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Histo Final Exam Extravaganza! > Cardiology > Flashcards

Cardiology Flashcards

1
Q

secondary functions of the heart

A

delivery of oxygen, nutrients, and water to the living tissues as well as hormones
Removes carbon dioxide and metabolic wastes.
Thermoregulation
Supports blood flow dependent function including urine formation in the kidneys, gas exchange in the lungs, metabolism in working skeletal muscle, digestive processes and absorption, and reproductive system functions

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2
Q

3 layers of the heart

A
  1. endocardium: inner layer; single layer of endothelial cells
  2. Myocardium: middle layer thicker layer of cardiac muscle
  3. Epicardium: the outer layer of the heart that is made of a thin layer of mesothelial cells. visceral layer of serous pericardium
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3
Q

Pericardium

A

fibrous structure surrounding the heart to secure it within the mediastinal space and protect the heart. Thick outer layer of pericardium: true pericardium

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4
Q

Which animals have four chambered hearts?

A

mammals and birds

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5
Q

atria vs ventricles

A

Atria receive blood returning to the heart and the ventricles pump blood out of the heart.
Atria are low pressure and ventricles are high pressure.

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6
Q

What maintains the pressure gradient between the atria and ventricles?

A

valves

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7
Q

Which heart valve is most cranial? Is it on the right or left?

A

pulmonic valve, left

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8
Q

annulus ring

A

structure that attaches the valves.
annular stretch occurs when the heart dilates
Insulate the electrical contraction to the AV node

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9
Q

Rule 2 of the heart

A

it is a muscle

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10
Q

unique features of cardiac muscle

A

rapid depolarization and more glycogen and mitochondria to meet high energy needs
Branched with intercalated discs that facilitate rapid electrical conduction or adhere adjacent cells

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11
Q

sarcomere

A

contractile unit of the heart

contraction controlled by tropomyosin and troponin proteins

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12
Q

base vs apex

A

base is top of heart, apex is the bottom

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13
Q

heart murmurs

A

abnormal sounds that indicate turbulent blood flow and are often caused by leakage, or regurgitation of heart valves

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14
Q

A heart murmur on the left apex is likely due to which valve?

A

mitral valve

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15
Q

You auscultate a right apical murmur, Your patient likely has regurgitation of which heart valve?

A

Tricuspid valve

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16
Q

cardiac skeleton

A

provides structure for the heart. Prevents electrical activity from travelling from the atria to the ventricles. (Fibrous structures don’t conduct electricity). Insulates the bundle of His so it can conduct the signal

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17
Q

Pulmonic circulation

A

pumps blood to the lungs

Includes right heart, pulmonary arteries, pulmonary capillaries and pulmonary veins.

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18
Q

systemic circulation

A

pumps blood to the body

Includes left heart, systemic arteries, capillaries, and veins

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19
Q

“in series”

A

In a normal patient, a red blood cell will flow through the pulmonary circulation, followed by the systemic circulation.

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20
Q

Cardiac output

A

normally equal between right and left ventricles
Rate at which blood is pumped out of the ventricles per minute
= stroke volume * heart rate

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21
Q

Rule 1 of the heart

A

There are two circulations arranged in series

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22
Q

Rule 5 of the heart

A

Blood is lazy. Flows down its pressure gradient

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23
Q

For blood to flow, the circulatory system must have _____

A

a pressure gradient

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24
Q

The systemic circulation is a ____ pressure system

A

high

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25
Q

The pulmonary circulation is a ______ pressure system

A

low

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26
Q

What do these numbers mean? 120/80

A

first is the systolic pressure and the second is the diastolic pressure

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27
Q

Which organ(s) receive(s) the majority of the cardiac output?

A

Gastrointestinal tract and liver

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28
Q

Coronary circulation

A

vessels that provide oxygenated blood to the heart muscle

Vessels branch from the aorta, travel on the epicardial (outer) surface, and enter into the myocardium

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29
Q

Bronchial circulation

A

Vessels that provide oxygenated blood to the lung tissues for the metabolic needs of the lungs. Includes bronchial artery and veins.
Distinct from the pulmonary circulation

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30
Q

ischemia

A

abnormal delivery of blood

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31
Q

cyanosis

A

blue tinged mucous membranes
more than 5 g/dL of deoxygenated hemoglobin
Could be due to less oxygen due to higher altitude or pulmonary disease, tumor compressing the pulmonary artery, arterial vasoconstriction, or right to left shunts.

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32
Q

After travelling through the systemic capillary beds, how is blood returned to the right atrium?

A

Vena cavae

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33
Q

What is the direction of blood flow through the ductus arteriosus? Why?

A

From main pulmonary artery to the aorta because pulmonary is under higher pressure than the aorta because the lungs have not yet created low pressure in the pulmonary arteries

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34
Q

Explain the flow through the foramen ovale

A

Blood flow from the high pressure in the right atrium to the low pressure in the left atrium.
These pressures are flipped after birth.

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35
Q

What is a continuous murmur?

A

occurs throughout the heart cycle

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36
Q

thrill

A

the ability to feel the vibration of the murmur with your hand on the patient’s chest

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37
Q

patent ductus arteriosus

A

most common birth defect in dogs and results from failure of the fetal ductus arteriosus to close after birth.
Can be corrected with minimally invasive procedure to close the PDA with a ductal occluding device
Volume overload disease, eccentric dilation of left atrium and ventricle.
Hyperkinetic pulses
Continuous murmur cranial to the left base in the triceps brachii muscle

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38
Q

Which direction does the blood flow through a PDA in systole? Diastole?

A

from aorta to pulmonary artery in both phases (thus continuous murmur)

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39
Q

Where does gas exchange occur in the fetus vs the adult?

A

fetus uses placenta, adult uses the lungs

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40
Q

Is the pulmonary circulation a high or low pressure system in the fetus? Adult?

A

High pressure system in the fetus, low pressure system in the adult

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41
Q

Is the circuitry in the fetus parallel of systemic? Adult

A

Systemic in adult, parallel in the fetus (both the right and left ventricle pump blood into the systemic circulation)

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42
Q

ligamentum venosum

A

remnant of ductus venosus,

Failure to close results in portosystemic shunt as blood bypasses the liver

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43
Q

histologic makeup of arteries

A 
high pressure system.
3 tunics (intima, media, externa)
small lumen and thick walls
more muscle and elastin fibers
no valves
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44
Q

histologic makeup of capillaries

A

very tiny lumen
thin walls with only tunica intima
Large cross-sectional area as when considering all combined capillaries
No elastin, muscle fibers (no contraction or relaxation), or valves
Only let one blood cell pass through at a time

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45
Q

histologic makeup of veins

A 
low pressure system
3 tunic (intima, media, externa)
Large lumen and thin walls
fewer muscle and elastin fibers
valves
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46
Q

Compare histology of arteries and veins

A

Because arteries have thicker walls and smaller lumen than veins, they maintain their circular shape during slide preparation while veins usually have a collapsed shape

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47
Q

tunica externa

A

outermost layer of blood vessels, made of loose connective tissue

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48
Q

tunica media

A

middle layer of blood vessel, smooth muscle

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49
Q

compliance

A

volume divided by pressure, ability for vessels to stretch (distensibility), higher for veins

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50
Q

capacitance

A

ability for vessels to hold a large volume under low pressures, higher for veins

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51
Q

How does severe vasodilation effect the venous return to the heart? How would you treat this?

A

Less venous return, and less cardiac output,

Treatment: could give a shock bolus, norepinephrine and ADH (vasopressin) for vasoconstriction

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52
Q

elastic artery

A

large vessels like the aorta
deliver blood to the organs or lungs
Thick walls with a lot of elastin tissue, smooth muscle, and connective tissue
Walls allow these vessels to absorb the high-pressure blood flow as blood is pumped from the ventricles into the elastic arteries
Relatively thin tunica externa

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53
Q

Muscluar artery

A

medium sized vessels like the subclavian artery
Deliver oxygenated blood to the organs
Moderately thick walls with moderate amounts of elastin tissue, smooth, and connective tissue

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54
Q

arteriole

A

smallest branches of the arteries
function as the site of highest resistance to blood flow.
Alterations in the resistance occur in response to sympathetic nervous system activity

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55
Q

What are the receptors that cause vasoconstriction or vasodilation?

A

alpha 1 stimulation causes vasoconstriction

beta-2 stimulation causes vasodilation

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56
Q

continuous capillaries

A

least permeability, located in skin and muscle
Passage of lipid soluble molecules via diffusion across the lipid membrane
Passage of very small water soluble molecules through intracellular clefts

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57
Q

Fenestrated capillaries

A

moderate permeability, located in small intestine, kidneys, fenestrations allow passage of small molecules

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58
Q

sinusoidal cappilaries

A

most permeability
located in the liver, bone, marrow, spleen
Large fenestrations and incomplete basement membrane allow for exchange of large molecules (whole cells)

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59
Q

High elastic content of the large arteries results in which of the following properties?

a. increased compliance and increased capacitance
b. decreased compliance and decreased capacitance
c. increased compliance and decreased capacitance
d. decreased compliance and increased capacitance

A

b. decreased compliance and decreased capacitance

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60
Q

vaso vasorum

A

Vessels of the vessels, blood supply to large arteries and veins, found within tunica externa

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61
Q

Relationship between cross sectional area and blood flow

A

Velocity of of blood flow is inversely proportional to cross sectional area and directly proportional to flow in mL/sec

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62
Q

What factors determine flow?

A

Ohm’s law, Flow is directly related to change in pressure (pressure gradient) and inversely related to resistance

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63
Q

What factors determine resistance to flow?

A

Poiseuille’s law, Resistance to flow is directly proportional to viscosity and length of vessel and inversely proportional to the radius to the 4th power

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64
Q

hypovolemic shock

A

the inability to adequately perfuse the body due to severely reduced blood volume
Treat with fluid bolus
Hypokinetic pulses

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65
Q

how does needle size relate to rate of fluid administration?

A

to deliver fluids, quickly want a smaller gauge needle (wider) that is short to minimize resistance

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66
Q

laminar vs. turbulent flow

A

normally, blood flow is laminar or streamlined.

In disease, blood flow may become turbulent resulting in a heart murmur

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67
Q

Reynolds number

A

describes turbulence
= density of blood multiplied by diameter of vessel and velocity of flow, all divided by viscosity of blood
velocity and viscosity are main determinants

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68
Q

What is polycythemia and how would it impact blood viscosity?

A

increased red blood cells, increased blood viscosity

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69
Q

How do the following conditions impact blood viscosity?
Anemia
Intravenous fluids
Dehydration

A

Anemia: decreased viscosity
Intravenous fluids: decreased viscosity
Dehydration: increased viscosity
Therefore anemic patients or those receiving intravenous fluids can present with heart murmurs.

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70
Q

ventricular septal defects

A

VSD, most common cardiac birth defect in cats
Characterized by hole in interventricular septum
Volume overload disease

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71
Q

How does size of a VSD impact flow velocity and loudness of murmur?

A

Kittens with a small VSD have high velocity flow across the VSD. Kittens with a large VSD have lower velocity flow across the VSD. Murmur is louder with the small VSD.

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72
Q

A patient with a severe intestinal parasite presents with anemia and a soft murmur. Once the anemia resolves, so does the murmur. Which hemodynamic equation can be used to explain the resolution of the murmur?

A

Reynold’s number

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73
Q

Gradation of murmurs

A

based on loudness only with a I-VI scale. I is softest, VI is very loud
Soft murmurs are more focal and only in one quadrant

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74
Q

What is rule 6 of the heart? (equation)

A

Blood pressure is a product of cardiac output and vascular resistance.
BP= CO * VR

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75
Q

How does blood pressure change throughout the systemic circulatory system?

A

The mean arterial blood pressure is highest in the large arteries and falls as the arteries get smaller due to increased resistance. The pressure is the lowest in the venae cavae.
The largest drop in pressure is within the arterioles because they have the highest resistance.

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76
Q

Causes of falling pressure in arterioles, capillaries and venules/veins?

A

Arterioles: due to high resistance to flow
Capillaries: due to high frictional resistance and loss of fluid
Venules/veins: due to high capacitance and low resistance (large lumen)

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77
Q

Systolic pressure

A

during systole, the ventricles pump blood into the arteries generating the highest arterial pressures (systemic not pulmonary)

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78
Q

diastolic pressure

A

the ventricles relax, blood is no longer being ejected from the left ventricle, and the pressure falls to its lowest point
Generated by elastic properties of the aorta that continue flow of blood

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79
Q

mean arterial pressure

A

The average pressure in a complete cardiac cycle and is the driving force for perfusion. Tightly regulated
=systolic pressure + 2 diastolic pressures all divided by 3.

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80
Q

pulse pressure

A

systolic pressure minus diastolic pressure,

Represents the stroke volume

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81
Q

stroke volume

A

the volume of blood pumped out of the heart with each beat/contraction, represented by pulse pressure,
can be palpated in the arterial vessels
Consists of preload, afterload and contractility

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82
Q

subaortic stenosis

A

(SAS) congenital heart disease characterized by a narrowing of the outflow tract that carries blood from the left ventricle to the aorta
Presents with loud murmur at left base and weak femoral pulses (hypokinetic)
Pressure overload disease, increased afterload
concentric hypertrophy

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83
Q

What conditions might cause hyperkinetic pulses?

A

large pulse pressure due to PDA, severe aortic regurgitation, bradycardia, decreased vascular resistance, high sympathetic tone

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84
Q

What conditions might cause hypokinetic pulses?

A

weak thready pulses,

subaortic stenosis, hypovolemia, some arrhythmias, lower stroke volume

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85
Q

How do the pressures in pulmonary circulation compare to systemic pressures?

A

pulmonary pressures are about 1/5 of the systemic pressures

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86
Q

What is changed in the pulmonary circulation to maintain the same flow rate at lower pressures?

A

The pulmonary resistance is much lower

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87
Q

You are performing a blood pressure measurement and obtain a systolic pressure of 120 mmHg and a diastolic pressure of 40 mmHg. How do you expect the femoral pulses to feel?

A

Hyperkinetic

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88
Q

Are cardiac output and vascular resistance independently or dependently related?

A

They are dependent in that if one changes, the other will increase as a regulatory mechanism

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89
Q

Why do arterioles have high resistance?

A

small lumens causing increased friction

Lot of smooth muscle with basal tone that can constrict or dilate to regulate flow

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90
Q

How do the two arms of the autonomic nervous system impact heart rate and blood pressure?

A

Sympathetic system increases heart rate and blood pressure.

Parasympathetic decrease heart rate and blood pressure

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91
Q

Baroreceptors

A

specialized cells in aortic arch and carotid sinuses that monitor the blood pressure by detecting changes in the stretch of the vessel walls (mechanoreceptors)
They are always firing at a basal rate, but more when blood pressure increases. Response in seconds to minutes because it is neutrally mediated

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92
Q

Impact of signal from baroreceptors

A

signal travels via vagus and glossopharyngeal nerves to nucleus tractus solitarius in the medulla oblongata
Cardiovascular centers in the pons are stimulated or inhibited to adjust the parasympathetic and sympathetic balance in the autonomic nervous system

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93
Q

vasomotor control center

A

controls sympathetic tone for decreasing diameter of blood vessels

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94
Q

How does vascular resistance related to sympathetic tone?

A

Increased sympathetic tone will have greater vascular resistance

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95
Q

What factors of the blood pressure equations do baroreceptors change as a result of increased blood pressure?

A

Reflex bradycardia (lower heart rate and cardiac output), arteriolar vasodilation (lower vascular resistance), and decreased contractility (decreased stroke volume and cardiac output)

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96
Q

In response to a sudden decrease in the blood pressure, the baroreceptor sends _____ signals to the brain resulting in _____ sympathetic tone and _______ parasympathetic tone. The shift towards a _______ tone predominance results in _______ heart rate, arteriolar vaso______ and _______ contractility that work to normalize blood pressure.

A 
fewer signals
increased sympathetic
decreased parasympathetic
sympathetic predominance
increased heart rate
vasoconstriction
increased contractility
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97
Q

RAAS system

A

Renin angiotensin-aldosterone system
Corrects low blood pressure via two mechanisms and is slower than baroreceptor response because it is hormonally mediated

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98
Q

RAAS stimuli

A
  1. mechanoreceptors in the juxtaglomerular apparatus detect low blood pressure in afferent arteriole.
  2. Increased sympathetic nervous system stimulation
  3. Chemoreceptors in the macula densa detect low renal blood flow or low sodium
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99
Q

A car almost hits you in an intersection and you have a sudden increase in blood pressure. Which blood pressure regulatory action occurs first?

A

increased baroreceptor firing rates

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100
Q

How are the regulatory mechanisms of baroreceptors and RAAS related?

A

Both involve vasoconstriction to increase a lower blood pressure.
When arteriolar baroreceptors detect low pressures, they stimulate increased sympathetic output that stimulates renin release from the JG cells

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101
Q

Aldosterone

A

acts in the distal convoluted tubule and collecting ducts to increase sodium and water reabsorption and potassium excretion

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102
Q

What controls the flow of blood through capillary beds?

A

smooth muscle in the arterioles

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103
Q

metarterioles

A

metarterioles and the precapillary sphincters act as on/off switches for capillary blood flow

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104
Q

local blood flow vasodilators

A

low tissue O2 or high CO2, histamine, adenosine, bradykinin,

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105
Q

local blood flow vasoconstrictors

A

angiotensin II, epinephrine/ norepinephrine (catecholamines), endothelin (produced by vessel trauma), acute stretch of the arterioles after acute increase in blood pressure (myogenic autoregulation)

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106
Q

microcirculation

A

the exchange of substances across the capillaries occurs via simple diffusion

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107
Q

lymphatic vessels: function and histology

A

reabsorb excess fluid and proteins from interstitial space (the fluid filled space between cells)
histologically have thin walls with smooth muscle and one-way valves that allow for reabsorption of fluid and proteins to maintain the low hydrostatic and oncotic pressures in the interstitial space.
Difficult to visualize on slide because they are very thin and collapsible with no red blood cells in the lumen

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108
Q

edema

A

increased interstitial fluid volume due to increased filtration (increased Pc or Kf) and/or decreased absorption or drainage (decreased pi c or lymphatic drainage)

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109
Q

What cardiac conditions cause increased capillary hydrostatic pressure?

A 
arteriolar dilation
venous constriction
increased venous pressure
heart failure
extracellular fluid volume expansion
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110
Q

What conditions cause increased capillary permeability (Kf)?

A

burns, inflammation, toxins

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111
Q

What conditions cause decreased capillary oncotic pressure?

A

loss of plasma proteins (urinary or GI protein loss)

decreased production of proteins (liver failure or malnutrition)

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112
Q

What conditions cause decreased lymphatic drainage?

A

standing (decreased skeletal muscle compression of lymph vessels)
lymphatic obstruction

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113
Q

fluid exchange across capillaries

A

dictated by Starling forces
Net - causes fluid reabsorption
Net + causes fluid filtration

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114
Q

tachypnea

A

increased respiration rate

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115
Q

DMVD

A

degenerative mitral valve disease, common acquired heart disease in middle aged to older small breed dogs, thickened valve leaflets, can cause left sided congestive heart failure
volume overload disease in left atrium causing dilation, regurgitation during systole, increased preload causes dilation of left ventricle. causing increased pressure, making less of pressure difference and less venous return from the lungs (ohm’s law)
eccentric hypertrophy
Pulmonary edema.
RAAS is activated by the reduced blood pressure and retains fluid in the kidneys and causes vasoconstriction.
Murmur can be heard at left apex during systole

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116
Q

left sided congestive heart failure

A

severe heart disease leading to back up of fluid into the lungs and leakage of fluid into the interstitial spaces in the lungs

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117
Q

Which starling’s force is impacted in DMVD?

A

increased capillary hydrostatic pressure (Pc)

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118
Q

subcutaneous edema

A

accumulation of fluid in tissues such as swollen skin in distal limbs and ventral abdomen

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119
Q

panhypoproteinemia

A

reduced blood protein levels with severely reduced albumin and globulin levels

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120
Q

protein losing enteropathy

A

chronic condition characterized by loss of proteins through the gastrointestinal tract
Presents with panhypoproteinemia resulting in subcutaneous edema or thoracic or abdominal effusion

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121
Q

Which of the following treatments is used to treat DMVD and which to treat PLE?

a. furosemide is a diuretic that reduces the circulating blood volume
b. colloid fluids are intravenous fluids that contain large proteins

A

Furosemide to treat DMVD

Colloids to treat PLE

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122
Q

What compounds can leak through capillary beds in burns and why?

A

increased capillary bed permeability causes leakage of albumin and other proteins as well as electrolytes

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123
Q

A patient has subcutaneous edema caused by hypoproteinemia (low blood albumin levels). How are Starling’s forces altered?

A

low capillary oncotic pressure

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124
Q

Electrophysiology

A

study of the electrical activation of the heart and is the foundation for understanding and treatment of arrhythmias.

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125
Q

Are there ways to improve the function of the lymphatic system?

A

Not in the lungs other than medication, but compression in the limbs and contraction of these muscles can help push fluid back to the heart, so improving patient mobility helps.

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126
Q

What is required to come before cardiac contraction and relaxation can occur?

A

electrical depolarization and repolarization

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127
Q

What are the functions of the heart (rule 4)?

A
  1. Electrical conduction
  2. Contraction during systole
  3. Relaxation during diastole
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128
Q

chronotropy

A

heart rate

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129
Q

dromotropy

A

speed of conduction

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130
Q

inotropy

A

contractility, strength of contraction of the heart, modulated by drug or autonomic tone influences
Increased inotropy/contractility means stronger contractions

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131
Q

lusitropy

A

relaxation function of the heart

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132
Q

membrane polarity

A

transmembrane potential, voltage difference across the membrane in mV

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133
Q

membrane permeability

A

how easily an ion can move across the membrane. Different for each ion. Higher the permeability, the more the ion can move across the membrane

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134
Q

action potentials

A

marker of electrical stimulation in the cells of the heart.

Provide a visual representation of the changes in the membrane polarity that occurs over time during the cardiac cycle

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135
Q

What are the three states a cardiomyocyte can be in?

A
  1. Resting (polarized)
  2. Depolarization
  3. Repolarization
136
Q

What do changes in polarity require?

A

movement of ion across membranes, which require a driving force (electrochemical gradient).

137
Q

Resting state (polarized)

A

created by Na K ATPase pump and selective permeability to K (primary determinant)
a.k.a electrochemical gradient, resting membrane potential, phase 4 of action potential, transmembrane potential

138
Q

ion movement by Na K ATPase pump

A

3 Na pumped out of cell per 2 K into the cell

139
Q

How might a urethral obstruction in a cat alter the electrochemical gradient in cardiomyocytes?

A

Less K excretion, hyperkalemia (high extracellular K), less K leaving the cell, K accumulates in the cell, RMP is less negative (more positive), reduced driving force for ion movement

140
Q

Which of the following is the primary determinant of resting membrane potential?

a. passive diffusion through the sodium potassium pump
b. selective membrane permeability to sodium at rest
c. selective membrane permeability to potassium at rest
d. energy dependent transport of 2 Na ions out of the cell and 3 K ions into the cell

A

c. selective membrane permeability to potassium at rest

141
Q

Order of electrical activation

A
  1. SA node
  2. Atrial myocardium
  3. AV node
  4. Bundle of His
  5. Bundle branches
  6. Purkinje fibers
  7. Ventricular myocardium
142
Q

Bachmann’s bundle

A

transmits the electrical impulse from the right to left atrium

143
Q

Fast response action potentials

A

occur in the atrial and ventricular myocytes and Purkinje cells

144
Q

Phase 4 of fast response action potential

A

RMP, membrane potential is -90 in fast response, no ion movement

145
Q

phase 0 of fast response action potential

A

stimulus from adjacent cells (a small influx of positive ions) reduces the transmembrane potential enough to reach threshold
rapid influx of Na occurs through voltage-gated and time gated, fast Na channels
the interior of the cell rapidly becomes more positive
The rate of phase 0 is key determinant of cell to cell conduction velocity

146
Q

m gate of sodium channel

A

extracellular part, allows the Na in, closed at rest, opens quickly

147
Q

h gate of sodium channel

A

intracellular part, closes off entry of sodium, closes slowly, open at rest

148
Q

phase 1 of fast response action potential

A

initial repolarization via opening of K channels, K efflux

149
Q

Phase 2 of fast response action potential

A

membrane potential is relatively stable

Na channels inactivated, Long acting Ca channels opened, Ca influx, K channels opened, K efflux

150
Q

phase 3 of fast response action potential

A

Completion of repolarization,

K channels are fully activated and opened allowing for efflux of K, membrane potential is returned to RMP (-90 mV)

151
Q

slow response action potentials

A

occur in sinus and atrioventricular nodes
No phases 1 or 2 (initial repolarization and plateau)

Note: phase 2 can be present, but it is not distinct

152
Q

phase 4 of slow response action potential

A

less negative RMP (-60 mV)
continuously drifting towards threshold via funny current (If) allowing for spontaneous depolarization of the pacemaker cells in SA node

153
Q

phase 0 of slow response action potential

A

slow upstroke via a slow influx of Ca

154
Q

Why do slow response action potentials use Ca influx to depolarize instead of Na influx?

A

sodium channels cannot work at the RMP used in slow action potentials

155
Q

Phase 3 of slow response action potential

A

potassium currents are responsible for repolarization, the K channels are open allowing for efflux of K ions
as the inside of the cell becomes more negative, the RMP is restored

156
Q

escape beats

A

if the SA node fails to discharge, some other parts of the heart can display automaticity and act as subsidiary pacemakers
Depolarization rates in subsidiary pacemakers varies depending on their location. (Farther away from SA node= slower)

157
Q

How does parasympathetic stimulation impact action potentials? Sympathetic?

A

Parasympathetic: Cell is hyperpolarized, depolarization rate of SA node decreases as well as conduction velocity through the AV node with bradycardia
Sympathetic: Cell has faster depolarization rate of SA node and conduction velocity through AV node with tachycardia

158
Q

What allows for propagation of depolarization?

A

Gap junctions allow ions to pass from the depolarized cell to the adjacent cell

159
Q

Refractory period

A

cells are unresponsive to restimulation,

dictated by the balance of inactive vs reactivated/ resting Na channels

160
Q

relative refractory period

A

a stronger than normal stimulus from an adjacent cell can prematurely excite the cells

161
Q

ventricular premature complexes

A

VPC: an arrhythmia caused by abnormally early depolarization of ventricular cardiomyocytes
Treatment can include drugs that prolong refractory period (sotalol)

162
Q

mechanism of sotalol

A

drug that blocks beta receptors and K channels
Blocked K channels means repolarization is slower with a longer refractory period to prevent arrhythmias
Also blocks beta-2 receptors to prevent vasodilation and the beta-1 receptors that are responsible for increasing heart rate (sympathetic system)

163
Q

Which of the following action potential events allows sinoatrial nodal cells to act as the pacemaker of the heart

a. a slower depolarization during phase 0
b. spontaneous diastolic depolarization during phase 4
c. a less negative resting membrane potential
d. the influx of calcium through the L-type calcium channel during phase 2

A

b. spontaneous diastolic depolarization during phase 4

164
Q

electrocardiograms

A

the clinical diagnostic used to evaluate the heart rate and rhythm i patients
Summation of all the action potential from the electrical conducting portions of the heart

165
Q

What do ECGs tell us, what don’t they tell us?

A

Great for heart rate, arrhythmias, conduction abnormalities and good for chamber enlargement (specific but not sensitive).
Bad for anything regarding mechanical activity such as strength of beats.

166
Q

arrhythmia

A

electrical activity with irregular rhythm and/or an abnormal heart rate

167
Q

p wave

A

atrial depolarization

168
Q

QRS complex

A

ventricular depolarization

169
Q

t wave

A

ventricular repolarization

170
Q

ECG leads

A

have positive and negative poles (left caudal and right cranial for lead II, respectively) that serve as a point of reference to code the depolarization wave’s amplitude and direction on the ECG

171
Q

isoelectric line

A

flat line on ECG

172
Q

amplitude of deflection on ECG

A

dictated by the amount of tissue being depolarized (more tissue, more amplitude) and the orientation of the waveform relative to the lead

173
Q

What color electrode goes where on the patient?

A

in a dog, white on right and smoke over fire, so white is right front, black, left front, red left back and green right back
In horse, white on right jugular furrow, red and black are at left lower thorax behind elbow, green is not placed

174
Q

what position is the patient in for an ECG?

A

right lateral recumbency

175
Q

Purkinje fibers

A

specialized myocardial cells capable of conducting electrical signals in the heart
Located in the subendocardial layer.
Larger than cardiomyocytes with 1-2 nuclei. Less glycogen and fewer myofibrils so stain paler.

176
Q

Compare Purkinje cell network in small vs large animals

A

Humans and small animals have subendothelial Purkinje cells that require cell to cell conduction of the depolarization wave to stimulate the outer myocardial layers.
Birds and large animals like horses have extensive branching Purkinje network that extends deeper into the myocardium, providing direct stimulation to all myocardial layers. Allows for very rapid spread of the impulse to the larger ventricular mass. Therefore the ECG cannot detect ventricular enlargement in these animals

177
Q

How might ECGs be different in large animals (particularly horses)?

A

single lead system, predominantly negative QRS (deep S wave), notched P waves are normal in horses

178
Q

mean electrical axis

A

helps determine which side of the heart has disease (enlargement)

179
Q

K channels

A

both voltage and ligand gated

Opened by increases in acetylcholine (parasympathetic tone), extracellular K, adenosine, muscle stretch

180
Q

Which tissues are more or less impacted by hyperkalemia?

A

atrial are most sensitive, then ventricular, then nodal tissues where hyperkalemia reduces funny current and slows the rate of spontaneous phase 4 depolarization (mimics increased parasympathetic tone)

181
Q

Why is the QRS complex often the equal or narrower width than the P wave?

A

The His-Purkinje system is a superhighway that allows very rapid conduction through the ventricles

182
Q

How is the ECG impacted by hyperkalemia?

A

bradycardia, loss of P waves to smaller or absent, Wide QRS, narrower Tented t wave (faster repolarization and greater amplitude)
This is because hyperkalemia mimics increased parasympathetic tone and nodal cells are slower to depolarize. P waves are lost when the atrial tissue becomes inexcitable.

183
Q

associated vs dissociated beats

A

Associated: the Ps and QRSs are related to each other because they are part of the same electrical chain of events
Dissociated: the Ps and QRSs are independent rhythms, superimposed overtop of one another on the ECG because they are not part of the same electrical chain of events

184
Q

equation for heart rate calculation

A

25mm/sec: 15 big boxes x 20 (maybe 30 x 10 same as bic pen)

50 mm/sec: 30 big boxes x 20 or bic pen x 20

185
Q

Bradycardia and bradyarrhythmia

A

heart rates are slower than normal

Hyperkalemia is a common cause in cats

186
Q

tachycardia and tachyarrhythmia

A

heart rates are faster than normal

187
Q

Normal heart rates for these species:

Canine, Feline, Bovine, Equine

A

Canine: 60-160 bpm
Feline: 140-240 bpm
Bovine: 60-88 bpm
Equine: 28-44 bpm

188
Q

Does normal heart rate different across species? Within a species?

A

Heart rate differs across different species, but not within a single species.

189
Q

What would cause differering heart beats between healthy individuals of a species?

A

Differences in sympathetic or parasympathetic tone

190
Q

transient atrial standstill

A

bradycardia, absent P waves, and narrow QRS complex

Can be caused by hyperkalemia

191
Q

Is the direction of the T wave positive or negative?

A

It can be either with no significant clinical correlation.

192
Q

What does the PQ or PR interval represent?

A

rate of conduction through the AV node

193
Q

What does the QT interval represent?

A

Total interval from start of ventricular depolarization to end of repolarization

194
Q

P pulmonale

A

tall P wave, could be due to right atrial enlargement in dogs (>0.4 mV) or right or left atrial enlargement in cats (>0.2 mV)

195
Q

P mitrale

A

wide P wave, due to left atrial enlargement in dogs (>0.04 sec or 0.05 sec in giant breeds) or cats (>0.035 seconds)

196
Q

The PR interval or PQ interval is a measurement of the time the impulse takes to travel through what portions of the conducting system?

a. the atria and atrioventricular node
b. the atrioventricular node and ventricle
c. the atria and ventricles
d. the bundle branches and Purkinje fibers

A

a. the atria and atrioventricular node

197
Q

Which vessel type has an internal elastic lamina?

A

arteries

198
Q

Why is sodium nitroprusside used to treat DMVD?

A

It is converted to nitric oxide which is a powerful vasodilator to dilated the arteries and veins. The disease has caused a loss of pressure gradient so the vascular resistance must decrease with it to maintain the same flow (Ohm’s law).

199
Q

Pulmonary hypertension

A

high blood pressure in the lungs
Can be associated with high altitude disease
Pressure overload disease, concentric hypertrophy, increased afterload

200
Q

High altitude disease

A

characterized by pulmonary hypertension caused by vasoconstriction of the vessels in the lungs in response to hypoxia. Presents with bottle jaw, brisket edema, and peritoneal effusion

201
Q

What type of capillaries are present in the portal capillary beds?

A

sinusoidal capillaries

202
Q

Mean electrical axis

A

the average path of electrical activity during ventricular depolarization
Normal values are species dependent (+40 to +100 degrees in dogs, 0 to +150 degrees in cats)

203
Q

What is the normal direction of depolarization in the heart?

A

going from right to left and cranial to caudal

204
Q

Which diseases are associated with a left axis shift? Right axis shift?

A

Left axis shift: left ventricular enlargement, Left bundle branch block
Right axis shift: right ventricular enlargement, Right bundle branch block

205
Q

Diseases with low heart rates?

A

sinus bradycardia

second or third degree atrioventricular block, atrial standstill, sinus node dysfunction

206
Q

Cardiac conditions that would have a normal heart rate?

A

sinus rhythm, first degree atrioventricular block, sinus with ventricular ectopic (ventricular premature complexes or escape beats) sinus with supraventricular premature complexes (SVPC)

207
Q

Diseases associated with high heart rate?

A

sinus tachycardia, ventricular tachycardia, supraventricular tachycardia, atrial fibrillation

208
Q

block or unconducted P waves

A

sinus origin P waves that are not conducted through the AV node, dissociated
(NOT to be confused with a p wave that never occurs, it happens and doesn’t make it to the ventricle)

209
Q

sinus arrhythmia

A

can be normal in dogs because healthy dogs have a predominance of parasympathetic tone
Cyclic changes in heart rate may or may not vary with the respiratory phase. Usually faster during inspiration and slower during expiration.

210
Q

physiologic vagal tone

A

a predominance of parasympathetic tone

211
Q

pathologic vagal tone

A

increased vagal tone caused by disease (gastrointestinal, ocular, central nervous system, or respiratory systems)

212
Q

What are the ECG features in sinus arrhythmia?

A

Wandering atrial pacemaker (variable P wave heights)
Low heart rate, regularly irregular rhythm, PQRST waves present, associated
Origin of QRS: sinus

213
Q

wandering atrial pacemaker

A

variable P wave heights, commonly seen with sinus arrhythmia

214
Q

atrial fibrillation

A

Afib, disorganized electrical activity that reaches the AV node at irregular time intervals,
f waves, small wavelets of depolarization of the atria
Sometimes AV node is in the refractory period and cannot conduct the impulse and sometimes conducts the impulses very quickly. So the impulse is passed to ventricles in rapid irregular fashion. Following depolarization of AV node, the impulse is propagated along the normal path of conduction to the ventricles
decreased preload

215
Q

ECG features of Afib

A

high heart rate, irregularly irregular rhythm, QRS and T, true p is absent, supraventricular ectopic beats
dissociated

216
Q

sinus bradycardia (description and ECG features)

A

SA node discharging at slower than normal rate in regular fashion. Following depolarization of SA node, the impulse is propagated along the normal path of conduction in the heart.
ECG features: low heart rate, regular rhythm, PQRST waves seen. Origin of QRS: sinus

217
Q

A right axis shift may be present on an ECG for a patient with which of the following diseases?

a. Mitral valve regurgitation
b. pulmonary hypertension
c. systemic hypertension
d. subaortic stenosis

A

B. pulmonary hypertension

218
Q

excitation-contraction coupling

A

describes how the electrical activity leads to the mechanical contraction of the heart
The electrical events occur on the surface (sarcolemma) but must stimulate contractile elements located throughout the myocardial cell

219
Q

What relationship facilitates excitation-contraction coupling?

A

The spatial relationship between the sarcolemma, T tubules, and Sarcoplasmic reticulum facilitates excitation contraction coupling.

220
Q

T-tubules

A

invagination of sarcolemma that transmit outer electrical events deeper into the cell

221
Q

What mediates excitation-contraction coupling?

A

Mediated by changes in sarcoplasmic calcium levels

222
Q

Step one of E-C coupling

A

small Ca influx during phase 2 of action potential.

Calcium enters the cell through the voltage gated long acting Ca channel (Ca-L)

223
Q

Step 2 of E-C coupling

A

Calcium induced calcium release: small influx of Ca from step one triggers larger release of Ca from the sarcoplasmic reticulum by binding to the calcium release receptor called the ryanodine receptor

224
Q

Step 3 of E-C coupling

A

Ventricular contraction during systole: Ca binds cardiac troponin C and goes on to cause contraction

225
Q

Step 4 of E-C coupling

A

Ventricular relaxation during diastole: Ca is removed from the sarcoplasm via re-sequestration of Ca into the SR by SERCA (phospholamban/PL is gatekeeper) then elimination of Ca from the cell by the Na-Ca exchanger and Ca-ATPase pump

226
Q

Major determinant of inotrpy

A

cytosolic Ca concentration determines the force of contraction. Increased intracellular calcium has stronger contractions and decreased intracellular calcium has weaker contractions

227
Q

Relationship of actin, myosin, tropomyosin and troponin

A

Tropomyosin wraps around the actin filament blocking the myosin binding sites and prevents actin-myosin interaction in the resting state. Cardiac troponin (cTn) complex regulates tropomyosin position and inhibitory function. When calcium enters the sarcoplasm and binds cardiac troponin C, a morphologic change to the troponin complex pulls the tropomyosin to the side, exposing the myosin binding site.
Once the myosin binds to actin to form a cross bridge, the myosin releases phosphate and creates a power stroke resulting in myocardial contraction

228
Q

What are the parts of the cardiac troponin complex and what is their function?

A

cTn I- inhibits myosin binding
cTn C- binds calcium
CTn T- binds tropomyosin

229
Q

phospholamban

A

PL, regulates sarco(endo)plasmic reticulum calcium ATPase (SERCA) by acting as a gatekeeper and only phosphorylated PL “opens the gate” for resequestration

230
Q

How would sympathetic or parasympathetic stimulation impact SERCA?

A

Parasympathetic stimulation of muscarinic receptors inactivates SERCA and PL closes gate. Results in negative contractility and relaxation.
Sympathetic stimulation of beta 1 receptors activates SERCA as PL is phosphorylated and opens gate. Results in increased contractility and relaxation.

231
Q

How do positive and negative inotropic drugs impact the heart?

A

During systole, positive inotropes increase contractility and negative inotropes decreased contractility

232
Q

How do lusitropic drugs impact the heart?

A

During diastole, positive lusitropes increase relaxation and negative lusitropes decrease relaxation.

233
Q

If you are designing a drug to increase contractility, what effect would it have on intracellular calcium levels? What kind of drug is it?

A

positive inotrope that increased intracellular Ca by increasing release into the sarcoplasm or decreasing removal from the sarcoplasm

234
Q

mechanism for Pimobendan

A

acts as a “calcium sensitizer by increasing the affinity of cTn-C for calcium
Positive inotrope

235
Q

mechanism of Diltiazem

A

calcium channel blocker (long acting Ca channels) that is used to treat arrhythmias.
Negative inotrope

236
Q

mechanism of Dubutamine

A

stimulates beta receptors

beta agonist activity, positive inotrope

237
Q

mechanism of Theophylline

A

binds to and stimulates beta receptors

beta agonst, positive inotrope

238
Q

mechanism of Atendol

A

beta blocker medication that inhibits beta receptors

beta antagonist activity, negative inotrope

239
Q

mechanism of Amlodipine

A

calcium channel blocker (long acting Ca channels) that is used to treat systemic hypertension
Negative inotrope

240
Q

When calcium is released from the sarcoplasmic reticulum into the sarcoplasm, what protein does calcium bind to?

A

Troponin C

241
Q

Dihydropyridine calcium channel blockers

A

eg. amlodipine, bind “peripherally” in the vascular smooth muscle causing vasodilation

242
Q

Non-dihydropyridine calcium channel blockers

A

eg. diltiazem, act “centrally” binding to the calcium channel blockers in the cardiomyocytes and have negative chronotropic effects (by slowing depolarization rates in AV and SA nodes) and negative inotropic effects (by reducing Ca influx)

243
Q

agonist

A

substance that binds and stimulates the receptor

244
Q

antagonist

A

binds and inhibits the receptor

245
Q

What does stimulation of beta receptors do?

A

Increases all of the “tropy”s

246
Q

What are two ways to increase pressure in a chamber?

A
  1. fill with more blood/ increase volume

2. Contraction/ squeezing

247
Q

When is the mitral valve open? Closed?

A

Open when atrial pressure is greater than ventricular pressure (early rapid filling, diastasis, atrial contraction), closed when ventricular pressure is greater than atrial pressure (Isovolumic contraction, ejection, isovolumic relaxation)

248
Q

When is the aortic valve open? Closed?

A

Open when pressure in the ventricle is greater than the pressure in the aorta (ejection). Closed when the pressure in the ventricle is less than the pressure in the aorta. (isovolumic relaxation through isovolumic contraction)

249
Q

Atrial contraction

A

Final phase of diastole, the atrium contracts and empties the last 20% of blood into the ventricle

250
Q

isovolumic contraction

A

Occurs during systole. Followed by ventricular depolarization (QRS complex) the ventricles begin to contract, increased the pressure in the ventricles greater than the atrium so the mitral valve closes.
The volume does not change because all the valves remain closed until the pressure in the ventricles exceed that of the aorta or pulmonary artery.

251
Q

Ejection

A

Occurs during systole.
As soon as the ventricular pressures exceed the aortic pressures, the aortic valve opens and blood is ejected into the artery. The pressures in the ventricle and aorta and the ventricle are changing. Initially, both are increasing as the ventricle is still contracting. Then these pressures gradually reduce following ventricular repolarization (t wave) until the aortic valve closes.
The atria are filling while the ventricles are contracting.

252
Q

S1 heart sound

A

(lub) occurs at the time of the mitral valve closure and marks the start of systole
Associated with QRS complex, ventricular depolarization and ventricular contraction
heart best at left or right apex

253
Q

S2 heart sound

A

(dub) occurs at the time of aortic valve closure and marks the end of systole
heard best at left base

254
Q

systolic dysfunction

A

characterized by reduced pumping function and progressive heart dilation and can have various causes.

255
Q

Primary diseases causing systolic dysfunction

A 
dilated cardiomyopathy (DCM)
Arrhythmogenic right ventricular cardiomyopathy ARVC)
256
Q

What diseases have systolic dysfunction as a secondary symptom?

A 
inflammation/infection
Toxins/drugs
diet associated cardiomyopathies
tachycardia induced cardiomyopathy
hypothyroidism
257
Q

preload

A

ventricular wall tension at the end of diastole. The stretch on the ventricular fibers at the end of diastole that is best estimated by the end diastolic volume or pressure. As this volume increases, so does preload.

258
Q

Afterload

A

ventricular wall tension during contraction. The amount of force that must be generated to eject blood. Systolic blood pressure/ arterial blood pressure is used to estimate afterload. As systolic blood pressure increases, so dues afterload.

259
Q

Dilated cardiomyopathy

A

DCM, common disease in Dobermans caused by genetic mutation of sarcomeric proteins (titin) or a microbial PDK4 protein. Acquired disease because signs do not present until adulthood
Characterized by systolic dysfunction and progressive dilation of the heart chambers. Eccentric hypertrophy
Results in myocyte atrophy, degeneration and death that appears on a slide as attenuated (thin) wavy fibers and fibrosis (blue w/ trichrome stain)
Fibrosis and dilation can result in arrhythmia or failure
Presents with hypokinetic pulses, regular sinus rhythm tachycardia (compensating for P mitrale with left atrial enlargement)
Compensatory increase in heart rate by baroreceptors and RAAS system to improve blood pressure. Low pressure causes lethargy and exercise intolerance.
Higher heart rate causes higher cardiac output and more blood remains in the ventricle (ESV increases) causing progressive ventricular dilation.
Ventricle is stiff and dilated so S3 heart sound is created by oscillation of the structures during early rapid filling (mid diastole). Lub dub ah, S3 heard at left apex. Murmur heard during systole more commonly at left apex
Forward heart failure.
Usually left ventricle is effected first, but both right and left can be effected when severe.
Treat with Pimobendan to increase contractility

260
Q

cardiomyopathy

A

disease of the heart muscle

261
Q

Ejection fraction percentage

A

EF%, represents the percent change in left ventricular volume before and after contraction of the ventricle (normal >50%)
=(EDV-ESV)/ EDV x 100%

262
Q

Fractional shortening percentage

A

FS%, the percent change in the width of the left ventricular chamber between systole and diastole (normal>30%)
=(LVd-LVs)/ LVd x 100%

263
Q

end diastolic volume

A

EDV, the maximum volume of blood in the ventricle at the end of diastole

264
Q

End systolic volume

A

ESV, the minimum volume of blood in the ventricle at the end of systole
(yes, some is still left over)

265
Q

left ventricular internal dimension in diastole

A

LVd, left ventricular width at the end of diastole

266
Q

left ventricular internal dimension in systole

A

LVs, left ventricular width at the end of systole

267
Q

Treatment for DCM

A

Pimobendan increases contractility and this is the source of the issue

268
Q

A heart murmur is heard between the S1 and S2 heart sounds. During what phase of the cardiac cycle is this murmur occuring?

A

Systole, either isovolumic contraction or ejection, probably ejection

269
Q

isovolumic relaxation

A

During diastole following ventricular repolarization (T wave). Begins once aortic valve closes. When the ventricle is relaxing and the ventricular pressures are rapidly reduced, but the volume remains unchanged because the valves are closed. Atrium is completing the filling process while atrial pressure reaches a maximum of 10 mmHg
Can be associated with S2 heart sound

270
Q

early rapid filling

A

during diastole, as soon as the pressure in the ventricle is less than the atrium, the mitral valve opens. The ventricle rapidly fills with blood because of the large pressure gradient between the atrium and the ventricle.

271
Q

Diastasis

A

during diastole, as the atrium empties and the ventricle and the ventricle fills, the pressures in each chamber nearly equilibrate and the ventricular filling is less rapid. The atrial pressures remain mildly higher than the ventricular pressures, barely keeping the mitral valve open.

272
Q

atrial contraction

A

aka atrial kick, during diastole, immediately following atrial depolarization (P wave) the atrium contracts, resulting in an increased atrial pressure, and empties the last 20% of blood into the ventricle, causing a small increase in both the atrial and ventricular pressures.

273
Q

Which is longer systole or diastole?

A

diastole is 2/3 of the cardiac cycle

274
Q

Does diastole require energy, why or why not?

A

Yes, ATP is required for SERCA resequestration of Ca and to reset the myosin head.

275
Q

What stage of the cardiac cycle does blood enter the coronary arteries?

A

Diastole, coronary arteries carry blood to the heart muscle. During the elastic recoil of the aorta.

276
Q

Which heart sounds are normal in small animal patients? large animals?

A

S1 and S2 are normal in small animals will all four can normally be heard in large animals

277
Q

hypertrophic cardiomyopathy

A

HCM, most common acquired heart disease in cats, Commonly middle-aged or older cats.
Caused by genetic malformation in one of the myosin binding proteins in Ragdoll and Maine Coon breeds.
due to diastolic dysfunction, incomplete ventricular filling with decreased preload, stroke volume, cardiac output, and blood pressure.
involves S4 heart sound during filling of stiffened ventricle during atrial contraction. Bah lub dub.
Murmur heard during diastole at left apex
Involves thickened left ventricle dilated and left atrium from backup of blood. Concentric hypertrophy.
Moderate to severe dilation can cause clot formation and/or back up of fluid into the lungs with pulmonary edema or pleural effusion.
Decreased compliance of the ventricle results in decreased relaxation (lusitropy) of the ventricular myocardium
Presents with normokinetic or hypokinetic pulses

278
Q

ventricular compliance

A

describes the stiffness of the ventricle.
= change in volume divided by change in pressure
When normal, ventricle easily distends to accommodate the end diastolic volume (EDV) with a relatively small increase in the interventricular pressure

279
Q

What happens when ventricular compliance is decreased?

A

the stiff ventricle doesn’t relax well (decreased lusitropy) with a larger increase in pressure for the same EDV

280
Q

S4 heart sound

A

occurs during atrial contraction (P wave) in late diastole in patients with thickened hearts (concentric hypertrophy). Ventricle has poor compliance so filling causes oscillation of hemodynamic structures
heard at apex or base

281
Q

How is coronary perfusion to the heart muscle altered in patients with diastolic dysfunction?

A

decreased coronary perfusion, ischemia. There is more muscle to perfuse and the coronary vessels are not developing along with the muscle.

282
Q

How is the flow of blood impacted in patients with HCM?

A

diastolic dysfunction disease, incomplete ventricular filling means a decreased preload, therefore also decreased stroke volume, cardiac output, and blood pressure.
Backup of blood into the atrium and progressive dilation.
Moderate to severe atrial dilation can result in blood stasis and clot formation (treated with Piavix), and/or backup of fluid from the left atrium to the lungs resulting in pulmonary edema or pleural effusion.

283
Q

What conditions increase preload?

A

intravenous fluid administration, mitral or tricuspid valve regurgitation

284
Q

What conditions decrease preload?

A

Dehydration, atrial fibrillation, HCM

285
Q

What conditions increase afterload?

A

arterial hypertension, stenosis of aortic or pulmonic valve, arterial vasoconstrictor medication

286
Q

What conditions decrease afterload?

A

arterial vasodilator medication

287
Q

rule 3 of the heart

A

its response to disease is predictable (concentric vs eccentric hypertrophy)

288
Q

concentric hypertrophy

A

appears as an increased wall thickness and small chamber

289
Q

eccentric hypertrophy

A

appears as a normal wall thickness with a dilated chamber

290
Q

Frank-Starling mechanism

A

When the preload increases the force of contraction increases by increasing cTN-C affinity for Ca when stretched and increasing actin myosin interaction when stretched

291
Q

Pathophysiology of a volume overload disease

A

eg. DMVD
1. disease causes excess volume in atrial and ventricular chambers.
2. Atria and ventricles dilate because of increased preload
3. Wall tension is increased and results in compensatory ventricular eccentric hypertrophy
4. When cardiac output is reduced, the RAAS system provides a long term compensatory mechanism for maintaining a normal blood pressure
5. Moderate to severe atrial dilation can result in backup of fluid from the atrium to the lungs, resulting in congestive heart failure. Left sided causing pulmonary edema and right sided heart failure causing cavitary effusions.

292
Q

systemic hypertension

A

SHT, common disease in middle aged to older cats that results in left ventricular hypertrophy. Also associated with dilation of the left atrium and poor relaxation (negative lusitropy) of the ventricle.
The thickened left ventricular muscle in response to pressure overload, concentric hypertrophy (not associated with diseased muscle) narrowing the tract that takes blood from the left ventricle to the aorta resulting in turbulent blood flow and a heart murmur.
Increased afterload
Commonly associated with other systemic diseases such as kidney disease or elevated thyroid hormone (hyperthyroidism).
Treated with Amlodipine to to block calcium channels, negative inotrope

293
Q

pulmonic stenosis

A

PS, congenital malformation of the pulmonic valve characterized by fusion of the valve leaflets that prevents them from fully opening during systole and results in right heart enlargement. Concentric hypertrophy. Pressure overload disease, increased afterload
ECG has regular sinus rhythm with right axis shift
Murmur heard during systole at left base
Jugular pulses or distension

294
Q

Law of LaPlase

A

Tension= pressure multiplied by radius divided by wall thickness.
Therefore ventricular hypertrophy reduces the ventricular wall tension

295
Q

Pathophysiology of pressure overload disease

A

eg. pulmonic stenosis or hypertension.
Results from high afterload that requires the ventricle to generate a higher than normal pressure during systole to eject blood
Increased tension in the wall is normalized by concentric hypertrophy
The hypertrophied, thickened ventricle is poorly compliant and causes poor relaxation lusitropy. Therefore the atrium cannot empty as much blood into the ventricle, resulting in progressive atrial dilation
Moderate to severe atrial dilation can result in blood stasis and clot formation and/or backup of fluid from the left atrium to the lungs, resulting in congestive heart failure.
Poor relaxation also results in poor coronary perfusion of the cardiac muscle, ischemia, and myocardial fibrosis that can predispose patients to arrhythmias.

296
Q 
Categorize the following as systolic dysfunction, diastolic dysfunction, volume overload or pressure overload:
Degenerative mitral valve disease
Patent ductus arteriosus 
Systemic hypertension
Pulmonic stenosis
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Pulmonary hypertension
Ventricular septal defect
Subaortic stenosis
A

DMVD: volume overload
PDA: volume overload
Systemic hypertension: pressure overload
Pulmonic stenosis: pressure overload
HCM: diastolic dysfunction
DCM: systolic dysfunction
Pulmonary hypertension: pressure overload disease
Ventricular septal defect: volume overload disease
Subaortic stenosis: pressure overload disease

297
Q

You have diagnosed a patient with systemic hypertension. Which of the following structural changes do yo expect to see on the cardiac ultrasound (echocardiogram)

a. Eccentric hypertrophy of the left ventricle.
b. Eccentric hypertrophy of the right ventricle
c. concentric hypertrophy of the left ventricle
d. concentric hypertrophy of the right ventricle

A

c. concentric hypertrophy of the left ventricle

298
Q

ECG features of sinus rhythm with ventricular ectopics

A

Normal heart rate unless the escape complexes occur frequently. Irregular rhythm. QRST and ventricular ectopics, QRS is of ventricular origin

299
Q

supraventricular premature complexes

A

(SVPC) may be caused by atrial enlargement, inflammation or infection of the atrial myocardium, atrial masses, or pressure from masses in the thorax pressing on the myocardium.
aka atrial premature complexes (APC)
When atrial myocytes depolarizes the heart earlier than expected.

300
Q

P prime waves

A

P waves with a different morphology from sinus P waves

found with supraventricular QRS complexes

301
Q

ECG features of SVPC

A

heart rate is normal unless the supraventricular ectopic complexes occur very frequently. Irregular rhythm. P prime, PQRST, supraventricular ectopic, Origin of QRS: supraventricular (normal QRS width)

302
Q

Third degree atrioventricular block (AVB)

A

Unlike first and second degree, third degree is almost always pathologic and due to disease of the AV node (fibrosis, neoplasia, inflammation/infection due to Chagas disease or Lyme disease. This rhythm is treated with a pacemaker implant.
ECG features: low heart rate, regular rhythm, QRST, ventricular ectopic and unconducted P waves, Origin of QRS: ventricular
markedly dissociated atrial and ventricular QRS rhythms

303
Q

Common causes of ventricular arrhythmias (HEADS)

A

Heart disease (ventricular chamber enlargement, fibrosis, ischemia)
Electrolyte imbalances, endocrine (hyperthyroidism, pheochromocytoma)
Altered autonomic tone, intra Abdominal disease
Drugs and toxicities (eg digoxin)
stuff surgeons see (gastric dilation and volvulus, splenic disease, sepsis)

304
Q

Which of these medications would slow the depolarization phase of the ventricular cardiomyocyte?

a. diltiazem (a calcium channel blocker)
b. ivabradine (a funny channel blocker)
c. Lidocaine (a sodium channel blocker)

A

Lidocaine

305
Q

ECG features of ventricular tachycardia

A

high heart rate, regular rhythm, QRST, ventricular ectopic
Origin of QRS: ventricular
dissociated

306
Q

stenosis

A

fusion of valves making a smaller opening, a type of pressure overload disease, increased afterload

307
Q

Wigger’s diagram

A

illustrates relationship during the cardiac cycle between:
pressures in the atria, ventricles, and great vessels,
electrical and mechanical events,
the mechanical events and heart sound

308
Q

What is the mechanical event and heart sound(s) associated with T wave?

A

(ventricular repolarization) isovolumic relaxation, S2 and S3 heart sounds

309
Q

heart failure

A

heart pumps an inadequate volume of blood to meet O2 demands of tissue and prevent fluid accumulation
Occurs in the face of adequate or high venous return (shock is low venous return)
Not a primary diagnosis
Can be result from all 4 categories of heart disease

310
Q

clinical signs of forward heart failure

A

syncope (fainting), pallor, cyanosis, hypokinetic pulses, azotemia
Contractile dysfunction

311
Q

clinical signs of backward heart failure

A 
(congestive heart failure) pulmonary edema
Pleural effusion
Ascites/ hepatomegaly
Pericardial effusion
Peripheral edema
312
Q

Signs of left vs right sided heart disease in dogs

A

Left: pulmonary edema with rarely any other signs
Right: Ascites with occasional pleaural effusion, pericardial effusion, peripheral edema

313
Q

Sings of left vs right sided heart disease in cats

A

left: pulmonary edema, pleural effusion, pericardial effusion
right: pleural effusion, ascites, pericardial effusion

314
Q

Long term impacts of RAAS activation

A

myocardial remodeling and fibrosis, renal and arteriolar sclerosis, cytokine activation

315
Q

long term impacts of baroreceptor activation

A

myocardial remodeling and fibrosis, cytokine activation

316
Q

How does vasoconstriction by the RAAS system and baroreceptors contribute to progressive left ventricular dilation in DCM?

A

arterial vasoconstriction causes increased resistance. Ventricular vasoconstriction increases venous return and preload

317
Q

tricuspid valve dysplasia

A

TVD, congenital malformation of the tricuspid valve that results in regurgitation. Severe regurgitation is a volume overload disease that results in dilation and eccentric hypertrophy, increased preload
Presents with brisket edema and loud right apical heart murmur during systole. dilated right ventricle with normal wall measure, and moderate peritoneal effusion. hepatomegaly

318
Q

Visual exam findings that can indicate heart disease

A

Cachexia (muscle atrophy), abdominal distension due to peritoneal effusion, mucous membranes with pallor or cyanosis, peripheral edema

319
Q

venous assesment

A

visual assessment of the jugular vein that is performed in standing patients

320
Q

jugular pulsation

A

wave-like motion in the jugular vein that moves up the neck

Normal when seen in the lower 1/3 of neck in large animals

321
Q

jugular distension

A

the jugular vein remains full of blood

322
Q

causes of jugular pulsation or distension

A

back of fluid due to changed pressure in right atrium caused by any right heart pressure or volume overload disease.
Possibly due to obstruction in cranial vena cava, pericardial effusion, pulmonic stenosis

323
Q

Three features of arterial assessment

A

strength, synchronous, symmetry

324
Q

Where are arterial pulses palpated?

A

Small animals: femoral artery in the femoral triangle

Large animals: facial artery on medial aspect of the ramus of the mandible

325
Q

snchronous

A

hearing a heartbeat that is almost immediately followed by a palpable pulse.
Evaluate by listening and feeling pulse at same time

326
Q

symmetrical

A

whether right and left arterial pulses are the same strength

327
Q

pulse deficit

A

heart beat with no palpable pulse (ventricular premature beat)

328
Q

bell

A

smaller part of stethoscope, best for listening to low frequency sounds like heart sounds and gallops

329
Q

diaphragm

A

larger stretched part of stethoscope,

best for listening to high frequency sounds like murmurs

330
Q

tunable diaphragm

A

behaves as a bell with gentle pressure and as a diaphragm with firm pressure

331
Q

precordium

A

palpation of the chest wall, normally on the left side near the elbow (left apex)
Note: can probably be felt on both sides in normal chested dogs

332
Q

precordial thrill

A

ability to feel the vibrations of a murmur

333
Q

point of maximal intensity

A

the location on the chest where the murmur is loudest (left or right, apex or base)

334
Q

You are listening to a patient and hear a grade IV/VI left apical systolic murmur. Which of the following heart diseases could be the cause?

a. Mitral valve dysplasia
b. tricuspid valve dysplasia
c. pulmonic stenosis
d. patent ductus arteriosus

A

a. Mitral valve dysplasia

335
Q

Common diagnostics for heart disease

A

Blood pressure, ECG, x-ray, cardiac ultrasound,

Labs: CBC, chemistry, urinalysis, cTn- I (released into blood in patients with myocarditis

336
Q

Murmurs vs heart sounds (gallops)

A

heart sounds are short and transient and murmurs are long sounds,
These can be heard at different times in one disease

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