Cardiology Flashcards
(336 cards)
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
2
Q
3 layers of the heart
A
- endocardium: inner layer; single layer of endothelial cells
- Myocardium: middle layer thicker layer of cardiac muscle
- Epicardium: the outer layer of the heart that is made of a thin layer of mesothelial cells. visceral layer of serous pericardium
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
4
Q
Which animals have four chambered hearts?
A
mammals and birds
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.
6
Q
What maintains the pressure gradient between the atria and ventricles?
A
valves
7
Q
Which heart valve is most cranial? Is it on the right or left?
A
pulmonic valve, left
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
9
Q
Rule 2 of the heart
A
it is a muscle
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
11
Q
sarcomere
A
contractile unit of the heart
contraction controlled by tropomyosin and troponin proteins
12
Q
base vs apex
A
base is top of heart, apex is the bottom
13
Q
heart murmurs
A
abnormal sounds that indicate turbulent blood flow and are often caused by leakage, or regurgitation of heart valves
14
Q
A heart murmur on the left apex is likely due to which valve?
A
mitral valve
15
Q
You auscultate a right apical murmur, Your patient likely has regurgitation of which heart valve?
A
Tricuspid valve
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
17
Q
Pulmonic circulation
A
pumps blood to the lungs
Includes right heart, pulmonary arteries, pulmonary capillaries and pulmonary veins.
18
Q
systemic circulation
A
pumps blood to the body
Includes left heart, systemic arteries, capillaries, and veins
19
Q
“in series”
A
In a normal patient, a red blood cell will flow through the pulmonary circulation, followed by the systemic circulation.
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
21
Q
Rule 1 of the heart
A
There are two circulations arranged in series
22
Q
Rule 5 of the heart
A
Blood is lazy. Flows down its pressure gradient
23
Q
For blood to flow, the circulatory system must have _____
A
a pressure gradient
24
Q
The systemic circulation is a ____ pressure system
A
high
25
The pulmonary circulation is a ______ pressure system
low
26
What do these numbers mean? 120/80
first is the systolic pressure and the second is the diastolic pressure
27
Which organ(s) receive(s) the majority of the cardiac output?
Gastrointestinal tract and liver
28
Coronary circulation
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
29
Bronchial circulation
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
30
ischemia
abnormal delivery of blood
31
cyanosis
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.
32
After travelling through the systemic capillary beds, how is blood returned to the right atrium?
Vena cavae
33
What is the direction of blood flow through the ductus arteriosus? Why?
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
34
Explain the flow through the foramen ovale
Blood flow from the high pressure in the right atrium to the low pressure in the left atrium.
These pressures are flipped after birth.
35
What is a continuous murmur?
occurs throughout the heart cycle
36
thrill
the ability to feel the vibration of the murmur with your hand on the patient's chest
37
patent ductus arteriosus
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
38
Which direction does the blood flow through a PDA in systole? Diastole?
from aorta to pulmonary artery in both phases (thus continuous murmur)
39
Where does gas exchange occur in the fetus vs the adult?
fetus uses placenta, adult uses the lungs
40
Is the pulmonary circulation a high or low pressure system in the fetus? Adult?
High pressure system in the fetus, low pressure system in the adult
41
Is the circuitry in the fetus parallel of systemic? Adult
Systemic in adult, parallel in the fetus (both the right and left ventricle pump blood into the systemic circulation)
42
ligamentum venosum
remnant of ductus venosus,
| Failure to close results in portosystemic shunt as blood bypasses the liver
43
histologic makeup of arteries
```
high pressure system.
3 tunics (intima, media, externa)
small lumen and thick walls
more muscle and elastin fibers
no valves
```
44
histologic makeup of capillaries
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
45
histologic makeup of veins
```
low pressure system
3 tunic (intima, media, externa)
Large lumen and thin walls
fewer muscle and elastin fibers
valves
```
46
Compare histology of arteries and veins
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
47
tunica externa
outermost layer of blood vessels, made of loose connective tissue
48
tunica media
middle layer of blood vessel, smooth muscle
49
compliance
volume divided by pressure, ability for vessels to stretch (distensibility), higher for veins
50
capacitance
ability for vessels to hold a large volume under low pressures, higher for veins
51
How does severe vasodilation effect the venous return to the heart? How would you treat this?
Less venous return, and less cardiac output,
| Treatment: could give a shock bolus, norepinephrine and ADH (vasopressin) for vasoconstriction
52
elastic artery
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
53
Muscluar artery
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
54
arteriole
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
55
What are the receptors that cause vasoconstriction or vasodilation?
alpha 1 stimulation causes vasoconstriction
| beta-2 stimulation causes vasodilation
56
continuous capillaries
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
57
Fenestrated capillaries
moderate permeability, located in small intestine, kidneys, fenestrations allow passage of small molecules
58
sinusoidal cappilaries
most permeability
located in the liver, bone, marrow, spleen
Large fenestrations and incomplete basement membrane allow for exchange of large molecules (whole cells)
59
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
b. decreased compliance and decreased capacitance
60
vaso vasorum
Vessels of the vessels, blood supply to large arteries and veins, found within tunica externa
61
Relationship between cross sectional area and blood flow
Velocity of of blood flow is inversely proportional to cross sectional area and directly proportional to flow in mL/sec
62
What factors determine flow?
Ohm's law, Flow is directly related to change in pressure (pressure gradient) and inversely related to resistance
63
What factors determine resistance to flow?
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
64
hypovolemic shock
the inability to adequately perfuse the body due to severely reduced blood volume
Treat with fluid bolus
Hypokinetic pulses
65
how does needle size relate to rate of fluid administration?
to deliver fluids, quickly want a smaller gauge needle (wider) that is short to minimize resistance
66
laminar vs. turbulent flow
normally, blood flow is laminar or streamlined.
| In disease, blood flow may become turbulent resulting in a heart murmur
67
Reynolds number
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
68
What is polycythemia and how would it impact blood viscosity?
increased red blood cells, increased blood viscosity
69
How do the following conditions impact blood viscosity?
Anemia
Intravenous fluids
Dehydration
Anemia: decreased viscosity
Intravenous fluids: decreased viscosity
Dehydration: increased viscosity
Therefore anemic patients or those receiving intravenous fluids can present with heart murmurs.
70
ventricular septal defects
VSD, most common cardiac birth defect in cats
Characterized by hole in interventricular septum
Volume overload disease
71
How does size of a VSD impact flow velocity and loudness of murmur?
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.
72
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?
Reynold's number
73
Gradation of murmurs
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
74
What is rule 6 of the heart? (equation)
Blood pressure is a product of cardiac output and vascular resistance.
BP= CO * VR
75
How does blood pressure change throughout the systemic circulatory system?
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.
76
Causes of falling pressure in arterioles, capillaries and venules/veins?
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)
77
Systolic pressure
during systole, the ventricles pump blood into the arteries generating the highest arterial pressures (systemic not pulmonary)
78
diastolic pressure
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
79
mean arterial pressure
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.
80
pulse pressure
systolic pressure minus diastolic pressure,
| Represents the stroke volume
81
stroke volume
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
82
subaortic stenosis
(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
83
What conditions might cause hyperkinetic pulses?
large pulse pressure due to PDA, severe aortic regurgitation, bradycardia, decreased vascular resistance, high sympathetic tone
84
What conditions might cause hypokinetic pulses?
weak thready pulses,
| subaortic stenosis, hypovolemia, some arrhythmias, lower stroke volume
85
How do the pressures in pulmonary circulation compare to systemic pressures?
pulmonary pressures are about 1/5 of the systemic pressures
86
What is changed in the pulmonary circulation to maintain the same flow rate at lower pressures?
The pulmonary resistance is much lower
87
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?
Hyperkinetic
88
Are cardiac output and vascular resistance independently or dependently related?
They are dependent in that if one changes, the other will increase as a regulatory mechanism
89
Why do arterioles have high resistance?
small lumens causing increased friction
| Lot of smooth muscle with basal tone that can constrict or dilate to regulate flow
90
How do the two arms of the autonomic nervous system impact heart rate and blood pressure?
Sympathetic system increases heart rate and blood pressure.
| Parasympathetic decrease heart rate and blood pressure
91
Baroreceptors
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
92
Impact of signal from baroreceptors
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
93
vasomotor control center
controls sympathetic tone for decreasing diameter of blood vessels
94
How does vascular resistance related to sympathetic tone?
Increased sympathetic tone will have greater vascular resistance
95
What factors of the blood pressure equations do baroreceptors change as a result of increased blood pressure?
Reflex bradycardia (lower heart rate and cardiac output), arteriolar vasodilation (lower vascular resistance), and decreased contractility (decreased stroke volume and cardiac output)
96
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.
```
fewer signals
increased sympathetic
decreased parasympathetic
sympathetic predominance
increased heart rate
vasoconstriction
increased contractility
```
97
RAAS system
Renin angiotensin-aldosterone system
Corrects low blood pressure via two mechanisms and is slower than baroreceptor response because it is hormonally mediated
98
RAAS stimuli
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
99
A car almost hits you in an intersection and you have a sudden increase in blood pressure. Which blood pressure regulatory action occurs first?
increased baroreceptor firing rates
100
How are the regulatory mechanisms of baroreceptors and RAAS related?
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
101
Aldosterone
acts in the distal convoluted tubule and collecting ducts to increase sodium and water reabsorption and potassium excretion
102
What controls the flow of blood through capillary beds?
smooth muscle in the arterioles
103
metarterioles
metarterioles and the precapillary sphincters act as on/off switches for capillary blood flow
104
local blood flow vasodilators
low tissue O2 or high CO2, histamine, adenosine, bradykinin,
105
local blood flow vasoconstrictors
angiotensin II, epinephrine/ norepinephrine (catecholamines), endothelin (produced by vessel trauma), acute stretch of the arterioles after acute increase in blood pressure (myogenic autoregulation)
106
microcirculation
the exchange of substances across the capillaries occurs via simple diffusion
107
lymphatic vessels: function and histology
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
108
edema
increased interstitial fluid volume due to increased filtration (increased Pc or Kf) and/or decreased absorption or drainage (decreased pi c or lymphatic drainage)
109
What cardiac conditions cause increased capillary hydrostatic pressure?
```
arteriolar dilation
venous constriction
increased venous pressure
heart failure
extracellular fluid volume expansion
```
110
What conditions cause increased capillary permeability (Kf)?
burns, inflammation, toxins
111
What conditions cause decreased capillary oncotic pressure?
loss of plasma proteins (urinary or GI protein loss)
| decreased production of proteins (liver failure or malnutrition)
112
What conditions cause decreased lymphatic drainage?
standing (decreased skeletal muscle compression of lymph vessels)
lymphatic obstruction
113
fluid exchange across capillaries
dictated by Starling forces
Net - causes fluid reabsorption
Net + causes fluid filtration
114
tachypnea
increased respiration rate
115
DMVD
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
116
left sided congestive heart failure
severe heart disease leading to back up of fluid into the lungs and leakage of fluid into the interstitial spaces in the lungs
117
Which starling's force is impacted in DMVD?
increased capillary hydrostatic pressure (Pc)
118
subcutaneous edema
accumulation of fluid in tissues such as swollen skin in distal limbs and ventral abdomen
119
panhypoproteinemia
reduced blood protein levels with severely reduced albumin and globulin levels
120
protein losing enteropathy
chronic condition characterized by loss of proteins through the gastrointestinal tract
Presents with panhypoproteinemia resulting in subcutaneous edema or thoracic or abdominal effusion
121
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
Furosemide to treat DMVD
| Colloids to treat PLE
122
What compounds can leak through capillary beds in burns and why?
increased capillary bed permeability causes leakage of albumin and other proteins as well as electrolytes
123
A patient has subcutaneous edema caused by hypoproteinemia (low blood albumin levels). How are Starling's forces altered?
low capillary oncotic pressure
124
Electrophysiology
study of the electrical activation of the heart and is the foundation for understanding and treatment of arrhythmias.
125
Are there ways to improve the function of the lymphatic system?
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.
126
What is required to come before cardiac contraction and relaxation can occur?
electrical depolarization and repolarization
127
What are the functions of the heart (rule 4)?
1. Electrical conduction
2. Contraction during systole
3. Relaxation during diastole
128
chronotropy
heart rate
129
dromotropy
speed of conduction
130
inotropy
contractility, strength of contraction of the heart, modulated by drug or autonomic tone influences
Increased inotropy/contractility means stronger contractions
131
lusitropy
relaxation function of the heart
132
membrane polarity
transmembrane potential, voltage difference across the membrane in mV
133
membrane permeability
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
134
action potentials
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
135
What are the three states a cardiomyocyte can be in?
1. Resting (polarized)
2. Depolarization
3. Repolarization
136
What do changes in polarity require?
movement of ion across membranes, which require a driving force (electrochemical gradient).
137
Resting state (polarized)
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
ion movement by Na K ATPase pump
3 Na pumped out of cell per 2 K into the cell
139
How might a urethral obstruction in a cat alter the electrochemical gradient in cardiomyocytes?
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
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
c. selective membrane permeability to potassium at rest
141
Order of electrical activation
1. SA node
2. Atrial myocardium
3. AV node
4. Bundle of His
5. Bundle branches
6. Purkinje fibers
7. Ventricular myocardium
142
Bachmann's bundle
transmits the electrical impulse from the right to left atrium
143
Fast response action potentials
occur in the atrial and ventricular myocytes and Purkinje cells
144
Phase 4 of fast response action potential
RMP, membrane potential is -90 in fast response, no ion movement
145
phase 0 of fast response action potential
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
m gate of sodium channel
extracellular part, allows the Na in, closed at rest, opens quickly
147
h gate of sodium channel
intracellular part, closes off entry of sodium, closes slowly, open at rest
148
phase 1 of fast response action potential
initial repolarization via opening of K channels, K efflux
149
Phase 2 of fast response action potential
membrane potential is relatively stable
| Na channels inactivated, Long acting Ca channels opened, Ca influx, K channels opened, K efflux
150
phase 3 of fast response action potential
Completion of repolarization,
| K channels are fully activated and opened allowing for efflux of K, membrane potential is returned to RMP (-90 mV)
151
slow response action potentials
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
phase 4 of slow response action potential
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
phase 0 of slow response action potential
slow upstroke via a slow influx of Ca
154
Why do slow response action potentials use Ca influx to depolarize instead of Na influx?
sodium channels cannot work at the RMP used in slow action potentials
155
Phase 3 of slow response action potential
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
escape beats
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
How does parasympathetic stimulation impact action potentials? Sympathetic?
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
What allows for propagation of depolarization?
Gap junctions allow ions to pass from the depolarized cell to the adjacent cell
159
Refractory period
cells are unresponsive to restimulation,
| dictated by the balance of inactive vs reactivated/ resting Na channels
160
relative refractory period
a stronger than normal stimulus from an adjacent cell can prematurely excite the cells
161
ventricular premature complexes
VPC: an arrhythmia caused by abnormally early depolarization of ventricular cardiomyocytes
Treatment can include drugs that prolong refractory period (sotalol)
162
mechanism of sotalol
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
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
b. spontaneous diastolic depolarization during phase 4
164
electrocardiograms
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
What do ECGs tell us, what don't they tell us?
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
arrhythmia
electrical activity with irregular rhythm and/or an abnormal heart rate
167
p wave
atrial depolarization
168
QRS complex
ventricular depolarization
169
t wave
ventricular repolarization
170
ECG leads
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
isoelectric line
flat line on ECG
172
amplitude of deflection on ECG
dictated by the amount of tissue being depolarized (more tissue, more amplitude) and the orientation of the waveform relative to the lead
173
What color electrode goes where on the patient?
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
what position is the patient in for an ECG?
right lateral recumbency
175
Purkinje fibers
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
Compare Purkinje cell network in small vs large animals
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
How might ECGs be different in large animals (particularly horses)?
single lead system, predominantly negative QRS (deep S wave), notched P waves are normal in horses
178
mean electrical axis
helps determine which side of the heart has disease (enlargement)
179
K channels
both voltage and ligand gated
| Opened by increases in acetylcholine (parasympathetic tone), extracellular K, adenosine, muscle stretch
180
Which tissues are more or less impacted by hyperkalemia?
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
Why is the QRS complex often the equal or narrower width than the P wave?
The His-Purkinje system is a superhighway that allows very rapid conduction through the ventricles
182
How is the ECG impacted by hyperkalemia?
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
associated vs dissociated beats
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
equation for heart rate calculation
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
Bradycardia and bradyarrhythmia
heart rates are slower than normal
| Hyperkalemia is a common cause in cats
186
tachycardia and tachyarrhythmia
heart rates are faster than normal
187
Normal heart rates for these species:
| Canine, Feline, Bovine, Equine
Canine: 60-160 bpm
Feline: 140-240 bpm
Bovine: 60-88 bpm
Equine: 28-44 bpm
188
Does normal heart rate different across species? Within a species?
Heart rate differs across different species, but not within a single species.
189
What would cause differering heart beats between healthy individuals of a species?
Differences in sympathetic or parasympathetic tone
190
transient atrial standstill
bradycardia, absent P waves, and narrow QRS complex
| Can be caused by hyperkalemia
191
Is the direction of the T wave positive or negative?
It can be either with no significant clinical correlation.
192
What does the PQ or PR interval represent?
rate of conduction through the AV node
193
What does the QT interval represent?
Total interval from start of ventricular depolarization to end of repolarization
194
P pulmonale
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
P mitrale
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
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. the atria and atrioventricular node
197
Which vessel type has an internal elastic lamina?
arteries
198
Why is sodium nitroprusside used to treat DMVD?
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
Pulmonary hypertension
high blood pressure in the lungs
Can be associated with high altitude disease
Pressure overload disease, concentric hypertrophy, increased afterload
200
High altitude disease
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
What type of capillaries are present in the portal capillary beds?
sinusoidal capillaries
202
Mean electrical axis
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
What is the normal direction of depolarization in the heart?
going from right to left and cranial to caudal
204
Which diseases are associated with a left axis shift? Right axis shift?
Left axis shift: left ventricular enlargement, Left bundle branch block
Right axis shift: right ventricular enlargement, Right bundle branch block
205
Diseases with low heart rates?
sinus bradycardia
| second or third degree atrioventricular block, atrial standstill, sinus node dysfunction
206
Cardiac conditions that would have a normal heart rate?
sinus rhythm, first degree atrioventricular block, sinus with ventricular ectopic (ventricular premature complexes or escape beats) sinus with supraventricular premature complexes (SVPC)
207
Diseases associated with high heart rate?
sinus tachycardia, ventricular tachycardia, supraventricular tachycardia, atrial fibrillation
208
block or unconducted P waves
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
sinus arrhythmia
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
physiologic vagal tone
a predominance of parasympathetic tone
211
pathologic vagal tone
increased vagal tone caused by disease (gastrointestinal, ocular, central nervous system, or respiratory systems)
212
What are the ECG features in sinus arrhythmia?
Wandering atrial pacemaker (variable P wave heights)
Low heart rate, regularly irregular rhythm, PQRST waves present, associated
Origin of QRS: sinus
213
wandering atrial pacemaker
variable P wave heights, commonly seen with sinus arrhythmia
214
atrial fibrillation
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
ECG features of Afib
high heart rate, irregularly irregular rhythm, QRS and T, true p is absent, supraventricular ectopic beats
dissociated
216
sinus bradycardia (description and ECG features)
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
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
B. pulmonary hypertension
218
excitation-contraction coupling
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
What relationship facilitates excitation-contraction coupling?
The spatial relationship between the sarcolemma, T tubules, and Sarcoplasmic reticulum facilitates excitation contraction coupling.
220
T-tubules
invagination of sarcolemma that transmit outer electrical events deeper into the cell
221
What mediates excitation-contraction coupling?
Mediated by changes in sarcoplasmic calcium levels
222
Step one of E-C coupling
small Ca influx during phase 2 of action potential.
| Calcium enters the cell through the voltage gated long acting Ca channel (Ca-L)
223
Step 2 of E-C coupling
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
Step 3 of E-C coupling
Ventricular contraction during systole: Ca binds cardiac troponin C and goes on to cause contraction
225
Step 4 of E-C coupling
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
Major determinant of inotrpy
cytosolic Ca concentration determines the force of contraction. Increased intracellular calcium has stronger contractions and decreased intracellular calcium has weaker contractions
227
Relationship of actin, myosin, tropomyosin and troponin
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
What are the parts of the cardiac troponin complex and what is their function?
cTn I- inhibits myosin binding
cTn C- binds calcium
CTn T- binds tropomyosin
229
phospholamban
PL, regulates sarco(endo)plasmic reticulum calcium ATPase (SERCA) by acting as a gatekeeper and only phosphorylated PL "opens the gate" for resequestration
230
How would sympathetic or parasympathetic stimulation impact SERCA?
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
How do positive and negative inotropic drugs impact the heart?
During systole, positive inotropes increase contractility and negative inotropes decreased contractility
232
How do lusitropic drugs impact the heart?
During diastole, positive lusitropes increase relaxation and negative lusitropes decrease relaxation.
233
If you are designing a drug to increase contractility, what effect would it have on intracellular calcium levels? What kind of drug is it?
positive inotrope that increased intracellular Ca by increasing release into the sarcoplasm or decreasing removal from the sarcoplasm
234
mechanism for Pimobendan
acts as a "calcium sensitizer by increasing the affinity of cTn-C for calcium
Positive inotrope
235
mechanism of Diltiazem
calcium channel blocker (long acting Ca channels) that is used to treat arrhythmias.
Negative inotrope
236
mechanism of Dubutamine
stimulates beta receptors
| beta agonist activity, positive inotrope
237
mechanism of Theophylline
binds to and stimulates beta receptors
| beta agonst, positive inotrope
238
mechanism of Atendol
beta blocker medication that inhibits beta receptors
| beta antagonist activity, negative inotrope
239
mechanism of Amlodipine
calcium channel blocker (long acting Ca channels) that is used to treat systemic hypertension
Negative inotrope
240
When calcium is released from the sarcoplasmic reticulum into the sarcoplasm, what protein does calcium bind to?
Troponin C
241
Dihydropyridine calcium channel blockers
eg. amlodipine, bind "peripherally" in the vascular smooth muscle causing vasodilation
242
Non-dihydropyridine calcium channel blockers
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
agonist
substance that binds and stimulates the receptor
244
antagonist
binds and inhibits the receptor
245
What does stimulation of beta receptors do?
Increases all of the "tropy"s
246
What are two ways to increase pressure in a chamber?
1. fill with more blood/ increase volume
| 2. Contraction/ squeezing
247
When is the mitral valve open? Closed?
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
When is the aortic valve open? Closed?
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
Atrial contraction
Final phase of diastole, the atrium contracts and empties the last 20% of blood into the ventricle
250
isovolumic contraction
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
Ejection
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
S1 heart sound
(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
S2 heart sound
(dub) occurs at the time of aortic valve closure and marks the end of systole
heard best at left base
254
systolic dysfunction
characterized by reduced pumping function and progressive heart dilation and can have various causes.
255
Primary diseases causing systolic dysfunction
```
dilated cardiomyopathy (DCM)
Arrhythmogenic right ventricular cardiomyopathy ARVC)
```
256
What diseases have systolic dysfunction as a secondary symptom?
```
inflammation/infection
Toxins/drugs
diet associated cardiomyopathies
tachycardia induced cardiomyopathy
hypothyroidism
```
257
preload
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
Afterload
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
Dilated cardiomyopathy
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
cardiomyopathy
disease of the heart muscle
261
Ejection fraction percentage
EF%, represents the percent change in left ventricular volume before and after contraction of the ventricle (normal >50%)
=(EDV-ESV)/ EDV x 100%
262
Fractional shortening percentage
FS%, the percent change in the width of the left ventricular chamber between systole and diastole (normal>30%)
=(LVd-LVs)/ LVd x 100%
263
end diastolic volume
EDV, the maximum volume of blood in the ventricle at the end of diastole
264
End systolic volume
ESV, the minimum volume of blood in the ventricle at the end of systole
(yes, some is still left over)
265
left ventricular internal dimension in diastole
LVd, left ventricular width at the end of diastole
266
left ventricular internal dimension in systole
LVs, left ventricular width at the end of systole
267
Treatment for DCM
Pimobendan increases contractility and this is the source of the issue
268
A heart murmur is heard between the S1 and S2 heart sounds. During what phase of the cardiac cycle is this murmur occuring?
Systole, either isovolumic contraction or ejection, probably ejection
269
isovolumic relaxation
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
early rapid filling
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
Diastasis
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
atrial contraction
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
Which is longer systole or diastole?
diastole is 2/3 of the cardiac cycle
274
Does diastole require energy, why or why not?
Yes, ATP is required for SERCA resequestration of Ca and to reset the myosin head.
275
What stage of the cardiac cycle does blood enter the coronary arteries?
Diastole, coronary arteries carry blood to the heart muscle. During the elastic recoil of the aorta.
276
Which heart sounds are normal in small animal patients? large animals?
S1 and S2 are normal in small animals will all four can normally be heard in large animals
277
hypertrophic cardiomyopathy
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
ventricular compliance
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
What happens when ventricular compliance is decreased?
the stiff ventricle doesn't relax well (decreased lusitropy) with a larger increase in pressure for the same EDV
280
S4 heart sound
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
How is coronary perfusion to the heart muscle altered in patients with diastolic dysfunction?
decreased coronary perfusion, ischemia. There is more muscle to perfuse and the coronary vessels are not developing along with the muscle.
282
How is the flow of blood impacted in patients with HCM?
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
What conditions increase preload?
intravenous fluid administration, mitral or tricuspid valve regurgitation
284
What conditions decrease preload?
Dehydration, atrial fibrillation, HCM
285
What conditions increase afterload?
arterial hypertension, stenosis of aortic or pulmonic valve, arterial vasoconstrictor medication
286
What conditions decrease afterload?
arterial vasodilator medication
287
rule 3 of the heart
its response to disease is predictable (concentric vs eccentric hypertrophy)
288
concentric hypertrophy
appears as an increased wall thickness and small chamber
289
eccentric hypertrophy
appears as a normal wall thickness with a dilated chamber
290
Frank-Starling mechanism
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
Pathophysiology of a volume overload disease
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
systemic hypertension
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
pulmonic stenosis
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
Law of LaPlase
Tension= pressure multiplied by radius divided by wall thickness.
Therefore ventricular hypertrophy reduces the ventricular wall tension
295
Pathophysiology of pressure overload disease
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
```
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
```
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
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
c. concentric hypertrophy of the left ventricle
298
ECG features of sinus rhythm with ventricular ectopics
Normal heart rate unless the escape complexes occur frequently. Irregular rhythm. QRST and ventricular ectopics, QRS is of ventricular origin
299
supraventricular premature complexes
(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
P prime waves
P waves with a different morphology from sinus P waves
| found with supraventricular QRS complexes
301
ECG features of SVPC
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
Third degree atrioventricular block (AVB)
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
Common causes of ventricular arrhythmias (HEADS)
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
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)
Lidocaine
305
ECG features of ventricular tachycardia
high heart rate, regular rhythm, QRST, ventricular ectopic
Origin of QRS: ventricular
dissociated
306
stenosis
fusion of valves making a smaller opening, a type of pressure overload disease, increased afterload
307
Wigger's diagram
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
What is the mechanical event and heart sound(s) associated with T wave?
(ventricular repolarization) isovolumic relaxation, S2 and S3 heart sounds
309
heart failure
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
clinical signs of forward heart failure
syncope (fainting), pallor, cyanosis, hypokinetic pulses, azotemia
Contractile dysfunction
311
clinical signs of backward heart failure
```
(congestive heart failure) pulmonary edema
Pleural effusion
Ascites/ hepatomegaly
Pericardial effusion
Peripheral edema
```
312
Signs of left vs right sided heart disease in dogs
Left: pulmonary edema with rarely any other signs
Right: Ascites with occasional pleaural effusion, pericardial effusion, peripheral edema
313
Sings of left vs right sided heart disease in cats
left: pulmonary edema, pleural effusion, pericardial effusion
right: pleural effusion, ascites, pericardial effusion
314
Long term impacts of RAAS activation
myocardial remodeling and fibrosis, renal and arteriolar sclerosis, cytokine activation
315
long term impacts of baroreceptor activation
myocardial remodeling and fibrosis, cytokine activation
316
How does vasoconstriction by the RAAS system and baroreceptors contribute to progressive left ventricular dilation in DCM?
arterial vasoconstriction causes increased resistance. Ventricular vasoconstriction increases venous return and preload
317
tricuspid valve dysplasia
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
Visual exam findings that can indicate heart disease
Cachexia (muscle atrophy), abdominal distension due to peritoneal effusion, mucous membranes with pallor or cyanosis, peripheral edema
319
venous assesment
visual assessment of the jugular vein that is performed in standing patients
320
jugular pulsation
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
jugular distension
the jugular vein remains full of blood
322
causes of jugular pulsation or distension
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
Three features of arterial assessment
strength, synchronous, symmetry
324
Where are arterial pulses palpated?
Small animals: femoral artery in the femoral triangle
| Large animals: facial artery on medial aspect of the ramus of the mandible
325
snchronous
hearing a heartbeat that is almost immediately followed by a palpable pulse.
Evaluate by listening and feeling pulse at same time
326
symmetrical
whether right and left arterial pulses are the same strength
327
pulse deficit
heart beat with no palpable pulse (ventricular premature beat)
328
bell
smaller part of stethoscope, best for listening to low frequency sounds like heart sounds and gallops
329
diaphragm
larger stretched part of stethoscope,
| best for listening to high frequency sounds like murmurs
330
tunable diaphragm
behaves as a bell with gentle pressure and as a diaphragm with firm pressure
331
precordium
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
precordial thrill
ability to feel the vibrations of a murmur
333
point of maximal intensity
the location on the chest where the murmur is loudest (left or right, apex or base)
334
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. Mitral valve dysplasia
335
Common diagnostics for heart disease
Blood pressure, ECG, x-ray, cardiac ultrasound,
| Labs: CBC, chemistry, urinalysis, cTn- I (released into blood in patients with myocarditis
336
Murmurs vs heart sounds (gallops)
heart sounds are short and transient and murmurs are long sounds,
These can be heard at different times in one disease
