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Board Review 2020 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the classes of antiarrhythmic drugs:

A

Class 1: Inhibiting the fast sodium channel decreasing the slope of phase 0
Class 2: Beta adrenergic antagonists (blockers)
Class 3: Potassium channel blocker Ik
Class 4: Calcium channel blockers

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2
Q

What is the MOA of Class 1a antiarrhythmic drugs and give two examples?

A

Procainamide, quinidine, dispyramide

Fast sodium channel blocking effects, modreate blockade of the the delayed rectifier potassium current Ikr

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3
Q

What is the MOA of Class 1b antiarrhythmic drugs and give two examples

A

Lidocaine, Mexiletine
Inhibit fast Na channel primarily in the open state with rapid onset/offset kinetics
Enhanced ability with acidosis, hyperkalemia and partially depolarized cells

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4
Q

What is the MOA of Class 1c antiarrhythmic drugs and give two examples

A

Flecainide, propafenone; potent blockade of fast sodium channels with greater effects as the depolarization rate increases

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5
Q

What is the MOA of Class 2 antiarrhythmic drugs and give two examples

A

Esmolol, atenolol, propranolol
Inhibit the current If , important pacemaker current- also promotes proarrhythmic depolarization in damaged myocytes
Inhibit the inward calcium current Ica-L indirectly by decreasing cAMP

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6
Q

What is the MOA of Class 3 antiarrhythmic drugs and give two examples

A

Sotalol, Amiodarone

Block repolarizing of Ik results in prolongation of action ptoeintal during and effective refractory period

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7
Q

What is the MOA of Class 4 antiarrhythmic drugs and give two examples

A

Diltizam and verapimil
Slow AV nodal conduction, Prolong refractory period of nodal tissue
Inhibits the inflow of Ca via voltage sensitive Ca channels during depolarization

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8
Q

How are lidocaine and mexiletine excreted

A

Hepatic clearance determines serum concentration

Mexiletine: Highly protien bound with renal clearance

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9
Q

When are beta blockers contraindicated

A

sinus nodal dysfunction, AV nodal conduction disturbances, pulmonary disease or overt CHF

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10
Q

What is the difference between atenolol metroprol and propanolol

A

B1 selectivity: Atenolol, Esmolol, metroprol
Kidney excreted atenolol
Proparanolol- non specific beta blocker

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11
Q

What are the additional benefits of Amiodarone

A

Has properties of all 4 classes of antiarrhythmic

Negative sided effects hepatopathies, and thrombocytopenia

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12
Q

What is the MOA of digioxin

A

autonomic nervous system by enhancing central and peripheral vagal tone

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13
Q

When is magnesium sulfate administered

A

Torsades de pointes

When suspected is low secondary to furosemide administration

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14
Q

What are additional benifits of Sotalol

A

Non selective beta blocked with Ikr inhibition at lower doses…. Higher doses see Class 3 efffects.
Excreted soley by the kidneys

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15
Q

Describe the events in a cardiac cycle starting with diastolic

A

: Diastolic- Mitral valve opens (right side would be pulmonic) once the left ventricular pressure is lower then left atrial pressure. There is rapid filling initially, then filling of both the atria and ventricle simultaneously. Finally after a p-wave there is contraction of the atria
Systole: Action potential passes through AV node- Contraction of the ventricles allows ventricular pressure to rise above atrium and the mitral valve closes due to increased pressure. Period called isovolumetric contraction. As contraction continues the LV pressure continues to increase when exceeds that of aorta it opens.
Initial rapid entry of blood into the aorta causing a rise in pressure then drops off. Then when the ventricular pressure drops below that of the aortic pressure. Dicrotic notch in pressure wave is due to back flow of blood through the valve leaflets as the pressure drops. Closure of aortic valve. Isovolumetric relaxation phase as the mitral valve is closed, when the pressure falls below that of the atria it opens again

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16
Q

Describe the pressure and volume changes in the atria, ventricles, and aorta during each phase of the cardiac cycle

A

Diastole: AP High to low, AVol High then decrease to small; VP Low to high, VVol Low to high; Aortic Pressure Low, AVol Low
Systole: AP Low to high, Avol Small then fills; V Pres High to low, VVol High to low; Aortic Press High then drops
A Volu High to low

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17
Q

Compare and contrast the mechanical events in the left and right heart pump

A

The events are the same, with equal volume; the difference right side is low pressure as there is less resistance in the lungs compared to the high pressure side of the left.

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18
Q

How do the cardiac sounds correlate to the electrical and mechanical events of the cardiac cycle?

A

S1: Corresponds with closure of the mitral/tricuspid valves
S2: corresponds with closing of the aortic/pulmonic valves
S3 Ventricle, S4 atrial gallop

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19
Q

The pressure in the ventricles is directly linked to the volume and the stretch of the heart muscle. Describe these relationships and discuss how changes in one variable alters the other variables.

A

Pressure and volume are linked to the tension and length of the cardiac muscle cells in the ventricular wall.
Diastolic filling increase in pressure causes a corresponding increase in muscle tension which passively stretches the resting cardiac muscle to greater lengths. End diastolic pressure = ventricular preload it sets the end diastolic volume and resting length of the cardiac muscle fibers at end diastole.
Systemic atrial pressure= ventricular afterload because it determines the tension that must be developed by cardiac muscle fibers before they can shorten

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20
Q

What is the Frank Starling Law of the heart

A

Stroke volume increases as cardiac filling increases.

All factors have to remain the same…. More your stretch the more you snap

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21
Q
  1. How do changes in ventricular preload affect the stroke volume? What about the ventricular pressure-volume relationship?
A

The relationship is curvilinear, (at very high filling pressures) it is nearly linear over the normal operation range of the heart.

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22
Q
  1. What is the effect of altered ventricular after load on stroke volume and the ventricular pressure-volume relationship?
A

An increased afterload, at a constant preload, has a negative effect on cardiac muscle cell shortening.
Ventricular function is adversely influenced by abnormally high ventricular afterload… less stroke volume is decreased because end-systolic volume is increased
The effect of changes on end-systolic volume (stroke volume) is quite small- normal function hear

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23
Q

What is ejection fraction

A

(end diastolic volume-end systolic volume)/end diastolic volume

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24
Q

Cardiac function curves plot cardiac output against cardiac filling pressure. Describe and diagram how cardiac sympathetic nerve activity affects these curves.

A

CO increases at a constant filling pressure with an increase in cardiac sympathetic acitivity: 1) increased activity increases heart rate 2) increases stroke volume by increasing cardiac contractility.

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25
Q

What are the effects of the sympathetic nervous system on the heart

A

Inotropy- contractility – ventricles Harder
Chronotropy- Rate- SA Node faster
Dromotropy- conduction velocity in the AV node faster
Lusitropy – Relaxation ventricles faster

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26
Q

What are the determinants of myocardial oxygen demand and consumption? Which of these things are fixed/determined, and which things can we alter when managing critically ill patients?

A

Myocardial oxygen consumption is directly related to energy use as an aerobic process. The highest energy expenditure is during isovolumetric contraction (50%). The work is determined by cardiac afterload.
More efficient- less oxygen with lower heart rate and higher stroke volume to maintain cardiac output.

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27
Q

How will an increase in contractility change the slope of the line on the pressure volume loop of the heart

A

Increased contractility will increase the slope of the ling and shift it to the left.

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28
Q

What is the Fick Principle and how do we use this to determine cardiac output?

A

The amount of substance consumed by an organ/tissue is equal to what goes in minus what goes out. This is rearranged algebreically to solve for blood flow through an organ.
CO is then generally with oxygen content with a arterial- venous (at the level of the right heart)
CO= L blood/min

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29
Q
  1. What is the cardiac index? How is it different from cardiac output?
A

Cardiac index is equal to cardiac output corrected for the individuals size Generally in m^2
Dog 150-200 ml/kg/min
Cat 200 ml/kg/min

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30
Q

What is Ohm’s law of hydrodynamics and what are the implications of this in relation to tissue perfusion

A

The pressure difference (driving pressure) between two sites is the flow between the sites X the resistance between theses sites.
ABP= CO X SVR

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31
Q

What are the determinants of central venous pressure

A

Effecitve blood volume at site of measurement, pleural pressure (which influeneces transmural pressure across the great veins and heart), venous vascular resistance, and right heart ‘function’

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32
Q

What are the determinants of the pulmonary artery pressure? Why would we want to measure the pulmonary arterial pressure?

A

Analogous to ABP, but is of the pulmonary circulation.
CO X PVR
Pulmonary vascular resistance affected by pleural pressure variation (disease vs. respiratory cycle) and pulmonary venous pressures

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33
Q

What is a water manometer, how is it used, and which measurements (ABP, CVP, PAOP, etc) can we obtain with it

A

Fluid filled system of tubing and manometer- water is continuous from catheter to the manometer; pressure is reported as the height of the fluid within the column direct measurement at the catheter tip. Used for CVP only (ABP is too high). Measured in cmH2O.
Report a single value considered the mean intravascular pressure in the cavity.

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34
Q
  1. What are the components of a fluid-filled hemodynamic monitoring system?
A

Manometer: tubing, three way stopcock, water monometer and fluid reservoir
Electronic system: tubing, at least one stopcock, pressure transducer, pressurized fluid reservoir, a flush device a cable connecting the transducer to a processor and the processor-display

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35
Q

Describe how to set up a direct arterial blood pressure system

A

Arterial catheter is in place. The transducer is flushed with hepranized saline ( using 1 liter bag 0.9% NaCl with 1 unit per ml of heparin). There is a semi rigid line that goes from the transducer to the patient and from the transducer to the bag. The bag is maintained pressured at 300 mmHg The entire line should be primed with heparin saline above. The monitor is turned on and the connection from the transducer to the monitor plugged in. The transducer should be at the level of the heart and flushed once connected. Once connected (transducer to arterial line) and flushed A waveform should appear on the screen. The line should be flushed to ensure an adequate waveform appears. A square test may be preformed.

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36
Q

Describe how to zero a direct arterial blood pressure system

A

Zeroied- opening the tranducer’s stopcock port to the atmosphere and depressing the zero button on the electronic monitoring; done at initial set up and anytime systme components are removed or replaced or if any problems occur with reading.

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37
Q

Describe how to calibrate a direct arterial blood pressure system

A

after it is zeroied, must be calibrated prior to use. Per monitor’s manufacture guidelines.

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38
Q

Describe how level a direct arterial blood pressure system

A

eliminate the influence of gravity- the reference point is the right atrium (zero reference point). The tranducer placed at the level of the RA and zeroed at that point by opening the three-way valve to air. Should be performed prior to every measurement. Sternum is good landmark.

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39
Q

What is the natural frequency in a direct arterial blood pressure system

A

very structure when stimulated naturally vibrates at a characteristic frequency which is cycles per second or hertz (Hz). Adding components together alters a systems natural frequency.

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40
Q

What is damping in a direct arterial blood pressure system

A

is measures as coefficeitn. Higher is more significant damping— overdamped has slurred upstrokes/downstrokes, loss of detail and generally flatened appearance (falsely narrowed low systolic high diastolic. Underdamped contain non physiologic points/spikes, extra waves and exaggerated falsely high systolic and low diastolic

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41
Q

What is a square test in a direct arterial blood pressure system

A

fast flush will allow you to evaluate

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42
Q

How is MAP calculated from a direct arterial pressure waveform

A

DAP + (SAP-DAP)/3

Underestimated with tachycardia as have decreased filling time

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43
Q

What are the determinants of systolic arterial pressure

A

stroke volume, velocity of left ventricular ejection, SVR, arterial distensibility, and left ventricular preload.

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44
Q

Define pulse pressure

A

The difference between SAP and DAP. This is what is palpated

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45
Q

How do you calculate systolic pressure variation

A

SP max-SP Min

Humans SPV > 10 mmHg has been show to correlate with hypovolemia

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46
Q

How do you calculate Delta up and delta down

A 
Up= SP Max- SP Ref
Down= SP Ref-SP Min

SP ref= Meausring SP During an end expiratory pause
No better correlation than systolic pressure variation in human patients with sepsis for hypovolemia

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47
Q

How do you calculate the pulse pressure variation

A

% = (PPmax-PPmin)/ [(PPmax+PPmin)/2]

This is over a single breath. 
Higher PPV (>15%) are most likely to correlate with hypovolemia and volume responsiveness
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48
Q

What is the distal pulse amplification

A

changes that occur to the pressure wave moves from central arterial circulation out to the periphery.

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49
Q

Name three indirect blood pressure measurements

A

Doppler flow
Oscillometric
Plethysmograph

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50
Q

Describe doppler flow indirect blood pressure measurements and list two advantages/disadvantages

A

A cuff is placed above the piezo crystal. The crystal is placed over the artery with ultrasound gel. Generally, need to shave to have good contact. The cuff attached to a syphgometer and inflated until pulse is no longer heard. Slowly release the cuff until the pulse is heard.
Advantage: Good for patients that are small (<10 kg)
Patients in low flow states
Disadvantage: In cats likely represents mean, wears in dogs more likely to be systolic
Difficult to obtain if patient hairy- requires clipping of fur
Requires patient handling which may be difficult

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51
Q

Describe Oscillometric

indirect blood pressure measurements and list two advantages/disadvantages

A

Cuff is placed on the antebrachium, over the tibia, metatarsus or the tail. Cuff should measure 40% of the circumference as with above. The cuff is fully inflated to a pressure where there is no blood flow through artery. As it decreases blood flow returns causing dectable vibrations in the arterial wall. Dependent on pulses pressures and artery stiffness
Advantage- Minimal training/expertise needed
Don’t need to restrain patient once cuff is placed.
Disadvantage- While generally gives you systolic/diastolic mean it is all calculated based on mean and therefore only one value is a true measured value.
Requires appropriate cuff size. If too big may get falsely low reading or too high falsely high readings.

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52
Q

Describe plethysmograph indirect blood pressure measurements and list two advantages/disadvantages

A

Technique where use a cuff as with doppler above. Monitor for when the waveform returns use a pulse oximetry. The pulse ox monitor is placed distal to the cuff. Once the duff is inflated the waveform will not be present. Once waveform is first detected this is systolic pressure.
Advantages: requires less restraint than with doppler
Good for patients with low flow states
Disadvantages: May be difficult to obtain waveform on hairy or pigmented skin.
Dependent on accurate cuff size for accurate measurement

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53
Q

Describe how to place an pulmonary artery catheter

A

The patient is appropriately sedated. The right jugular vein is clipped and sterile prepped while patient is in left lateral or dorsal recumbency. ECG monitor should be in place. An 18 ga catheter is placed into the jugular vien. An guide wire is placed to the level of the thoracic inlet. The catheter is removed. A dilator is introduced then removed. Prior to placement integrity of balloon is tested. The pulmonary artery catheter (Swan-Ganz) is placed. The distal hole should lie within the pulmonary artery and the proximal hole in the atrium to take measurements. The ECG should be monitored as the tip of the catheter passes through the right atrium, right ventricle and into the right atrium. Besides taking measurements, fluoroscopy may be used to visualize placement

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54
Q

List 2 advantages and disadvantages of placing a pulmonary artery catheter

A

Advantage: Able to measure pulmonary artery pressures and central venous pressures.
Using thermodilution may measure cardiac output
Disadvantages: placement requires sedation; Complications such as damage to cardiac structures

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55
Q

What are the normal pressures that are anticipated as the catheter passes through the chambers

A

a. Right atrium: 4/0 mmHg
b. Right ventricle: 15-30/4 mmHg
c. Pulmonary artery: 15/6 mmHg
d. Wedged pulmonary artery: 5-12 mmHg

56
Q

What is a PAOP and how do you interpret the value

A

Pulmonary wedge pressure: Balloon is inflated in the distal branch of the pulmonary artery. Measured pressure reflects the left atrial filling pressure as it equilibrates across the pulmonary capillary bed. Left ventricular preload. Deflate balloon once measured.
Low- volume depletion the need for fluid administration
Increased: volume overload or cardiac dysfunction. Fluid is contraindicated.

57
Q

What are the parts to a CVP waveform

A
  • a wave: atrial contraction at end-diastole
  • c wave: The pressure increases due to tricuspid bulging into the atrium as a result of isovolumic ventricular contraction; Early systole
  • v wave: increase in pressure during atrium begins to fill during late systole
  • x descent: Drop in atrial pressure during ventricular systole causes by atrial relaxation
  • y descent: Drop in atrial pressure as blood enters the ventricle during diastole, emptying
58
Q

List 4 possible causes of elevated PAOP

A

Volume overload
Cardiac dysfunction
Measured at peak inspiration
High PEEP with mechanical ventilation or other pleural space disease.

59
Q

What can be calculated after you have determined cardiac output

A

DO2 (oxygen delivery): CO x CaO2
VO2 (oxygen consumption): CO x (CaO2-CvO2)
SVR: (MAP – Right Arterial Pressure)/Cardiac Output
PVR: (Mean PAP – PAOP)/ Cardiac Output

60
Q

Describe two methods of deteriming cardiac output with a pulmonary artery catheter

A

Thermodilution Technique: known Volume of a known temperature injected into the right side of circulation, a thermalcouple to follow the dilution of this sample in the blood volume. In use of a PA catheter dilution is injected into the right atrium and then measures in the pulmonary artery.

Fick Principle: the total update of a substance by the peripheral tissues is equal to the produc of the blood flow to the peripheral tissues and the arteriovenous concentration difference of the substance. Original method is by measuring oxygen concentration difference in inhaled air and the exhaled air collected over time. However can use the arteriovenous oxygen content difference by measuring an arterial and mixed venous blood sample. (using PA cath).

61
Q

How is stroke volume calculated from Left ventricular outlfow tract

A

Stroke volume = Pi x (LVOT^2/2) x LVOT Velocity
This would be calculated by getting the diameter of the LVOT in the first view and the LVOT velocity in the second view (doppler)- the peak (below the line)

62
Q

How does PEEP effect PAOP

A

PEEP will increase PAOP due to the increased in pressure within the thoracic cavity.
- PAOP is depending on continuous fluid column between the left atrium and the distal catheter tip. If the pressure from PEEP surrounding the alveoli exceeds capillary pressures the capillary will be compressed and the tip will reflect alveoli pressure

63
Q
  1. The central venous pressure (CVP) was measured, and its waveform was obtained at the right atrium using the pulmonary arterial catheter. The value was 13 cmH2O without any apparent arrhythmia on ECG. Interpret these CVP results
A

The elevated CVP >10 likely supports adequate volume to too much fluid volume. A wave is tall and could also represent right sided heart failure or significant pleural effusion. The depressed y descent suggests restriction to right ventricular filling. TFAST evaluation for fluid should be performed. Consider judicious fluids should be given in accordance with any ongoing loss, but replacement is not indicated at this time.

64
Q

List and briefly describe 5 methods of cardiac output monitoring

A

1) Bio-impedance: uses the principles of Ohm’s laws of voltage, current, and resistance. Difference in voltage from sensors
2) Transthoracic and transesophageal echocardiogram: Measuring the LVEDV and LVESV to calculate CO
3) Thermodilution: uses Fick principle, volume of room temp saline into a PA cath to the proximal injection port in the RA, and the measure of the temperature at the PA
4) Dye dilution: Inject dye into a central vein or RA and measure at a distal arterial site
5) Ion dilution: lithium chloride injected via venous catheter and lithium measured at an electrode in an arterial catheter

65
Q

How do you maintain and care for a central cath for CVP

A

periodically fast flush once every 4 hours.
Zeroed every 12 hours.
Change flush solution every 48 hours
No air bubbles in the line at any time.
Inspect and reinflate pressure bag of flush

66
Q
  1. What CAN the CVP tell us about the patient? What can the CVP NOT tell us about the patient? Discuss how monitoring CVP might be helpful in critically ill patients.
A

Best used in serial measurements over time.
Rational is its ability to serve as an estimate of right atrial pressure.
Estimate of pre-load.
Probable inidcator of volume status—in normal cardiac function likely to determine if more likely to respond.
Trends are clinically meaningful. Progressive drop look for losses, if rising look for cardiac dysfunction or fluid loading is not indicated.

*Can not: does not correlate well with intravascular volume, and predict stroke volume or cardiac output following a fluid chanllenge.

**elevated CVP may mean normal volume with cardiac disfunction or hypervolemia with normal cardiac function

67
Q
  1. Discuss driving pressure and transmural pressure as they relate to CVP.
A

Driving pressure is a pressure gradient. Is small on the venous side averages 5-10 mmHg

Higher CVP generated by elevation in thoracic or intra-abdominal pressure does not necessarily result in change in driving pressure or venous return because of the change in transmural pressure.
Pressure exerted outside of the vessel wall.

Splanchnic circulation 20-65% of the venous circulation (65% of blood)

68
Q
  1. Discuss how to perform a fluid challenge, and how to interpret the results of the fluid challenge using CVP
A

Rapidly infusing small volume of fluid (colloid or crystalloid) 15 ml/kg in dog 5 ml/kg cat crystalloid
Given over 10-15 minutes
Normal patient is rise of 2-4 cmH20 and return to baseline over 15 minutes. If low and returns to baseline early then it is indication that hypovolemia is likely.

Fall is due to redistribution of fluid from the intravascular to the interstitial space, stress induced relaxation of venous tone and pooling within the splanchnic vascular bed.
persistently high over 30 minutes may support volume overload decreased cardiac performance or restrict pericardial disease

69
Q
  1. How do you determine the CVP from the CVP waveform
A

(a wave peak + x descent base)/2

A wave is ventricular end diastole

70
Q

How are PICCO2 and LiDCO cardiac output monitors work

A

PICCO2: requires central venous and arterial catheter. Uses transpulmonary thermodilution to intermittently measure cardiac output.
Saline at a known temp
Compares well to thermodilution in people and pigs
LiDCO- pulse power analysis algorith- to calcoulat stroke volume
It requires lithium indicator dilution cardiac output to calibrate
Accuracy falls off time from aclibration. May be needed ever 1-2 hours

71
Q

What are the phases of a Cardiac fast response action potential

A

0: Depolarization: Fast Na channels open. Na rushes intracellular becomes slightly less positive than outside
1: small amount of K+ leaves the cell (the tip)
2: Ca+ influx through L-type Ca channels over time less permeable to Ca (allows for contraction)
3: Repolarization; K+ channels open and K+ effluxes and membrane returns to -90 mV
4: resting phase: Na not considered leaky at this stage

72
Q

What are the phases of a cardiac slow response action potential

A

4: Constantly leaky Na+ through Ifunny: Slope of phase 4 and the threshold potential determine the discharge rate
0: influx of Ca through Slow L-type Channels, Na Channels and T-type channels close
3: Repolarization— K+ efflux through iKto phase ends when resting potential is reached

73
Q

Write out the blood flow through the heart

A

Caudal/cranial vena cava –> right atrium –> tricuspid valve –> right ventricle –> pulmonic valve –> pulmonary artery –> pulmonary artery tree –> Pulmonary vein –> left atrium –> mitral valve –> left ventricle –> aortic valve –> aorta

74
Q

What is coronary perfusion pressure

A

Difference between diastolic aortic pressure and right atrial end diastolic pressure
Perfused during diastole; pressure gradient that drives coronary blood flow

75
Q

How are cardiac action potentials different

A

Self generative potential
conducted from cell to cell
they have a long duration which precludes fusion of individual twitch contractions

76
Q

What is the sympathetitic effect on the heart (specific ion channels)

A

Increase heart rate by increasing the inward currents of iNa funny and Ca T-type during diastolic intervals
Speeds conduction velocity in AV node and working myoctes

77
Q

What is the parasympathetic effect on the heart

A

Vagus nerve release of ACTH on the SA nod to increase permeability of resting K+ and decrease permeability of diastolic Na prolongs the time for resting membrane potential to reach threshold level

78
Q

What are the effects of atenolol

A

Beta adrengeric antagonist
Limits myocardial O2 consumption
Decreased HR
Decreased contractility

79
Q

What is cor tratriatum dexter

A

Persistence of the right venouse valve causes pertitioning of the right atrial into cranial and caudal chambers

80
Q

What is the MOA of telemisartin

A

Angiotensin II rectport antagonist

Binds to AT1

81
Q

How might chronic RAAS activtation lead to systemic hypertension

A

Systemic vasoconstriction, IV fluid expansion, sympathetic activation mediated by Ang type 1 Recpetor

82
Q

What are the stages of MMVD

A

A: High risk but not identifiable structual disease
B: structual heart disease but no clinical signs
1) No evidence on radiographs/echo of cardiac remodeling or not severe enough to warrant tx
2) Severe enough/ long standing enough to cause LA and LV enlargement on imaging:
La:AO >/= 1.6; LV internal diameter in diastole >/= 1.7
VHS > 10.5 with breed adjustments
C: current or past signs of CHF due to MMVD
D: End stage MMVD refractory to standard Tx

83
Q

What is the Bainbridge reflex

A

Stimulation of atrial stretch receptors in responses to an increase in blood volume

84
Q

What is the MOA of torasemide and possible benefits

A

Loop diuretic with increase in 1/2 life and bioavailability compared to furosmide (also longer duration of action)
Has anti-aldosterone effect

85
Q

What are the three types of cardiac troponin

A

cTnT: aids with contraction
CTnI- inhibits in abscesce of Ca
CTnC- calcium binding subunit (homogeneous with skeletal)

86
Q

What are two mechanisms for the body to treat increased potassium

A

Intracellular shift mediated by insulin, B2 adrengicer receptors and K itself
Increase renal excretion via aldosterone by princple cells in the DCT

87
Q

What are possible reasons for troponin release from myocytes

A

Dying Cell destruction: Necrosis, apoptosis, cell turnover

Viable Cell Leakage: increase permeability, intracellular proteolysis, formation of vesicles

88
Q

How does cardiogenic pulmonary edema develop

A

Neurohormonal activation leads to Na and H20 retention expansion of plasma volume (up to 30%)
Increase volume increases in pulmonary venous capillary increase oncotic pressure which then leaks fluid into interstitum and alveolar
Pulmonary venous pressure > 25 mmHg

89
Q

What are reasons why furosemide dose may need to be increased

A

Poor renal perfusion, NSAIDs, or severe hypoalbuminemia

90
Q

What is the MOA of nitroglycerin

A

Increase concentration of cGMP by NO release
Venous vasodilator
Increase venous capacity reduced preload by redistrbution to central venous resivors

91
Q

What is the MOA of hydralazine

A

Effects through arterial vasodilation via smooth muscle relaxation
Decreased afterload in MMVD

92
Q

What is the MOA of nitroprusside

A

Increase concentration of cGMP by NO release

Mixed vasodilator

93
Q

What is the MOA of pimobendan (both vasodilatory and inotropy)

A

Inotropy: Calcium sensitizer– Increase affinitiy of cardiac troponin to Ca
arterial vasodilator: Prevents breakdown of cAMP, more cAMP prevents cross bridging of actin/myosin

94
Q

What are side effects of high doses of dobutamine or dopamine

A

Sinus tachycardia, arrhythmias, alpha receptor vasoconstriction

95
Q

What is the MOA of milirone

A

increase in cytsolic cAMP to increase Calcium

arterial vasodilator and positive inotrope

96
Q

Define heart failure

A

Inability of heart to adequately meet the metabolic demands of the peripheral tissues

97
Q

What is the MOA of CHF

A

Demand is met by increase venouts filling pressures and fluid bild up
RAAS activiation, chronic SNS activation

98
Q

What are nauteritic peptides effect on the heart

A

Neuroendocrine that is cardioprotective
B-type and atrial naturetic peptides elicit vasodilation and fluid/Na excretion
Down regulated with chronic disease

99
Q

What does endothelin 1 do for the CV system

A

Potent vasoconstrictor produced by endothelial cells to mechanical disruption sheer stress, Ang II, and cytokines

100
Q

How does vasopressin affect CHF

A

Increase H20 Absorption restults in Hyponatremia

HypoNa with CHF is a poor prognostic indicator

101
Q

Describe eccentric cardiac hypertrophy

A

End to end increase in sarcomeres
MMVD, DCM, PDA
Increase stress on myocardial cells, increase myocardial O2 demand, decrease myocyte contractility

102
Q

Describe concentric cardiac hypertrophy

A

Side by side (parallel) incrase in sarcomperes: Thickness
HCM, Hypertension (systemic/pulmonary), Subaortic stenosis
Increase myocardial O2 demand, impaired diastolic relaxation

103
Q

What is tetralogy of fallot

A

VSD, Overriding aorta, pulmonic stenosis, right ventricular hypertrophy
Right to left shunting

104
Q

How do you know how much blood to remove in polycythemia

A

Kg x Blood volume x [(PCV current-PCV desirec)/PCV Current)]

105
Q

Why does pulses paradoxus occur

A

Inspiration allows increase right side filling and pulmonic blood flow. Blood pools in pulmonary circulation due to decreased LV preload and SV resuting in decreased arterial pressure during inspiration
Exaggerated with PCE and tamponade

106
Q

In the V/D radiograph view describe the position of the anatomical structures

A 
12-1: arotic arch
1-2: main pulmonic trunk
2-3: Left aurical
3-6: left ventricle
6-9: right ventricle
9-12: Right atrium
107
Q

How do phsophodiesterases inhibit vasodilation

A

Inhibits cGMP inhibition of Ca release

108
Q

What are the grades of pulmonary hypertension

A

Mild < 50 mmHg
Moderate 50-74
Severe > 75 mmHg

109
Q

What are the classes of pulmonary hyper tension and an example

A

1) Primary: HWT, VSD, PDAS
2) Left sided heart disease
3) Pulmonary disease: Tracheal collapse, fibrosis, chronic bronchitis
4) thromboemolic disease
5) Unclear cause/multifactorial (doesnt really occur in VET)

110
Q

What is the kussmal sign in Cardiorespiratory

A

increased jugular venous distension during inspiration

111
Q

What is the modified bernouli equation to measure pulmonary hypertension

A

Uses tricuspid regurgitation in the right short axis view

Max TR velocity squared x 4

112
Q

What is the MOA of sildenafil

A

Phosphodiesterase 5 inhibitor

leads to increase of cGMP concentration to vasodilation

113
Q

What antiarrythmic would you use to treat SVT

A

Diltazeam IV or beta blocker (propanolol or esmolol) IV

Beta blockers negatively affect systolic function

114
Q

What antiarrythmic would you use to treat VT

A

Dogs Lidocaine

Cats propanolol

115
Q

How would you determine if a bradycardia is vagally mediated

A

atropine response test= tachycardia at 15-30 minutes

116
Q

List 5 causes of myocarditis

A 
Parvo virus
chagas disease (trypanosoma cruzi)
Lyme dz
Bartonella
Toxoplasmosis (cats only)
117
Q

List 6 causes of DCM

A 
Genetics
Parvo virus
Chagas disease
Doxorubicin 
Taurine deficency
Tachycardia induced cardiomyopathy
118
Q

In medical management of bradyarryhtmia what would you do to treat a calcium channel or beta blocker overdose

A

Isoproterenol (beta agonist) or dopamine (increase HR and AV conduction)

119
Q

List two types of temporary pacing

A

Transvenous: using left jugular or lateral saphenous placed into the right ventricle
Trans thoracic pacing: place pads over shaved skin directly over apex of heart on both sides of thorax: very painful requires GA

120
Q

List the 4 ACVIM stages of systemic hypertension

A

1: < 140 mmHg min risk of TOD
2: 140-159 mmHg Low risk TOD
3: 160-179 mmHg mod risk of TOD
4: > 180 mmHg Severe risk of TOD

121
Q

What are 4 target organ damages from systemic hypertension and which might not require ER intervention

A

Neuro: white matter interstital edema, hyperplastic vascular lesions and parenchymal microhemorrages
Ocular: retinal detachment, hemorrage, edema, viteral hemorrhage secondary glaucoma
CV: concentric hypertrophy due to increased afterload (Not Generally ER tx)
Renal: with CKD glomerulosclerosis and tubulointerstitial fibrosis (ER tx generally not indicated)

122
Q

What is the treatment goal of hypertensive emergency

A

Decrease 25% in first 1 hr then cautious reduction to 160 mmHg over 2-6 hrs Then < 150 mmHg in 24-48 hrs

123
Q

Contrast hypertensive urgency vs. emergency

A

Urgency: critically increased BP without target organ damage

Emergency with target organ damage

124
Q

What are the most common underlying diseases in dogs for systemic hypertension

A

CKD, DM, HAC, Hyper T4

125
Q

What is the MOA of amlodipine

A

Inhibits voltaged gated L-type channels
Used for Cats with CKD- long acting
May decrease GFR, nausea, tachycardia, constipation

126
Q

What is the MOA of fenodapam

A

Peripheral dopamine-1 agonist
Maintains or increases renal perfusion while lowering BP
No rebound post CRI
Adverse: Reflex tachycardia, increased IOP

127
Q

What are the adverse effects of hydralazine

A

reflex tachycardia, weakness, GI upset

128
Q

What are the adverse effects of nitroprusside

A

Shock- severe hypotension
Hepatic dysfucntion
Cyanide intoxication

129
Q

What is the MOA of spironolactone

A

Aldosterone antagonist at the DCT and CD
Decreased Na reabsorption and K excretion
Used in Hyper aldosterone, iatrogenic steroid edema, and refractory edema

130
Q

What are the adverse effects of spironolactone

A

Hyper K

Uncommon with out CKD or concomitant use of beta blockers, ace i; ARBs and potassium supplements

131
Q

How are beta blockers useful for hypertension

A

Inhbit release of renin, decrease heart rate and contractility
Reduce Peripheral vascular resistance and reduced central adrenergic drive
Useful as second line in cats with HCM or tacchyarrythmias

132
Q

What are adverse effects of beta blockers

A

cats- asthma broncho constriction

Hyper K, bradycardia, insulin resistance, depression

133
Q

Briefly describe how myocardial muscle contracts

A

ADP bind to myosin= contraction
ATP bind to myosin= relaxation/ release of actin
L-type calcium channel voltage gated; ca to RyR at sarcoplasum reticulum to release of Ca. Calcium spark binds to troponin
Clacium back to SR via ATP, and some out of cell via Na/Ca exchanger. Na then exits the cell via 3Na/2K atp ase pump

134
Q

Where are alpha 1 and alpha2 adrenergic receptors found

A

1: central arteries and veins –> Vasoconstriction
2: GI Tract decrease secretions, motility, tone
Peripheral arteries and veins –> Vasoconstriction

135
Q

Where are beta 1 and beta 2 receptors found

A

1: Heart Increase inotropy and chronotropy
2: skeletal muscle vessels and coronary artery: Vasodilation
bronchial smooth muscle Relaxation

136
Q

What are the various mechanisms of dopamine based on dose

A

Low: D1 and D2— controversilly improve urine output
Medium: Inotrope (Beta 1)
High: Alpha agonist

137
Q

What are the vasopression receptors and where are they located

A

V1: Smooth muscle- G-coupled leads to phospholipase C –> ca from SR to cell
Lung- pulmonary vasodilator
V2: cAMP in the renal CD
V3: Pituitary release of ACTH
Also get vasodilation via oxytocin release which leads to NO release

Board Review 2020 (37 decks)

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