Cardiovascular Flashcards

Question

What is the sarcolemma

Answer 1

True cell membrane surrounding each muscle fiber Each muscle fiber contains hundreds to thousands of muscle myofibrils

Answer 2

The spaces between the myofibrils are filled with intracellular fluid called sarcoplasm It contains larges amounts of K, Mg and Ph and a lot of mitochondria that supply with energy for the contraction.

Answer 3

o Same as for skeletal muscle, when an action potential reaches the cardiac muscle membrane, it spreads to the interior of the cardiac muscle fiber along the membranes of the transverse (T) tubules. o The T tubule action potentials in turn act on the membranes of the longitudinal sarcoplasmic tubules to cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum. o The calcium will promote sliding of the actin and myosin filaments along one another, which produces the muscle contraction. o In the cardiac muscle, addition to the calcium ions that are released into the sarcoplasm from the cisternae of the sarcoplasmic reticulum, calcium ions also diffuse into the sarcoplasm from the T tubules themselves at the time of the action potential, which opens voltage-dependent calcium channels in the membrane of the T tubule. o Ca entering the cell then activates Ca release channels (ryanodine receptor channels), in the sarcoplasmic reticulum membrane, triggering the release of Ca into the sarcoplasm. Calcium ions in the sarcoplasm then interact with troponin to initiate cross-bridge formation and contraction. o Without the calcium from the T tubules, the strength of cardiac muscle contraction would be reduced considerably because the sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle and does not store enough calcium to provide full contraction.

Answer 4

Ryanodine receptor channel

Answer 5

Via the NCX anti porter (3Na in, 2Ca out) Via the Na/K ATPase

Answer 6

0.1 sec This delay is important to allow the atria contract ahead of the ventricles, therefore pumping blood into them.

Answer 7

Events that occur from the beginning of one heartbeat to the beginning of the next one.

Answer 8

o The duration of the action potential and the systole decreases, but not by as great a percentage as does the diastole. o Because the heart beating at a very fast rate does not remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction.

Answer 9

TRUE - when the atria fail to function, the difference is unlikely to be noticed unless a person exercises.

Answer 10

Is caused by atrial contraction. The right atrial pressure increases 4 to 6 mm Hg during atrial contraction, and the left atrial pressure increases about 7 to 8 mm Hg.

Answer 11

Occurs when the ventricles begin to contract; it is caused partly by slight back flow of blood into the atria at the onset of ventricular contraction but mainly by bulging of the A-V valves backward toward the atria because of increasing pressure in the ventricles.

Answer 12

Occurs toward the end of ventricular contraction; it results from slow flow of blood into the atria from the veins while the A-V valves are closed during ven- tricular contraction. Then, when ventricular contraction is over, the A-V valves open, allowing this stored atrial blood to flow rapidly into the ventricles and causing the v wave to disappear.

Answer 13

As soon as systole is over and the ventricular pressures fall to their low diastolic values, the moderately increased pressures that have developed in the atria during ventricular systole immediately push the A-V valves open and allow blood to flow rapidly into the ventricles.

Answer 14

1/3 of the diastole

Answer 15

o Immediately after ventricular contraction begins, the ventricular pressure rises abruptly causing the A-V valves to close. o Then an additional 0.02 to 0.03 second is required for the ventricle to build up sufficient pressure to push the aortic and pulmonary valves open against the pressures in the aorta and pulmonary artery. o Therefore, during this period, contraction is occurring in the ventricles, but no emptying occurs. Cardiac muscle tension is increasing but little or no shortening of the muscle fibers is occurring.

Answer 16

When the LV pressure rises slightly above 80 mm Hg (and the RV pressure rises slightly above 8 mm Hg), the ventricular pressures push the semilunar valves open. Immediately, blood begins to pour out of the ventricles.

Answer 17

o 70% of the blood ejected by the ventricles flows out during the first third of the ejection period -> rapid ejection period. o Remaining 30% empties during the next 2/3 of systole -> slow ejection period.

Answer 18

o At the end of systole, ventricular relaxation begins suddenly, allowing both the right and left intraventricular pressures to decrease rapidly. o The elevated pressures in the distended large arteries that have just been filled with blood from the contracted ventricles immediately push blood back toward the ventricles, which snaps the aortic and pulmonary valves closed. o For another 0.03 to 0.06 second, the ventricular muscle continues to relax, even though the ventricular volume does not change as the AV valves are still closed -> period of isovolumic or isometric relaxation. o During this period, the intraventricular pressures rapidly decrease back to their low diastolic levels. Then the A-V valves open to begin a new cycle of ventricular pumping.

Answer 19

o During diastole, normal filling of the ventricles increases the volume of each ventricle to about 110 to 120mL. o This volume is called the end- diastolic volume.

Answer 20

o As the ventricles empty during systole, the volume decreases about 70mL, which is called the stroke volume output.

Answer 21

o The remaining volume in each ventricle after systole, about 40 to 50mL

Answer 22

The fraction of the end-diastolic volume that is ejected — usually equal to about 0.6 (or 60 percent).

Answer 23

FALSE - They close and open passively. They close when a backward pressure gradient pushes blood backward, and they open when a forward pressure gradient forces blood in the forward direction.

Answer 24

FALSE - They contract when the ventricular walls contract.

Answer 25

FALSE - they pull the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction.

Answer 26

o High pressures in the arteries at the end of systole cause the semilunar valves to snap closed, in contrast to the much softer closure of the A-V valves. o Because of smaller openings, the velocity of blood ejection through the aortic and pulmonary valves is far greater than that through the much larger A-V valves. o Because of the rapid closure and rapid ejection, the edges of the aortic and pulmonary valves are subjected to much greater mechanical abrasion than are the A-V valves. o The A-V valves are supported by the chordae tendineae, which is not true for the semilunar valves.

Answer 27

o An incisura occurs in the aortic pressure curve when the aortic valve closes. o This is caused by a short period of backward flow of blood immediately before closure of the valve, followed by sudden cessation of the back flow.

Answer 28

Around 80mmHg

Answer 29

Close of AV valves

Answer 30

Close of semilunar valves

Answer 31

150mL Partly because of fibrous tissue in the heart that will stretch no more and partly because the pericardium that surrounds the heart becomes filled nearly to its limit.

Answer 32

150-170mL o As the volume increases further, the systolic pressure actually decreases, because at these great volumes, the actin and myosin filaments of the cardiac muscle fibers are pulled apart far enough that the strength of each cardiac fiber contraction decreases.

Answer 33

250-300mmHg

Answer 34

Usually considered to be the end-diastolic pressure when the ventricle has become filled.

Answer 35

o The pressure in the aorta leading from the ventricle. o Sometimes the afterload is loosely considered to be the resistance in the circulation rather than the pressure.

Answer 36

Because approximately 70 to 90 percent of this energy is normally derived from oxidative metabolism of fatty acids, with about 10 to 30 percent coming from other nutrients, especially lactate and glucose.

Answer 37

1) Intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart - Frank Starling mechanism and increased stretch of RA. 2) Control of HR and contractility by the ANS

Answer 38

Amount of blood that flows into the heart from the veins

Answer 39

Frank-Starling mechanism of the heart.

Answer 40

That the greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater the quantity of blood pumped into the aorta.

Answer 41

o When an extra amount of blood flows into the ventricles, the cardiac muscle is stretched to a greater length. o This stretching in turn causes the muscle to contract with increased force because the actin and myosin filaments are brought to a more nearly optimal degree of overlap for force generation. o Therefore, the ventricle, because of its increased pumping, automatically pumps the extra blood into the arteries. o This ability of stretched muscle, up to an optimal length, to contract with increased work output is characteristic of all striated muscle, not only the cardiac muscle. o Stretch of the right atrial wall directly increases the heart rate by 10 to 20 percent, which also helps increase the CO, although its contribution is much less than that of the Frank-Starling mechanism.

Answer 42

o The pumping effectiveness of the heart also is controlled by the sympathetic and parasympathetic (vagus) nerves. o Sympathetic nerves -> can increase the heart rate from the normal rate of 70bpm up to 180 to 200 and, rarely, 250bpm. o Sympathetic stimulation increases the force of heart contraction to as much as double the normal rate -> increases the volume of blood pumped and increases the ejection pressure. o Sympathetic stimulation often can increase the maximum cardiac output as much as twofold to threefold, in addition to the increased output caused by the Frank-Starling mechanism. o Inhibition of the sympathetic nerves to the heart can decrease cardiac pumping to a moderate extent. Under normal conditions, the sympathetic nerve fibers to the heart discharge continuously at a slow rate that maintains pumping at about 30 percent above that with no sympathetic stimulation. o When the activity of the sympathetic nervous system is depressed below normal, both the heart rate and strength of ventricular muscle contraction decrease, decreasing the level of cardiac pumping as much as 30 percent below normal

Answer 43

o Strong stimulation of the parasympathetic nerve fibers in the vagus nerves to the heart can stop the heartbeat for a few seconds, but then the heart usually “escapes” and beats at a rate of 20 to 40 beats/min as long as the parasympathetic stimulation continues. o In addition, strong vagal stimulation can decrease the strength of heart muscle contraction by 20 to 30 percent. o The vagal fibers are distributed mainly to the atria and not much to the ventricles, where the power contraction of the heart occurs -> the effect of vagal stimulation is mainly to decrease the heart rate rather than to decrease the strength of contractility. o However, the great decrease in heart rate combined with a slight decrease in contractility can decrease ventricular pumping 50% or more.

Answer 44

o The ventricular function curves here represent the function of the entire heart rather than of a single ventricle. o It shows the relation between right atrial pressure at the input of the right heart and cardiac output from the left ventricle into the aorta. o At any given right atrial pressure, the cardiac output increases during increased sympathetic stimulation and decreases during increased parasympathetic stimulation.

Answer 45

o Heart becomes dilated and flaccid and slows heart rate down. o Large quantities of potassium can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle. o Elevation of K to only 8 to 12 mEq/L can cause severe weakness of the heart, abnormal rhythm, and death. o High extracellular fluid potassium concentration partially depolarizes the cell membrane, causing the membrane potential to be less negative. o As the membrane potential decreases, the intensity of the action potential also decreases, which makes contraction of the heart progressively weaker.

Answer 46

o Excess calcium ions cause effects almost exactly opposite to those of potassium ions, causing the heart to move toward spastic contraction. o This effect is caused by a direct effect of calcium ions to initiate the cardiac contractile process. o Deficiency of calcium ions causes cardiac weakness, similar to the effect of high potassium. o Calcium ion levels in the blood normally are regulated within a very narrow range.

Answer 47

o Increased body temperature (like fever,) greatly increases the heart rate, sometimes to double the normal rate. o Decreased temperature greatly decreases heart rate, which may fall to as low as a few beats per minute when a person is near death from hypothermia in the body temperature range of 60° to 70°F. o These effects presumably result from the fact that heat increases the permeability of the cardiac muscle membrane to ions that control heart rate, resulting in acceleration of the self-excitation process. o Contractile strength of the heart often is enhanced temporarily by a moderate increase in temperature, such as that which occurs during body exercise, but prolonged elevation of temperature exhausts the metabolic systems of the heart and eventually causes weakness. o Optimal function of the heart depends greatly on proper control of body temperature.

Answer 48

o Small, flattened, ellipsoid strip of specialized cardiac muscle localized on the right atrium. o The fibers of this node have almost no contractile muscle filaments o The sinus nodal fibers connect directly with the atrial muscle fibers so that any action potential that begins in the sinus node spreads immediately into the atrial muscle wall.

Answer 49

o Some cardiac fibers have the capability of self-excitation -> can cause automatic rhythmical discharge and contraction. o This capability is especially true of the fibers of the heart’s specialized conducting system, including the fibers of the sinus node. o The sinus node ordinarily controls the rate of beat of the entire heart.

Answer 50

o Sinus nodal fiber between discharges has a negativity of about −55 to −60mV o Ventricular fibers at −85 to −90mV o The reason is that the cell membranes of the sinus fibers are naturally leaky to Na and Ca (leak IN), and positive charges of the entering Na and Ca neutralize some of the intracellular negativity.

Answer 51

o At -55mV (SA node), fast Na channels are probably inactivated -> any time the membrane potential remains less negative than about −55 millivolts for more than a few milliseconds, the inactivation gates on the inside of the cell membrane close the fast Na channels and remain so. o Only the slow Ca channels can open and cause the action potential. o As a result, the atrial nodal action potential is slower to develop than the action potential of the ventricular muscle. o After the action potential does occur, return of the potential to its negative state occurs slowly as well, rather than the abrupt return that occurs for the ventricular fiber.

Answer 52

o Because of the high Na concentration in the extracellular fluid outside the nodal fiber, as well as a moderate number of already open sodium channels, positive sodium ions from outside the fibers normally tend to leak to the inside. o Therefore, between heartbeats, influx of positively charged sodium ions causes a slow rise in the resting membrane potential in the positive direction. o The resting potential gradually rises and becomes less negative between each two heartbeats. o When the potential reaches a threshold voltage of about −40mV, the L-type calcium channels become activated, thus causing the action potential. o Therefore, the inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.

Answer 53

o Two events occur to prevent such a constant state of depolarization. 1) The L-type Ca channels close within about 100 to 150msec after opening. 2) At about the same time, greatly increased numbers of potassium channels open. o Both of these effects reduce the intracellular potential back to its negative resting level and therefore terminate the action potential.

Answer 54

o The potassium channels remain open for another few tenths of a second, temporarily continuing movement of positive charges out of the cell. o That results in excess negativity inside the fiber -> hyperpolarization. o The hyperpolarization state is what carries the resting membrane potential down to about −55 to −60mV at the termination of the action potential.

Answer 55

FALSE - it will inhibit the SNS causing vasodilation and stimulate the PNS causing bradycardia

Answer 56

o The endothelium communicates with the vascular smooth muscle.

Answer 57

Inhibition o Stimulation of M2 receptors leads to inability of the Gs protein to stimulate adenylate cyclase to produce cAMP

Answer 58

TRUE Primary effect on VENOUS vascular tone, does not regulate arterial BP.

Answer 59

The conversion of tyrosine to DOPA via the enzyme tyrosine hydroxylase

Answer 60

o Presynaptic - like the alpha2 that modulate the release of NE o Postsynaptic - on effector organs

Answer 61

o Junctional - immediately associated with a sympathetic nerve (nerve -> tissue) o Non-junctional - not directly associated with a nerve - mainly affected by circulating E/NE

Answer 62

Stimulated Inhibited

Answer 63

Because all B receptors will be blocked, and glucagon can have the same effects -> increase cAMP -> increase HR and contractility, independent of the B receptors

Answer 64

Add a phosphorus - phosphorylates

Answer 65

Remove phosphate group from its substrate - dephosphorylation -> opposite of kinases. Usually inactivates.

Answer 66

o It will increase the rate of depolarization increasing the If (funny current) o Opening of L-type voltage gated Ca channels - lower threshold potential

Answer 67

o Decreases in If (funny current) -> decreased rate of depolarization o Inhibition of L-type voltage gated Ca channels -> increases threshold o Activation of GIRKach (K channels) -> membrane hyperpolarization

Answer 68

TRUE E/NE -> alpha 1 receptors Vasopressin -> V1 receptors Ach -> M3 -> if it binds M2 on the endothelial effects -> release of NO, vasodilation AgII -> AT1 ET1 (endothelin 1) -> ETA

Answer 69

Via myosin light chain kinase, MLCK (phosphorylation of myosin -> vasocontration) and myosin phosphatase, MMP (dephosphorylation of myosin -> vasodilation).

Answer 70

TRUE Once myosin is phosphorylated it allows a good positioning of acting and myosin.

Answer 71

TRUE Change in conformation in the troponin complex and contraction can occur TN-C -> calcium binding site -> regulates contraction TN-I -> inhibits active site on actin TN-T -> tropomyosin binding protein

Answer 72

o Non-selective PDEI o- Chocolate components (theobromine), theophylline - spread effects throughout the body - increased cAMP generalized - increased HR and BP

Answer 73

o Calcium sensitizer -> troponin regulatory complex does a better job binding Ca -> increase contractility w/o increasing intracellular calcium. o Vascular smooth muscle vasodilator -> via PDEI3, increased cAMP

Answer 74

sGC - soluble guanyl cyclase

Answer 75

o Thick filament regulated - myosin o Thin filament regulated - troponin complex on actin

Answer 76

SERCA2 Inhibited by phospholamban -> more Ca in cytosol If phospholamban is inactivated -> more Ca pumped in the SR -> B adrenergic stimulation is one of the ways with increased relaxation Because in the next cycle there will be more Ca in the SR, more Ca will be released -> increase force of contraction This is how there is both increased lusitropy and inotropy

Answer 77

o A branch of the internodal tract o From the right atrium directed towards the left atrium

Answer 78

o Blood flow to most tissues is controlled according to the tissue need. When a particular tissue demands increased flow -> the microvessels of each tissue continuously monitor tissue needs, and in turn act directly on the local blood vessels, dilating or constricting them, to control local blood flow. o Cardiac output is the sum of all local tissue flows o Arterial pressure regulation is generally independent of either local blood flow control or cardiac output control.

Answer 79

o Pressure difference of the blood between the 2 ends of the vessel (pressure gradient) o Vascular resistance - as a result of the friction between the flowing blood and the intravascular endothelium o Can be calculated using Ohm's law: F = P1-P2 / R Be also familiar with o R = P1-P2 / F o P1-P2 = F x R

Answer 80

o When blood flows at a steady rate through a long, smooth blood vessel, it flows in streamlines, with each layer of blood remaining the same distance from the vessel wall. o When laminar flow occurs, the velocity of flow in the center of the vessel is far greater than that toward the outer edges. o The fluid in the middle of the vessel can move rapidly because many layers of slipping molecules exist between the middle of the vessel and the vessel wall; thus, each layer toward the center flows progressively more rapidly than the outer layers.

Answer 81

o When the rate of blood flow becomes too great, when it passes by an obstruction in a vessel, when it makes a sharp turn, or when it passes over a rough surface. o The blood flows crosswise in the vessel and along the vessel, usually forming whorls in the blood, called eddy currents. o The blood flows with much greater resistance -> eddies add tremendously to the overall friction of flow in the vessel.

Answer 82

o The measure of the tendency for turbulence to occur o Proportional to velocity of blood flow (v, in cm/sec), diameter (d, in cm) of blood vessel and density of blood o Inversely proportional to viscosity of blood (in poise). o If it is > 2000 -> turbulence will happen in a straight, smooth vessel o Normally between 200-400 -> turbulent flow will occur at some branches but die pretty quick.

Answer 83

1mmHg = 1.36cm H2O

Answer 84

Inverse of resistance C = 1/R

Answer 85

o F is the rate of blood flow. o ΔP is the pressure difference between the ends of the vessel. o r is the radius of the vessel. o l is length of the vessel. o η is viscosity of the blood. o The rate of blood flow is directly proportional to the fourth power of the radius of the vessel.

Answer 86

Hematocrit and plasma proteins

Answer 87

The ability of each tissue to adjust its vascular resistance and to maintain normal blood flow during changes in arterial pressure between approximately 70 and 175 mmHg

Answer 88

TRUE - the veins, on average are about eight times more distensible than the arteries.

Answer 89

o The total quantity of blood that can be stored in a given portion of the circulation for each mm Hg pressure rise o Vascular compliance = increase in V / increase in P

Answer 90

o Stroke volume o Compliance of the arterial tree Pulse pressure = stroke volume / arterial compliance

Answer 91

Because there is no aortic valve to close

Answer 92

TRUE o The cause of this damping is for 2 reasons: 1) Resistance to blood movement in the vessels. the greater the resistance, the more difficult the flow. 2) Compliance of the vessels -> the more compliant a vessel, the greater the quantity of blood required at the pulse wave front to cause an increase in pressure. o The degree of damping is almost directly proportional to the product of resistance times compliance.

Answer 93

o Caused mainly by blood jetting through the partly occluded vessel (when measuring a BP) and by vibrations of the vessel wall. o The jet causes turbulence in the vessel beyond the cuff, and this turbulence sets up the vibrations heard through the stethoscope.

Answer 94

Pressure in the RA

Answer 95

Starling forces: Capillary and interstitial hydrostatic pressure Capillary and interstitial oncotic presure

Answer 96

o Intermittent contraction of the metarterioles and precapillary sphincters o Blood usually does not flow continuously through the capillaries. Instead, it flows intermittently, turning on and off every few seconds or minutes due to vasomotion

Answer 97

o The most important factor affecting the degree of opening and closing of the metarterioles and precapillary sphincters is the concentration of oxygen in the tissues. o When the rate of oxygen usage by the tissue is great so that tissue oxygen concentration decreases below normal, the intermittent periods of capillary blood flow occur more often, and the duration of each period of flow lasts longer.

Answer 98

TRUE - for example, the membranes of the liver capillary sinusoids are so permeable that even plasma proteins pass through these walls, almost as easily as water and other substances.

Answer 99

o Oxygen -> reduced O2 availability causes vasodilation o Autoregulation of blood flow: * Metabolic theory -> if BP increases -> too much flow -> too much nutrients -> washes out vasodilatory substances -> vasoconstriction * Myogenic mechanism -> present in other organs too -> high BP -> stretch of blood vessels -> vasoconstriction o Endothelial-derived substances (relaxing or constricting factors): * NO -> released from healthy endothelial cells in response to different stimuli * Endothelin -> released from damaged endothelium and causes vasoconstriction.

Answer 100

o Changes in tissue vascularity - creating new vessels as a result of a chronic increased demand of blood flow. o Development of collateral circulation - when a blood vessel gets blocked o Vascular remodeling in response to chronic changes in BP / blood flow

Answer 101

Vasoconstrictor agents: E/NE AgII Vasopressin Vasodilatory agents: Bradykinin Histamine

Answer 102

Bradycardia associated with clinical sings (dog <60bpm, cats <100bpm)

Answer 103

Alterations in autonomic tone Electrolyte imbalances Drug exposure Trauma Hypoxia Inflammation / infiltration of myocardium Degenerative disease of the conduction system

Answer 104

Changes in p wave amplitude in relation to the respiratory cycle and it is normally when vagotonia is the cause of bradycardia

Answer 105

o Disease of the conduction system o Periods of normal SR or sinus bradycardia o Periods of long sinus arrest that can last up to 10-12 seconds because junctional and ventricular pacemakers fail to initiate escape beats. o Variant - bradycardia tachycardia syndrome -> periods of paroxysmal tachycardia followed by a temporal failure of the sinus rhythm to resume when tachycardia ends. * It is due to an exaggerated normal physiologic response of the sinus node to the effect of the tachyarrhythmia - called overdrive suppression o Old mini Schnauzers and Terrier breeds commonly affected by SSS

Answer 106

o Prolonged PR interval o AV node fibrosis, increased vagal tone, drugs that delay AV conduction (digoxin, Ca channel blockers, B blockers)

Answer 107

o When some p not followed by QRS o High grade -> when more atrial impulses fail to be conducted than are conducted. o Mobitz type I - progressive PR interval ending by a blocked P wave (Wenckebach's phenomenon) - usually bening and does not require treatment o Mobitz type II - unexpected blocked p waves. PR before and after are normal. More likely to worsen and result in clinical signs.

Answer 108

Atropine - 0.04mg/Kg IV or glycopyrrolate 0.01mg/kg IV Mobitz I will improve. Mobitz II unchanged or worsens.

Answer 109

o Absence of conducted p waves to ventricles. o Electrical ventricular activation depends on scape beats o Ventricular rate normally 20-60bpm in dogs and 60-120bpm in cats. o Myocardial fibrosis, inflammation or infiltration, potentially drug toxicity (Ca2+ channel blockers) o In cats often associated with structural heart disease.

Answer 110

o Lack of visible atrial activity on EKG o Temporary or persistent - persistent is rare. o Persistent - English Springer Spaniels, predisposed to developing AV block. Young dogs. genetic etiology. Long term prognosis guarded. o Hyperkalemia most common cause * First change is narrowing and taller T wave * Decrease HR with reduced p amplitude and WRS widening * Undetectable p waves

Answer 111

o Parasympathicolytic meds (atropine / glycopyrrolate) o Dopamine / dobutamine - increased HR and systolic function. Indicated in B blocker overdose o Isoproterenol (pure B agonist) - improves conduction in AV node. Given as CRI. o Terbutaline / aminophylline - mild chronotropic effects, can temporarily increase HR in dogs with SSS.

Answer 112

o Transcuteanous pacing -> in emergency situations, painful, only under general anesthesia. o Temporary transvenous pacing -> lead in R side of heart connected to a generator external to the patient. Can be done under sedation. * Can be used as stabilization until permanent pacemaker improving patient stability. * Can be used to support patients with transient bradycardia (diltiazem toxicity)

Answer 113

o Rapid cardiac rhythm that originate t¡in the atria or AV junction (about bundle of His) o Or, it involves the atria or AV junction as critical component of a tachyarrhythmia circuit o Classified into atrial tachyarrhythmias or AV node dependent tachyarrhythmias - helps guide therapy.

Answer 114

We cannot. Once treatment is started, tachycardia-induced cardiomyopathy can be partially or completely reversed.

Answer 115

o Identification of p waves -> if there are p waves related to QRS, indicative of SVT with aberration. o QRS fusion completes -> hallmark of ventricular tachyarrhythmia o If tachycardia terminates with vagal maneuvers -> supraventricular in origin. If not, it can be both. o If tachycardia ends with administration of lidocaine -> most likely ventricular in origin.

Answer 116

o If an SVT continues despite AV block - atrial in origin o If a VPC terminates the SVT - more likely that is AV node dependent o if vagal maneuver terminates the SVT - more likely AV node.

Answer 117

o Carotid sinus massage o Sustained, gentle compression applied for 5-10 seconds over the carotid sinus -> immediately caudal to the dorsal aspect of the larynx.

Answer 118

B-blockers Ca channel blockers Digitalis Class III (amiodarone, stall)

Answer 119

Main ones: B blockers Ca channel blockers Digitalis glycosides Others that can be used: Class IC Class III Adenosine

Answer 120

Class IA Class IC Class III

Answer 121

Class IA Class IC Class III

Answer 122

Diltiazem - slowed AV node conduction while maintaining good hemodynamic parameters. Esmolol - caused severe drop in LV contractility Adenosine at 2mg/kg was ineffective.

Answer 123

Inotropy - contractility Chronotropy - rate Dromotropy - conduction Lusitropy - relaxation

Answer 124

Hypotension Negative chronotropy Negative dromotropy Negative isotropy Impared insulin release Effects on peripheral vasculature, cardiac muscle and pancreatic B cells -> can lead to hemodynamic collapse with high doses.

Answer 125

FALSE - they are effective in terminating reentries rather than abnormal automaticity

Answer 126

2 One to decrease conduction through AV node Second to terminate the atrial tachyarrhythmia itself. AV node dependent tachyarrhythmias will sometimes respond to single-agent therapy aimed at slowing AV nodal conduction

Answer 127

Orthodromic impulse -> conduction in normal direction Antidromic impulse -> conduction opposite of the normal direction.

Answer 128

Because diltiazem has a more favorable hemodynamic profile at effective anti arrhythmic doses.

Answer 129

Catheter ablation

Answer 130

FALSE - when it lasts < 30sec

Answer 131

o Broad QRS tachycardia with complexes wider than 0.06sec in dogs and 0.04sec in cats. o Each QRS complex is followed by a large T wave directed opposite to the QRS deflection

Answer 132

AV dissociation Fusion beats Capture beats

Answer 133

P waves are occasionally seen on the ECG tracing but are not related to ventricular complexes

Answer 134

Result from the summation of a ventricular impulse and a simultaneous supra ventricular impulse resulting in a QRS complex of intermediate morphology and proceeded by a p wave (unless concurrent afib)

Answer 135

Supraventricular impulse conducting through the normal conduction pathways to the ventricle during an episode of VT or AIVR

Answer 136

Hypoxemia AB and electrolyte disturbances - hypokalemia most important Sympathetic stimulation Drugs

Answer 137

Digoxin competes with K on its receptors -> hypoK increases risk of digoxin toxicity

Answer 138

Mg is necessary for proper functioning (activation) of the Na/K ATPase pump

Answer 139

Cardiac tumors (w or w/o cardiac tamponade) Myocarditis Endocarditis Ischemia DCM ARVC Severe SAS and PS Cats - idiopathic HCM and concentric hypertrophy secondary to hypertension/hyperthyroidism.

Answer 140

21% in a pool of breeds 16% in Newfoundlands 92% in Doberman

Answer 141

o Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) o Adult onset disease o Occasional VPCs o Overt VT associated with exercise intolerance and collapse o Sometimes myocardial failure can be observed o Sometimes ventricular ectopics have a LBBB morphology, indicating their right side origin.

Answer 142

o Sustained ( >30sec ) o Polymorphic complexes o HR > 180-200bpm o R-on-T phenomenon

Answer 143

o Lidocaine - max of 8mg/kg due to neurotoxic effects. In cats, B blockers preferred. o Procainamide - for VT that do not respond to lidocaine. Rapid IV -> hypotension. o B-blockers - esmolol CRI can help with VT associated w/ pheochromocytoma or thyrotoxic disease in cats. o Sotalol - main anti arrhythmic for long-term management of VT especially in Boxers with ARVC. o Amiodarone - anaphylaxis-like reactions can occur o Mg2+ sulfate

Answer 144

How easy it is for albumin to move from the capillaries to interstitium

Answer 145

How easy it is for water to move from capillaries to interstitium

Answer 146

Glycocalyx

Answer 147

o Complex gel between plasma and endothelium forming an endothelial surface layer o Mostly glycoproteins and proteoglycans o Thickness varies between 0.1 to 1um o It is inert and has plasma proteins that get bound to it

Answer 148

o Regulates permeability o Influences blood cell-vessel interactions o Affects rheology o Controls microenvironment

Answer 149

o Has a net negative charge that is depending on GAG side chain sulfation and it is affected by physiologic/pathophysiologic stimulation o Charged mesh acts as a sieve - repels negatively charged molecules, RBCs and WBCs and molecules >70kDa o Albumin can enter the glycocalyx and enter it due to its amphoteric nature -> reduces water conductivity across endothelium.

Answer 150

o Now instead of oncotic pressure of interstitial space, we replace if for oncotic pressure of subglycocalyx space, that is much lower. o Subglycocalyx is almost protein free, oncotic pressure much lower compared to interstitium. o The membrane osmotic reflection coefficient now it has to be that of the glycocalyx rather than the endothelium.

Answer 151

o Interstitial oncotic pressure replaced for subglycocalyx oncotic pressure o Instead of having filtration at the pre-capillary arterioles and absorption at the post-capillary venules, we have NO absorption at the post-capillary venules, just les filtration

Answer 152

Inotrpy (contractility) and afterload Not the preload as preload is basically the x axis

Answer 153

Instead of LVEDV on x axis, we have the R atrial pressures (basically CVP) On Y axis the CO in L/min (Frank Starling curve can have CO (L/min) or stroke volume (mL) on the Y axis)

Answer 154

Same as FS, inotropy and afterload Not preload as it is the x axis of the graph

Answer 155

Because in a patient breathing spontaneously -> negative intrathoracic pressures that will lead to negative RA pressures

Answer 156

Cardiac output. It is depicted on the Y axis to be able to superimpose the cardiac function curves

Answer 157

Because blood is being drawn into the ventricle with each beat of the heart and moved into the arterial system, leading to a drop in atrial (and venous) pressure.

Answer 158

Because at <0mmHg of the RA, the vena cava collapses, limiting venous return therefore CO plateaus.

Answer 159

o Aortic pressure falls and right atrial pressure increases as blood redistributes between the arterial and venous systems until they reach the same pressure. o Since there is no flow, the pressures in the entire circulatory system will be equal. o This is called the mean circulatory filling pressure and in healthy animals is about 8mmHg

Answer 160

Because the venous system has a higher capacitance, it will accommodate between 10-20% more volume than arteries when CO is zero

Answer 161

Intravascular volume and venous compliance

Answer 162

o With an increased in volume, the mean filling pressure will increase because there is greater volume in the circuit. o Since the mean vascular filling pressure is more affected by the high compliance of the venous system than the low compliance of the arterial system, it will shift to a higher value when venous compliance decreases (ie, the veins become stiffer).

Answer 163

The RA pressure

Answer 164

RA - mean of 0-5mmHg RV - systolic of 15-30mmHg, diastolic of 0-5mmHg LA - mean of 4-12mmHg LV - systolic of 90-150mmHg, diastolic of 4-12mmHg Aorta - systolic 90-150mmHg, diastolic 60-100mmHg, mean 70-100mmHg.

Answer 165

o It’s the LV pressure generated by a set volume of blood within the ventricle when the ventricle is relaxed and not contracting o You would inject blood into an isolated ventricle and record the pressure in the heart resulting from each volume.

Answer 166

o It’s the pressure generated in the ventricle when a range of volumes are present in the ventricle. o In this case, the ventricle is maximally contracting (at the end of systole). o The curve is significantly higher and shifted to the left.

Answer 167

MPP = Diastolic aortic pressure – right atrial pressure

Answer 168

HR, MM, CRT, mental status, temperature, pulse quality, lactate, SI, MAP, CVP * CVP considered no longer clinically valuable

Answer 169

CO monitoring (thermodilution, LiDCO), Surrogates for CO - pulse pressure variation, systolic pressure variation, stroke volume variation

Answer 170

Hemostasis is a physiological phenomenon that leads to blood clot formation. Thrombosis is a pathological hemostasis leading to occlusion of blood supply and ischemia

Answer 171

Thrombus -> aggregation of PLT and fibrin with entrapped blood cells Thrombo-emboli -> migration of the thrombus

Answer 172

Blood stasis Hypercoagulability Endothelial damage

Answer 173

o Venous thrombi -> created under low shear stress rates -> fibrin generation plays a major role. o Venous thrombus is primarily composed of RBCs embedded within a fibrin meshwork. o Arterial thrombosis -> high shear stress conditions predominate -> PLT adhesion to endothelium is the most important part of thrombus formation. o Arterial thrombus is primarily composed of PLT.

Answer 174

o Between 7-12yo o Males predisposed -> 2/3 of cases are males o 75% of cases have both limbs affected. o 90% have underlying cardiomyopathy but <10% were previously diagnosed w/ cardiac dz.

Answer 175

Reduced blood velocity Reduced or turbulent flow (often caused by vascular, valves or chambers abnormalities)

Answer 176

Platelet activation Activated clotting factors

Answer 177

o Mostly clinical o Palor (purple or pale toes) o Polar (cold extremities) o Pulselessness o Paralysis o Pain

Answer 178

o Glucose/lactate differential between the affected limb and normal limbs - glucose lower and lactate higher in affected limbs compared to the normal ones. o BLASTT study - lactate might be a more robust diagnostic tool compared to glucose. o The use of infrared thermography used in 16 cats to differentiate FATE from non-ischemic conditions, a 2.4C difference was wound between ipsilateral affected and non-affected limbs. o Infrared thermography had a sensitivity of 85%, specificity of 100%, PPV of 100% and a NPV of 80% to diagnose ATE as cause of paralysis. Can also be used to assess repercussion of affected limbs.

Answer 179

Between 27-45%

Answer 180

o The use of clopidogrel, UF or LMWH o Clopidogrel at 18.75mg PO SID. Loading dose suggested to obtain therapeutic plasma concentrations rapidly. o If using heparin, initial SQ dosage of UFH of 250U/kg QID or dalteparin 75 U/kg QID o Enoxaparin 0.75-1mg/kg SQ BID to QID for cats at risk for venous thromboembolism but no specific recommendations for LMWH.

Answer 181

FALSE - they recommend against aspirin as the sole antithrombotic and do NOT recommend an appropriate dosage in cats.

Answer 182

They suggest warfarin not to be used because of marked inter-individual variation coupled with a narrow therapeutic index.

Answer 183

o Appears safe and well tolerated. o Dose of 0.5-1mg/kg/day recommended in cats.

Answer 184

o Yes o Results have been mixed o Repercussion injury - cats after receiving t-PA developed hyperK, neurological sings leading to respiratory arrest and hemorrhagic complications in one study.

Answer 185

o Furosemide 1-2mg/kg until resolution of pulmonary signs o 2% nitroglycerine crea for potential ventilatory effect o +/- sedation with butorphanol or methane of pain. o FATE is painful, recommended full mu opioids with methadone followed by fentanyl CRI o Physical therapy with PROM and leg warming can be attempted if tolerated by the patient

Answer 186

o PLN o Cushing's o DM o Hypothyroidism o Liver disease o Neoplasia o Infective endocarditis o Immune mediated diseases requiring high steroid doses (IMHA, ITP, Addison's)

Answer 187

o Visualization of the thrombus in the aorta on ultrasound o Glucose differential has been used in 1 study - a difference of >30mg/dL corresponded to 100% sensitivity and specificity.

Answer 188

o Varies based on presentation and clinical signs o In the largest case series published - discharge rate of 57% and 63% with severe enough clinical signs to be hospitalized.

Answer 189

Suggest that antiplatelets might be more effective than anticoagulants for prevention of CATh, but anticoagulants may also be effective for prevention.

Answer 190

mL/kg/min or mL/kg/m2 Dogs - 100-150 Cats 80-130

Answer 191

Fick principle states that blood flow to an organ can be calculated using a marker substance if the following information is known: Amount of marker substance taken up by the organ per unit time Concentration of marker substance in arterial blood supplying the organ Concentration of marker substance in venous blood leaving the organ

Answer 192

o CO2 clearance is another marker to determine CO o Can be performed "non-invasively" through the NICO (rebreathing) system (non-invasive cardiac output) o Measurement of ETCO2 to determine arterial CO2 (ETCO2N = CaO2) o Use of partial rebreathing ETCO2 for mixed venous CO2 (ETCO2R = CvCO2) o Measurement of CO2 expired (produced) (VO2) o CO = ΔVO2 / (S * ΔETCO2)

Answer 193

They involve the injection of a known volume of fluid (V1) with a known concentration of an indicator (C1) into an unknown larger volume (V2) and then measuring the concentration of the indicator in the larger volume of fluid (C2). The unknown volume (V2) can be calculated: V1 x C1 = V2 x C2

Answer 194

Any indicator can be used as long as it can be measured with a rapidly responding sensor.

Answer 195

o Temperature o It involves measurement of temperature at two distinct locations o Pulmonary artery catheter - Swan-Ganz catheter o Injection of cold saline in proximal port, temperature measured at the tip of the PAC o Multiple dilutions performed, average for each CO o Thermistor tip can allow continuous CO monitor o Can be also used to assess PCWP (LA pressures) and obtain samples for SvO2

Answer 196

o Accuracy and reliability questioned o Can be affected by blood temperature, concurrent fluid administration and sample handling o Inaccuracy with valvular regurgitation (blood not mixed completely due to regurg) and anatomical shunts o Potential complications: pneumothorax, infection, bleeding, clot/PTE o Limited use in vet med due to cost, availability and potential complications

Answer 197

o Injecting lithium chloride o Peripherally or centrally, IV bolus - it stays in the intravascular compartment o Ion selective electrode attached to arterial line o CO computed o CO = (Indicator dose x 60) / total dose x (1-PCV) o Need to measure Na and PCV before each dilution o Validated in multiple veterinary species o Lithium accumulation with repeated measurements - background interferences, potential toxicity o Volume of blood withdrawn may limit repeated measures

Answer 198

o Correlate arterial blood pressure tracing AUC to stroke volume o Potential limitations * Non-linear relationship between pressure and volume (effect of arterial compliance, resistance...) * Damping of the pressure waveform (arterial catheter, fluid tubing, pressure transducer)

Answer 199

o The pathophysiology of sepsis involves the release of cytokines, some of which are associated with abnormal calcium handling by the cardiac myocytes, leading to reduced myocardial contraction. o Because of the simultaneous tachycardia and reduced vascular tone, however, afterload is reduced – and cardiac output can therefore be maintained or even increased. "

Answer 200

RAAS and SNS. The natriuretic peptides, endothelin, and vasopressin systems also play a role.

Answer 201

o Renal sodium and water retention o Production of aldosterone o Myocardial apoptosis o Cardiac and vascular remodeling and fibrosis o Increased thirst o Vasoconstriction

Answer 202

Natriuretic system

Answer 203

o Atrial natriuretic peptide (ANP) o B-type natriuretic peptide (BNP)

Answer 204

o Natriuretic peptide receptor downregulation o Inappropriate or inadequate production or processing of the peptides o Increased peptide clearance or degradation

Answer 205

Endothelin 1

Answer 206

o Indicates heightened free water retention to the extent that serum sodium concentrations are decreased, despite an overall excess of body-wide sodium. o In both humans and veterinary patients, dilutional hyponatremia is a marker of severe neurohormonal activation and is a poor prognostic sign.

Answer 207

o Is a response to conditions causing pressure overload (i.e., increased afterload), as in the case of systemic hypertension or subaortic stenosis. o Increased afterload triggers replication of sarcomeres in parallel -> increase in the relative thickness of the ventricular walls. o Consequences -> increased myocardial oxygen demand, endocardial ischemia, fibrosis, collagen disruption, and injury to small coronary vessels.

Answer 208

o In instances of volume overload, such as mitral regurgitation or dilated cardiomyopathy. o Sarcomeres replicate in series leading to elongation of myocytes and dilation of the ventricular chamber. o The limitations of concentric hypertrophy include increased myocardial wall stress, myocyte injury or necrosis, and myocyte slippage.

Answer 209

Glucose and free fatty acids Glucose -> requires less oxygen than fatty acids

Answer 210

o Arterial vasodilators (amlodipine or hydralazine) -> shift the curve upward in a manner similar to a positive inotrope. o Venous vasodilators (nitrates) -> reduce preload through an increase the capacitance of the venous system and shift the curve leftward, similar to diuretics. o Mixed vasodilators (ACE inhibitors) result in a combination of both upward and leftward adjustment"

Answer 211

HCM in cats

Answer 212

o Primary impairments of ventricular relaxation, filling or compliance o Secondary to disease of the pericardium

Answer 213

o Thickness of the ventricular wall (concentric hypertrophy) o Changes in the cytoskeleton and extracellular matrix (fibrosis) o Function of the pericardium (pericardial disease or effusion)

Answer 214

TRUE - SERCA is an ATPase pump. o Then, in myocardial ischemia and energy deficit, active relaxation is delayed and early filling of the ventricle is diminished.

Answer 215

TRUE - In the absence of obvious pericardial disease, treatment focuses on increasing the time available for diastolic filling by decreasing heart rate, suppression of arrhythmias, and alleviation of congestion through the use of diuretics and vasodilators.

Answer 216

Class A o Overtly healthy animals that are at risk for developing heart disease. o Doberman Pinschers over the age of 4 or adult Maine Coon cats. o Might benefit from screening programs to detect the possible onset of disease Class B o Diagnostic evidence of heart disease but without clinical signs o ex. Dogs with a murmur, cats with arrhythmias o B1 - no radiographic or echocardiographic evidence of cardiac remodeling, as well as those in which remodeling changes are present, but not severe enough to meet current clinical trial criteria used to determine that initiating treatment is warranted o B2 - with radiographic or echocardiographic evidence of cardiac remodeling, that meet clinical trial criteria used to identify dogs that clearly should benefit from initiating pharmacologic treatment to delay the onset of heart failure Class C o With cardiac remodeling, as well as current or historical clinical signs of heart failure Class D o Patients with severe and debilitating signs of heart failure even at rest. clinical signs of heart failure are refractory to standard treatment.

Answer 217

25mmHg 20mmHg

Answer 218

o In patients with severe myocardial dysfunction, cardiac performance is insufficient to provide adequate cardiac output and animals present with signs of low-output heart failure. o Common clinical signs include weakness, depressed mentation, cardiac shock, and syncope. o Diagnostic testing in these patients commonly reveals hypothermia, hypotension, azotemia, anuria or oliguria, and lactic acidosis. Patients with low-output heart failure require positive ino tropes to improve contractility"

Answer 219

Common causes of left-sided heart failure in dogs: o Degenerative mitral valve disease o Dilated cardiomyopathy o Patent ductus arteriosus Common causes of left-sided heart failure in cats: o HCM o Restrictive cardiomyopathy"

Answer 220

o Dilated cardiomyopathy o Degenerative or congenital tricuspid valve disease o Pulmonary hypertension. "

Answer 221

FALSE - Ascites as a sign of right- sided heart failure in cats is relatively uncommon, and most cats with ascites are afflicted with noncardiac diseases Right-sided heart failure is relatively rare in cats and most cases of cardiogenic pleural effusion in cats actually are due to left-sided disease.

Answer 222

Forward flow failure

Answer 223

o Backward flow failure -> secondary to elevated venous pressures o Forward flow failure (left ventricular failure) -> reduced forward flow into the aorta and systemic circulation • Most patients deteriorate secondary to the increase in preload and subsequent congestive (backward) heart failure and pulmonary edema • Some patients may suffer from concurrent forward and backward failure (e.g., dogs with dilated cardiomyopathy)."

Answer 224

o Enlarged pulmonary veins o An alveolar or interstitial pattern in the perihilar region (in dogs only; infiltrates are often patchy or diffuse in cats) o Pleural effusion In L-CHF * Increased VHS * Dorsal displacement of trachea due to LA enlargement R-sided disease * Reverse D cardiac sillhouette * Increased sternal contact * Enlarged CVC * Ascites

Answer 225

1. A decrease in cardiac contractility * DCM * ARVC * Sepsis * Endomyocarditis * Myocardial infarction 2. Decreased flow through the left ventricular outflow tract (mechanical failure). *Functional obstruction (e.g., aortic stenosis or hypertrophic obstructive cardiomyopathy) * Severe retrograde blood flow (e.g., chordae tendineae rupture and acute, severe mitral regurgitation)"

Answer 226

o Progressive decrease in myocardial contractility that occurs over months to years -> gradual decrease in stroke volume and forward failure -> activation of the RAAS system and SNS -> increased intravascular volume -> increased end-diastolic volume -> eccentric hypertrophy secondary to cardiac myocardial stretch. o Compensatory mechanisms will maintain cardiac output until the myocardial failure becomes so severe that the cardiac chambers cannot sustain further enlargement -> increase in pulmonary capillary hydrostatic pressure and cardiogenic pulmonary edema or ascites. o An electrocardiogram may show a sinus tachycardia or arrhythmias such as atrial fibrillation or ventricular tachycardia.

Answer 227

Endomyocarditis hyperechoic neutrophilic inflammation and fibroplasia.

Answer 228

Hypovolemia Physical restriction. Ex: Tamponade Inhability to relax: HCM Inadequate time to fill: Tachycardia

Answer 229

Severe high-grade second-degree AV block

Answer 230

o Bundle of His producing 40 to 60 beats/min o Bundle branches or distal Purkinje fibers producing 20 to 40 beats/min o Cats with third- degree AV block typically have a higher ventricular escape rhythm of 100 to 140 beat/min and thus less commonly present for cardiogenic shock or syncope.

Answer 231

Tachycardia-induced cardiomyopathy

Answer 232

cTnI --> rises rapidly after myocardial cell damage (myocarditis) cTnT

Answer 233

Occurs when there is impaired ventricular filling in the absence of myocardial hypertrophy or pericardial disease. Left atrial enlargement with normal ventricle.

Answer 234

Diastolic dysfunction

Answer 235

Abnormal drag forces are responsible for systolic movement of the MV leaflets toward the septum that results in dynamic—as opposed to fixed—left ventricular outflow tract obstruction and, usually, concurrent mitral valve regurgitation

Answer 236

SAM Decreases in preload and afterload or increases in contractility may provoke or augment SAM, and this may explain the fact that the intensity of the associated murmur may vary from moment to moment

Answer 237

LA - specifically the appendage

Answer 238

Aortic trifurcation

Answer 239

o Left atrial enlargement o Echocardiographic findings of spontaneous contrast and systolic myocardial dysfunction.

Answer 240

FALSE - long-term prognosis for cats with glucocorticoid-associated CHF may be better than for those with CHF from more typical causes.

Answer 241

near 90% high 80s

Answer 242

FALSE - tachypnea was identified in 89% of patients with FATE in the absence of CHF (presumably as a result of pain).

Answer 243

TRUE - 50% short-term survival for patients with a body temperature of 37.2° C (98.9F)

Answer 244

Causes venodilation as well as dilation of specific arteriolar beds, including those of the coronary circulation

Answer 245

o Antagonist of ""funny"" lf sodium channel o Slow heart rate but do not exert a negatively inotropic effect

Answer 246

Prolongs the time to onset of clinical signs and extends survival

Answer 247

Calstabin-2

Answer 248

Portuguese water dog

Answer 249

Has a longer half-life in circulation and therefore is easier to measure. Pulmonary hypertension, renal dysfunction.

Answer 250

o Pimobendan 0.25-0.3 mg/kg PO q12h. o Mild dietary sodium restriction and provision of a highly palatable diet with adequate protein and calories for maintaining optimal body condition o Clinical trials addressing the efficacy of ACEI for treatment of dogs in Stage B have shown mixed results - 5 (of 10) panelists recommend treatment o Cough suppressants useful in occasional patients in advanced Stage B2 when their cough is thought to be the result of pressure from cardiac enlargement o Surgical intervention in advanced Stage B2 is possible and recommended by some panelists.

Answer 251

In stage C patients with acute signs (hospital based treatment) in patients that fail to respond adequately to diuretics, pimobendan, sedation, oxygen, and comfort care measures Dobutamine (2.5-10 μg/kg/min CRI, starting at 2.5 μg/kg/min and increasing the dosage incrementally) ** Continuous ECG monitoring is recommended, with dosage reduction indicated if tachycardia or ectopic beats occur

Answer 252

* noncompliance (not receiving the drug) * high sodium intake, slow absorption (gut edema) * impaired secretion into the renal tubular lumen (CKD, advanced age, concurrent NSAIDs use) * hypoproteinemia, hypotension, nephron remodeling, and neurohormonal activation

Answer 253

Right atrial collapse

Answer 254

Neoplastic - Idiopathic

Answer 255

Left atrial rupture secondary to severe MVD - coagulopathy (rodenticide/DIC) - Trauma

Answer 256

Chemodectoma (aortic body tumor)- arises from the chemoreceptor cells at the base of the aorta

Answer 257

Pericardial mesothelioma - cardiac lymphoma - Malignant Histiocytosis - metastatic carcinoma

Answer 258

Pure transudate = Cell count <1000/uL - SG: <1012 - TP: <2.5g/dL / Modified transudate = Cell count 1000-8000/uL - SG: 1015-1030 - TP: 2.5 - 5g/dL

Answer 259

CHF, Hypoproteinemia, vasculitis (ex. Toxicities that increase vascular permeability, uremia), congenital pericardial malformations, cardiac lymphoma in cats

Answer 260

Migrating foreign body (plant awn), infection (extension of pleural or mediastinal infection, bite wound)

Answer 261

Actinomycosis, coccidiomycosis, Aspergillus, tuberculosis, systemic protozoal infections (rare)----------- Dogs = distemper, leptospirosis Cats= FIP

Answer 262

When intrapericardial pressure rises toward and exceeds normal cardiac diastolic pressures

Answer 263

A fall in arterial pressure during inspiration of 10 mm Hg or more

Answer 264

DCM, marked tricuspid (with or without mitral) insuficiency

Answer 265

o Reduced amplitude QRS complexes (less than 1 mV in dogs) o Electrical alternans (recurring, beat-to-beat alteration in the size or configuration of the QRS complex (and sometimes T wave) o Atrial and ventricular tachyarrhythmias occur in some cases

Answer 266

Cardiac tamponade commonly produces CVP measurements of 10 to 12 cm H2O or higher

Answer 267

Many neoplastic (and other noninflammatory) effusions have a pH of 7.0 or greater, whereas inflammatory effusions generally have lower pH. However, there is too much overlap for pericardial effusion pH to be a reliable discriminator.

Answer 268

Right side of the chest. This minimizes the risk of trauma to the lung (via the cardiac notch) and major coronary vessels, most of which are located on the left.

Answer 269

Ventricular arrhytmias, hemorrhage, myocardial injury (coronary artery laceration, myocardial infarction), infection, lung laceration, pneumothorax, diseemination of neoplasia into pleural space

Answer 270

Subtotal pericardiectomy - techniques = thoracoscopy (allows biopsy or resection of small right auricular masses); thoracoscopic partial pericardectomy, percutaneous ballon pericardiotomy

Answer 271

o Pericardiocentesis prn o Infusion of antimicrobial agents might help o Indweling pericardial catheter o Surgical debridement

Answer 272

When thickening of the visceral or parietal pericardium impairs ventricular diastolic expansion and prevents cardiac filling

Answer 273

Peritoneopericardial diaphragmatic hernia (PPDH)

Answer 274

bradycardia (heart rate below than 60 beats/min in dogs, 100 beats/min in cats) associated with clinical signs, such as lethargy, decreased appetite, exercise intolerance, CHF, and syncope.

Answer 275

Hypothermia, hyperkalemia, GI/ocular/neurologic/respiratory disease, Hypertension (reflex bradycardia), hypothyroidism / Iatrogenic (ABCD opioids, alpha-2 agonists, anesthetics)

Answer 276

Bundle branch blocks, first, second and third degree AV blocks. - Bundle branch and first degree AV blocks are not associated with clinical signs

Answer 277

6 to 8 seconds

Answer 278

Periods of normal sinus rhythm or sinus bradycardia intercalated with prolonged pauses that can be as long as 10 to 12 seconds because the junctional and ventricular pacemarkers fail to generate escape beats.

Answer 279

Older miniature schnauzers,Terrier breeds, Cocker Spaniel, Daschunds

Answer 280

All the atrial impulses are conducted but the PR interval is prolonged - causes= increased vagal tone, fibrosis, medications that delay AV conduction (Ca channel blockers, B blockers, digoxin)

Answer 281

Mobitz type I --> progressive increase in PR interval ending by a blocked P wave (alson known as Wenckebach's phenomenom). Usually improves with atropine. Mobitz type II --> unexpected ocurrence of blocked P waves, PR intervals before and after the block are identical. Usually does not change with atropine or worsens.

Answer 282

Abscense of conducted P waves to the ventricles. Atrial and vetricular activities are independent. QRS complexes depend on escape rhythm beyond the site of block

Answer 283

QRS complexes depend on escape rhythm beyond the site of block and rates are usually 20-60bpm in dogs and 60-120bpm in cats

Answer 284

age-related fibrodegenerative disease

Answer 285

Absent p waves with regular ventricular or AV nodal escape rhythm at rates of 20 to 60bpm in dogs.

Answer 286

o Persistent Atrial Standstill (PAS) English Springer Spaniels predisposed, genetic etiology is likely, usually afecting young dogs. Atria fail to depolarize despite normal Sinus node discharge - Generally a significant myocardial pathologic condition is present and the long-term prognosis is guarded o Cardiac glycoside toxicity o Hypothermia (temporary atrial standstill)

Answer 287

Atropine 0.04mg/kg IV or IM with ECG trace. Repeat ECG in 15 and 30 min. --> should demostrate sinus tachycardia (~140bpm within 30min) if the bradycardia is vagally mediated.

Answer 288

o Mydriasis, dry mouth, constipation, urinary retention, neurologic signs, symptoms of poor arterial perfusion (syncope) o Terbutaline or Theophylline can be used

Answer 289

o Isoproterenol and dobutamine might be effective in stabilizing the patient o Most likely diagnoses: sick sinus syndrome, third degree AV block, high grade second degree AV block.

Answer 290

Terbutalline, Theophilline, Hyoscynamine, propantheline --> they are rarely effective long term and are associated with significant side effects

Answer 291

o Advantages = pure B blocker, can improve conduction in the AV node and His-Purkinje system. Can be considered if pacing is unavailable, or in B blocker or Ca channel blocker toxicities o Disadvantages= B2 efect can cause significant decrease in dyastolic pressure, also acidosis decreases its effectiveness.

Answer 292

The stimulation of the local skeletal mucles can be painful, so usually is used only on anesthetized patients.

Answer 293

Because the myocyte to myocyte conduction is smaller than a normal conduction transmited thorugh the ventricles His-Purkinje system

Answer 294

Ventricular ectopic beat / Right axis deviation due to right ventricular enlargement or cardiac displacement / hyperkalemia / Bunddle branch block

Answer 295

High grade second degree AVB lacking sufficient escape activity

Answer 296

A lead is placed in the right side of the heart, usually the right ventricle - Jugular, spahenous or femoral vein can be used, fluoroscopy guidance is recommended - a HR rate is programed to 80-100 bpm - can be done in awake or mildly sedated patients.

Answer 297

rapid heart rhythm that: originates or involves the SA node, atrial myocardium, AV node (before the bundle of his) or great vessels conecting to the atria.

Answer 298

Myocardial ischemia thas gives rise to VT and fibrilation

Answer 299

SVT can be partially or completely reversible

Answer 300

A narrow QRS complex tachyarrhythmia will almost always be an SVT / The vast majority of wide complex tachyarrhythmias are ventricular tachyarrhythmias / Identification of P′ waves with a consistent relationship to the QRS is indicative of an SVT / QRS fusion complexes are a hallmark of ventricular tachyarrhythmia / If the tachycardia terminates in response to a vagal maneuver, this indicates that the tachycardia is supraventricular in origin. /If the tachycardia does not terminate with a vagal maneuver, it may be of either supraventricular or ventricular origin./ If the tachycardia terminates with the administration of IV lidocaine, the wide complex tachyarrhythmia is most likely ventricular in origin. Rarely, an atrial tachycardia will convert with lidocaine therapy

Answer 301

More likely AV (not atrial)

Answer 302

Sinus tachycardia and atrial arrhythmias (atrial fibrilation, atrial flutter, Intra-atrial reentrant tachycardia, orthodromic AV reciprocating tachycardia, automatic atrial tachycardia, sinus node re-entranrt tachycardia, AV nodal re-entrant tachycardia, automatic junctional tachycardia)

Answer 303

When atrial activity is excesively rapid, the AV node might limit the P waves that will be conducted to the ventricles (in a 2:1 ration, being 1:1 normal). If the ratio is 3:1 it is considered a second degree AV block)

Answer 304

Atrial tachyarrhythmias are best addressed by dual therapy: one drug to slow AV nodal conduction and a second drug to inhibit the atrial automatic focus or interrupt conduction in an atrial reentrant circuit.

Answer 305

First approach in an animal with tachycardia --> the goal is to increase the parasympathetic tone to the SA and AV nodes

Answer 306

Carotid sinus massage -> sustained, gentle compression is applied for 5 to 10 seconds over the carotid sinus, which is located immediately caudal to the dorsal aspect of the larynx

Answer 307

Diltiazem = intermitent dosing 0.125-0.35 mg/kg IV over 2 to 3 min. CRI 0.125 - 0.35mg/kg/h if frequent reocurrence

Answer 308

Esmolol (ultra-short selective B1 blocker 0.5mg/kg IV over 1 to 2 min) / contraindication = patient with decreased ventricular systolic function (it can cause a severe drop in L ventricular contractility at dosages that prolong AV nodal conduction)

Answer 309

negative dromothropic, inotropic and chronotropic effect, hypotension, bradycardia, impaired insulin release (acts in pancreatic B cells --> hyperglycemia)

Answer 310

B1 receptors couple with adenyl cyclase resulting in enhanced cyclic AMP production --> HR increases due to stimulation of funny current (If) and L-type calcium channels/ Myocardial contractility increases due to L-type Ca current influx stimulating release of Ca from sarcoplasmic reticulum / Increased myocardial relaxation occurs due to phosphorilation of phospholamban

Answer 311

Bradyarrhytmias, bronchospasms, impaired contractility, impaired glycogenolysis, gluconeogenesis and lypolysis

Answer 312

To convert SVT to sinus rhytm, shockable rhytms in CPR when defibirlator not available / sharp concussive blow in left precordium (patient in right lateral) --> this could cause myocardial depolarization that can disrupt a reentrant tachycardia circuit

Answer 313

Direct current cardioversion / overdrive pacing / Transvenous frequency catheter ablation

Answer 314

Animals with systolic dysfunction classically are placed on digoxin as a first-line negative dromotrope -> however, the ventricular rate is almost never slowed adequately and other drugs must be added -> diltiazem is effective in prolonging the effective and functional refractory periods of the AV node

Answer 315

o B1 selective blocker --> because of its negative inotropic effects, the dosages required to significantly affect AV nodal conduction are often not well tolerated by animals with ventricular systolic dysfunction. o Is particularly useful in cats with hypertrophic cardiomyopathy and SVTs

Answer 316

Frequent dosing needed (2 to 4h), GI effects, proarrhythmic properties

Answer 317

Hypoxia, acid-base disturbances, electrolyte disturbances, drugs

Answer 318

occurrence of 4 or more VPCs in a row and a HR of 240 or more

Answer 319

ARVC in boxers, DCM

Answer 320

When the Purkinje fibers work as a pacemaker if the impulse cannot be generated or conducted in the SA or AV nodes.

Answer 321

Reentry / enhanced automatocity / triggered activity

Answer 322

When the ventricular rhythm is faster than the sinus rhythm but slower than VT

Answer 323

More than 30sec

Answer 324

broad QRS tachycardia with complexes wider than 0.06 second in dogs and 0.04 second in cats. Each QRS complex is followed by a large T wave, directed opposite to the QRS deflection / the three most reliable diagnostic criteria of VT are: AV dissociation/fusion beats/capture beats

Answer 325

Treat as Ventricular --> Managing SVT as VT is usually less dangerous than the opposite, because drugs used to stop SVT or to slow the ventricular response rate to rapid atrial impulses (i.e., calcium channel blockers and β-blockers) do not interrupt VT and worsen hypotension with their vasodilatory or negative inotropic effects

Answer 326

Hypokalemia / decreases the difference in resting potential and threshold potential --> increases phase 4 depolarization, increasing spontaneous automaticity and prolonging action potential duration (cell more exitable) --> promotes arrhytmias

Answer 327

digoxin --> conpetes with K on its receptors

Answer 328

Mg is necessary for proper functioning of the sodium-potassium ATP pump, which maintains normal intracellular potassium concentration / hypomagnesemia can contribute to ventricular arrhythmias

Answer 329

Procainamide, sotalol, domperidone, cisapride, chlorpromazine, erythromycin

Answer 330

A study --> 21% in general, but 92% in Doberman Pinschers

Answer 331

Doberman pinschers (DCM), Boxers (ARVC), German Shepherds (inherited ventricular arrhythmias)

Answer 332

Idiopathic HCM and concentric HCM secondary to hypertension and hyperthyroidism

Answer 333

Supportive tx for underlying condition, no Tx specific for the arrhythmia. Those usually resolve spontaneously within 4 days.

Answer 334

sustained VT with a HR>180 / R on T phenomenum / polymorphic Vtaq

Answer 335

No - only works on damaged myocardium lidocaine activity is enhanced by acidosis, hyperkalemia and partially depolarized cells

Answer 336

8mg/kg/h to avoid neurologic effects

Answer 337

B blockers

Answer 338

Mexiletine with atenolol for control Sotalol as long term management

Answer 339

o Sympathetic activation has been implicated in the pathogenesis of ventricular arrhytmias o Sustained VT causing hemodynamic instability can increase circulating chatecholamines and B-blockers activity may help control these arrhythmias. --> Diseases where sympathetically driven VTs can develop include = pheochromocytoma, thyrotoxic disease in cats.

Answer 340

Dogs = bradycardias associated with clinical signs or high degree second AV block or third degree AV block Cats: Severe refractory clinical signs secondary to a pathologic arrhythmia (they generaly tolerate well AVB without treatment, regardless of structural disease or CHF being present)

Answer 341

Anesthesia/sedation = decreases high sympathetic output --> benzodiazepines or propofol are used in humans / electrical therapies --> rapid pacing/synchronized electrical cardioversion

Answer 342

Sinus nodal AV nodal Atria ventricles *the pacing lead is located dorsal to the heart

Answer 343

Transvenous Transcutaneous Transesophageal

Answer 344

V fib Pulseless Vtaq Rapid polymorphic Vtaq

Answer 345

R wave The R wave is the absolute refractory period of the myocytes. This mode prevents delivery of a shock around the peak of the T wave, which represents the vulnerable period of the ventricles. Delivery of a shock during the vulnerable period increases the risk of initiating ventricular fibrillation because the electrical impulse reaches the ventricles during their repolarization phase, which is characterized by tissue heterogeneity.

Answer 346

SVT or monomorphic ventricular tachyarrhythmias refractory to antiarrhythmic drug therapy

Answer 347

Vfib very irregular and rapid polymorphic Vtaq

Answer 348

Amount of energy delivered Thoracic impedance Path of the current relative to the position of the heart

Answer 349

Direct current

Answer 350

Monophasic defibrillators generate a uni- directional flow of current through the heart. Conversely, biphasic shocks are characterized by an initial positive current flow followed by a negative current flow in the opposite direction. These waveforms have been shown to be more effective than the monophasic configu- ration in terminating ventricular fibrillation at a lower energy setting, which may also decrease the severity of myocardial damage. Indeed, it appears that the second wave of current eliminates charges from cells that were only partially depolarized by the first phase of the shock and “heals” cell membranes damaged by the first wave of current

Answer 351

1 to 2J/Kg

Answer 352

o The main complication of cardioversion is induction of ventricular fibrillation if the shock is not synchronized to the R wave. o Ventricular fibrillation should be treated rapidly with a high-energy asynchronous shock.

Answer 353

Parvovirus (still rare) - Distemper (experimental infections) - West Nile virus (1 report in a wolf)

Answer 354

Trypanosoma cruzi

Answer 355

Acute syndrome = sudden right sided CHF, circulating trypomastigotes may be seen in circulation / Chronic syndrome = free of clinical signs for months or years, Nervous system damage: atazia and weakness.

Answer 356

Streptococcus and staphylococcus (most common) - Lyme disease (Borrelia burgdorferi), rickettsial organisms (Erlichia canis, Rocky mountain spotted fever (Rickettsia ricketsii)), Bartonella.

Answer 357

Doxorubicin treatment (usually cumulative doses >250mg/m2) - vasculitis - Heat stroke - Radiation - Immune mediated polymyositis - catecholamine toxicity

Answer 358

Digoxin increased expression of proinflammatory cytokines and increased mortality in experimental myocarditis, so it is recommended to be used with caution and at low dosages

Answer 359

mild ( < 50 mmHg), moderate (51–75 mmHg), or severe ( > 75 mmHg)

Answer 360

NO is produced from L-arginine and oxygen by the enzyme nitric oxide synthase (NOS). Nitric oxide travels to smooth muscle, where it stimulates the enzyme guanylate cyclase (GC) to convert guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP). cGMP inhibits calcium release and ultimately leads to pulmonary vasodilation; cGMP is inactivated by phosphodiesterases

Answer 361

Prostaglandin I2 (prostacyclin or PGI2) is an eicosanoid produced by vascular endothelial cells via prostacyclin synthase. PGI2 stimulates adenylate cyclase (AC) and enhances the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). cAMP decreases intracellular calcium stores, leading to pulmonary vasodilation

Answer 362

Alveolar hypoxia is associated with pulmonary vaso-constriction. This response targets perfusion to better ventilated lung regions, improving ventilation:perfusion matching

Answer 363

Class I pulmonary arterial hypertension (PAH) Class 2 PH due to left-sided heart disease Class 3 PH due to pulmonary disease Class 4 PH due to thromboembolic disease Class 5 PH due to unclear or multifactorial mechanisms

Answer 364

HW disease, congenital shunts (PDA, atrial/ventricular septal defects)

Answer 365

A large or chronic left-to-right shunt allows significant blood flow to the right side of the heart, leading to severe pulmonary vascular changes. These changes promote increased right- sided cardiac pressures, and eventually the right-sided cardiac pressures exceed left-sided pressures; due to the pressure differences, shunt reversal occurs, and blood flows through the shunt from the right side of the heart to the left. As a result of right-to-left shunting through the defect, deoxygenated blood enters the systemic circulation and leads to cyanosis and polycythemia.

Answer 366

Increased jugular distension during inspiration

Answer 367

Bubble study??

Answer 368

Pulmonary Artery Pressure (PAP)

Answer 369

Right parasternal short axis basilar view and left parasternal apical view

Answer 370

Using the modified Bernoulli equation (pressure gradient (mmHG) = maximum TR velocity (m/s)2 × 4), the TR velocity is converted to pressure and is considered an adequate indirect measurement of PAP

Answer 371

Right heart catheterization and direct measurement of PAP

Answer 372

Pulmonary artery profile Measurement of pulmonary artery acceleration time and ejection time Tricuspid annular plane systolic excursion (TAPSE) Assessment of right ventricular myocardial function via the TEI Index Tissue Doppler imaging

Answer 373

Moderate to seere right sided cardiac changes: RA enlargement, RV dilation and/or hypertrophy, septal flattening, pulmonary artery dilation.

Answer 374

o Antiplatelet therapy should be instituted in cases of PH due to thromboembolic disease o Given that PH is associated with cellular changes that promote platelet-induced vascular changes, such as serotonin-associated vascular remodeling, there is some rationale for use of platelet inhibitors in other classes of PH

Answer 375

Phosphodiesterase 5 (PDE-5) is highly concentrated in pulmonary vessels, leads to the breakdown of cGMP. Inhibition of PDE-5 at higher concentrations of cGMP, decreased Ca release, and therefore improved vasodilation

Answer 376

Prostaglandin I2 (prostacyclin or PGI2) is an eicosanoid produced by vascular endothelial cells via prostacyclin synthase. PGI2 stimulates adenylate cyclase (AC) and enhances the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). cAMP decreases intracellular calcium stores, leading to pulmonary vasodilation.

Answer 377

blood stasis, hypercoagulability, and endothelial damage. It is generally believed that two factors have to be present for thrombosis, but one also influences the others.

Answer 378

o Venous thrombus à at low shear stress rates (0–1000 s−1), fibrin generation (i.e. secondary hemostasis) plays a major role. Therefore, a venous thrombus is primarily composed of red blood cells embedded within a fibrin meshwork o Arterial thrombosis --> where high shear stress conditions (>10 000 s−1) predominate, and platelet adhesion to the endothelium is the most important part of thrombus formation. Therefore, an arterial thrombus is primarily composed of platelets

Answer 379

Low platelet count, fibrin degradation products, D dimers / Hypercoagulable TEG VCM

Answer 380

Tissue plasminogen Activator, urokinase, streptokinase

Answer 381

Acts on the arachidonic acid pathway and irreversibly inhibits the COX pathways. These enzymes (COX 1 and COX 2) catalyze the conversion of arachidonic acid to PGH2, the pre- cursor for several metabolites including thromboxane A2 (TXA2). TXA2 enhances platelet function and promotes platelet aggregation and vasoconstriction / Also produces a permanent defect in platelet TXA2 synthesis during the entire life of the platelet (7–10 days).

Answer 382

Thienopyridine that selectively inhibits ADP-induced platelet aggregation but has no direct effects on arachidonic acid metabolism. It requires hepatic biotransformation to produce the active metabolite.

Answer 383

It complexed with antithrombin to form heparin:antithrombin complex --> catalyzes the activity of it. Inhibits coagulation factors II, IX, X, XI, XII

Answer 384

UF: mean of 15.000 / LMWG 4000 to 5000

Answer 385

They depend on the proportion of heparin molecules large enough to bind thrombin

Answer 386

aPTT therapeutic target range 1.5 to 2.5 times normal control value

Answer 387

only 25–50% of the heparin molecules in LMWH are large enough to inhibit factor IIa, although all retain the capacity to inactivate factor Xa.

Answer 388

it’s a reflexion of the inhibition of factor IIa

Answer 389

LMWH has a reduced affinity for binding to plasma proteins or cells compared with UFH --> more predictable dose–response relationship and longer half-life

Answer 390

Chromogenic assay of anti-factor Xa activity

Answer 391

10% (90% of cats have underlying cardiomyopathy, but less than 10% are previously diagnosed with cardiac disease)

Answer 392

Glucose and lactate peripheral compared with affected limb, Lack of doppler flow, direct visualizetion of the thrombus on US, angiography

Answer 393

FATCAT study -> Clopidogrel administration was associated with significantly reduced likelihood of recurrent FATE compared to aspirin and had a longer median time to recurrence. Recurrence rates of 75% and 49% with aspirin and clopidogrel respectively.

Answer 394

# of limbs affected (1 limb = 70% survival to discharge / 2 limbs = 25% survival to discharge) Motor function CHF Hypothermia Bradycardia Phosphorus levels

Answer 395

o PLN / PLE - Endocrinopathies: hyperadrenocorticism, diabetes mellitus, hypothyroidism - liver disease - neoplasia - infective endocarditis - Immune-mediated diseases where chronic or higher doses of steroids are required à IMHA, ITP or Addison’s disease.

Answer 396

Flowmeter - surgically applied surrounding a vessel and measures the SV - only used in research

Answer 397

o PV loop diagram o Catheter inside the LV with ultrasound waves attached to the catheter and will give several volumes that will be added and give us PV loops. o Why is it not used clinically? If there is a tiny bubble of air, goes straight into the brain, will not pass through lungs to be caught. Much more dangerous.

Answer 398

o Clinical gold standard. o CO = vol indicator (temp patient - temp indicator) / f time

Answer 399

o They all measure things that go in and out of the heart, an indicator. Depending on which indicator it has different names. o Swan Ganz - with temperature o LiDCO - lithium o CO status - ultrasound dilution o PiCCO o The AUC is inversely proportional to CO

Answer 400

o From Ra -> RV -> PA o Measures temperature changes - we inject a big bolus of 0.9%NaCl o There is a thermometer at the tip of the catheter that will measure temperature drops. o Temperature in graph is negative cause it is less than initial temperature o Curve will tell us CO

Answer 401

o PAP - resistance for lungs o PCWP - pulmonary circulation, resistance and how volume status is.

Answer 402

o Size of the patient - only made for humans and babies, not possible to use it in large animals o We need a cut down to introduce it o Myocardium damage o Pulmonary rupture - if balloon ruptures o Contraindications - LBBB - risk of complete block. Hypocoagulation.

Answer 403

o Instead of finishing in the PA, finish in the RV or even vena cava o Transpulmonary thermodilution - PiCCO plus o PiCCO stands for Pulse Contour Cardiac Output. The “i” in PiCCO was added to create a pronounceable word. o The PiCCO Technology is based on transpulmonary thermodilution and arterial pulse contour analysis. The thermodilution measurement needs to be performed correctly and the arterial pressure curve needs to be of a certain quality. o Limitations - requires femoral artery catheterization, indicator loss over time, charge per catheter

Answer 404

o Lithium dilution cardiac output is a minimally invasive indicator dilution technique for the measurement of cardiac output. o Any arterial line works, does not need to be the femoral (like with PiCCO) o Lithium injected via central line. From an artery, sample is collected and machine detects amount of lithium. o Limitations: bleeding out (operator, depending on how much sampling, blood loss over time), indicator stable over time (will not leave the body easy over time), clots, cytokines inflammation.

Answer 405

o Saline velocity dilution method (aka ultrasound velocity dilution method) o Ultrasound dilution method. Injects saline in the system and causes hemodilution. The viscosity of the blood changes for that period of time. That is the indicator, the viscosity change, not the saline itself. o In this case arterial catheter is connected to a central line, there is no blood loss like in LiDCO methods. o Less invasive than PAC, blood returned to the patient, no indicator accumulation. o Reasonable bias and limits of agreement. o Limitations - placement of arterial line. Patient should be sedated. Not bad for small patients.

Answer 406

They are very expensive

Answer 407

o Arterial line -> arterial pulse wave. The stronger the heart pumps, the stronger the arteries pump. o Had good correlation in humans the AUC from the arterial line. For every AUC it gives you a SV. o It correlates well in stable patients where CO is constant, when it changes there is not good correlation

Answer 408

o Pulse pressure variation = (PPmax - PPmin / PPmean) x 100 o PPmean = (PPmax + PPmin) / 2 o To predict fluid responsiveness in MV patients o MV - BP increases on inspiration, decreases on expiration (opposite of spontaneous breathing) o Normally PPV <5mmHg

Answer 409

o Requires a PAC o Helps to measure the oxygen consumption based on SvO2

Brainscape's Knowledge GenomeTM

Cardiovascular Flashcards

Brainscape's Knowledge Genome^TM