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First Year Veterinary School > Physiology I- Cardiology/ Blood Exam 3 study > Flashcards

Physiology I- Cardiology/ Blood Exam 3 study Flashcards

1
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Sinus Arrhythmia

Variable heart rate ( increases and decreases in frequency within the same strip)

Originates in the SA Node ( is often benign)

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2
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Premature atrial complex.

Caused by irritation of atria, increased automacity. Classically seen as narrow QRS with upright P wave and sometimes different morphology.

Originates in the SA node.

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3
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Premature Ventricular Complex.

Comes from irritation of ventricle. Wide QRS complex, no P wave, Twave opposite R wave (usually benign)

  • lead one will show positive voltage in abnormal complex
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4
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Sinus bradycardia

HR <60 bpm, athletic dogs may have decreased hr. Can be signs of nervous system issue, medication side effect disease ect.

Seen as Narrow QRS, with an upright P wave.

SA node is pacemaker but rate is abnormally slow and irregular. (Arrhythmias present)

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5
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Sinus Tachycardia

HR >100 ( also depends on size of dog)

Causes: Increased sympathetic response, pain, fever, hypovolemia, increased O2 demand.

Characteristics: Narrow QRS, Upright P wave followed by positve T wave.

Rapid HR initiated by SA node.

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6
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Supraventricular tachycardia

Characteristics: Indistinguishable P wave narrow QRS, Fairly regular rhythm

Causes: Same as Sinus Tachy/ increase sympathetic response.

Origine: AV node

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7
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Atrial Fibrilation

Characteristics: Chaotic rhythm (not organised), No atrial kick, decreased preload, can affect BP. Narrow QRS, Absent/ chaotic P wave, irregular, F waves present.

Causes: Damage to structure.

Concerns: Blood doesnt move as it should so patient is at high risk of thrombus.

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8
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Ventricular Tachycardia

Characteristics: P waves if present are obsucred by large ventricular complexes. Sometimes you can see normal complexes trying to reestablish NSR. Degenerates frequently into V fib.

Causes: Cardiac drug toxicity, electrolyte imbalance, ventricular irritation, ect.

Origin: Ectopic pacemajers in ventricles

***Potentially leathal Rhythm***

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9
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Ventricular Fibrillation

Characteristics: Chaotic with no discernable pattern. Atria may / may not be fibrillating. Ventricles are just quivering and cannot pump significant cardiac output even if atria continues to pump. NO QRS.

*** LEATHAL RHYTHM, CAN ONLY BE REVERSED WITH MECHANICAL FIBRILLATION***

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10
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

1st Degree AV Block

PR interval: Dogs: >0.13 secs , Cats: >0.09 secs

Abnormally slow AV conduction, Each QRS has postive P wave and is followed by a negative T wave.

Origin: AV node

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11
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

2nd Degree AV Block

Characteristics: p waves alone sometimes, not with QRS at all times, indicates some atrial depolarization outside of AV node. Delay present between QRS and T wave. PR interval normal when p wave followed by QRS.

Not life threatening unless there is so many missed ventricular beats that cardiac output falls to dangerous levels.

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12
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

3rd Degree AV Block

Characteristics: QRS not preceeded by p waves. QRS-T waves made by auxillary (emergency) pacemakers. Atrial rate much higher than ventricular rate. Ventricles beat slowly in response to auxillary pacemaker down AV node. ST depression also present but is irrelavent to AV Block diagnosis.

Origin: Auxillary emergency pacemakers.

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13
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Right Ventricular Hypertrophy

Characteristics: polarity of QRS on lead I usually is negative, which indicates a right shift or that the mass of the right ventricle has increased or both. Abnormally high voltages of QRS are recorded on leads II and III which indicate ventricular hypertropy. Pronounced negative components in the QRS recorded in leads II and III suggest that ventricular depolarization, the prominent direction is away from the LHL.

Causes: Usually caused by lung issue/ issue with heart structure.

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14
Q

What rhythm is presented here? What is the classic characteristics? In what location does it originate?

A

Tamponade or Pericardial Effusion ( similar EKG seen in Pleural effusion as well)

-Characteristics: Abnormally low EKG Voltage. This occurs because pericardial fluid creates a short circut for the ionic currents that would normally flow to the surface. The voltages are smaller than normal created at body surface.

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15
Q

What is the function of blood?

A

Transport of nutrients, oxygen, carbon dioxide, waste products, hormones, heat, and immune system
components

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16
Q

What is the pH of blood?

A

about 7.4 (venous is slightly more acidic then arterial blood)

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17
Q

What makes up blood plasma?

A

Mostly water, protiens (albumin, globulins, fibrinogen, ect), other solutes (electrolytes, nutrients, BUN/Creat) Nutrients, Gases, Hormones, Enzymes.

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18
Q

What is a hematocrit?

A

Amount of cellular components of the blood ( 99% erythrocytes, 1% leukocytes) (other 99% leukocytes in lymphatic organs)

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19
Q

What is the reason for the hematocrit difference in cold blooded and warm blooded horses?

A

Cold blooded (28-44%)

Warm blooded ( 32-53%)

Metabolism difference.

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20
Q

What can account for differences in hematocrit values?

A

Altitude changes ( higher altitude = increased RBC production, Erythropoetin is incerased)

Differences in the number or size of RBC

Nutrition, Physical activity, metabolism.

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21
Q

How does exercise affect hematocrit?

A

Increased hematocrit during exercise is due to increased sympathetic nervous system which mobilizes erythrocytes both from the spleen and other parts of cardiovascular system.

More work = more RBC being released from reserves.

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22
Q

What does a erythrocyte look like? What do they do?

A

Circular, flattened, bi concave in most species wirh thin middle part (pallor). Non nucleated except in avian. reptile, amphibian. Diameter 4-8 um

Cammelids ( oval RBC), Cats ( smaller pallor), Horses (Rouloux), Cows (varied sizes)

Chickens have lowest number but RBC are larger so they are not anemic.

Goats have small rbc but they have alot more then other species so it also does not affect anemia.

RBC transport O2 to the cells of the body via hemaglobin and remove CO2 from tissues.

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23
Q

What must be part of Hemaglobin for it to bind to O2?

A

Must have divalent Fe (iron)

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24
Q

What is hematopoiesis?

A

Formation of blood cells

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25
Q

What is erythropoeisis?

A

Formation of RBC

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26
Q

Where does erythropoeisis occur in fetal life?

A

Liver and Spleen

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27
Q

Where does erythropoeisis occur from birth until adolesence ?

A

Long bones ( tibia and femur)

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28
Q

Where does erythropoeisis occur in from adolescence onward?

A

Flat bones (vertebrae, pelvis, sternum, ribs)

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29
Q

What is the stem cell that all blood cells are derrived from?

A

Pluripotent stem cell

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30
Q

What cells are predestined to become erythrocytes?

A

Pro erythroblasts and erythroblasts.

The hemaglobin concentration will gradually increase, and the nucleus will become smaller and finally disapears (reticulocytes)

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31
Q

What is needed for proper erythropoeisis?

A

Iron ( for Hb synthesis)

Vitamin B12 and folic acid ( synthesis for DNA for cell division)

Erythropoietin (34 kDa glycoprotien, produced in kidney and upregulated by low O2 tension in tissues)

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32
Q

What is polycythemia?

A

An increased number of erythrocytes ( seen at high altitudes, and in erythropoietin doping)

  • When hematocrit increases so does blood viscosity. Increased viscosity makes it difficult for the heart to pump polycythemia blood. Therefore polycythemia causes a heavy workload for the heart and can lead to failure. Particularly if the cardiac muscle is not healthy.
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33
Q

What mediates the destruction of old erythrocytes, and where does it occur?

A

Macrophages, and occurs in liver, spleen, and bone marrow.

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34
Q

What is anemia and what are the causes/ symptoms?

A

Conditions where the capacity of blood to transport O2 is reduced.

Causes: Blood loss (hemorrhage), RBC destruction ( hemolysis), Decreased RBC production (erythroid hypoplasia)

Symptoms: Pale MM, Depression, Lethargy, Weakness, Exercise intolerance, Jaundice (icterus if Bilirubin concentration is > 2mg/dL), Splenomegaly, Recombancy, seizures, syncope, coma.

* Could be low Hematocrit ( abnormally few RBCs in each deciliter blood) or Low MCH and or MCHC: abnormally low hemoglobin concentration in each RBC. Cardiac increase must be increased above normal to deliver normal O2 to tissues each minute. Necessity to increase cardiac output also imposes increased workload on heart and can lead to failure in diseased heart.

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35
Q

How are anemias classified?

A

Morphology ( erythrocytes in micro, macro, and normocytic)

Hb content ( in erythrocytes in hypo, hyper, normochromic)

Regeneration (ability of bone marrow in regenerative and non regenerative)

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36
Q

What is values helps you determine anemia types and how?

A

Mean corpuscular volume (MCV) If increased macrocytic anemia, if decreased microcytic anemia.

Mean corpuscular hemoglobin (MCH) If increased hyperchrome, if decreasd hypochrome

Mean corpuscular hemoglobin concentration (MCHC) avg # of hemaglobin within erythrocytes

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37
Q

How do you determine regenerative vs. non regenerative anemias?

Regenerative

A

Regenerative anemia will have increased #’s of circulating reticulocutes which indicates increased bone marrow erythropoiesis

Causes: hemorrhage ( gastric ulcer, trauma, hemostasis defect, parisitism)

Hemolysis:

  • Intrinsic defects ( mostly congenital: hemoglobin defects, sickle cell, membrane deformation, enzyme deficiencies)

Extrinsic defects ( mostly acquired): chemicals ( methemoglobin formation, denaturation of Hb), Parisitism (bartonella, babesia, mycoplasm, rikettsia), immune mediated ( hemolytic anemia of newborn)

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38
Q

How do you determine regenerative vs. non regenerative anemias?

Non- Regenerative

A

Non- Regenerative: low number of reticulocytes, no increased erythropoiesis

Function of bone marrow impaired: FELV, Chemo, Congenital

Extramarrow diseases: Chronic renal failure, liver disease, B12 deficiency, Iron deficiency.

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39
Q

Piglets with microcytic, hypochromic anemia: Tell me about them?

A

Piglets grow rapidly in first few weeks, in modern rearing they dont get access to soil/ other iron sources. Iron pool is only sufficient for first few days. Must be supplemented with Iron to help piglets thrive. Given within first 2 weeks of life. Those who got it sooner increased in body mass quicker.

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40
Q

What are WBC and what are their characteristics.?

A

WBC

Big nucleus (sometimes segmented), with many organelles

No hemoglobin

Function is immune response, and perform at sites of inflammation, infection ect.

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41
Q

What is the functions of lymphatic system?

A

Transport of fluid, protiens, fat, pathogens and antigens.

Big lymph vessels are surrounded by smooth muscle cells, and have endothelial valves which enable lymph to move in one direction.

  • recovered lymph makes its way to the thoracic duct and then to the blood.
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42
Q

What are platelets derrived from?

A

Megakaryocytes

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43
Q

Innate vs. Adaptive immunity

A

Innate: Immediate destruction ( phagocytosis) and alert immune system.

  • Cell mediated: macrophages, granulocytes, dendritic cells.

Adaptive immunity: Creates memory, delayed/ acts later

  • Cell mediated: T lymphocytes ( Helper T cells and Cytotoxic T cells)
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44
Q

What cells are granulocytes and what to they do in general terms?

A

Granulocytes are the Neutrophils, Eosinophils, and Basophils. Each have specific functions/ triggers but in general they engage in phagocytosis.

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45
Q

What are Agranulocutes and what do they do in simple terms?

A

Agranulocytes include lymphocytes and monocytes.

Lymphocytes will become B lymphocytes, T lymphocytes, or natural killer cells.

Monocytes will become tissue specific macrophages ( which have Toll like receptors) and participate in phagocytosis and cytokine release.

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46
Q

What are the mechanisms of hemostasis that minimize or prevent blood loss?

A

Contraction of injured vessel, formation of platelet plug, and coagulation of blood.

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47
Q

What is the job of prostacyclin?

A

Inhibits activation of blood platelets.

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48
Q

What increases the adhesiveness of blood platelets within a wound?

A

ADP and TXA2 ( thromboxane A2)

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49
Q

In the coagulation cascade what is intrinsic activation?

A

All factors participating in the cascade are present in the blood. Occurs when blood comes into contact with collagen fibers or with surfaces other from endothelium (this also occurs inside a test tube

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50
Q

In the Coagulation cascade what is Extrinsic activation?

A

Triggered by a tissue factor (tissue thromboplastin, factor III) that is not present in the blood but is released from surrounding tissues upon tissue damage

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51
Q

What electrolyte is needed for blood coagulation?

A

Calcium

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52
Q

What is fibrinolysis and what is plasmin?

A

Fibrinolysis is slow process and begins right after clot formation

Plasmin is an active proteolytic enzyme that will slowly dissolve clot.

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53
Q

What are some clinical considerations in regards to the clotting cascade?

A

Hemophillia: congenital deficiency of coag factors VIII (Hemophillia A) and IX (hemophilla B)

Vitamin K: Required by liver for synthesis of coag factors.

Warfarin ( present in rat posion): inhibits action of Vitamin K and because of that reduces concentration of several clotting factors.

Acetylsalicylic acid (asprin) inhibits synthesis of thromboxane X2 so it inhibits formation of platelet plugs

Many anticoagulants are Ca++ chelators ( edta, citrate)

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54
Q

What are ABO blood group antigens?

A

Glycosphingolipids ( and the difference is just one additional compound at the end of the chain. )

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55
Q

How does blood donor- recipient interaction work?

A

Universal donors are type O blood because they dont have A or B antigens. They cannot receive blood with A or B antigens however. AB blood type can receive blood from anyone.

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56
Q

What can happen with administration of the wrong transfusion?

A

Anaphylaxis, hemolytic anemia, agglutination, destruction of RBC

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57
Q

What is the significance of RhD ( Rhesus blood group D antigen) ?

A

RhD allel is mutated in 15 % of population (deletion).

Generation of antibodies against Rh+ patients.

This is extremely dangerous when transfusing blood from an incompatible donor.

Pregnant women who are Rh- and have a fetus that is Rh+ can pass antibodies through placenta and can cause hemolytic anemia in the fetus, first pregnancy is normally unproblematic though.

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58
Q

What is Neonatal isoerytholysis?

A

Hemolytic disease of newborn.

During pregnancy Aa- mares can be immunized by Aa+ fetuses during pregnancy.

Upon second antigen contact the mother will have IgGs against Aa+ RBC of the fetus. After birth IgGs will be taken up by foal from colostrum and this will go to blood stream and cause hemolytic anemia in the foal.

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59
Q

TRUE or FALSE: If you are doing a cross match and the final match has agglutination you should use the transfusion.

A

FALSE

Positive cross match = do not transfuse with that unit.

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60
Q

In Ischemic / infarcted areas of the ventricle, how does that affect the AP within the heart?

A

The portion of the ventricle that is infarcted remains depolarized at all times, and cannot return to resting membrane potential.

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61
Q

What are the major components of the cardiovascular system?

A

The major and broad components of the cardiovascular system consists of Heart blood vessels and blood. This helps to transport blood, O2 to brain and other organs. These “tubes”/ vessels also transport blood / CO2 to the lungs to be oxygenated, and carries waste for appropriate disposal.

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62
Q

What are the four valves in the heart and their functions?

A

Mitral Valve, Aortic Valve,Tricuspid Valve, Pulmonary Valve: Their job is to keep blood flowing in one direction/ prevent back flow.

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63
Q

Which circulation provides the blood supply to the heart itself?

A

Central circulation: specifically coronary arteries

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64
Q

What are the 3 kinds of circulation?

A

◦ Pulmonary circulation: Blood vessels of lungs, including pulmonary arteries and veins.
◦ Systemic circulation: The blood vessels between the aorta and venae cavae are collectively called systemic circulation.
◦ Central circulation: The heart and pulmonary circulation

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65
Q

What are the systolic aortic pressure and the diastolic pressure?

A

Systolic aortic pressure: Aortic blood pressure at peak after aorta is distended with blood from left ventricular contraction. (Approximately 120 mmHg)

Diastolic pressure: Minimal value or aortic BP before next cardiac ejection ( blood continues to flow between ejection into downstream arteries, this cause aortic pressure to decrease) (Approximately: 80 mmHG)

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66
Q

What are the systemic perfusion pressure, pulmonary perfusion pressure, and their differences?

A
  • Systemic Perfusion Pressure: mean aortic pressure - mean venae Cavae pressure = systemic perfusion pressure
  • Pulmonary Perfusion pressure: pulmonary artery blood pressure - mean pressure in pulmonary veins= Pulmonary Perfusion pressure
  • Perfusion pressure for systemic circulation is much greater than the perfusion pressure for pulmonary circulation.

Systemic = high pressure, high resistance

Pulmonary circulation = low pressure, low resistance.

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67
Q

What are the major functions of the splanchnic portal system, renal portal system and hypothalamic/ hypophyseal portal system?

A

◦ Splachnic portal system: Directs blood flow to the abdominal GI organs including, stomach spleen, small and large intestines, pancreas, and liver.
◦ Renal portal system: blood from caudal vein to kidneys via two renal portal veins.
◦ Hypothalmic- hypophyseal portal system: System of blood vessels in the microcirculation at the back of the brain.

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68
Q

What are the differences between serum and plasma?

A
  • Plasma is the liquid, cell - free part of blood that has been treated with anticoagulants. ( contains clotting factors)
  • Serum: is the liquid part of blood after coagulation, therefore devoid of clotting factors.
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69
Q

What is the mean corpuscular hemoglobin (MCH)?

A

The mean quantity of hemoglobin in each RBC. (Normal is: 21-26 pga)

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70
Q

What is the mean corpuscular hemoglobin concentration (MCHC)?

A

The mean quantity of hemoglobin in each Deciliter of packed RBCs. (Normal is: 32-36 g/dL)

71
Q

What is hematocrit?

A

Percent by volume of RBC in blood. (Normal is 35-57%)

72
Q

How is carbon dioxide (CO2) transported?

A

Most of CO2 becomes hydrated to form bicarbonate (HCO3-) or combines with hemoglobin or plasma proteins to form carbamino compounds. Only small portion of CO2 in blood is carried in dissolved form.

73
Q

What are bulk transportation and its driving force?

A

Bulk transportation is the transport of blood through the heart and blood vessels. The source of energy for bulk flow is its perfusion pressure. Perfusion pressure is the pressure difference that causes blood to flow through blood vessels.

• Transmural pressure (distending pressure) is pressure difference between blood pressure inside vessel and fluid pressure in tissue immediately outside vessel.
◦ Equations:
‣ Perfusion Pressure = P[inlet] - P[outlet]
‣ Transmural Pressure = P[inside] - P[outside]

74
Q

What is diffusion and its driving force?

A

Diffusion is the slow transport of nutrients and wastes from an area of high concentration to low concentration. It is a major mode of transport that occurs at capillaries, and every metabolically active cell in the body must be close to a capillary carrying blood via bulk flow.

75
Q

What are the locations and characteristics of sinoatrial and atrioventricular pacemaker cells?

A

◦ The SA node is in the right atrial wall, near where the venae cavae enter the right atrium. SA nodes spontaneously depolarize most quickly to threshold. In resting dog the ventricular rate from SA node cells is 80-90 BPM. Each heartbeat is initiated by a spontaneous action potentials in one of the pacemaker cells of the SA node.
◦ AV Node and bundle of his is in the interventricular septum. The only route of propogation of action potentials is from the atria to the ventricles. Slow conduction of action potentials which creates delay between atrial and ventricular contractions. AV node also exhibits spontaneous pacemaker activity.

76
Q

What are the characteristics of ectopic pacemaker cells?

A

twin properties of slow conduction of action potentials and an ability to conduct action potentials in only one direction. Occurs in damaged heart cells.

77
Q

How do Na+, Ca2+, and K+ channel changes correspond to the action potential phases in pacemaker cells?

A

◦ Pre-potential: K+ channels close and open Na+ channels, Na+ slowly influxes in.
◦ Depolarization: (atria contraction) Ca2+ channel opens and there is a rapid influx of CA2+.
◦ Repolarization: Open of K+ channel which allows outflow of K+

78
Q

How do Na+, K+, and Ca2+ channel changes correspond to the action potential phases in cardiac
muscle cells?

A

◦ Phase 0: Sodium channels are open due to depolarization threshold. Causing rapid depolarization
◦ Phase 1: Na+ channels inactivate which causes Na+ permeability to decrease quickly. Membrane begins to repolarize.
◦ Phase 2: Subsequently, some types of K+ channels close so K+ permeability decreases. In addition many gated Ca2+ channels open so Ca2+ permeability increases. These actions keep the cell membrane in the depolarized state for 200ms which causes the prolonged plateau of depolarization. (Ca2+ entering cell triggers more Ca2+ to be released from the sarcoplasmic reticulum.
◦ Phase 3 and 4: K+ channels reopen and Ca2+ channels close, which causes the cell to repolarize (Phase 3) and eventually return to its stable negative resting potential (phase 4)

79
Q

How is resting membrane potential created in cardiac muscle cells?

A

◦ With each pump cycle a Na+,K+ exchanger transfers three Na+ out of a cell and 2 K+ cells into a cell. This imbalance creates a small negative resting membrane potential.
◦ There are also many K+ leakage channels and very few open Na+ channels, so their is a greater tendency for positive K+ to exit the cell then for positive Na+ to enter. This charge imbalance is the main contributor to the normal, negative resting membrane potential.
◦ In resting cardiac cells the membrane Ca2+ channels are closed so Ca2+ permeability is low and extracellular Ca2+ is prevented from entering cardiac cells.

80
Q

What are the differences in action potentials between skeletal and cardiac muscle cells?

A

◦ Cardiac muscle cells are electrically linked to one another with specialized gap junctions allowing ionic currents to flow into neighboring cells and initiate action potentials. Cardiac cells form a functional syncytium. Skeletal Muscles are electrically isolated from one another
◦ Action potential lasts 100x longer than in skeletal muscle. Cardiac: 200-250 ms. Skeletal: 1-2 ms. Cardiac muscle cells also has long refractory period.

81
Q

How do the norepinephrine and epinephrine (sympathetic nerve) regulate pacemaker cells and cardiac muscle cells?

A

◦ They activate B-adrenergic receptors on the cell membranes of pacemaker cells and leads to elevated HR.
◦ In cardiac muscle cells: B adrenergic receptors lead to taller (more positive) plateau, Shorter duration of action potentials, and quicker, stronger, and shorter duration contractions.

82
Q

How does acetylcholine (parasympathetic nerve) regulate pacemaker cells and cardiac muscle cells?

A

◦ Acetylcholine activates muscarinic cholinergic receptors on the cell membranes of pacemaker cells which decrease heart rate.
◦ Does the opposite of above and exert strong anti-sympathetic influences on all the atrial cells. (Not ventricular because very few ventricular cells receive direct parasympathetic innervation).

83
Q

What are the differences in functions between the sympathetic nerve and parasympathetic nerve in
ventricular muscle cells?

A

◦ Parasympathetic neurons exert indirect effect on ventricular muscles. Parasympathetic neurons release their acetylcholine onto sympathetic neuron terminals. This inhibits release of norepinephrine, and weakens the effects of sympathetic activation on ventricular cells.

84
Q

How do the sympathetic and parasympathetic activities change in a dog’s daily life?

A

Overlapping control- varies based on activity/ behavior.

Stressed/ animals exerting = more sympathetic nerve activity

S leeping or resting/ non exerting = more parasympathetic nerve activity.

Walking or doing minimal exertion will be at the intrinsic rate/ have equal parasympathetic and sympathetic influence or if they have an absence of both.

85
Q

What is the characteristics and treatment of sick sinus syndrome?

A

◦ Characteristic:
‣ Extreme: Sinus arrest. SA node completely fails to form action potentials. Auxilary pace maker function fo AV node keeps ventricles beating at very low rate.
‣ Less Extreme: Sluggish depolarization of SA node pacemaker cells, abnormally low intrinsic HR. Usually exhibit bradycardia and insufficient increase in HR during exercise.
◦ Treatment: Atropine (cholinergic muscarinic antagonist drug), Isoproterenol ( B-adrenergic agonist drug), Artificial cardiac pacemaker.

86
Q

What is the characteristics/ treatment of tachycardia?

A

Dependent on the type but would say usually some sort of Beta1adrenergic antagonist and/ or some sort of muscurinic agonist/ chollinergic substance

87
Q

What is the characteristics/ treatment of ventricular fibrillation?

A

◦ Characteristic: Each tiny region of ventricular wall contracts and relaxes at random in response to action potentials that propagate randomly and continuous throughout ventricles. Synonymous with sudden cardiac death.
◦ Treatment: Only treatment is electrical defib

88
Q

What are the types of av blocks, their characteristics, and possible treatments?

A

◦ Characteristics:
‣ 1st degree: AV node transmits all action potentials but slowly. Calm dog transmits even slower.
‣ 2nd degree: AV node transmits some action potentials. Some Action potentials pass.
‣ 3rd degree: Complete block of AV node. No action potentials pass from atria to ventricles
◦ Treatment:
‣ Must be treated if resulting ventricular rate is too low or to maintain adequate blood flow to body,
‣ Atropine (cholinergic muscarinic antagonist drug), Isoproterenol ( B-adrenergic agonist drug), Artificial pacemaker- applied to ventricles .
◦ Causes: Cardiac trauma, toxins, viral/bacterial infection, ischemia, congenital heart defects, cardiac fibrosis, inadvertent damage of AV node during surgical repair of a ventricular septal defect.

89
Q

What is the working mechanisms of the major antiarrhythmic drugs? Specifically Local anesthetics?

A

Examples: quinidine, lidocaine, procaine

Act by binding to some of the
voltage-gated Na+ channels (fast Na+ channels) in cardiac muscle cells and preventing them from opening, which counteracts membrane depolarization and action potential formation.

90
Q

What is the working mechanisms of the major antiarrhythmic drugs? Specifically Cardiac glycosides?

A

Example: Digitalis

Inhibits the Na+,K+ pump in cell membranes. Increase cardiac contractility. Keeps resting membrane potential less negative as normal, cardiac cells do not repolarize fully at end of action potential. Acts on CNS and causes increase PNS tone. Allow more Ca2+ to accumulate inside cardiac cells, which increases strength of cardiac contraction.

91
Q

What is the working mechanisms of the major antiarrhythmic drugs? Specifically calcium channel blockers?

A

Examples: verapamil, diltiazem, and nifedipine

Bind to L- type (slow) Ca2+ channels and prevent them from opening, this decreases the entry of Ca2+ into cardiac muscle cells during action potential. This lowers the plateau ( membrane potential less positive) and lengthen the action potential (Slower opening of K+ channels. Also decrease strength of cardiac contractions.

92
Q

What is the working mechanisms of the major antiarrhythmic drugs? Specifically Beta adrenergic antagonists?

A

Example: propranolol

Bind to some of the b-adrenergic receptors
on cardiac cells and prevent their activation by norepinephrine from sympathetic nerves or
by circulating epinephrine and norepinephrine from the adrenal medulla.

A. Decreasing heart rate;

B. Lengthening refractory period;

C. Slowing conduction of action potentials, especially through the AV node.

D. Reverse sympathetic-induced increases in cardiac contractility.

93
Q

The two atria act like one giant cell, and the same is the two ventricles. What is the difference in
extracellular voltage between the side that depolarizes first and the side that that depolarizes later?

A

Positive wave. Action potential moves from right to left, right being negative, left being positive so you will see positive wave

94
Q

What do the six ECG leads record?

A

Measures voltage differences from right fore limb, left hind limb, and left forelimb and compares with the average voltage of the other leads.

95
Q

What do the P waves correspond to the electrical events in the heart?

A

Atrial Depolarization

96
Q

What do the QRS complex correspond to the electrical events in the heart?

A

Intraventricular septum depolarization, ventricular depolarization, depolarization of ventricular base

97
Q

What does the Q wave correspond to the electrical events in the heart?

A

Depolarization that spreads from left to right across the interventricular septum. This is the small voltage difference between left and right forelimb, with left forelimb being slightly negative compared to right.

98
Q

What does the T waves correspond to the electrical events in the heart?

A

Corresponds to repolarization of both ventricles. Not predictable. In normal dogs it follows same direction of depolarization (from inside out), creating negative T wave.

99
Q

How is the ECG chart calibrated?

A

◦ Vertical calibration: The standardized vertical calibration on an ECG is that 10 mm (two major division) equals 1 millivolt (mV).

100
Q

What do PR intervals correspond to the electrical events in the heart?

A

Time between start of atrial depolarization (start of P wave) and start of ventricular depolarization (QRS complex)

101
Q

What do QRS intervals correspond to the electrical events in the heart?

A

Time it takes for the ventricles to depolarize, once the Cardiac AP emerges from AV node/ AV bundle ( Normal: <0.1 sec)

102
Q

What do QT intervals correspond to the electrical events in the heart?

A

Beginning of ventricular depolarization to the end of ventricular repolarization. This approximates the duration of an AP in ventricular tissue (Normal: ~ 0.2 secs)

103
Q

What do PP intervals correspond to the electrical events in the heart?

A

Time between atrial depolarization/ contraction and the next atrial depolarization/ contractions. Can be used to determine atrial rate.

104
Q

What do RR intervals correspond to the electrical events in the heart?

A

Time between ventricular depolarization/ contractions and the next ventricular depolarization/contraction. Can be used to determine ventricular rate.
‣ Usually Atrial rate = ventricular rate.

105
Q

How does ECG vary among small and big animals?

A

◦ less consistent pathways followed by cardiac depolarization in atria and ventricles of large animals lead to variability with small animals
◦ ECG not useful in detecting structural cardiac abnormalities in large animals.
◦ There is consistency in basic sequence of electrical events in hearts of normal animals large and small, so ECG is useful in large animals for detecting/ categorizing cardiac arrhythmias.
◦ Lead / electrode placement that yields clearly discernible complexes is sufficient.

106
Q

How does the blood pressure change when the blood flows through the systemic circulation?

A

Blood pressure decreases as it flows through systemic circulation.

Pressure will be greatest in aorta (98 mm Hg) and least in the venacavae (~ 3 mm Hg)

107
Q

What is the mean circulatory filling pressure?

A

The blood pressure of static circulation when the heart is not pumping blood ( ~7 mm Hg)

108
Q

What are the two factors that determine the mean aortic blood pressure?

A

◦ Mean aortic blood pressure is determined by two, and only two, factors. Cardiac output and TPR or Total peripheral resistance (systemic vascular resistance)

Mean aortic pressure = CO x TPR

109
Q

How is the blood flow regulated and redistributed during exercise?

A

Cardiac output is increased and is redistributed from brain, splanchnic, and other muscles and is redistributed to skeletal muscles.

110
Q

What is the primary mechanism that controls the blood flow in an organ?

A

Vascular resistance. Specifically arteriolar resistance

111
Q

Why is the resistance of a single arteriole greater than the resistance of a capillary network?

A

This is because the resistance must be divided over the total surface area and the surface area will be larger in a capillary network, hence a lower resistance overall.

112
Q

Which has more resistance , a single capillary or a single arteriole?

A

a single capillary has more resistance then a single arteriole.

113
Q

What is the equation to find resistance? What about to find flow rate?

A

Resistance= change in pressure/ blood flow

Flow = change in pressure/ resistance

114
Q

TRUE or FALSE: Arteriolar vasoconstriction increases blood flow to the brain.

A

FALSE: It is vasodialation that can increase bloodflow to brain

115
Q

How is the mean aortic pressure regulated during hypertension?

A

cardiac output is normal. But the blood pressure is elevated because of excessively constricted systemic arterioles, which increases TPR above normal. Naturally occurring hypertension is rare in veterinary species.

116
Q

How is the mean aortic pressure regulated during severe hemorrhage?

A

The arteriole pressure is reduced in these conditions, not elevated because of decreased cardiac output. TPR is actually increased above normal because the body constricts the arterioles in the kidneys, splanchnic circulation, and resting skeletal muscle. The vasoconstriction in these organs minimizes the fall in arterial pressure.

However over time the blood pressure will decrease, and this is usually due to severe hemorrhage and decreased blood volume. ( Hypovolemia from decrease of fluid (severe dehydration) or blood volume ( hemorrhage)

117
Q

How is the mean aortic pressure regulated during exercise?

A

Cardiac output is elevated. TPR is decreased ( arterioles in exercising skeletal muscle dilates which increases skeletal muscle blood flow).

118
Q

What is the point of greatest pressure decrease in circulation?

A

The greatest pressure decrease occurs as blood flows through arterioles; that is because, the resistance to
blood flow is greater in the arterioles than in any
other segment of the systemic circulation.

119
Q

What is compliance?

A

The change in the volume within a vessel or a chamber divided by the
associated change in distending (transmural) pressure

Compliance=ΔVolume ÷ Δtransmural Pressure

120
Q

Which are more compliant, Veins or arteries?

A

Veins are about 20 times more compliant than arteries: Veins thus function as
the major blood volume reservoirs of the body.
Arteries function as pressure reservoirs. Arteries are tough vessels with low
compliance. Arteries accommodate a large increase in pressure during a cardiac
ejection and then sustain the pressure high enough between cardiac ejections to
provide a continuous flow of blood through the systemic circulation.

121
Q

What are systolic, diastolic, and pulse pressures?

A

◦ Systolic: The pressures in the aorta and pulmonary artery during each cardiac ejection.
◦ Diastolic: The minimal pressures in the aorta and pulmonary artery before each new cardiac ejection.
◦ Pulse Pressure: The amplitude of the pressure pulsations in an artery.

122
Q

How do stroke volume and heart rate affect pulse pressure?

A

◦ Increase in stroke volume increases pulse pressure (larger ejections, larger pulses) (also increase MAP/ Cardiac output
◦ Decrease in Heart rate increases pulse pressure (longer time between ejections, more blood runs out of aorta) also decreases MAP and cardiac output.
◦ Increase stroke volume + decrease in heart rate = greatly increased pulse pressures. Unchanged MAP and unchanged cardiac output. Ex: athlete, strong slow pulse at rest.

123
Q

How does arterial compliance affect pulse pressure?

A

Decrease in arterial compliance = increase of pulse pressure with unchanged MAP.

124
Q

How does patent ductus arteriosus affect pulse pressure?

A

PDA = elevated aortic systolic pressure, decreased aortic diastolic pressure ( because of the two pathways from the PDA) and this greatly increases aortic pulse pressures.

125
Q

How does aortic regurgitation affect pulse pressure?

A

Blood flows back into heart, Decrease in diastolic pressure, increase in systolic pressure, increase in pulse pressure. Heart working harder.

126
Q

What are the unique characteristics of aorta/large arteries?

A

◦ Aorta/ Large arteries:
‣ are elastic and low compliant vessels.
‣ Aorta: Wall thickness: 2 mm, Inside Diameter: 25 mm
‣ Artery: Wall thickness: 1mm, Inside diameter: 4mm

127
Q

What are the unique characteristics of arterioles?

A

◦ Arterioles:
‣ Adjust blood flow to an organ. Small arteries are called muscular vessels, and have relatively thick walls with less elastic tissue and predominance of smooth muscle. Muscular vessels vary the total peripheral resistance and direct blood flow toward or away from particular organs/ organ regions.
‣ Wall thickness: 20 um, Inside diameter: 30 um

128
Q

What are the unique characteristics of capillaries?

A

‣ Are where fluid exchange takes place. Smallest vessels are usually 0.5 mm long. Walls are especially adapted for exchange functions. Sometimes called microcirculation or exchange vessels. Have single layer of epithelial cells, form network, each cell of a tissue is within 100um of a capillary. Not all capillaries of a tissue carry blood flow at all times, pre-capillary sphincters can reduce or stop blood flow in individual capillaries. At max metabolic rate, arterioles become maximally dilated, and blood flows through all the capillaries all the time.
‣ Wall thickness: 1 um. Inside Diameter: 8um

129
Q

What are the unique characteristics of venules/veins?

A

enules/ veins:
‣ Veins are compliant vessels and are reservoir vessels. Venules and veins are larger than capillaries but capillaries have thicker walls. Primary role of veins is to serve as reservoir vessel. Veins are very complaint and can accommodate substantial changes in blood volume without much change in venous pressure.
‣ Venule: Wall thickness: 2 um, Inside diameter: 20 um
‣ Vein: Wall thicknessL 0.5 um, Inside diameter: 5 um

130
Q

What are the unique characteristics and locations of continuous, discontinuous, and fenestrated
capillaries?

A

◦ Continuous:
‣ Most widespread in body. Lipid soluble substances readily diffuse. Pores diameter is typically 4 nm. Can permit passage of water, ions, glucose and amino acids. No plasma proteins/ blood cells. Main route for delivery of plasma proteins to interstitial fluid us transcytosis. This is very slow compared to passage of small lipid insoluble substances through capillary pores and extremely slow compared to the diffusion of lipid soluble substances through endothelial cells. Can be found in fat, muscles, and nervous system.
◦ Sinusoidal/ Discontinuous:
‣ have clefts between capillary endothelial cells which are typically longer than 100 nm width. Plasma proteins (like albumin and globulin can pass through clefts. Found in liver, spleen, and bone marrow. Allows liver to transport newly synthesized proteins to enter blood and allows toxins bound to plasma proteins to get into liver and be detoxified.
◦ Fenestrated capillaries:
‣ have holes/ perforations through (not between) endothelial cells. These perforations are usually 50-80 nm in diameter, and are found in places where large amounts of fluid and solutes must pass in or out of capillaries ( like gi, endocrine glands, and kidneys)

131
Q

How is the diffusion rate altered during exercise based on Fick’s law of diffusion?

A

◦ During exercise the arterioles dilate and more of them remain open. Areolar vasodilation speeds the delivery of O2 and increases diffusion rate by increasing the area available for diffusion, decreasing the distance between each exercising muscle cell and the nearest open capillaries, and the driving force for the diffusion of O2 and metabolic substrates are increased.

132
Q

How does osmosis affect the water movement across capillaries?

A

Actual rate of water movement across capillaries is affected by both the magnitude of the imbalence between hydrostatic and oncotic forces and by the permeability of the capillary wall to water.

133
Q

What are the physical prerequisites for osmosis?

A

◦ Semipermeable membrane
◦ Difference in total concentration of the impermeable solutes on the two sides of the membrane.

134
Q

How does hydrostatic pressure affect the water movement across capillaries?

A

Hydrostatic pressure is greater on inside (18 mm Hg) then on outside (- 7 mm Hg), creating a difference of 25 mm Hg. This difference drives filtration.

135
Q

What are the functions of lymphatic vessels in water movement?

A

◦ Since there is a small net filtration between net hydrostatic and osmotic pressure of water reabsorption it allows for excess interstitial fluid and plasma proteins to be removed from the interstitial space via lymph flow.

136
Q

What are the two causes of edema?

A

◦ Excessive filtration of fluid out of capillaries.
◦ Depressed removal of excess interstitial fluid by lymph system.

137
Q

What are the factors that can cause excessive fluid filtration?

A

◦ Increase in venous BP
◦ hypoproteinemia
◦ Physical Injury/ Allergic reaction to antigen challenge

138
Q

What are the pathological conditions that can increase venous blood pressure, leading to edema?

A

◦ Application of too tight dressing on extremity.
◦ Severe pulmonic stenosis (can be caused by HW disease)
◦ Failure of right ventricle: cause increase in systemic venous pressure
◦ Failure of left ventricle: cause pulmonary edema.

139
Q

What are the pathological conditions that can cause hypoproteinemia, leading to edema?

A

◦ Decrease plasma protein production in liver
◦ Plasma protein loss from kidney diseases
◦ Severe burns

140
Q

What are the pathological conditions that can cause depressed removal of excess interstitial fluid by the lymph system?

A 
Impairment by inflammation of nodal tissue or neoplasia/tumors growing within nodes
Parasitical diseases (microfilarie lodge in lymph nodes and obstruct outflow)
141
Q

What are the intrinsic mechanisms that control vascular resistance?

A

Act within an organ or tissue and do not rely on an external influence. Histamine: acts on the arteriolar smooth muscle to relax it. Dilation of the arterioles decrease arteriolar resistance and therefore increases blood flow to the tissues), Exercise (increases metabolic rate in skeletal muscle)

142
Q

What are the extrinsic mechanisms that control vascular resistance?

A

Act from outside organ/ tissue, through nerves or hormones to alter arteriolar resistance. (Include nerve and hormones)

143
Q

When a tissue’s metabolic rate increases, what are the subsequent events that lead to an increased
supply of oxygen (O2) and washout of vasodilators?

A

First there us a release of metabolic products which are vasodialators ( ex: K+, CO2, adenosine, lactic acid)

Then this triggers a decrease in the O2 concentration and an increase in concentration of vasodialators.

Next you will have a decrease in precapilary sphincter tone, and vasodialation will occur.

Because of the decrease in precapillary sphincter tone you will have an increase in the number of open capillaries. Vasodialation will cause an decrease in arteriolar resistance .

The increase in number of open capillaries and a decrease in diffusion difference. Because of the decreased in arteriolar resistance you will have an increase in blood flow, these three things will lead to an increased supply of O2 and an increase in the washout of vasodialators.

144
Q

What are the different effects of oxygen on systemic and pulmonary vessels?

A

A high level of oxygen, for example, causes dilation of pulmonary vessels, whereas the effect in systemic vessels is vasoconstriction.

145
Q

What mechanisms cause a temporary increase above normal blood flow to the tissue after a period of blood flow restriction (reactive hyperemia)?

A

During the period when mechanical compression restricts blood flow, metabolism continues in the compressed tissue, metabolic products accumulate, and the local concentration of oxygen decreases. These metabolic effects cause dilation of the arterioles and a decrease in arteriolar resistance. Then the mechanical obstruction to flow is removed, blood flow increases above normal until the “oxygen debt” is repaid and the excess metabolic products have been removed from the compressed tissue.

146
Q

How is the autoregulation of blood flow in an organ achieved?

A

Same as reactive hyperemia but also Other mechanisms also contribute to autoregulation. However, metabolic control plays a major role in the autoregulation of blood flow, particularly in the critical tissues of a body (brain, coronary vessels, and exercising skeletal muscle)
Regardless of the status of arterioles, mechanical compression can reduce blood flow to a
tissue.

147
Q

How does mechanical compression affect coronary blood supply in the heart?

A

◦ Long-term mechanical pressure causes a prolonged period of subnormal blood flow (ischemia), which can lead to reversible tissue damage, then irreversible tissue damage, and eventually to cell death (necrosis).
◦ Mechanical compression during ventricular systole reduces the blood flow to left but not right coronary blood vessels.

148
Q

. What can cause mechanical compression in pulmonary vessels?

A

◦ Pulmonary vessels are susceptible to narrowing under the influence of mechanical compression.
◦ An abnormal elevation in airway pressure can compress pulmonary blood vessels, which could happen when a tracheal tube is attached to a source of elevated pressure. An increase in airway pressure exerts a compressing force on the pulmonary blood vessels.

149
Q

What is occuring and causes the first heart sound (S1)?

A

Associated with the closure of the AV valves (the mitral
and tricuspid valves).

150
Q

What is occuring and causes the second heart sound (S2)?

A

S2 (Second heart sound): Associated with closure of the aortic valve on the left
side of the heart and the pulmonic valve on the right side of the heart.

151
Q

What is occuring and what causes the third heart sound (S3)?

A
  1. S3 (Third heart sound): In early diastole, the rush of blood into the ventricles can
    create sufficient turbulence to vibrate the ventricular walls and create this sound.
152
Q

What is occuring and what causes the fourth heart sound (S4)?

A

If audible, occurs at the very end of diastole, as atrial systole causes a sudden rush of blood into the ventricle

153
Q

What causes a systolic murmur?

A

Mitral/ Tricuspid regurgitation/ incompetence ( the large pressure difference between ventricle and atrium causes rapid/ backward flow through partially closed valve. present in 8% of dogs over 5 years old)

Ventricular septal defect (hole/ cleft in interventricular septum)

Pulmonic/ Aortic stenosis (common congenital defect, valve fails to open widely enough)

154
Q

What causes a diastolic murmur?

A

THIS TYPE IS RARE

Tricuspid/ Mitral stenosis - atroventricular valve fails to open widely enough, filling of ventricle occurs through a stenotic valve, which creates turbulent flow and diastolic murmur. Mitral is common among humans with calcification of mitral valve from rheumatic heart disease. Tricuspid is not common as congenital defect but can occur with heavy infestion in right heart which can create a functional stenosis.

Aortic/ Pulmonic regurgitation ( insufficiency) - Aortic/ pulmonary valve does not close tightly during diastole, turbulent flow of blood regurgitates from aorta to ventricle.

Aortic regurg common in horses not dogs.

Pulmonic regurg is not common.

155
Q

What is the causes of a continuous murmur?

A

PDA: Persistence after birth of the opening between the aorta and pulmonary artery. Sometimes called machinery murmur because it sounds like rumble of machinery. Common in young dogs, more prevelant in females.

Arteriovenous fistulae: Abnormal openings between peripheral arteries and peripheral veins. Carries turbulent blood flow during both systole and diastole. Is audible at body surface close to point of fistula

156
Q

What can cardiac defects lead to?

A

Abnormally high/ low blood flow to a region of the body

Abnormally high or low blood pressure in a region of the body

Cardiac hypertrophy (enlargement of cardiac muscle)

157
Q

What are the consequences of mitral reguritation?

A

Increased volume work of Left ventricle and thus left ventricle hypertrophy. Also causes an increase left atrial pressure which leads to an increase in pulmonary venous pressure and the onset of pulmonary edema.

Consequences are usually more noticable during exercise then at rest.

158
Q

What are the consequences of mitral stenosis?

A

Increased left atrial pressure which leads to increased left atrial size and an increase of pulmonary venous pressure. The increase of left atrial size leads to afib, while the increase of pulmonary venous pressure leads to pulmonary edema.

Right ventricular hypertrophy occurs. Animals with greatly elevated left atrial pressures uusually die of the effects of pulmonary edema before they have a chance to develop right ventricular hypertrophy

159
Q

What is the consequences of PDA?

A

Increased volume work of Left ventricle and increased pulmonary artery pressure. The increase volume work of left ventricle leads to left ventricular hypertrophy, while an increase in pulmonary artery pressure increases the pressure work of Right ventricle which will then lead to right ventricular hypertrophy as well.

PDA causes exercise intolerance. Surgical repair in a young animal leads to rapid reveral of all these abnormalities

160
Q

What is the consequences for aortic stenosis?

A

A patient with aortic stenosis may be able to function normally at rest but
characteristically exhibits exercise intolerance.

161
Q

What is the consequence for aortic regurgitation?

A

Left ventricular hypertrophy; pulmonary edema may develop.

162
Q

What is the consequences of ventricular septum defect?

A

Moderate left ventricular hypertrophy; pronounced right ventricular
hypertrophy; possible pulmonary edema; probable exercise intolerance.

163
Q

What is the consequence for pulmonic stenosis?

A

Pronounced right ventricular hypertrophy.

164
Q

What part of the heart uses up the most metabolic energy / oxygen/ and coronary blood flow?

A

Left ventricle

165
Q

Which ventricle of the heart has thicker muscle?

A

Because of the high amount of pressure work done by the left ventricle compared with the right
ventricle, the left ventricle normally develops much heavier and thicker muscle walls than the right
ventricle.

166
Q

Which ventricle completes more external work?

A

Because the systolic pressure generated is about five times higher in the left ventricle
than in the right, the external work done by the left ventricle is approximately five
times greater than the external work done by the right ventricle.

167
Q

What is some characteristics of veins/ venules?

A

Veins are compliant vessels and are reservoir vessels:
• Venules and veins are larger than capillaries, but have thicker walls.
• The primary role of veins is to serve as reservoir vessels.
• Veins are very compliant and can accommodate substantial changes in blood volume
without much change in venous pressure.

  • contain some elastic tissue and some smooth muscle
168
Q

What is some characteristics of capillaries?

A

Capillaries are where the fluid exchange takes place: Capillaries are the smallest vessels, being
about 8 mm in diameter and about 0.5 mm long. Walls of capillaries are especially well adapted for their
exchange function. Capillaries are sometimes called microcirculation or exchange vessels.
They have a single layer of endothelial cells.
Capillaries form network. In most tissues, each cell of a tissue is within 100 mm of a capillary.
However, not all the capillaries of a tissue carry blood flow at all times. Contraction of precapillary
sphincters can reduce or stop the flow of blood in individual capillaries.
At maximal metabolic rate, arterioles become maximally dilated, and blood flows through all the
capillaries all the time.
- capillaries have no smooth muscle or elastic tissue.

169
Q

What is some characteristics of Arterioles?

A

Arterioles adjust blood flow to an organ: Small arteries are called muscular vessels. They have
relatively thick walls with less elastic tissue and a predominance of smooth muscle. The muscular vessels
vary the total peripheral resistance and direct blood flow toward or away from particular organs or regions
within an organ.
- contains the most muscle

170
Q

What are some characteristics of Arteries/ Aorta?

A

Aorta and large arteries are elastic and low compliant vessels: Aorta and large arteries are called
elastic vessels. They have a large amount of elastic material along with smooth muscle. However, They have low compliance. Elasticity denotes dispensability and an ability to return to the original shape after the distending force or pressure is removed.

Compliance is a measure of how much force or pressure is required to achieve distention.
Therefore, there is no contradiction in saying that the arteries are both elastic and stiff.

171
Q

TRUE or FALSE: Atrial cells have shorter action potentials then ventricular cells

A

TRUE.

Atrial cells also have shorter refractory periods, and can preform more action potentials per minuter then ventricular cells.

172
Q
  1. The two atria act like one giant cell, and the same is the two ventricles. What is the difference in
    extracellular voltage between the side that depolarizes first and the side that that depolarizes later?
A

AP moves from right to left

Right side is negative, left side is postive so you will see a positive wave between the two

173
Q

Which leads for an EKG correspond to which area?

A

Lead I: Voltage in left forelimb compared to right forelimb

Lead II: Voltage in left hind limb compared to right forelimb

Lead III: voltage in the left hind limb compared to the left forelimb.

aVr: Measures voltage from right forelimb electrode compared to all other leads

aVl: Measures voltage from left forelimb electrode compared to all other leads

aVf: Measures voltage from left hindlimb compared to all other leads.

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Q
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First Year Veterinary School (43 decks)

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