterium

Question 84

Where on the action potential does lidocaine work?

Answer 84

Depresses phase 0 in abnormal tissue (no effect in normal tissue), little effect on sinus rate, AV conduction, or action potential duration and refractoriness

Question 85

What does a positive deflection in an EKG signify?

Answer 85

the sum of the heart’s electrical impulses was moving toward the positive electrode at that time

Question 86

What does a negative deflection in the EKG signify?

Answer 86

the sum of the heart’s impulses was moving away from the positive electrode

Question 87

T/F: impulses traveling perpendicular to the heart can cause a deflection in the EKG?

Answer 87

false

Question 88

What is excitation-contraction coupling?

Answer 88

Ca influx during phase 2 of cardiac cell activation triggers the intracellular release of more Ca from the sarcoplasmic reticulum. The increase in free intracellular Ca leads to contraction.

Question 89

What are the functions of troponin I and C?

Answer 89

I: inhibits cross-bridge formation during diastole when intracellular Ca is low. When Ca is available it activates troponin C

C: Binds to troponin I to reduce its inhibitory effect which allows interaction between adjacent actin and myosin filaments

Question 90

Describe the Frank-Starling relationship

Answer 90

As end-diastolic volume (preload) increases, the volume with each contraction increases

Diastolic stretch of the sarcomeres increases the myofilament Ca affinity

Question 91

True or false: Contractility depends on the amount of free intracellular Ca available

Answer 91

True

It also depends to some degree on ATP availability

Question 92

Describe what happens with calcium in the myocyte at the end of systole

Answer 92

Ca influx stops, the sarcoplasmic reticulum actively takes up Ca. Some Ca is transported out of the cell via a membrane Na/Ca exchange and Ca pump mechanisms

Question 93

What is the normal canine resting cardiac index (CO/body size)?

Answer 93

3.1-4.7 liters/minute/m^2

Question 94

What percentage of the end-diastolic volume is ejected with each contraction of the heart?

Answer 94

65%

Question 95

What determines the stroke volume?

Answer 95

SV is directly related to the level of myocardial contractility and preload, and inversely related to afterload

Question 96

Chronic increases in ventricular volume stimulate what changes in the sarcomeres?

Answer 96

It stimulates the formation of new sarcomeres in series, lengthening the myofibers and creating a larger ventricle of normal wall thickness aka eccentric hypertrophy

Question 97

Chronic increases in systolic pressure stimulate what changes in the sarcomeres?

Answer 97

It stimulates formation of new sarcomeres in parallel, increasing myofiber diameter and ventricular wall thickness aka concentric hypertrophy

Question 98

What is responsible for the generation of the S1 heart sound?

Answer 98

Vibration associated with closing and tensing of the AV valves (when ventricular pressure exceeds atrial pressure)

Question 99

What is responsible for the generation of the S2 heart sound?

Answer 99

Vibrations associated with the closing of the semilunar valve (ventricular pressure drops below that in the associated great artery)

Question 100

What is responsible for the generation of the S3 heart sound?

Answer 100

Accentuated low-frequency vibrations associated with the end of early diastolic filling. It is most likely to be heard in animals with LV dilation and failure.

It is sometimes called the ventricular gallop sound.

Question 101

What is responsible for the generation of the S4 heart sound?

Answer 101

It is associated with blood and tissue oscillations at the time of atrial contraction. It may be heard with an abnormally stiff or hypertrophied LV.

It is sometimes called the atrial gallop sound.

Question 102

What is diastasis and what determines the duration of diastasis?

Answer 102

It is the slow filling phase of the ventricles (after the rapid filling phase that happens with the opening of the AV valves).

Duration depends on heart rate.

Question 103

Describe the effects of sympathetic stimulation on beta receptors

Answer 103

Contractility is increased as more Ca enters the myocytes and more Ca is released from the sarcoplasmic reticulum. Relaxation is also accelerated via reduced troponin affinity for Ca as well as accelerated SR reuptake of Ca.

Sympathetic stimulation of the Sa node hyperpolarizes the cells and activates and inward flux of Na and K which causes faster spontaneous diastolic depolarization

Question 104

Describe the layers of the heart from outside to inside

Answer 104

Parietal pericardium–>visceral pericardium (epicardium)–> myocardium–> endocardium

Question 105

T/F: the RV wall thickness is approximately 1/4 of the thickness of the LV wall

Answer 105

false- RV is 1/3 LV thickness

Question 106

What helps facilitate conduction through the RA and LA to the AV node once the SA node has fired?

Answer 106

specialized fibers called internodal pathways

Question 107

What is it about the AV node that makes it have a slower conduction?

Answer 107

AV nodal cells are small and branching; this allows time for atrial contraction before ventricular activation

Question 108

Where do electrical impulses go after the AV node?

Answer 108

bundle of His

Question 109

T/F: conduction is fast through the His bundle and into the RBB & LBB?

Answer 109

true

Question 110

Which part of the heart is activated by the RBB?

Answer 110

right ventricular free wall

Question 111

How many branches of the LBB? What does each one activate?

Answer 111

3 branches:

1. septal fascicle
2. posterior fascicle- conducts to ventrocaudal aspect of LV wall
3. anterior fascicle- craniolateral LV wall

Question 112

Where do purkinje fibers transmit their electrical pulses?

Answer 112

ventricular myocardium

Question 113

T/F: the duration of cardiac action potential is longer than that of noncardiac tissues?

Answer 113

true

Question 114

Describe the 2 types of cardiac action potentials

Answer 114

1. Fast response- atrial and ventricular muscle cells, purkinje fibers
2. Slow response- SA and AV nodal cells

Question 115

What is the normal resting membrane potential for myocardial cells?

Answer 115

-90 mV… this means that inside the cell is negative compared with the outside of the cell

Question 116

For each major electrolyte (Na, Ca, K) state whether the concentration is higher outside the cell or inside the cell

Answer 116

Na- higher outside
Ca- higher outside
K- higher inside

Question 117

Which electrolyte is the most permeable into the resting sarcolemma?

Answer 117

K+- it tends to diffuse outward along its concentration gradient thru K specific chanels

Question 118

What is responsible for maintaining the normal resting membrane potential?

Answer 118

the electrogenic Na, K-ATPase pump, which moves 3 Na ions out for every 2 K ions in

Question 119

Describe the cardiac action potential

Answer 119

Phase 0=influx of Na
Phase 1= brief partial repolarization
Phase 2=Ca influx
Phase 3=K efflux

Question 120

What is the effective refractory period?

Answer 120

period of time from phase 0 until membrane potential reaches -50 mV during phase 3; a time when the cell cannot be reexcited

Question 121

What is the relative refractory period?

Answer 121

a stronger than normal stimulus may elicit another action potential but velocity may be slowed b/c partial Na channel inactivation

Question 122

Describe the effects of vagal (parasympathetic) stimulation on the heart

Answer 122

Vagal innervation to the heart is mainly localized to the SA and AV nodes. Vagal stimulation slows the SA node rate by reducing the slope of diastolic depolarization via and acetycholine-activated outward K current.

Question 123

What is responsible for the variation in heart rate seen with a sinus arrhythmia?

Answer 123

It is related to reflexly-mediated fluctuations in vagal tone associated with the respiratory cycle.

Increase in HR occurs with inspiration, and decreases with expiration.

Question 124

What is the major source of energy for the heart?

Answer 124

Fatty acids

Question 125

What is the equation for coronary blood flow?

Answer 125

(Aortic pressure - coronary sinus pressure) / coronary vascular resistance

Question 126

What direction does coronary flow move within the heart?

Answer 126

From epicardium to endocardium (because the majority of major coronary arteries lie on the surface of the heart).

Question 127

During what phase of the cardiac cycle does most coronary flow occur?

Answer 127

During diastole (lower intraventricular pressure allows flow)

Question 128

What are the consequence of inadequate coronary blood flow?

Answer 128

It promotes myocardial ischemia which leads to replacement fibrosis. This contributes to diastolic dysfunction (inability to relax the ventricles) and can be seen in diseases such as HCM and SAS.

Question 129

What determines blood flow through any part of the circulation?

Answer 129

Blood flow is directly dependent on the driving pressure and inversely dependent on vascular resistance.

Q = Change in P / R

Q is blood flow, P is pressure, R is resistance

Question 130

The pressures at which location determine the change in pressure for both systemic and pulmonary circulation?

Answer 130

Systemic change in pressure is calculated from the difference between aortic pressure and right atrial pressure. This averaged over time is equal to Mean Arterial Pressure (MAP).

Pulmonary change in pressure is calculated from the difference between pulmonary arterial pressure and left atrial pressure.

Question 131

TRUE OR FALSE:

Resistance in the systemic circulation is generally less than in the pulmonary circulation.

Answer 131

FALSE
Resistance in the pulmonary circulation is generally less than in the systemic circulation. This allows perfusion of the lungs at relatively low pressures.

Question 132

According to Poiseuille’s law, what determines resistance?

Answer 132

Resistance is inversely proportional to vessel radius to the fourth power, and directly proportional to blood viscosity.

Question 133

What does laminar flow mean?

Answer 133

Blood flowing in smooth vessels forms layers (streamlines) that slip over each other. Flow is faster towards the center of the vessel, while the outer layers drag against the vessel wall.

Question 134

What factors promote turbulent flow?

Answer 134

High flow velocity (ventricular outflow obstruction)
Low blood viscosity (anemia)
Wide vessel diameter
Sudden change in vessel diameter or direction
Pulsatile flow

Question 135

What is Reynold’s number?

Answer 135

It is a measure of the tendency for turbulence to occur. Numbers over a critical level (~2,000) are likely to be associated with an audible murmur.

Question 136

Name several causes of an under circulation pattern in the lungs

Answer 136

Severe dehydration
Hypovolemia
Obstruction to RV inflow
Right sided CHF
Tetralogy of Fallot

Question 137

Name several causes of an over circulation pattern in the lungs

Answer 137

Left-to-right cardiac shunts
Overhydration
Other hyper dynamic states

Question 138

What effect does enlargement of either ventricle have on the orientation of the caudal vena cava radiographically?

Answer 138

It pushes the caudal venal cava - heart junction dorsally, which results in a more horizontal caudal vena cava orientation

Question 139

True or false: The caudal vena cava should have a similar diameter to that of the descending thoracic aorta

Answer 139

True

The size of the vena cava does change with respiration however

Question 140

What conditions can result in a widening of the caudal vena cava?

Answer 140

RV failure
Cardiac tamponade
Pericardial constriction
Other obstruction to right heart inflow

Question 141

What conditions can result in a narrowing of the caudal vena cava?

Answer 141

Hypovolemia
Poor venous return
Pulmonary overinflation

Question 142

Name several conditions that can result in an alveolar lung pattern

Answer 142

Hemorrhage
Neoplasia
Edema
Pneumonia
Lung lobe torsion

Question 143

What findings may be seen radiographically in conjunction with cardiogenic pleural effusion?

Answer 143

Wide caudal vena cava
Cardiomegaly
Hepatomegaly
Ascites

Question 144

What is the most sensitive radiographic view for identifying pneumothorax?

Answer 144

The lateral view

The lung border appears separated from the diaphragm and dorsal thoracic wall; the heart shifts toward the dependent lung and looks elevated off the sternum

Question 145

On which view (DV or VD) can you most easily identify a pneumothorax?

Answer 145

Pneumothorax is best seen on the DV as the air rises to the widest (most dorsal) part of the thorax

Question 146

True or false: The cardiac silhouette is best visualized on the DV view in a patient with pleural effusion

Answer 146

False

Its better visualized on the VD view as the fluid collects at the dorsal aspect of the thorax. This view may cause more respiratory compromise however.

Question 147

What determines the magnitude of a deflection in an ECG?

Answer 147

The angle between the lead axis and the direction of the myocardial activation wave. As the angle between the lead and the activation wave increases (approaches 90 degrees), the ECG deflection in that lead becomes smaller.

Question 148

If the deflection in the ECG is positive, in what direction is the myocardial activation wave traveling?

Answer 148

Towards the positive pole of the lead

Question 149

What does the P wave represent?

Answer 149

Atrial muscle activation

Question 150

What does the PR interval represent?

Answer 150

Duration of atrial muscle activation, conduction over the AV node, bundle of His, and Purkinje fibers

Question 151

What does the QRS complex represent?

Answer 151

Ventricular muscle activation

Question 152

What does the ST segment represent?

Answer 152

Period between ventricular depolarization and repolarization (phase 2 of the action potential)

Question 153

What does the T wave represent?

Answer 153

Ventricular muscle repolarization

Question 154

What does the QT interval represent?

Answer 154

Total time of ventricular depolarization and repolarization

Question 155

The standard limb lead system records electrical activity in what plane?

Answer 155

The frontal plane (similar to that seen on a VD radiograph)

Left to right and cranial to caudal currents are recorded

Question 156

How do you determine the heart rate on an ECG?

Answer 156

Count the number of complexes within a 3 or 6 second period and multiple by 20 or 10 respectively

At 25 mm/s 30 blocks equals 6 seconds

At 50 mm/s 60 blocks equals 6 seconds

Question 157

What structures are better visualized on a thoracic DV as opposed to a VD view?

Answer 157

hilar area and caudal pulmonary vessels

Question 158

What structures are better visualized on a thoracic VD as opposed to a VD view?

Answer 158

lung disease, small volume pleural effusion

Question 159

What type of radiographic considerations/technique should be used for cardiac evaluation (kVp, mAs)

Answer 159

high kVp, low mAs

Question 160

List some artifacts that occur during expiration on chest radiographs?

Answer 160

increased lung opacity, larger heart, diaphragm overlapping caudal heart border, pulmonary vessels difficult to delineate

Question 161

T/F: displacement of the heart into the right hemithorax could be a normal variant?

Answer 161

true

Question 162

Normal VHS for most dogs? Dogs with long thorax? Short thorax?

Answer 162

Most dogs 8.5-10.5
Short thorax: 11
Long thorax: 9.5

Question 163

Normal VHS for cats?

Answer 163

6.7-8.1

Question 164

How do you objectively measure the cardiac dimensions on a VD/DV radiograph in cats? What is the normal value?

Answer 164

Similar to the VHS- compare the mean short axis cardiac dimension with the thoracic spine starting at T4 on the lateral view. Normal is 3.4-3.5 (up to 4)

Question 165

List some differentials for generalized cardiomegaly on radiographs

Answer 165

DCM, mitral and tricuspid insufficiency, pericardial effusion, PPDH, intrapericardial mass, VSD or ASD, PDA, systemic hypertension, athletic heart, hyperthyroidism, acromegaly, AV vistula, chronic anemia, intracardiac mass, intrapericardial fat

Question 166

Where is the LA located on lateral and VD/DV thoracic radiographs?

Answer 166

Lateral: dorsocaudal aspect of the heart, with the auricular appendage extending cranially
VD/DV: caudal heartbase, with auricle at 2-3 o clock

Question 167

How does LV enlargement manifest on lateral and VD/DV thoracic radiographs?

Answer 167

Lateral: taller heart, elevation of tracheal bifurcation

VD/DV: enlargement located at 2-6 o clock position

Question 168

What does RA enlargement do to the cardiac silhouette on radiographs?

Answer 168

Lateral: bulge of cranial heart border
VD/DV: bulging in 9-11 o clock position
*difficult to differentiate from LV enlargement**

Question 169

What does RV enlargement do to the cardiac silhouette on radiographs?

Answer 169

Lateral: increased widening and convexity of cranioventral heart border
VD/DV: reverse D appearance; widening at 6-9 o clock

Question 170

T/F: a wavy, undulated aorta is always abnormal in geriatric cats?

Answer 170

False- usually normal variant

Question 171

Where is the MPA located on lateral and v/d radiographs?

Answer 171

Lateral: overlaps trachea at cranial heart base (difficult to visualize)
VD/DV: 1-2 o clock position

Question 172

Where would a ductus bump be located on VD radiographs?

Answer 172

2-3 o clock area

Question 173

How do you objectively assess cranial pulmonary vessel size on thoracic XR?

Answer 173

on lateral view measure where vessel crosses proximal 1/3 of 4th rib. The vessels should be 0.5-1x the diameter of this part of the rib

Question 174

How do you objectively assess caudal pulmonary vessel size on thoracic XR?

Answer 174

on the VD view compare the vessel to the 9th rib where they cross; they should be 0.5-1x the size of this part of the 9th rib

Question 175

Describe the different murmur grades

Answer 175

I- very soft heard in quiet surroundings after listening intently
II- soft, easily heard
III- moderate intensity
IV- loud, no precordial thrill
V- loud, palpable precordial thrill
VI- very loud, can be heard without stethoscope, precordial thrill

Question 176

what “shape” of murmur does AV valve insufficiency usually have?

Answer 176

plateau-shaped or holosystolic; begins at S1 and is uniform throughout systole

Question 177

List some causes of functional murmurs

Answer 177

anemia, fever, high sympathetic tone, hyperthyroidism, peripheral AV fistulae, hypoproteinemia, athletic heart, extreme bradycardia

Question 178

Describe the typical characteristics of functional murmurs

Answer 178

soft to moderate intensity, crescendo-decrescendo, left heart base PMI

Question 179

At what age do puppy innocent murmurs typically disappear?

Answer 179

4-6 months

Question 180

T/F: the intensity of a MR murmur caused by valve dz is related to severity?

Answer 180

true

Question 181

What disease causes a murmur that is loudest at the left base and becomes louder as cardiac output or contractile strength increases?

Answer 181

ventricular outflow obstructions

Question 182

which disease can occasionally cause a murmur that can be heard over the skull?

Answer 182

subaortic stenosis- heard best at low left base and radiates up the aortic arch to the right base and carotid arteries

Question 183

T/F: most murmurs heard on the right cvhest wall are diastolic in nature?

Answer 183

false- most are holosystolic, plateau shaped with the exception of SAS murmurs

Question 184

What is the most common cause of diastolic murmurs in dogs and cats? What are some less common causes?

Answer 184

aortic regurgitation from bacterial endocarditis = most common
Others= ventricular septal defect, congenital malformation, degenerative aortic valve disase

Question 185

DDX for continuous murmur ?

Answer 185

PDA (most common), peripheral AV fistulae, aorticopulmonic window, ruptured sinus of Valsalva aneurysm

Question 186

What does a gallop sound indicate in dogs and cats?

Answer 186

ventricular diastolic dysfunction

Question 187

What does an audible S3 sound indicate in the dog/cat?

Answer 187

ventricular dilation with myocardial failure and poor compliance; may be the only abnormality in an animal with DCM

Question 188

An S4 sound indicates what?

Answer 188

abnormal ventricular relaxation, increased ventricular stiffness

Question 189

What causes a pericardial knock? What disease is it associated with?

Answer 189

early diastolic sound caused by sudden checking of ventricular filling by the restrictive pericardium; restrictive pericarditis

Question 190

List some mechanisms causing syncope

Answer 190

acutely reduced cardiac output (decreased filling, arrhythmias), outflow obstruction, hypoxia, hypoglycemia, decreased vascular resistance

Question 191

At what percentage of normal cerebral blood flow will syncope occur?

Answer 191

30-50% of normal CBF

Question 192

Equation for cardiac output?

Answer 192

CO=HR x SV

Question 193

equation for cerebral perfusion pressure?

Answer 193

CPP= MAP-ICP

Question 194

what is cough syncope?

Answer 194

syncope precipitated by coughing, more common in brachycephalic dogs or dogs with underlying airway disase or collapse; also chronic MMVD and marked LA enlargement

Question 195

what is the mechanism behind cough syncope?

Answer 195

coughing–>increased intrathoracic pressure–>reduced venous return to heart–>reduced ICP–>reduced CPP
Can also cause vagally mediated bradycardia and vasodilation

Question 196

How quick is the onset of action of furosemide? When do its effects peak? How long do the effects last?

Answer 196

Onset of action is 5 minutes

Effects peak by 30 minutes

Effects last 2 hours

Question 197

Why are arteriolar vasodilators generally not used in patients with left ventricular outflow obstruction?

Answer 197

They can exacerbate the obstruction and worsen forward flow

Ex. Hypertrophic obstructive cardiomyopathy

Question 198

How does nitroglycerin work?

Answer 198

It acts mainly on venous smooth muscle to increase venous capacitance and reduce cardiac filling pressure

Question 199

Why is dobutamine preferred over dopamine for inotropic support?

Answer 199

It has a lesser effect on heart rate and after load. Dobutamine primarily stimulates B1 receptors, and has weak action on beta2 and alpha receptors

Question 200

List 4 substances that are involved in local regulation of systemic vascular resistance

Answer 200

Vasodilatory substances: nitric oxide, histamine, prostacyclin, CO2

Vasoconstrictive substances: endothelin, thromboxane, thrombin

Question 201

List 2 substances that are involved in systemic regulation of SVR

Answer 201

Vasopression
Angiotensin
Catecholamines released from the SNS

Question 202

List the 3 major categories of causes of hypotension

Answer 202

Reduction in preload
Reduction in cardiac function
Reduction in SVR

Question 203

For reduction in preload resulting in hypotension, give the 2 main categories and examples of each

Answer 203

Hypovolemia: hemorrhage, severe dehydration, edema/cavitary effusion

Obstructive: GDV, mesenteric volvulus, caval/portal venous occlusion, pericardial effusion, severe pleural space disease, PTE

Question 204

For reduction in cardiac function resulting in hypotension, give the two main categories and examples of each

Answer 204

Primary: cardiomyopathy, valvular disease, tachy/brady-arrhythmias

Secondary: SIRS/Sepsis, electrolyte abnormalities, severe hypoxia, severe acidosis or alkalosis

Question 205

Give 4 examples of diseases that case a reduction in SVR resulting in hypotension

Answer 205

SIRS/Sepsis
Electrolyte abnormalities
Severe hypoxia 
Severe acidosis or alkalosis
Drugs or toxins
Anaphylaxis

Question 206

What is the primary mechanism of reduction in SVR is SIRS/sepsis?

Answer 206

Vasodilation related to excessive production of nitric oxide from upregulation of induced nitric oxide synthase by assorted cytokines (IL-1beta, IL-6, TNF alpha)

Question 207

Other than excessive production of NO, what other mechanisms have been proposed for reduction in SVR in SIRS/Sepsis?

Answer 207

Upregulation of ATP-sensitive potassium channels
Depletion of vasopressin stores
Vascular insensitivity to catecholamines

Question 208

What is responsible for the initial hyperdynamic state seen in SIRS/Sepsis?

Answer 208

In the early stages of SIRS/Sepsis, the afterload reduction from arterial vasodilation actually results in increase CO

Question 209

Describe the baroreceptor reflex system

Answer 209

Main moment-to-moment regulator of blood pressure

With decrease in BP, there is decreased stretch of baroreceptors (carotid sinus and aortic body), resulting in decreased stimulus to the vasomotor center of the medulla.

Results in increase in sympathetic and decrease in parasympathetic outflow

Shift in autonomic balance and release of catecholamines lead to vasoconstriction and increased HR and contractility

Question 210

Describe the chemoreceptor reflex system

Answer 210

Originates in chemoreceptor organs (carotid and aortic bodies) in response to decreased in tissue oxygen tension, increase in CO2, or decrease in pH.

Increased signalling from chemoreceptors results in excitement of the vasomotor center and promotes sympathetic outflow.

Question 211

Describe how the RAAS responds to hypotension

Answer 211

Decreased BP and blood flow to the kidneys results in activation of the RAAS.

Release of renin from the juxtaglomerular cells in response to decreased baroreceptor activity, sympathetic activation, or decreased tubular chloride as sensed by the macula densa.

Angiotensin II than causes vasoconstriction by direct (triggering vascular smooth muscle contraction) and indirect (stimulation of sympathetic activity and release of vasopressin) actions

Angiotensin II also promotes Na and water retention in the proximal tubule and alters GFR through preferential constriction of the efferent arteriole.

Aldosterone release from the adrenal cortex drives Na reabsorption and K excretion in the cortical collecting duct

Question 212

How does vasopressin act to counteract hypotension?

Answer 212

Release of vasopressin from the anterior pituitary is regulated by changes in blood osmolarity.

In significant hypovolemia/hypotension, release of vasopressin can increase significantly independent of osmolarity (nonosmotic stimulation of ADH)

V1 receptors are activated which causes vasoconstriction and an increase in SVR (binds to the receptor that results in activation of phospholipase C, and release of Ca from the sarcoplasmic reticulum and vasoconstriction)

Activation of V2 receptors in the renal collecting duct promotes water retention (though insertion of aquaporins) to help support blood volume and preload

Question 213

what is the equation for mean arterial blood pressure?

Answer 213

MAP= diastolic + [(systolic-diastolic)/3]

Question 214

what is the most frequent cause of secondary hypertension?

Answer 214

kidney injury/failure

Question 215

list diseases other than kidney disease that may cause secondary hypertension

Answer 215

hyperthyroidism, diabetes mellitus, hyperadrenocorticism, pheochromocytoma

Question 216

list medications that can cause hypertension

Answer 216

glucocorticoids, cyclosporine, phenylpropanolamine, erythropoietin

Question 217

what is the guideline for selection of a cuff for noninvasive BP measurement

Answer 217

dogs- 40% circumference of limb

cats- 30% circumference of limb

Question 218

a study in anesthetized cats showed that doppler is closest to what BP value?

Answer 218

more closely related to MAP; routinely underestimated systolic BP by 10-15 mm Hg

Question 219

which value of BP is the most accurate using oscillometric measurement? why?

Answer 219

mean; because mean is measured and systolic/diastolic are calculated using a built in algorithm

Question 220

what is high definition oscillometry

Answer 220

a newer modality for blood pressure monitoring; performs real-time analysis of arterial wall oscillations to obtain pressure-wave amplitudes; systolic and diastolic pressure are measured instead of calculated

Question 221

what is the reported range of detection for BP using HDO

Answer 221

5-300 mm Hg, even at 500 beats/min HR and arrhythmias

Question 222

what is photoplethysmography

Answer 222

based on the “volume clamp” principle; it measures BP based on cuff inflation/deflation

Question 223

t/f- photoplethysmography has been determined to be accurate in dogs/cats

Answer 223

true

Question 224

explain how you prime/connect an arterial catheter tubing system for direct BP monitoring

Answer 224

connect arterial catheter to a semirigid tubing primed with hep saline from 0.9% NaCl + 1 unit heparin/mL; pump fluid bag to 300 mm Hg; place transducer at level of patient’s heart

Question 225

what 3 things are visible on a direct BP waveform

Answer 225

peak systolic pressure, diastolic pressure, and dicrotic notch

Question 226

what does the dicrotic notch represent on the invasive BP waveform

Answer 226

closure of the aortic valve

Question 227

what things can interfere with accurate direct BP monitoring/waveform

Answer 227

noncompliant tubing, catheter lodged against artery wall, clot formation, air bubbles present, catheter/tubing kinking

Question 228

what is damping of the waveform

Answer 228

causes falsely low systolic and falsely high diastolic values

Question 229

complications assoc with direct BP monitoring?

Answer 229

thrombosis, hematoma, infection, necrosis (espec in cats with cath >6-12 hrs)

Question 230

what are the benefits of using telemetric blood pressure monitoring

Answer 230

you feed the catheter SQ into the femoral artery, allows free patient movement; handling and restraint don’t affect the values

Question 231

what is the cvp used to estimate?

Answer 231

RA pressure, which is equal to RV end diastolic pressure when the tricuspid valve is open; also gives a measure of relative ability of heart to pump the volume of blood that is returned to it

Question 232

what size catheter is typically used for cvp monitoring

Answer 232

16 g or 19g although size of catheter has no effect on measurement of cvp

Question 233

what is a normal cvp

Answer 233

0-5 cm H2O, although trends are most impt due to variaton

Question 234

t/f- in foxhounds, a multiple linear regression equation can be used to estimate the CVP using diameter of CVC, hepatic vein and velocity of the v wave

Answer 234

true

Question 235

t/f

during inspiration the cvp increases and during expiration it decreases

Answer 235

false; this would be true only for PPV

Question 236

List all the positive waveforms of the CVP and what they represent

Answer 236

a wave-R atrial contraction
c wave- caused by bulging of tricuspid valve into RA as R ventricle contracts
v wave- increasing pressure from blood flowing into RA before tricuspid valve opens

Question 237

list the negative waveforms/descents of the CVP and explain what they mean

Answer 237

x descent- decrease in atrial pressure during ventricular ejection
y descent- rapid emptying of R atrium and tricuspid valve opens

Question 238

what are large c waves on the CVP waveform assoc with

Answer 238

tricuspid regurgitation

Question 239

what CVP is assoc with edema formation or body cavity effusion

Answer 239

> 16 cm h2o

Question 240

a cvp <0 may represent?

Answer 240

hypovolemia due to fluid loss or vasodilation

Question 241

a cvp >10 may represent?

Answer 241

volume overload, right CHF, pleural effusion

Question 242

if a patient is hypovolemic, what will happen with a test bolus to the cvp?

Answer 242

transient increase toward normal or no change in cvp, rapid decrease back to baseline

Question 243

if a patient is euvolemic what will happen to the cvp with a test bolus?

Answer 243

small increase of 2-4 cm h2o with return to baseline in 15 min

Question 244

if a patient is hypervolemic what will happen to the cvp with a test bolus?

Answer 244

> 4 cm h2o or large increase in cvp then slow return to baseline (>30 min)

Question 245

contraindications to cvp measurement?

Answer 245

hypercoagulable state, increased ICP, coaglopathy

Question 246

what does a pulmonary artery catheter measure? pulmonary wedge cath?

Answer 246

left ventricular preload; left atrial pressure equals LV end diastolic pressure when mitral valve is open

PAOP measures left atrial filling pressure

Question 247

t/f- PAP and PAOP are best predictors of pulmonary edema secondary to fluid overload?

Answer 247

true

Question 248

what is normal PAOP?

Answer 248

5-12 mm Hg

Question 249

what else can be measured by a swan-ganz catheter besides PAP and PAOP?

Answer 249

cardiac output using thermodilution technique, RA pressure

Question 250

what is normal cardiac output for dog/cat?

Answer 250

dog 125-200 ml/kg/min, cat 120 ml/kg/min

Question 251

list other values that can be calculated with a pulmonary artery catheter

Answer 251

cardiac index, stroke volume, stroke volume index, systemic vascular resistance, pulmonary vascular resistance

Question 252

complications assoc with pulmonary artery catheterization?

Answer 252

arrhythmias, damage to tricuspid/pulmonic valves, rupture of pulmonary artery, PTE

Question 253

where is Scvo2 measurement taken? Svo2?

Answer 253

Scvo2= central vein such as vena cava or RA
Svo2= pulmonary artery

Question 254

normal values for Scvo2 and Svo2?

Answer 254

Scvo2= >65%
Svo2= >75%

Question 255

in a recent vet study looking at the best discrimators between survivors and nonsurvivors in dogs with severe sepsis or septic shock, what 2 values were the best?

Answer 255

base deficit and Scvo2

Question 256

what are limitations to svo2 and scvo2 measurement?

Answer 256

hgb and SaO2 can affect them; if there is underlying defect in O2 extraction, the values can be normal or high despite oxygen debt

Question 257

Name the types of vessels in order as they leave the heart and return to the heart

Answer 257

arteries -> arterioles -> capillaries -> venules -> veins

Question 258

What types of vessels are referred to as conduits and why?

Answer 258

Arteries

Because they have low and relatively unchanging resistance to flow

Question 259

How does the structure of arterioles differ from arteries?

Answer 259

Arterioles have much thicker walls with more smooth muscle and less elastic material

Question 260

What types of vessels are referred to as resistance vessels and why?

Answer 260

Arterioles

Because of their high and changeable resistance, this helps them to regulate flow through individual organs

Question 261

True or false:

Capillaries can change their diameter, but less so than arterioles

Answer 261

False

They lack smooth muscle so cannot actively change their diameter

Question 262

What types of vessels are referred to as exchange vessels and why?

Answer 262

Capillaries

They are composed of a single layer of cells separating them from the interstitium so solutes can diffuse through them

Question 263

What types of vessels are referred to as capacitance vessels and why?

Answer 263

Peripheral venules and veins

They can distend and contain more than 50% of the blood volume

Question 264

What percent of the blood volume can be contained in the peripheral venules and veins?

Answer 264

More than 50%

Question 265

Describe the innervation of arterioles

Answer 265

Sympathetic nerves innervate arterioles
These nerves release norepinephrine at their endings and interact with alpha-adrenergic receptors on the smooth muscle cells to cause contraction and arteriolar constriction

These neural fibers provide the most important means of REFLEX control of vascular resistance and organ blood flow

Question 266

True or false:

There is no important neural or local metabolic control of either arterial or capillary vessels

Answer 266

TRUE

Question 267

What is the equation for hematocrit?

Answer 267

Hct = cell volume / total blood volume

Question 268

What are the conditions necessary to control the composition of the interstitial fluid?

Answer 268

1- Adequate blood flow though the tissue capillary
2- Controlled chemical composition of the arterial blood to be optimal for the interstitium
3- Short diffusion distance

Question 269

What is the maximal distance between a cell and capillary?

Answer 269

10 um

Question 270

Which organ receives the most of the arterial blood?

Answer 270

Kidneys (about 22%)

Question 271

Define blood-conditioning organ

Answer 271

Systemic organ that receives blood flow that exceeds the amount of flow necessary to supply their nutrient need, and recondition the composition of blood (ex. lungs, kidney, liver, skin (heat))

Question 272

Name 3 organs in which blood flows solely to supply the metabolic needs of the tissue (as opposed as blood-conditioning organ)?

Answer 272

Brain
Heart muscle
Skeletal muscles

Question 273

What percentage of the oxygen supplied to the myocardium is consumed?

Answer 273

75%

Question 274

True or false: Active tension in the cardiac muscle cells is higher at very long muscle lengths

Answer 274

FALSE

Active tension is at its highest point at an intermediate muscle cell length

Question 275

What are the three mechanisms that explain the relationship between cardiac muscle length and tension

Answer 275

1) This relationship depends on the extent of overlap of thick and think filaments in the sarcomeres (at long lengths there might not be enough overlap and at short lengths, think filaments may overlap)
2) As muscle lengthens it has an increased sensitivity to calcium
3) After increasing the resting length of the cardiac muscle, there is an increase in the amount of calcium that is released with excitation, which leads to higher force

Question 276

Where is the sensor for cardiac muscle length-dependent activation?

Answer 276

Within the troponin C molecule

Question 277

Define isotonic contraction

Answer 277

A muscle shortens against a constant load

Question 278

True or false, as muscle shortens, its inherent contractile potential increases

Answer 278

FALSE

it decreases

Question 279

What determines resting cardiac muscle length?

Answer 279

Preload

Question 280

True or false, afterloaded cardiac muscle shortens less than non-afterloaded muscle

Answer 280

TRUE

Question 281

What is the most important physiologic regulator of cardiac muscle contractility?

Answer 281

Norepinephrine

Question 282

How does epinephrine affects cardiac muscle contractility?

Answer 282

Norepi interacts with the beta 1 adrenergic receptor -> activation of the G-protein-cAMP-protein kinase A -> which phosphorylates the Ca2+ channel-> which increases the inward calcium current during the plateau of the action potential

Question 283

What is a positive lusitropic effect?

Answer 283

Increased rate of relaxation of cardiac muscle

An example is norepinephrine causing phosphorylation of phospholamban on the SR Ca-ATPase pump, which leads to increased retrapping of calcium in the SR, and increased rate of relaxation

Question 284

What is the staircase phenomenon (or treppe)?

Answer 284

A sudden increase in beating rate of the heart is followed by a progressive increase in contracticle force to a higher plateau

Question 285

How do length-tension relationships of cardiac muscle fibers determine volume and pressure relationships of the ventricular chamber? (3 points)

Answer 285

1) An increase in ventricular volume causes an increase in ventricular circumference and therefore an increase in individual cardiac muscle cells -> extent of diastolic filling determines preload
2) At a given ventricular volume, an increase in the tension of individual cardiac cells causes an increase in intraventricular pressure
3) As ventricular volume decreases, a lesser total force is required by the muscle cells in the ventricular walls to produce a given intraventricular pressure

Question 286

What is the Law of Laplace?

Answer 286

T = P x r

Total wall tension equals intraventricular pressure times the internal radius

Question 287

What important implication does the Law of Laplace have for the heart?

Answer 287

Muscle cells in the ventricular wall have an easier job of producing internal pressure at the end of ejection (radius is small) than at the beginning of ejection (radius is large)

This is important in conditions like HCM and DCM

Question 288

How does the voltage of the heart corresponds with the P, QRS T waves and its intervals.

Answer 288

P is atrial depolarization
PR interval to the conduction time to the atria and AV node
QRS complex to ventricular depolarization
QT interval to the duration of ventricular systole
T ventricular repolarization

Question 289

What is the intrinsic rate

Answer 289

its the spontaneous electrical pacemaker activity, in the absence of outside influences. In humans about 100bpm. Its determined by how long it takes for the cells in the pacemaker (SA node) to spontaneously depolarize to the threshold level.

Question 290

What are the main two outside influences on the automaticity of the SA

Answer 290

The autonomous nervous system: Sympathetic and parasympathetic.

Question 291

what is the difference between chronotropic effect and dromotropic effect

Answer 291

Chonotropic effect are caused by factors that affect the HR.
Dromotropic effect is caused by factors that affect the conduction velocity (most notable at the AV node and can influence the duration of the PR interval

Question 292

What are the processes that participate in the reduction of intracellular calcium that terminates the contraction

Answer 292

80% of the calcium is actively taken back up into the SR by action of Ca ATPase pumps
20% is extruded from the cell into the extracellular fluid either via the Na-Ca exchanger in the sarcolema or via sarcolemmal Ca ATPase pumps

Question 293

What is the difference between Isomeric and isotonic contraction?

Answer 293

Isomeric: fixed length: maximum ability to develop tension
Isotonic: fixed tension: muscle shortens with its maximum possible velocity

Question 294

What 3 things make cardiac muscle cell action potentials differ from those of skeletal muscle cells?

Answer 294

1. They can be self-generating
2. They can be conducted directly from cell to cell
3. They have long-duration, which precludes fusion of individual twitch contraction

Question 295

What are three ions that are the most important determinants of cardiac trans-membrane?

Answer 295

1. Na (more concentrated in the interstitial fluid than intracellular)
2. Ca (more concentrated in the interstitial fluid than intracellular)
3. K (more intracellular than interstitial)

Question 296

What are three general types of transmembrane protein structures that are involved in ion movement across the cell membrane?

Answer 296

1. Ion channels
2. Ion exchangers
3. Ion pump

Question 297

What are 2 categories of cardiac cell action potentials, depends on “the speed of response”, and “the type of cells”?

Answer 297

1. Cardiac pacemaker-type cell, slow-response action potentials
2. Ordinary cardiac muscle cell, fast-response action potentials

Question 298

With regard to fast-response action potentials, what are 3 periods and what’s the significance?

Answer 298

1. Absolute refractory period (during the most of the action potential, they cannot be stimulated to fire another action potential)
2. Relative refractory period (near the end of action potential, can be re-excited only by a larger-than-normal stimuls)
3. Supranormal, or vulnerable period (immediately after the action potential, transiently hyperexcitable)

Question 299

True or false: During the resting phase, membranes are more permeable to K than Na or Ca. Therefore, the membrane potential are close to the potassium equilibrium potential (-90 mV) during this period

Answer 299

True

Question 300

True or false: During initial depolarization phase of action potential, sudden increase in Na permeability causes rapid rising phase of fast-response action potential. Whereas, it’s an inward movement of Ca ions that cause slower rising phase of slow-response action potential.

Answer 300

True

Question 301

What 5 improvements in cardiac performance are caused by the sympathetic nervous system?

Answer 301

1. Positive chronotropic effect
2. Decrease in cardiac action potential duration (minimizes the effect of high heart rate on diastolic filling time)
3. Positive dromotropic effect (increased rate of conduction of the action potential)
4. Positive inotropic effect
5. Positive lusotropic effect (increase in rate of cardiac relaxation)

Question 302

True or false:
Fetal and newborn hearts rely primarily on fatty acids for ATP; whereas, adults derive their ATP from glucose and lactate

Answer 302

FALSE

It is the opposite, adults derive 60-90% of ATP from fatty acids

Question 303

What percentage of ATP is generated by fatty acids in the adult myocardium?

Answer 303

60-90%

Question 304

What is the end product of metabolism of glycogen, glucose, fatty acids, triglycerides, pyruvate and lactate? And what happens to this molecule?

Answer 304

The end product is Acetyl CoA
It enters the citric acid cycle (Krebs cycle) in the mitochondria, whereby through a process of oxidative phosphorylation it is degraded to carbon dioxide and water and the energy is converted to ATP

Question 305

What characteristics of the heart are consistent with the fact that the majority of energy is derived from the aerobic pathways?

Answer 305

1. High number of mitochondria

2. Presence of high concentrations of oxygen-binding protein myoglobin within cardiac muscle cells

Question 306

What does myoglobin do within cardiac muscle cells?

Answer 306

It can release its oxygen to the mitochondrial cytochrome oxidase system when intracellular oxygen levels are lowered

Question 307

What percent of myocardial energy use is normally accounted for by the basal metabolism of the heart tissue?

And what percent is accounted for by muscle contraction?

Answer 307

25% for basal metabolism

75% for muscle contraction

Question 308

What phase of the cardiac cycle accounts for the largest portion of total myocardial oxygen consumption?

Answer 308

Isovolumetric contraction

Question 309

Are increases in the afterload or the stroke volume more costly to myocardial oxygen consumption?

Answer 309

Increased in the afterload

Question 310

In terms of myocardial oxygen consumption, is it more efficient for the heart to work at a low heart rate and high stroke volume, or at a high heart rate and low stroke volume?

Answer 310

It is more efficient to work at a low heart rate
This is due to the energy required during the pressure development phase of the cardiac cycle, the less pressure developed and the less often pressure development occurs, the better.

Question 311

3 condition of proper filling of the ventricles

Answer 311

1. Filling pressure of blood returning to the heart and atria
2. Ability of AV valves to open fully (not be stenotic)
3. Ability of ventricular wall to expand passively with little resistance (to have high compliance)

Question 312

True or false: atrial contraction is initiated near the end of ventricular diastole, which causes P waves. At normal resting heart rate, atrial contraction is NOT essential for adequate ventricular filling.

Answer 312

True: Atrial contraction plays an increasingly significant role in ventricular filling as HR increases, because the time interval between beats for passive filling becomes progressively shorter with increased HR. Throughout diastole, atrial and ventricular pressures are nearly identical, and normal open mitral valve has very little resistance to flow and thus only a very small atrial-ventricular pressure difference is necessary to produce ventricular filling.

Question 313

What is isovolumetric contraction phase and isovolumetric relaxation phase?

Answer 313

Both phase means that left ventricle is a closed chamber (both mitral valve and aortic valve are closed). Isovolumetric contraction phase: from mitral valve closure to opening of aortic valve when LV exceeds that in the aorta
Isovolumetric relaxation phase: from aortic valve closure to mitral valve opening (after aortic valve closure, intraventricular pressure falls rapidly as the ventricular muscle relaxes)

Question 314

What is stroke volume?

Answer 314

The amount of blood ejected from the ventricle during a single beat. It’s equal to ventricular end-diastolic volume minus ventricular end-systolic volume. In normal condition, heart ejects only 60% of its end-diastolic volume.

Question 315

True or false: At a resting HR, heart spend approximately ⅔ of cardiac cycle in diastole and ⅓ in systole.

Answer 315

True

Question 316

What’s the major difference between the right and left pumps? (1) pressure, (2) stroke volume. And why?

Answer 316

Pressure developed by right side is considerably lower than those for the left side. Because the lungs provide considerably less resistance to blood flow than that offered collectively by the systemic organs

Question 317

What is physiological splitting of the second heart sound?, and What are two factors that lead to this prolonged ejection time from the right ventricle?

Answer 317

Discrepancy that pulmonic valve usually closes slightly after the aortic valve.

(1) Inspiration-induced decrease in intrathoracic pressure, and increased filling of the right side of the heart. So this extra volume will be ejected, with a little extra time.
(2) Inspiration-induced decrease in pulmonary vascular resistance (increased pulmonary compliance), which reduces pulmonary artery pressure and right ventricular afterload. With reduced afterload, ventricular ejection can go on for a slightly longer period of time.

Question 318

What is gallop rhythm?

Answer 318

S3 and S4 are not normally present. When they are present along with S1 and S2, produce what are called gallop rhythm.
S3 along with S1 and S2: ventricular gallop rhythm.
S4 along with S2 and S2: atrial gallop rhythm.

Question 319

What is the mean electrical axis of the heart? How can we use it clinically?

Answer 319

It describes the orientation of the net dipole at the instant of maximum wavefront propagation during ventricular depolarization.

We can use it as an indicator of whether ventricular depolarization is proceeding over normal pathways.
It usually falls between 0 and +90 degrees

Question 320

How would affect a left ventricular hypertrophy to the mean electrical axis.

Answer 320

It would produce a left axis deviation: when the mean electrical axis falls in the patient’s upper left quadrant. Indicates physical displacement of the heart to the left.

Question 321

What principle do the most accurate methods to measure cardiac output follow? Give the formula

Answer 321

Fick principle
Q = Xtc / ([X]a - [X]b)
Q: blood flow rate
Xtc: amount of substance consumed by the tissue in time
[X]a: arterial concentration of the substance
[X]b: mixed venous concentration of the substance

Question 322

Where should we ideally collect the blood from to get mixed venous blood

Answer 322

Right ventricle or pulmonary artery

Question 323

What substance/marker do we most commonly use with the Fick principle to measure cardiac output

Answer 323

O2, dye, heat (thermodilution)

Question 324

What is cardiac index?

Answer 324

Cardiac output corrected for the individual’s size

Question 325

What are 3 imaging techniques to measure cardiac output?

Answer 325

• Echocardiography
• Cardiac angiography (radiopaque contrast medium and high-speed x-ray filming)
• Radionuclide ventriculography (radioactive isotope and measurement of radiation intensity changes over the ventricle)

Question 326

What is the formula to define ejection fraction (EF)? What is the normal range?

Answer 326

EF = SV / EDV -55-80%-
SV: stroke volume
EDV: end-diastolic volume

Question 327

How can we measure end-systolic pressure?

Answer 327

Obtaining arterial pressure at the point of the closure of the aortic valve (incisura)

Question 328

How can we assess myocardial contractility using the LV end-systolic pressure-volume relationship?

Answer 328

By looking at the slope of the line joining the point on the LV pressure-volume loop at the closure of the aortic valve, and the point 0
Steep slope: increased contractility (decreased end-diastolic volume for the same pressure)
Flat slop: decreased contractility (increased end-diastolic volume for the same pressure)

Question 329

What are the 3 things can be evaluated from ECG?

Answer 329

1. HR, 2. rhythm, 3. conduction characteristics

Question 330

What’s the significance of P, QRS, T wave, PR interval, QT interval?

Answer 330

P: atrial depolarization
QRS: ventricular depolarization
T: ventricular repolarization
PR interval: AV nodal transmission time (the time it takes for an action potential to spread through the atria and the AV node) = conduction from SA node through AV node to the ventricle
QT interval: duration of ventricular systole

Question 331

True or false: in normal healthy status, PR interval is longer than QT interval

Answer 331

False: PR interval is usually shorter than QT interval. If PR interval is longer than QT interval: 1st degree AV block

Question 332

True or false: during T wave, all the cells in the heart are in the resting state

Answer 332

True

Question 333

True or false: PR interval is from beginning of P wave until the R wave

Answer 333

False: PR interval is from beginning of P wave until the beginning of QRS complex
PR segment? baseline portion of PR interval

Question 334

True or false: QT interval is from the beginning of Q wave until the end of T wave

Answer 334

True. It’s not from the peak of Q wave to the end of T wave

Question 335

Describe Einthoven’s triangle (3 location of electrode, i.e. lead 1 connect from A to B)

Answer 335

From RA to LA: lead 1
From RA to LL: lead 2
From LA to LA: lead 3

Question 336

What is compliance when referring to the vascular system?

Answer 336

How much a volume changes in response to a given distending pressure

Question 337

When listening to a doppler while taking a blood pressure how you determine the systolic and diastolic values?

Answer 337

Systolic: highest cuff pressure at which heart sounds are heard

Diastolic: cuff pressure at which heart sounds become muffled or disappear

Question 338

What two major components affect the mean arterial pressure?

Answer 338

Cardiac output

Total peripheral resistance

Question 339

How do you calculate MAP?

Answer 339

MAP = Diastolic pressures + 1/3 (systolic - diastolic)

Question 340

How is pulse pressure calculated?

Answer 340

Pulse pressure = Systolic - diastolic

Question 341

Why does pulse pressure increase with age?

Answer 341

Decrease in arterial compliance

Question 342

True or false:

Changes in total peripheral resistance have little effect on pulse pressure

Answer 342

TRUE

Because a change in total peripheral resistance causes parallel changes in both systolic and diastolic pressures

Question 343

True or false

Blood flows most rapidly in the smallest total cross-sectional area or the capillaries

Answer 343

False, it does but the smallest total cross sectional area is the aorta, not the capillaries.

Question 344

True or false

With laminar flow each layer goes at different velocity

Answer 344

True. Velocity is fastest along the central axis.

Question 345

What are the peripheral and central venous pool ?

Answer 345

Peripheral: circulating blood contained within the veins of the systemic organs.

Central: is smaller. Blood in the great veins of the thorax and the right atrium

Question 346

How does the blood pressure changes from the aorta to the capillaries

Answer 346

At the arch of the aorta is about 100mmHG and is similar within the arterial system.
It drops at the arterioles, where it loses the pulsatile nature.
At the capillaries the pressure is 25mmHg
It continues to decrease in the venules and veins.
The central Venous pressure is close to 0mmHg

Question 347

What segment of the circulatory system regulates the peripheral vascular resistance.

Answer 347

The changes in the radius of the arterioles.

Question 348

What is the total peripheral resistance

Answer 348

It is the overall resistance to flow through the entire systemic circulation. The resistance of every organ contributes to the total peripheral resistance.

Question 349

How does histamine produce arteriolar vasodilation and tissue edema?

Answer 349

It produces arteriolar vasodilation via the cAMP pathway and tissue edema due to increased vascular permeability from separations in the junctions between the endothelial cells that line the vascular system

Question 350

In terms of vasodilatory potency, which is more potent, bradykinin or histamine?

Answer 350

Bradykinin is 10 times more potent than histamine

Question 351

What is the myogenic response when talking about arterioles?

Answer 351

Active constriction of the arteriole in response to passive distension produced by a sudden increase in the internal pressure of the arteriole

Question 352

What is active hyperemia and how is it produced?

Answer 352

Change in blood flow to skeletal muscles in response to muscle exercise. It results from local metabolic vasodilatory feedback on arteriolar smooth muscle. Endothelial flow-dependent mechanisms may assist in propagating the vasodilation to larger vessels

Question 353

What is reactive or post-occlusion hyperemia and what mechanisms are responsible for producing it?

Answer 353

Higher than normal blood that occurs transiently after the removal of any restriction that has caused a period of lower than normal blood blood flow.

Both local metabolic and myogenic mechanisms may be involved

Question 354

What is autoregulation?

Answer 354

The ability of organs to keep their blood flow constant despite variations in arterial pressure

Question 355

What mechanisms are responsible for the arteriolar vasoconstriction of the autoregulatory response and how do they work?

Answer 355

1) Local metabolic feedback: washout of metabolic vasodilator factors from the interstitium by the excessive initial blood flow
2) Myogenic response: increase in arteriolar tone stimulated by the increase in stretching forces that the increase in pressure imposes on the vessel walls

Question 356

What is the tissue pressure hypothesis of blood flow autoregulation?

Answer 356

An abrupt increase in arterial pressure causes transcapillary fluid filtration and thus leads to a gradual increase in interstitial fluid volume and pressure.

The increase in extravascular pressure would cause a decrease in vessel diameter by simple compression.

This may be particularly important in organs such as the kidney and brain whose volumes are constrained by external structures

Question 357

What are the purposes of the ability to make vascular diameter changes?

Answer 357

• To efficiently distribute the cardiac output among tissues with different current needs (arterioles)
• To regulate the distribution of blood volume and cardiac filling (venules)

Question 358

Where are vascular smooth muscle cells absent from?

Answer 358

Arterioles

Question 359

What are the differences in anatomic and functional characteristics between smooth muscle cells and other skeletal or cardiac muscle cells?

Answer 359

1- Contract and relax much more slowly
2- Develop active tension over a greater range of muscle lengths
3- Can change their contractile activity as a result of action potentials or changes in resting membrane potential
4- May change their contractile activity in the absence of changes in membrane potential (changes in the Ca2+ sensitivity of the contractile machinery / contractility changes in the absence of change in intracellular free Ca2+ levels)
5- Maintain tension for prolonged periods at low energy cost
6- Can be activated by stretch
7- Filaments (actin and myosin) are not arranged in regular, repeating sarcomere units (no visible striation), but many travel obliquely or even traversely to the long axis of the cell
8- Actin filaments do not attach to Z-lines in the interior of the cell, but to ‘'’dense bands’’
9- Sequence of steps linking an increase free Ca2+ level to contractile filament interaction is different -> Ca2+ and calmodulin complex formation -> Activation of the myosin light-chain kinase -> Phosphorylation of the light-chain protein (cross-bridge head of myosin) -> cross-bridge formation and cycling
10- Lower resting membrane potentials [-40 ; -65 mV]

Question 360

How are adjacent smooth muscle cells electrically connected?

Answer 360

Gap junctions similar to those found in the myocardium

Question 361

What type of channel is predominantly responsible for the resting membrane potential of the smooth muscle cells?

Answer 361

'’Inward rectifying-type K+’’ channel = K+ move slightly more easily into the cell than out
‘‘ATP-dependent K+’’ channels = open when ATP level falls —> important to match blood flow and metabolic state of an organ

Question 362

What are the channels involved in depolarization? Repolarization? of the smooth muscle cells

Answer 362

Depolarization (inward flux of Ca2+): voltage-operated calcium channel (VOC)
Repolarization (outward flux of K+): delayed K+ channels, and calcium -activated K+ channels

Question 363

What is Pharmacomechanical coupling?

Answer 363

Chemical agents (i.e. norepinephrine) can induce smooth muscle contraction without the need for a change in membrane potential.

Question 364

What are the two mechanisms initiated by alpha1- agonists that cause intracellular Ca2+ levels to increase in the absence of a change in membrane potential in smooth muscle cells?

Answer 364

• Activated receptor may induce the formation of an intracellular ‘‘second messenger’’ (IP3) that open specific channels that release Ca2+ from the intracellular sarcoplasmic reticulum stores
• Activated receptor may open surface membrane receptor-operated channels for Ca2+ (influx)

Question 365

What percentage of cardiac output do the splanchnic organs receive?

Answer 365

25%

Question 366

What percentage of oxygen do the splanchnic organs extract?

Answer 366

15-20

%

Question 367

When the sympathetic nervous system is activated, what percent reduction in flow to the splanchnic organs can occur?

Answer 367

80%

This results in a large amount of blood being returned to the central venous pool

Question 368

True or false: Changes in renal blood volume are inconsequential to overall cardiovascular hemodynamics

Answer 368

True

Control of renal blood flow is important to overall cardiovascular function

Question 369

How much of resting cardiac output does the skin receive?

Answer 369

6%

Question 370

What are venous plexuses and what is their function?

Answer 370

Interconnected veins

Heat transfer from the blood takes place across the large surface area

Question 371

True or false:

Pulmonary blood flow is slightly less than cardiac output

Answer 371

False

Pulmonary blood flow = cardiac output

Question 372

How does pulmonary vascular resistance compare to systemic vascular resistance?

Answer 372

Pulmonary resistance is 1/7th of total systemic vascular resistance

Question 373

What effect do changes in pulmonary arterial pressure have on pulmonary vascular resistance?

Answer 373

An increase in pulmonary arterial pressure DECREASES pulmonary vascular resistance because pulmonary arteries and arterioles are less muscular and more compliant

Question 374

What effect does hypoxia have on pulmonary arterioles?

Answer 374

Pulmonary arterioles constrict in response to hypoxia

Question 375

What role do autnomonic nerves play in pulmonary vascular activity?

Answer 375

No major role

Physical and local hypoxic influences are more important

Question 376

In the lungs is capillary hydrostatic pressure high or low?

Answer 376

It is LOW which promotes fluid reabsorption and prevents fluid accumulation in airways

Question 377

What is the driving force for myocardial blood flow?

Answer 377

systemic arterial blood pressure, just as it is for systemic organs

Question 378

True of false? increases in myocardial oxygen consumption must be accompanied by appropriate increases in coronary blood flow.

Answer 378

True. Because myocardial oxygen extraction cannot increase significantly from its high resting value.

Question 379

What is the most important influence on coronary blood flow?

Answer 379

Myocardial oxygen consumption

Question 380

Why coronary flow is lower during systole than during diastole, even though systemic arterial pressure (coronary perfusion pressure) is highest during systole?

Answer 380

Because of systolic compression and the associated collapse of coronary vessels (large force pressure is generated within the myocardial tissue during cardiac muscle contraction)

Question 381

True or false? Myocardial infarcts occur most frequently in the epicardial layers of the right ventricle.

Answer 381

False. endocardial layers of the left ventricle. systolic compressional forces on coronary vessels are greater in the endocardial layers of the left ventricular wall than in the epicardial layer.

Question 382

True or false? When the activity of the sympathetic nervous system increases, the coronary arterioles normally vasodilate rather than vasoconstric.

Answer 382

True. Because an increase in sympathetic tone increase myocardial oxygen consumption by increasing the heart rate and contractility.

Question 383

What are the name of two factors designed to keep mean arterial pressure constant in cerebral blood flow?

Answer 383

total peripheral resistance and cardiac output

Question 384

True or false? Cerebral blood flow decreases when arterial blood Pco2 rises.

Answer 384

False, Cerebral blood flow decreases when arterial blood Pco2 decreass.

Question 385

True or false? Sympathetic and parasympathetic neural influecens on cerebral blood flow are minimal.

Answer 385

True

Question 386

What determines where the cardiac function and venous function curves intersect?

Answer 386

Influences on the heart and on the peripheral vasculature

ie sympathetic tone, blood volume, etc

Question 387

If a patient has an abnormally high central venous pressure what might the cardiac function and venous function curves look like?

Answer 387

Depressed cardiac function curve (left shift), right shifted venous function curve, or both

Question 388

What conditions cause an abnormally high CVP?

Answer 388

CHF, fluid overload

Question 389

If a patient has an abnormally low central venous pressure what might the cardiac function and venous function curves look like?

Answer 389

Elevated cardiac function curve (right shift) or left shifted venous function curve

Question 390

What conditions cause an abnormally low CVP?

Answer 390

Most often caused by left shift of venous function curve either due to low blood volume or lack of venous tone

Question 391

What physical exam finding might indicate increased CVP?

Answer 391

Jugular venous distension and pulsation

Question 392

What is central comand? How does it affect BP?

Answer 392

Is the response from the cerebral cortex to lower brain centers during physical exercise.
Mean art BP and RR increases during exercise

Question 393

How dosuperficial and deep pain affect BP

Answer 393

Superficial or cutaneous causes a raise in BP
Deep from viscera or joints causes a decrease on sympathetic tone, increase on parasympathetic and a serious decrease in BP

Question 394

Where is the temperature regulation controlled?

Answer 394

In the hypothalamus. It controls the sympathetic activity to cutaneous vessels ansd thus skin blood flow.

Question 395

How does a raise in BP affects the UOP, how does the body compensates a raise in BP?

Answer 395

The UOP changes the total fluid volume. An increase in BP, increases UOP which reduces the fluid and blood volume, this reduces cardiac output thus reduces BP

Question 396

T/F: Peripheral vascular adjustments associated with arterial baroreceptor reflex take place primarily in organs with strong sympathetic vascular control.

Answer 396

True

Question 397

What’s general function of cardiopulmonary receptors?

Answer 397

Sensing the pressure (or volume) in atria and the central venous pool. Increased CVP cause receptor activation by stretch, which elicits a reflex decrease in sympathetic activity.

Question 398

T/F: cardiopulmonary baroreceptors normally exert a tonic excitatory on sympathetic activity.

Answer 398

False: inhibitory, not excitatory.

Question 399

Which receptors are responsible for increase RR and MAP in condition of low PO2 and high PCO2?

Answer 399

Arterial chemoreceptor (located in carotid arteries and aortic arch), central chemoreceptor (located somewhere in CNS)

Question 400

T/F: gravity change the arterio-venous pressure difference at any one height level.

Answer 400

False: because gravity has the same effect on arterial and venous pressure.

Question 401

Two major direct effects of the increased pressure in lower extremities due to gravity?

Answer 401

1. increase in venous transmural pressure distends compliant peripheral vein.
2. increase in capillary transmural hydrostatic pressure causes a tremendously high transcapillary filtration rate in the lower leg and feet.

Question 402

What two forces are counteracting venous blood pooling and edema formation in the lower extremeties during standing?

Answer 402

1. skeletal muscle pump
2. vasoconstriction from sympathetic activation (is only marginally effective in ameliorating the adverse effects of gravity on the lower extremities)

Question 403

Briefly explain orthostatic or postural hypotension

Answer 403

In long-term bed rest or zero gravity, patient become hypovolemic (by normal earth standpoint) which means substantial decrease in circulating blood volume. Upon standing, blood shift out of the central venous pool into peripheral veins, SV falls, and individual often becomes dizzy and may faint because of dramatic fall in blood pressure.

Question 404

What is the normal intrapleural pressure at the end of expiration? inspiration?

Answer 404

-2 mmHg / -7 mmHg

Question 405

What are the receptors involved in the sinus cardiac rhythm?

Answer 405

• Stretch of the airways receptors -> inhibition of the normal tonic vagal activity to the sinoatrial node -> transient increase in the heart rate
• Stretch of the low-pressure cardiopulmonary baroreceptors -> transient increase in the heart rate
• > Increased MAP -> Stretch of the high-pressure arterial baroreceptors -> Reflex adjustment (decreased sympathetic, increased parasympathetic)

Question 406

How is the venous return affected by inspiration?

Answer 406

Increased venous return (decreased intrathoracic pressure)

Question 407

How does respiration affect the venous return during exercise?

Answer 407

Deep and rapid breathing -> increased venous return

Question 408

How does yawning affect the venous return?

Answer 408

More negative intrathoracic pressure -> increased venous return

Question 409

How does coughing affect the venous return?

Answer 409

Increased intrathoracic pressure -> decreased venous return

Question 410

How does vasalva maneuver affect the cardiovascular parameters?

Answer 410

• 1 (first heart beats)- Increased arterial pressure due to increased intrathoracic pressure
• 2 - Compensation: increased HR and peripheral vasoconstriction (decreased venous return due to increased intrathoracic pressure - distended peripheral veins (facial))
• 3 - End of maneuver: decreased intrathoracic pressure and BP, Venous return restores -> increased SV, CO, BP and decreased HR

Question 411

How does positive pressure ventilation affect the venous return?

Answer 411

Increased intrathoracic pressure -> Decreased venous return

Increased RV afterload

Question 412

What are the 2 direct effects of gravity on vasculature?

Answer 412

• Increased venous transmural pressure -> distension of compliant veins
• Increased capillary transmural hydrostatic pressure -> increased transcapillary filtraton rate

Question 413

What are the 2 main compensatory mechanisms for gravity?

Answer 413

• Reflex activation of sympathetic nerves (marginal effects)

- Skeletal muscle pump (contraction exels both venous blood and lymphatic fluid)

Question 414

How does standing affect the blood volume?

Answer 414

Increased sympathetic activity -> fluid retention from kidneys

Question 415

What are potential causes of altered diastolic properties in heart failure?

Answer 415

1) Decreased cardiac tissue passive compliance due to extracellular remodeling,collagen cross-linking, and extracellular matrix protein alterations
2) Increased myofibrillar passive stiffness due to alterations in titin
3) Delayed myocyte relaxation early in diastole due to slow cytosolic calcium removal
4) Inadequate adenosine triphosphate levels required to disconnect the myofilament cross-bridges rapidly
5) Residual, low grade cross-bridge cycling during diastole due to calcium leaking from the SR

Question 416

What is cor pulmonale?

Answer 416

Right sided heart failure resulting from chronic pulmonary hypertension

Question 417

Hypertension is associated with an increase or decrease in total peripheral resistance

Answer 417

Increase

Question 418

What may cause the increase in total peripheral resistance from hypertension?

Answer 418

1) decrease in density of microvessels
2) pronounced structural adaptations that occur in the peripheral vascular bed
3) continuously increased activity of the vascular smooth muscle cells
4) an increased sensitivity and reactivity of the vascular smooth muscle cells to external vasoconstrictor stimuli
5) diminished production and/or effect of endogenous vasodilator substances such as nitric oxide

Question 419

Name six treatments for hypertension

Answer 419

1) Restricted salt intake
2) Diuretic therapy
3) Beta-adrenergic blockers
4) ACE inhibitors
5) Angiotensin II receptor blockers
6) Alpha-adrenergic receptor blockers

Question 420

How does a pulmonary embolus mimic hypovolemic shock?

Answer 420

Decreased left ventricular filling -> Decreased cardiac output (+ interferes with adequate gas exchange in the lungs)

Question 421

What substances (exemples) mediate anaphylactic shocks?

Answer 421

Histamine, prostaglandines, leukotrienes, bradykinin

Question 422

How does endotoxin induce vasodilation?

Answer 422

Endotoxin (lipopolysaccharide released from bacteria) -> induces formation nitric oxide synthase in endothelial cells, vascular smooth muscle and macrophages (inducible as opposed as constitutive) -> nitric oxide production

Question 423

Give two potential causes for neurogenic shock

Answer 423

• Deep general anesthesia

- Deep pain

Question 424

What are three mechanisms that stimulate sympathetic output during shock?

Answer 424

• Reduced arterial baroreceptor discharge
• Decrease in central venous pressure and/or volume
• Cerebral ischemia (when BP falls below 60 mmHg and brain blood flow falls / most intense of all activation of the activation of the sympathetic nerves)

Question 425

What are the additional compensatory mechanisms to shock in addition to the autonomic nervous system?

Answer 425

• Rapid and shallow breathing -> respiratory pump promoting venous return
• Release of renin from the kidneys (sympathetic stimulation) -> angiotensin II which is a potent vasoconstrictor and promote thirst sensation / aldosterone which promotes renal sodium retention
• Increased level of vasopressin from the posterior pituitary gland in response to decreased firing of the cardiopulmonary and arterial baroreceptors
• Increased level of circulating epinephrine (sympathetic stimulation)
• Net shift of fluid from the interstitial space into the vascular space (decreased capillary hydrostatic pressure due to arteriolar constriction)
• Increased glyconeogenesis by the liver (epinephrine and norepinephrine) increasing BG, increasing extracellular osmolarity by as many as 20 mOsm -> net shift of fluid from the intracellular space to the extracellular space

Question 426

Define heart failure

Answer 426

The hearts inability to meet the metabolic needs of the peripheral tissues, or instances when the heart can only do so in the presence of increased venous filling pressures

Question 427

Name two of the most important neuro-hormonal systems in regards to heart failure

Answer 427

SNS (sympathetic nervous system) and RAAS (renin-angiotensin-aldosterone system)

Question 428

Typical sigsn of low cardiac output

Answer 428

weakness, activity intolerance, hypothermia, depressed mentation

Question 429

Inadeqaute tissue perfusioin results in which labratory abnormalities?

Answer 429

azotemia, oliguria, lactic acidosis

Question 430

Name the primary trigger for activation of the RAAS

Answer 430

the heart’s inability to provide normal renal perfusion

Question 431

What induces renin release from the macula densa

Answer 431

decreased renal blood flow and sodium delivery to the distal portion of the neprhon

Question 432

Renin converts ____ to produce ____

Answer 432

angiotensinogen to angiotensin 1

Question 433

angiotensin 1 is rapidly converted to _____ by _______

Answer 433

angiotensin 2 by ACE (angiotensin-converting enzyme)

Question 434

where is angioten 1 converted to angiotensin 2 by ACE?

Answer 434

pulmonary vasculature

Question 435

list the maladaptive responses which result from angiotensin 2 in regards to cardiac injury

Answer 435

renal sodium and water retention, production of aldosterone, myocardial apoptosis, cardiac and vascular remodeling and fibrosis, increased thirst, and vasoconstriction

Question 436

Name the main effector molecules of the SNS

Answer 436

Nor-epi and epi

Question 437

In times of danger, the SNS has what effects through epi and norepi

Answer 437

increased HR, cardiac output, and increased blood flow to important stress response oprgans such as skeletal muscle

Question 438

chronic activation of the SNS leads to what?

Answer 438

adrenergic receptor downregulation, persistent tachycardia, increased myocardial oxygen demand and myocyte necrosis

Question 439

myocardial tissue produced what two main hormones that induce natriuresis, diuresis and vasodilation

Answer 439

ANP (atrial natriuretic peptide and BNP (b-type natriuretic peptide)

Question 440

ANP and BNP are produced in response to what

Answer 440

myocardial stretch

Question 441

reasons for loss of natriuretic peptide efficacy

Answer 441

natriuretic receptor downregulation , inappropriate or inadequate production, or increased peptide clearance or degredation

Question 442

Endothelin 1 is a potent vaso (constrictor/dialator)

Answer 442

constrictor

Question 443

What produces endothelin 1

Answer 443

vascualr endothelial cells in repsonse to sheer stress, angiotensin 2 and other various cytokines

Question 444

endothelin 1 works with angiotensin 2 to cause ______ and ______

Answer 444

vasoconstriction and increased cardiac afterload

Question 445

Dogs and cats in heart failure have an elevated/decreased endothelin 1 level

Answer 445

elevated

Question 446

In addition to its vascualr effects, endothelin 1 alters what else?

Answer 446

normal calcium cycling within muscle cells and is directly cytotoxic to myocardioctyes

Question 447

what is the function of ADH (vasopressin)

Answer 447

increases re-absorption of free water within the renal collecting duct

Question 448

how does vasopressin worsen heart disease?

Answer 448

the increase in fluid retention leads to fluid overload, congestive heart failure, and dilutional hyponatremia

Question 449

In both humans and veterinary pateitns, dilutional hyponatremia is a marker of what?

Answer 449

severe neurohormonal activation and is a poor prognostic signs

Question 450

name three signaling molecules that can cause cardiac hypertrophy

Answer 450

angiotensin 2, norepi, and aldosterone

Question 451

What conditions cause concentric hypertrophy?

Answer 451

conditions that cause pressure overload such as systemic hypertension or subaortic stenosis

Question 452

Pathophysiology of how concentric hypertrophy occurs

Answer 452

increased afterload triggers replications of sarcomeres in the parallel, resulting in an increase in the relative thickness of the ventricular walls

Question 453

List some limitations of concentric hypertrophy

Answer 453

increased myocardial oxygen demand, endocardial ischemia, fibrosis, collagen disruption, injury to small coronary vessels, myocardial slippage, wall stress

Question 454

Pathophysiology of myocardial remodeling in instances of volume overload

Answer 454

(mitral valve regurg, DCM, etc), sarcomeres replicate in series leading to elongation of myocytes and dilation of the ventricular chamber

Question 455

Overall myocardial contraction pathway

Answer 455

During systole Ca enters myocardial cell which striggers release of additional Ca from the SARCOPLASMIC RETICULUM Ca from the SR flows through the RYANODINE channel and binds to TROPONIN C located on the ACTIN/MYOSIN complex.

Question 456

The majority of Ca responsible for myocardial contraction comes from where?

Answer 456

the sarcoplasmic reticulum inside the cell

Question 457

What receptor is responsible for Ca release from the sarcoplasmic reticulum

Answer 457

Ryanodine

Question 458

Once Ca has been released from the SR, where does it go?

Answer 458

Ca binds to troponin C on the actin molecule

Question 459

Describe the pathophys pathway of myocardial relaxation

Answer 459

Ca ions are released from troponin C and sequestered back into the SR through the sarcoplasmic reticulum Ca ATPase (SERCA) channel. Other effector molecules such as PHOSPHOLAMBAN regulate the reuptake of Ca

Question 460

After Ca is released from troponin, where does it go?

Answer 460

Back to the sarcoplasmic reticulum

Question 461

what channel does Ca travel through to re-enter the SR?

Answer 461

Sarcoplasmic/endoplasmic reticulum Ca ATPase channel (SERCA)

Question 462

Does phospholamban allow or inhibit the reuptake of Ca via the SERCA channel?

Answer 462

inhibits

Question 463

Myocyte mitochondria provided high energy phosphate molecules that fuel ………..

Answer 463

Ca pumps, ion pumps, sarcomeres contraction, sarcomeres relaxation, maintencance of the resting cell membrane potential, and propagation of the cardiac action potential

Question 464

In heart failure, the heart preferentially uses what energy source and why?

Answer 464

glucose –> requries less oxygen to metaboilize than fatty acids

Question 465

Define the Frank starling law

Answer 465

A mechanism which states that an increase in the initial volume or pressure within the ventricles increases the strength of the subsequent ventricular contraction

Question 466

Excessive amounts of (preload/afterload) result in CHF

Answer 466

preload

Question 467

Classic example of diastolic heart disease

Answer 467

hypertoprhic cardiomyoiptahty in cats

Question 468

Three things that affect ventricular compliance

Answer 468

1 - thickness of ventricular wall, 2- changes in cytoskeleton, 3 - function of the pericardium

Question 469

TX of diastolic dysfunction

Answer 469

targeted at improving ventricular relaxation, increasing ventricular compliance, and alleviating existing pericardial disease

Question 470

Class A heart disease

Answer 470

Patients at risk - no detectable cardiac disease (IE, dobermans, maine coon cats)

Question 471

Class B heart disease

Answer 471

Patients with diagnostic evidence of heart disease

Question 472

Class B1 heart disease

Answer 472

Patients with no radiographicor echocardiographic evidence

Question 473

Class B2 heart disease

Answer 473

Patients with radiographic or echocardiogenic evidence

Question 474

Class C heart disease

Answer 474

Pateints which have ben in heart failure

Question 475

Class D heart disease

Answer 475

Patients with severe to debilitating heart disease even at rest

Question 476

Pulmonary venous pressures greater than ____ and systemic venous pressures greater than ____ are sufficient to produce congestion that manifests are pulmonary edema, pleural effusion, ascites

Answer 476

Pulmonary >25mmHg, systemic >20mmHg

Question 477

Common causes of left sides HF in dogs

Answer 477

mitral valve disease, DCM, PDA

Question 478

Common causes of left sides HF in cats

Answer 478

hypertrophic or restrictive cardiomyopathy

Question 479

common causes of right sided HF in dogs

Answer 479

DCM, degernative or congenital tricupside valve disease and pulmonary hypertension