Cardiovascular Flashcards

Question

Lidocaine is more effective with low pH and hyperkalemia

Answer 1

True: ideal anti-arrhythmic for damaged myocardial tissue

Answer 2

Dog: 125-200 ml/kg/min Cat: 120 ml/kg/min

Answer 3

DO2: 20-35 ml/kg/min VO2: 4-11 ml/kg/min

Answer 4

SAP < 90 mmHg or MAP < 60 mmHg

Answer 5

Renal Eyes Cardiovascular CNS

Answer 6

Falsely higher When the limb is below the level of the heart (and specifically the right atrium), gravity causes an increase in **hydrostatic pressure** in the blood vessels of the lower limb. This increased pressure adds to the actual blood pressure and is detected by the cuff, leading to a higher reading than the true systemic blood pressure. * Limb below RA: Causes a falsely higher BP reading. * Limb above RA: Would cause a falsely lower BP reading.

Answer 7

1) HDO can measure more accurately in a wider range 2) HDO can obtain a more accurate reading in the presence of arrhythmias 3) HDO can obtain SAP, MAP and DAP HDO devices perform realtime analysis of arterial wall oscillations to obtain pressure wave amplitudes →

Answer 8

1) Place an arterial line 2) Prepare a bag of 1L saline with heparin (1-2U/ml), a transducer, a monitor and non-compliant arterial line monitoring extension tube. Attach them together. 3) Fill the entire arterial monitoring system with heparinized saline. 4) Attach the arterial BP monitoring system to the arterial catheter and the monitor. 5) There should be a 3-way stopcock on the arterial BP monitoring system. Turn it to close the patient end and open the monitor end to the atmosphere. Keep the system at the level of RA and zero the system. 6) After the system is zero. Turn the 2-way stopcock to close the opening to the atmosphere and connect the monitor to the patient. You should be able to obtain the arterial waveform. 7) Perform a fast flush test to determine if it is necessary to adjust the system and optimize its dynamic's response

Answer 9

1) Zeroing 2) Calibration 3) Leveling

Answer 10

RV diastolic pressure (= filling pressure of right side of the heart)

Answer 11

0 - 5 cmH2O

Answer 12

1) Venous return - Circulating blood volume - Venous wall compliance 2) Right-sided cardiac diseases 3) Intrathoracic/intraperitoneal pressure

Answer 13

Vasodilation (venodilation) Decreased systemic circulating blood volume

Answer 14

Compensated hypovolemia Compensated hypervolemia

Answer 15

1) Hypervolemia 2) Systemic hypertension or marked vasoconstriction 3) Occlusion of the catheter 4) Right sided cardiac disease (e.g. tricuspid regurgitation, right sided systolic dysfunction) 5) Pulmonary hypertension 6) Pericardial effusion 7) Pneumothorax 8) Marked ascitis 9) Pleural effusion 10) Mechanical ventilation (PEEP) 11) Intrathoracic mass

Answer 16

1.36 cmH2O = 1 mmHg

Answer 17

Draw a vertical line from sternum to the top of spinous process caudal to the scapula. The RA is at about 40% of the height of the line.

Answer 18

When the pressure waves go through the vessels, the reflection will create multiple oscillating waves with different frequency and amplutide (Fourior series). The arterial waveform is the summation of those oscillating waves

Answer 19

1: Systolic upstroke 2: Systolic peak pressure 3: Systolic decline 4: Dicrotic notch (incisura) 5: Diastolic runoff 6: End-diastolic pressure

Answer 20

The elastic recoil of the arteries with the closed aortic valves cause a slight and transient increase of the arterial blood pressure.

Answer 21

The shaded area beneath the arterial pressure curve

Answer 22

1) System's dynamic response 2) Presence of air bubbles in the tubing 3) Respiration 4) Arrhythmias 5) Catheter location/placement

Answer 23

1) Natural frequency 2) Damping coefficient * They are determined by the system's physical properties, specifically mass, elasticity, and friction

Answer 24

The reading and the waveform will be exaggerated due to summation of the waveforms ("**summation effect**") → higher SAP and lower DAP → overshooting, ringing

Answer 25

Too low * Ideally need to > 12 Hz or as high as possible

Answer 26

Loss of the pulse pressure energy when the waves travel from the catheter to the transducer.

Answer 27

1) Friction resistance along the line 2) Absorption of energy by the tubing and system 3) Air bubbles 4) Line occlusion

Answer 28

Higher damping coefficient → more significant of the damping → overdamp

Answer 29

Overdamped: loss of details (e.g. dicrotic notch), slurred waveform Underdamped: falsely high SAP and falsely low DAP, extra spikes and details that are non-physiological

Answer 30

25/1.7 = 14.7 Hz * Note the number of blocks between oscillation peaks

Answer 31

17/24 = 0.71 (amplitude ratio) According to the chart, the damping coefficient is 0.11 * Measure the length of two successive oscillations (i.e., from peak to valley, and from that same valley to the next peak).

Answer 32

> 2 oscillations * Normally should be 2 oscillations

Answer 33

* Very small air bubble may cause underdamp (act as a spring as they compress and decompress easily. This allows the pressure waveform to oscillate excessively, leading to an amplified or exaggerated response) * Large bubble will cause overdamp (acts like a cushion, absorbing and dissipating the energy of the wave rather than transmitting it accurately to the transducer)

Answer 34

Initial upstroke becomes steeper Systolic peak gets higher End-diastolic pressure gets lower * The waveform is delayed; the dicrotic notch appears later and appears more slurred * distal pulse amplification

Answer 35

Increase * The opposite during spontaneous ventilation

Answer 36

1) Systolic upstroke becomes less steep 2) Loss of dicrotic notch 3) The systolic peak pressure may decrease in severe case

Answer 37

1) Very steep systolic upstrokes 2) Increased pulse pressure 3) Decreased end-diastolic pressure

Answer 38

Corrigan's pulses is the rapid elevated and collapse pulse (increased pulse pressure but very short duration for each pules). Aortic regurgitation, PDA, severe anemia, hypertension

Answer 39

1) Examine the patient to see if the patient's clinical signs fit hypotension 2) Check the ABP tubing to see if there is any kink, blood clot or air bubbles 3) Check the pressured fluid bag to make sure the pressure is higher than 250 mmHg 4) Check if the arterial catheter is patent 5) Check if the patient's position has change and if re-zeroing is needed.

Answer 40

1) Flush the patient's central venous catheter with heparinized saline to make sure it's patent 2) Keep the water manometer vertical (can use an IV pole). Collect the three way stopcock with manometer, fluid set and tubing toward the CVC (do not connect yet) 3) Close the manometer end. **Fill the entire non-compliant tubing with normal saline. Connect the tubing to CVC.** 4) Close the patient end. **Fill the water manometer with 10-20 cm of normal saline** 5) Keep the zero marker of the water manometer at the level of right atrium. 5) Close the fluid set end. Allow the water manometer and patient's end to equilibrate.

Answer 41

Transmural pressure = intravascular pressure - extravascular pressure

Answer 42

CVP usually will increase 2-5 cmH2O and will return to baseline after 15 min * Hypovolemic patient → CVP rises minimally or rapidly returns to baseline * CVP takes longer to return to baseline → volume overload, cardiac dysfunction, restrictive pericardial disease

Answer 43

a wave: end-diastolic; right atrial contraction c wave: early-systolic; isovolumetric ventricular contraction; tricuspid valves are pushed toward RA x descent: mid-systolic; right atrial relaxation v wave: end-systolic; systolic filling of RA (venous return) y descent: early-diastolic; early ventricular filling

Answer 44

CVP = (a wave peak + x descent base)/2

Answer 45

Cannon "a" wave

Answer 46

Absence of a wave and prominent c wave (due to overfilling of RA)

Answer 47

Broad, tall systolic c-v wave, beginning in early systole and obliterating the systolic x descent in atrial pressure.

Answer 48

- Thermistor port - Measure CVP (blue; proximal) - Measure pulmonary artery pressure, collect sample for SvO2 (yellow) - Drug administration port - Balloon inflation port; measure PAWP (red)

Answer 49

Preload: a measure of the ventricular myocardium stretch at the end of diastole Afterload: the force/resistance which the ventricles need to overcome to eject the blood

Answer 50

Cardiac index (L/min/m2) = cardiac output/body surface area in m2

Answer 51

Total uptake of the oxygen by the peripheral tissues equal the product of total **blood flow** through the tissues and the **arteriovenous oxygen concentration difference**. * it can also be used for CO2 production

Answer 52

1. the patient is anesthetized and intubated to measure the VO2 2. patient needs to be cardiovascularly stable 3. not a real-time measurement as blood gas analysis is required 4. requires a central line to have a mixed venous sample (PA)

Answer 53

Patient is anaesthetised, intubated and hooked to a proprietary rebreathing circuit containing CO2. If CO2 significantly increases CO is high as more blood reaches peripheral tissues and carries more CO2 vs low CO2 exhaled = low CO and low tissue perfusion

Answer 54

There are two methods: 1. transpulmonary: injection via jugular vein and sampling on peripheral vessels (i.e. femoral artery) 2. pulmonary artery Injection: injection and sensor within the PA

Answer 55

Cross-section area of left ventricular outflow tract & aortic blood velocity

Answer 56

3.5 - 5.5 L/min/m2

Answer 57

1.5-2 ml/kg/beat

Answer 58

SVR: 0.5-0.8 mmHg/kg/min PVR: 0.04-0.06 mmHg/kg/min 10x difference!

Answer 59

- Arrhythmias - Respiration (ideally measure at end-expiration) - Intracardiac shunt - Thermistor probe problems (malfunction, got blood clote) - Severe hypotension - Inadequate indicator injection - Concurrent large volume fluid/med administration

Answer 60

NICO * The equation is for partial rebreathing technique

Answer 61

b) indicates high cardiac output c) indicates low cardiac output

Answer 62

1) valve damage, endocarditis 2) rupture of RA or PA 3) blood clot formation, air embolism 4) arrhythmias

Answer 63

Transpulmonary thermodilution - Inject a cold fluid bolus in jugular vein and measure its changes in femoral artery - It can also analyze the pulse waveform contour and therefore obtain more information (e.g. preload, afterload...etc)

Answer 64

Inject a fixed dose of lithium chloride and then has a lithium-selective electrode placed at the peripheral arterial catheter - It can also analyze the arterial pulse waveform

Answer 65

PiCCO LiDCO

Answer 66

1) Attach **ECG** to the patient 2) Clip and aseptically prepare the jugular vein. Fill the introducer with heparinized saline and Insert the **introducing catheter**. 3) Get the **thermodilution catheter** and attach **distal port to pressure transducer **via a three-way stopcock and flush the system with heparinized saline. 4) Attach continuous flush line to the transducer and pressurize the bag to ≥200 mm Hg. 5) Zero the pressure transducer. 6) Insert the thermodilution catheter through the introducer catheter to about **20 cm** and verify that the pressure tracing reflects a central venous pressure waveform. 7) Advance the catheter with the natural curve of the catheter aimed toward the sternum of the animal; watch for a typical ventricular waveform. 8) If the catheter advances to the **50-cm mark **without entering the right ventricle, withdraw it to the 20-cm mark and start again. 9) If the pressure tracing becomes damped, flush the distal port with the transducer’s fast flush device; if the pressure tracing abruptly ceases followed by a rapid, linear increase, the end-hole has butted up against a vessel or heart chamber wall and should be withdrawn slightly and then reinserted. 10) Once the catheter tip has entered the right ventricle, **inflate the balloon with 1 mL of air** and advance it further until the pressure waveform indicates that the catheter tip has entered the pulmonary artery. 11) With the balloon inflated, advance the catheter until the pressure tracing reflects occlusion of a branch of the pulmonary artery; deflate the balloon and verify a good pulmonary artery tracing. 12) Bandage the catheter and introducer set aseptically and occlusively.

Answer 67

Arterial: 17.8 ml/dL Venous: 14.2 ml/dL

Answer 68

C → D → A → B

Answer 69

- Damping when the waveform travels from LA to pulmonary artery - There is shorter time between LA contraction and LV contraction compared to RA & RV contraction → a & c waves may superimposed -

Answer 70

1) Atrial/ventricular tachyarrhythmias 2) Prolonged QT interval 3) Decreased T wave amplitude 4) ST segment elevation/depression

Answer 71

Prolong QT interval * If hypercalcemia → shortening of QT interval

Answer 72

No more than 25% in 1 hour

Answer 73

It is used to evaluate the tendency of turbulence to occur

Answer 74

Small arterioles (2/3 of total resistance)

Answer 75

75 - 175 mmHg

Answer 76

1) Spleen 2) Liver 3) Large intra-abdominal veins 4) Venous plexus under the skin

Answer 77

False. The lymph from right side of the neck and head, right arm, and parts of the right thorax flows into the **right lymph duct** → right subclavian vein and internal jugular vein

Answer 78

Medulla and lower 1/3 of the pons

Answer 79

True From Guyton: "The lateral portions of the vasomotor center tran mit excitatory impulses through the sympathetic nerve fibers to the heart when there is a need to increase heart rate and contractility. Conversely, when there is a need to decrease heart pumping, the medial portion of the vasomotor center sends signals to the adjacent dorsal motor nuclei of the vagus nerves, which then transmit parasympathetic impulses through the vagus nerves to the heart to decrease heart rate and heart contractility."

Answer 80

False When BP below 50-60 mmHg, baroreceptors at the carotid sinus do not respond. When BP below 80 mmHg, baroreceptors at the aortic arch do not respond.

Answer 81

The baroreceptor signal enters the vasomotor center → the secondary signal inhibits the vasoconstrictor center and stimulates the vagal parasympathetic center → vasodilation, decrease heart rate and contractility

Answer 82

1) Low oxygen 2) High CO2 3) Increased H+ ion

Answer 83

2 carotid bodies locate at the carotid bifurcation; 1-3 aortic bodies locates adjacent to the aorta

Answer 84

Low-pressure receptors are stretch receptors in pulmonry artery, atria and vena cava. They respond to changes in blood volume. 1) decrease in SNS tone --> afferent renal vasodilation → increase GFR and fluid filtrated through the glomerulus 2) Decrease ADH release → decrease water reabsorption 3) Release atrial natriuretic peptide → decrease sodium and water reabsorption at the nephrons 4) Bainbridge reflex --> increased atrial stretch --> increase HR to avoid pooling of blood

Answer 85

Increased atrial pressure leads to increased heart rate and contractility. * The afferent limb of the reflex within this signal, when activated takes sensory information from the vagus nerve to medulla oblongata, and the efferent limb sends out inhibitory signals by reducing vagus nerve tone and increasing the sympathetic outflow.

Answer 86

Bainbridge reflex vs vagal reflex? Inspiration → increased HR Expiration → decreased HR

Answer 87

Increased sympathetic tone → HR and BP elevate

Answer 88

When the mitral and tricuspid valves close Isovolumetric contraction

Answer 89

When the aortic and pulmonic valves close Isovolumetric relaxation

Answer 90

S2 heart sound is composed of closing of aortic valve and closing of pulmonic valve. Aortic valve usually close very slightly before pulmonic valve. During inspiration, the intrathoracic pressure decreased → increased venous return → more blood in the RV → pulmonic valve open for a bit longer because more RV volume → less blood return to LA → slightly decreased LV volume → aortic valve closes earlier due to shortening emptying time

Answer 91

- It is also called ventricular gallop - When mitral or tricuspid valves open and the blood is passively filling the ventricular → S3 is the sound when the large volume of blood strikes a very compliant ventricle - Early diastole - Often heard in dogs with DVM

Answer 92

- It is also called atrial gallop - When atria contracts to force the blood into a very non-compliant ventricle - End diastole - Often heard in cats with HCM

Answer 93

Ventricular myocardium: -85 mV SA nodal cells: -55 ~ -60 mV

Answer 94

A: LBBB B: RBBB

Answer 95

1) action potential of myocardium is caused by fast sodium channels and L-type calcium channels; AP of skeletal muscles is caused by fast sodium channels only 2) The source of Ca in myocardium is from extracellular space; while in skeletal muscles it's from endoplasmic reticulum 3) There is no plateau phase in skeletal muscle AP

Answer 96

skeletal and myocardial muscles are THIN filament regulated (Calcium binding to troponin key step for shifting of tropomyosin interaction between actin and myosin) vs smooth muscle requires Ca binding to calmodulin to activate MLCK which will phosphorilate myosin head and allow detachment from actin

Answer 97

0: depolarization; fast Na channel open and close Kir channels 1: initial repolarization; fast Na channel close, transient outward K channel open (Kv channels ITO current), also Na/Ca exchanger open (Na from phase 0 exists while Ca starts to come in) 2: plateau; L-type Ca channel open, transient outward K channel close 3: rapid repolarization; L-type Ca channel close; slow and rapid dealyed K rectifier channel open 4: resting membrane potential; slow and fast delayed K rectifier channel closes, inward rectifier K channel open

Answer 98

Kir (K inward rectifiers) channels close - these are the one responsible to keep stable membrane potential

Answer 99

"m" gate is voltage dependent "h" gate is time dependent The "m" gate opens when depolarization of the myocyte occurs while the 'h' gate closes to terminate Na entry a few millisecond after 'm' have opened. 'h' then remains close until the cell has partially repolarized --> responsible for absolute refractory period (protects the myocardium from tetany). The 'm' gate closes at late phase 3 --> responsible for relative refractory period. When the 'm' is close, but 'h' is open a cell receiving a strong enough stimulus can be depolarized again.

Answer 100

inactivated: 'm' open but 'h' close (absolute refractory period, phase 1,2 and early 3) resting: 'm' close but 'h' open (late phase 3 and 4) open: both 'm' and 'h' open (only 1-2 milliseconds during rapid depolarization, phase 0)

Answer 101

Ion current in pacemaker cells. Inward flow of Na and outward flow of K via HCN channels (hyperpolarization cyclic nucleotide channels). HCN channels sensitive to cAMP --> action of sympathetic nervous system and beta blockers on HR.

Answer 102

Activates KAch channels --> otward flow of K ions --> hyperpolarization of pacemaker cells This channel is also acted upon by gamma subunit of Gi protein (A1 adenosine receptors and digoxin)

Answer 103

Muscarinic M2 receptors --> Gi coupled --> drop cAMP + activate KAch (gamma subunit) to hyperpolarize cell and pull the resting potential away from threshold

Answer 104

1) Action potential reaches the T tubules system which leads to depolarization 2) The voltage change will be sensed by dihydropyridine (DHP) receptors which link to the ryanodine receptor channels (Ca release channels) on the sarcoplasmic reticulum 3) The Ca release channels open and release many Ca ions and cause contraction 4) Ca ions are re-uptaken by active calcium channels called SERCA (sarcoplasmic reticulum Ca2+-ATPase). Ca ions are bound with calsequestrin in the sarcoplasmic reticulum

Answer 105

The Ca storage in the myocardium sarcoplasmic reticulum is not as abundant as skeletal muscles. The Ca ion inflow during the plateau phase of AP triggers the Ca release from the sarcoplasmic reticulum and the Ca from both extracellular fluid and SR cause muscle contraction * Myocardial contractility is heavily dependent on the extracellular Ca ion concentration

Answer 106

1) SERCA2 (sarcoplasmic reticulum Ca2+-ATPase) 2) Na-Ca exchanger on the sacrolemma

Answer 107

Relaxation is an. ATP-dependent mechanism (Na/Ca exchanger and SERCA need ATP)

Answer 108

It is a negatively charged cytosolic protein that binds to Ca++ and chaperones it into the SR This is part of the 'sarcoplasmic calcium buffering system'

Answer 109

Ejection fraction is the fraction of the blood in the ventricular chamber that is ejected during systole in relation to the total blood volume during end-diastole EF = SV/LVEDV Normal EF in dogs and cats: 50-70%

Answer 110

RV is about 1/6 of LV

Answer 111

**Slow Na channel** is very leaky and can cause continuous slow Na inflow. When the membrane potential reaches **-40 mV**, L-type Ca channels open, causing depolarization and generation of AP.

Answer 112

Hepatojugular reflex means when the pressure is applied on the liver, the jugular vein becomes distended. Positive hepatojugular reflex means the heart cannot compensate with increased venous return.

Answer 113

Situational hypertension - White coat hypertension Secondary hypertension (most common) Idiopathic hypertension

Answer 114

Cushing disease Hyperthyroidism Chronic kidney disease AKI Pheochromocytoma DM Primary hyperaldosteronism

Answer 115

The eyes are the most vulnerable organ for TOD. First manifestation is tortuous retinal vessels followed by multifocal retinal oedema and exudative retinal detachment. Early aggressive treatment can lead to physical retinal re-attachment but rarely resoration of vision.

Answer 116

Sonographic measure of blood flow resistance in arcuate arteries RIR = (peak systolic velocity - peak diastolic velocity) / peak systolic velocity RIR closely correlated with number of organ involved in TOD RI>0.7 = 3-4 organs involved

Answer 117

Posterior Reversible Encephalopathy syndrome Form of acute hypertensive encephalitis - treat with nicardipine (CCB similar to amlodipine but injectable form). Sudden increase in MAP overcomes autoregulation mechanism

Answer 118

Hypertensive emergency SAP>180 and evidence of TOD vs hypertensive urgency SAP>180 without evidence of TOD

Answer 119

Glucocorticoid Vasopressin Epinephrine Phenylephrine Minerocorticoid EPO Phenylpropranolamine

Answer 120

False * Patients > 9yrs will be reasonable

Answer 121

> 180 mmHg

Answer 122

Recheck in 3-6 months

Answer 123

Recheck twice in 8 weeks & recheck for TOD If the SBP is still persistently above 160mmHg, antihypertensive therapy is recommended.

Answer 124

Recheck twice in 14 days & recheck for TOD If the SBP is still persistently above 160mmHg, antihypertensive therapy is recommended.

Answer 125

1) Minimize the risk of TOD (SBP ≤ 140 mmHg; **optimal goal**) 2) Maintain the SBP ≤ 160 mmHg (**minimal goal**)

Answer 126

Recheck BP in 7-10 days if no TOD Recheck BP in 1-3 days if TOD presents *If BP < 160 mmHg on recheck, the next recheck can be 4-6 months.

Answer 127

Because calcium channel blockers mainly cause renal afferent arteriole dilation → may increase the glomerulus capillary hydrostatic pressure

Answer 128

Calcium channel blockers mainly cause renal afferent arteriole dilation; ACE inhibitors and ARB mainly cause renal efferent arteriole dilation → may not make much change of the glomerulus capillary hydrostatic pressure

Answer 129

Dogs: ACE inhibitor Cat: calcium channel blocker (because of established efficacy)

Answer 130

Proteinuria

Answer 131

Amlodipine Beta blocker (atenolol > propanolol as selective Beta 1 blocker and safer for asthmatic cats)

Answer 132

1) SBP > 180 mmHg 2) Signs consistent with intracranial TOD

Answer 133

**Dopamine-1 receptor agonist** -> vasodilation Dose: 0.1 μg/kg/min with careful (ie, at intervals of at least 10 minutes) monitoring of BP. The dosage can be titrated up by 0.1 μg/kg/min increments every 15 minutes to the desired SBP, to a maximal dosage of 1.6 μg/kg/min. No evidence of clinical improvement of AKI in either dogs (0.8 ug/kg/min) or cats (0.5ug/kg/min).

Answer 134

Direct smooth muscle relaxant **SSAO (semicarbazide-sensitive amine oxidase) inhibitor**. Interferes with **intracellular Ca metabolism**. Prevents inititation and maintenance of contractile state in smooth muscle. Specifically it is thought to interfere with IP3 receptor on SRS. Dog: 0.1 mg/kg IV over 2 minutes, followed by a CRI of 1.5-5.0 μg/kg/min Cat: 1.0-2.5 mg per cat SC

Answer 135

Nitroprusside: arterial and venous dilators Nutroglycerin: mainly venodilator

Answer 136

1) Hypertrophic cardiomyopathy 2) Restrictive cardiomyopathy - Endomyocardial form vs Myocardial form 3) Dilated cardiomyopathy 4) Arrhythmogenic cardiomyopathy 5) Nonspecific phenotype

Answer 137

HCM, RCM (restrictive)

Answer 138

A: Predisposed B1: Subclinical with low risk of developing CHF/ATE (normal, mild atrial enlargement) B2: Subclinical with high risk of developing CHF/ATE (moderate, severe atrial enlargement) C: Current/previous CHF/ATE D: Refractory CHF

Answer 139

15% * 29% in older cats

Answer 140

Maine Coon, Ragdoll, British Shorthair, Persian, Bengal, Sphynx, Norwegian Forest cat, Birman

Answer 141

Gallop sound or arrhythmia on PE Moderate to severe LA enlargement Decreased LA fractional shortening (LA FS%) Extreme LV hypertrophy Decreased LV systolic function Spontaneous echo-contrast or intracardiac thrombus Regional wall thinning with hypokinesis Restrictive diastolic filling pattern

Answer 142

thromboprophylaxis (e.g. clopidogrel; 18.75 mg/cat PO q24h, with food) * If patient has rapid ventricular rate or AF → Diltiazem, atenolol or sotalol

Answer 143

Diuretic Thromboprophylaxis Pimobendan may be considered if patient has poor contractility and absent of DLVOTO (or dobutamine CRI)

Answer 144

0.1-0.2 mg/kg PO q24h

Answer 145

PAP ≥ 25mmHg at rest

Answer 146

Pressure gradient = 4 x velocity^2 (m/s)

Answer 147

Patient needs to have tricuspid regurgitation Right atrial pressure + Pressure gradient

Answer 148

3.0 - 3.4 m/s

Answer 149

1) Evidence of left-sided heart disease 2) Unequivocal LA enlargement

Answer 150

1) Pulmonary arterial hypertension 2) Left-sided heart disease 3) Respiratory disease, hypoxia or both 4) Emboli/thrombus/thromboembolism 5) Parasitic disease (e.g. heart worm) 6) Multifactorial or unclear mechanism

Answer 151

West Highland White Terriers Pekingese dogs

Answer 152

It is a phosphadiesterase type 5 inhibitor. Phosphadiesterase type 5 can degrade cGMP to 5'-GMP and decrease the NO vasodilatory function. By inhibiting cGMP degradation, it leads to vasodilation.

Answer 153

False Pimobendan is a PDE3 inhibitor

Answer 154

degenerative valve disease

Answer 155

Systolic failure/dysfunction (**DCM** phenotype) * toxic damage to the **mitochondria** of cardiomyocytes

Answer 156

Compare the sum of cardiac long axis and short axis with vertebral lengths, starting at the cranial border of T4 Dog: < 10.7 Cat: < 8

Answer 157

- Subaortic stenosis - Hypertrophic obstructive cardiomyopathy - Acute mitral regurgitation secondary to ruptured chordae tendineae - DCM

Answer 158

- HCM - Cardiac tamponade - Tachyarrhythmias

Answer 159

Neutrophilic inflammation Fibroplasia

Answer 160

Hypothermia

Answer 161

furosemide dose > 8mg/kg/d

Answer 162

Cl <103.5 mmol/L

Answer 163

Because of a high degree of protein‐binding to albumin, furosemide is not filtered at the glomerulus, but rather is secreted from the blood into the proximal renal tubule by organic anion transporters. * NSAIDs can compete with these transporters, hypoalbuminemia can affect the transport ** once furosemide is transported into the nephron lumen, it must remain free of protein interactions so that it can bind to the NKCC transporters on the luminal side of the tubular epithelial cells of the loop of Henle. Diseases such as protein‐losing nephropathies can impair the availability of furosemide to bind to these transporters.

Answer 164

1) Draw a line from the centro-ventral carina to the most caudal aspect of left atria where it intersects with dorsal border of caudal vena cave on the lateral view. 2) Transport the line to the cranial edge of T4 vertebral body. VLAS ≥ 3 → likely heart failure

Answer 165

VLAS ≥ 2.5 (sensitivity 100%) VLAS ≥ 3 (specificity 100%) Reference:Mikawa S, Nagakawa M, Ogi H, Akabane R, Koyama Y, Sakatani A, Ogawa M, Miyakawa H, Shigemoto J, Tokuriki T, Toda N, Miyagawa Y, Takemura N. Use of vertebral left atrial size for staging of dogs with myxomatous valve disease. J Vet Cardiol. 2020 Aug;30:92-99.

Answer 166

calstabin-2

Answer 167

>0.34 ng/mL

Answer 168

prevalence is 45-63% 2 genetic mutation: - pyruvate dehydrogenase kinase 4 - titin

Answer 169

- Great danes - Irish wolfhound (secondary to primary congenital rhythm defect) - Standard poodle, Portuguese Waterdog, Toy Manchester Terrier (juvinile onset of DCM)

Answer 170

Biphasic because composed by occult and clinical phase Occult no overt clinical signs but can see increase in N-pro-BNP (Dobbermans). Cinical phase starts with increased frequency of VPCs or APCs, then AF, S3 sound and left apical murmur indicating dilation of valvular anulus and mitral valve regurgitation

Answer 171

Atrial fibrillation Bilateral CHF

Answer 172

In Dobermans in the occult phase of DCM treatment with pimobendan delayed onset of clinical signs by *9 months* and increased survival time by *3 months*

Answer 173

Morphology of LBBB on lead I, II, III and aVF

Answer 174

Muscular dystrophy due to dystrophin defect (x-linked inheritance)

Answer 175

Sotalol (1.5-3 mg/kg PO q12h) Mexiletine (5-8mg/kg PO q8h)

Answer 176

Taurine and L-carnitine deficiency Also Dalmatian fed low protein diet for urate crystal.

Answer 177

RAAS SNS * Others: natriuretic peptides, endothelin, vasopressin systems

Answer 178

Vasoconstrictor

Answer 179

Natriuretic Peptide system Atrial natriuretic peptide (ANP) & B-type natriuretic peptide (BNP)

Answer 180

Stimulation: shear stress, angiotensin II, epinephrine, vasopressin, thrombin (all the bad things causing vasoconstriction) Inhibition: NO, atrial natriuretic peptide, prostacyclin, bradykinin, cGMP

Answer 181

Concentric hypertrophy: pressure overload Eccentric hypertrophy: volume overload

Answer 182

It is a SERCA inhibitor

Answer 183

1) Myosin isoform switching 2) Impaired Ca2+ transients and ryanodine function 3) Phospholamban upregulation 4) SERCA downregulation

Answer 184

P mitrale: P wave width >40 msec - Usually seen in LA enlargement P pulmonale: P wave height >0.5 mV - Usually seen in RA enlargement

Answer 185

- Grade 3/6 systolic heart murmur - La:Ao ratio in right-sided short axis view in early diastole ≥ 1.6 - Breed-adjusted VHS > 10.5 - Left ventricular internal diameter in diastole, normalized by weight (LVIDDN) ≥ 1.7

Answer 186

0.66 - 1 mg/kg/hr

Answer 187

Low UNa after furosemide = longer O2 dependency and higher likelihood of diuretic resistance

Answer 188

at least 60kcal/kg, high protein content, low Na content, possible supplementation of K and Mg especially if on high doses of diuretics or on digoxin

Answer 189

1. impact in end-diastole (max ventricular filling) or end systole (max atrial filling) 2. sudden increase in pre-load due to abdominal or peripheral vessels compression 3. bidirectional forces compressing the heart 4. acceleration/deceleration forces 5. blast injury 6. concussion 7. cardiac penetration

Answer 190

1. myocardial rupture 2. septal injury (immediated or delayed due to extensive necrosis) 3. pericardial laceration (can lead to secondary cardiac herniation and strangulation or PPDH) 4. valvular rupture (most vulnerable when closed, so mitral/tricuspid when systole vs aortic/pulmonic in diastole) 5. myocardial contusions (haemorrhagic, necrotic - arrhythmogenic due to re-entry circuit formation - severity of arrhythmia proportional to kinetic force applied to myocardium) 6. commoto cordis (cardiac impact during ventricle repolarization - ST segment - R on T phenomenon - ventricular tachycardia - immediate death - no histopathological changes)

Answer 191

- premature ventricular contractions - ventricular tachycardia - nonspecific ST segment elevation or depression

Answer 192

4-6 hr 7 days

Answer 193

ECG abnormalities and/or cTnI >0.11 ng/mL Hospitalise and close monitoring for 48h telemetry

Answer 194

2-4 mg/kg 10-40 mcg/kg/min

Answer 195

class Ia antiarrhythmic and K channel blocker prolongation of AP and depression of conduction velocity --> pro-arrhythmic due to possible re-entry mechanism More effective than lidocaine in controlling VT in humans In boxers with ARVC proven to decrease VPCs but not syncopal events. Can trigger SLE

Answer 196

0.25 ml/kg

Answer 197

Dogs: - neoplastic - idiopathic Cats: - CHF - FIP

Answer 198

- vomit (51%) - if acute = drop of CO - if chronic = increase venous pressure

Answer 199

False: HSA is most commonly found in R atrium and represents up to 61% of neoplastic causes of pericardial effusion Chemodectoma arises from heart base aortic chemoreceptors.

Answer 200

Left-ventricular output and systemic arterial pressure normally decrease slightly during inspiration. Pulsus paradoxus is an exaggeration of this normal pressure difference with respirations; patients with pulsus paradoxus exhibit a fall in arterial pressure during inspiration of 10 mm Hg or more.

Answer 201

Variable hight of QRS due to swinging of the heart MEA as the hearts moves within the pericardial sac with every beat

Answer 202

N-pro-BNP is not increased as both atria and ventricle are not distended (they are actually compressed). cTnI is elevated in HSA cases and a cut-off of 0.25 ng/mL is 81% sensitive and 100% specific vs cTnI is WNL in idiopatic cases.

Answer 203

Trauma Neoplasia Idiopathic Coagulopathy Infectious

Answer 204

True: shedded neoplastic mesothelial cells can be difficult to differentiate from inflammatory ones If not responding to steroids and recurrence then pericardectomy and biopsy should be performed

Answer 205

subtotal pericardiectomy is the preferred method as it requires less dissection (below phrenic nerves) than total pericardiectomy and it seems more effective than both thotacoscopic pericardial window and fluoroscopy guided baloon pericardiotomy. The most severe intra-operative complication is VF - risk can be reduced by using harmonics, minimise heart manipulation, normalise acid-base and lytes status and discontiue any arrhythmogenic drug

Answer 206

Both will show tall a and c wave. In constrictive pericardial disease, the y descent will be tall (increased resistance to passive atrial filling) In cardiac tamponade, the y descent will be almost absent (no flow to the atria as collapsed)

Answer 207

6-8 seconds

Answer 208

100-140 bpm

Answer 209

False: cats are rarely symptomatic because the vetricular rhythm is still quite high and III degree AV block is usually due to primary structural heart disease

Answer 210

1. atropine or glycopyrrolate if vagally mediated 2. isoproterenol (beta agonist) 3. terbutaline (beta 2 agonist) 4. aminophylline (PDEi) 5. pacemaker

Answer 211

False Aortic and pulmonary valves do not have chordae tendinae

Answer 212

End-diastolic ventricular pressure volume relationship It implies ventricular compliance

Answer 213

End-systolic ventricular pressure volume relationship It implies inotropic state of the heart

Answer 214

The acetylcholine released at the vagal nerve endings → Fiber membranes permeability to K+ ↑ ↑ ↑ → Rapid leakage of K+ out of the conductive fibers → Membrane potential more negative → Hyperpolarization

Answer 215

Periods of paroxysmal atrial tachycardia followed by a temporary failure of the sinus rhythm to resume when the tachycardia abruptly terminates → overdriven suppression

Answer 216

Mobitz type I: progressive prolongation of PR interval before a complete block Mobitz type II: unexpected irregular absence of QRS complex after P waves

Answer 217

Dog > 130 msec Cat > 90 msec

Answer 218

To evaluate if the arrhythmias if vagal-induced Atropine 0.04 mg/kg IV, the positive response = 50-100% increase in HR * Side effect: dry mouth, mydriasis, constipation, urinary retention

Answer 219

1) Sinus tachycardia 2) SVT (AV nodal re-entry, AV re-entry, atrial tachycardia) 3) Atrial fibrillation 4) Atrial flutter

Answer 220

1. ectopic foci - usually at the junction between pulmonary vein and atrial tissue 2. re-entry phenomenon - premature beat starts a local abnormal circuit (wavelet hypothesis)

Answer 221

Initial foci causes paroxysmal AF (starts and stop by itself) --> electrical remodeling --> persistent AF --> atrial fibrosis --> long-standing persistent AF

Answer 222

1. rate control 2. rhythm control No definitive evidence of superiority (AFFIRM study found no difference and RACE study found that rate control had less drug-related side effects) Rate control often more achievable (especially if underlying cardiac disease/remodelling). Goal **HR<160** Beta blockers or CCB.

Answer 223

Each 10bpm drop = 29% increase in survival

Answer 224

First choice: diltiazem + digoxin Sotalol not effective by itself but can be combined with diltiazem especially if concurrent ventricular arrhythmia. However, amiodarone might be preferrable as no negative inotropic effect.

Answer 225

Pharmacological cardioversion with amiodarone IV Synchronized electrical cardioversion with pre-emptive amiodaronization

Answer 226

- young age at diagnosis - syncopal episodes - increase LA size Ventricular arrhythmias were NOT linked with increased risk of SCD In humans but not in dogs the use of digoxin, anticoagulants, sotalol and amiodarone were linked with increased risk of SCD

Answer 227

Pulmonary disease

Answer 228

Diltiazem 0.125-0.35 mg/kg slow IV over 2-3 minutes

Answer 229

Reentry *Not automaticity

Answer 230

- Reentry - Enhanced automaticity - Triggered activities

Answer 231

VT > 30 sec

Answer 232

Atrioventricular dissociation Fusion beats Capture beats * Capture beats: A supraventricular impulse conducting through the normal conduction pathways to the ventricle during an episode of VT or AIVR. The PR interval can be longer than normal.

Answer 233

Dogs: - DCM - subaortic and pulmonary stenosis - arrhtyhmogenic right ventricular cardiomyopathy (Boxer and English Bulldogs) - inherited ventricular arrhythmia (GSD) Cats: - HCM - Takutsubo

Answer 234

Disease of the desmosome --> fibrosis --> arrhythmogenic foci --> malignant re-entrant ventricular arrhythmias

Answer 235

triggered activity of the **LV Purkinje fibers** very young age (12 w) if surviving >2y self resolving (also called Idiopathic Juvinile Ventricular Arrhythmia - also seen in Rhodesian ridgeback). Possibly due to **abnormal sympathetic system maturation**

Answer 236

It is used to evaluate the LV diastolic function

Answer 237

0.8 ≤ E/A ratio < 2

Answer 238

Impaired relaxation (grade 1 diastolic dysfunction)

Answer 239

Pseudonormal filling pattern (grade 2 diastolic dysfunction) Progressive diastolic dysfunction causes LA pressure to rise. The latter increases the pressure gradient between the left atrium and the left ventricle and will act as a driving force to fill the ventricle during early diastole.

Answer 240

Restrictive filling pattern (grade 3 diastolic dysfunction) A further increase in filling pressure will increase the gradient between the left atrium and the left ventricle during early diastole. The E-wave will become even taller and the A-wave shorter. The E/A ratio will be ≥ 2. In severe forms the A-wave may be so small as to be nearly invisible, and the E/A ratio may reach very high values of 5 or more.

Answer 241

Atria Vascular smooth muscles Skeletal muscles

Answer 242

Chronotropic: HR Dromotropic: AV conduction Inotropic: contractility Lusiotropic: myocardial relaxation

Answer 243

Pancreatic beta cells have L-type Ca channels

Answer 244

heart, kidney, adipose tissue

Answer 245

erythrocyte esterases

Answer 246

1) Inhibit 𝜷1 receptor at the juxtaglomerular cells → decrease renin release → decrease aldosterone formation 2) Inhibit 𝜷2 receptor on the cells membrane → inhibit Na/K-ATPase → decrease potassium uptake

Answer 247

False They are both high-protein bound and lipophilic (high Vd). TPE can be an option fo severe cases of CCBs (rebound from tissues can happen and a second cycle might be necessary)

Answer 248

Glucagon can bypass 𝜷 receptors and directly activate Gs protein → activates adenylate cyclase (AC) → converts ATP to cAMP → activates protein kinase A (PKA) → enhancing the release of Ca2+ from the sarcoplasmic reticulum * Glucagon has inotropic, chronotropic, and dromotropic properties

Answer 249

Ventricular side of the aortic valve Atrial side of the mitral valve

Answer 250

Subaortic stenosis Cardiac catheterization procedure

Answer 251

Mechanical damage/Inflammation → disruption of the endothelium → exposed extracellular matrix proteins, thromboplastin, tissue factor → activates coagulation cascade (fibrinogen, fibrin, platelet) → blood clot is formed and can bind bacteria → fibronectin binding triggers endothelial cell internalization and local pro- inflammatory and procoagulant responses → endothelial cell expression of integrins → bind bacterias and fibronectin to the extracellular matrix

Answer 252

Microbial surface components recognizing adhesive matrix molecules (MSCRAMMS)

Answer 253

Polyarthritis (75%) Glomerulonephritis (36%)

Answer 254

Aortic valve

Answer 255

1) Fibrinous vegetative lesion - Shields bacteria from the blood stream and host defenses - Provides a barrier for antibiotic penetration 2) Be resistant to platelet bactericidal protein 3) Internalize within the endothelial cells (e.g. S. aureus, Bartonella) 4) Colonize RBC without causing hemolysis (e.g. Bartonella)

Answer 256

1) Staphylococcal spp (aureus, intermedius, coagulase positive, and coagulase negative) 2) Streptococcus spp (canis, bovis, and ß-hemolytic) 3) E. coli

Answer 257

Bartonella vinsonii ssp. berkhoffii

Answer 258

Diastolic murmur

Answer 259

Aortic valve

Answer 260

6-8 weeks * IV for the first 1-2 weeks * Higher end of the dose range

Answer 261

Higher mortality: 1) Aortic involvement (92% mortality at 5 months and 33% in first week) 2) Glucocorticoid administration 3) Thromboembolic event 4) AKI 5) thrombocytopenia Survival: 1) administration of antithrombotic Reagan KL, et al. Outcome and prognostic factors in infective endocarditis in dogs: 113 cases (2005-2020). J Vet Intern Med. 2022;36(2):429-440.

Answer 262

> 0.625 ng/mL - it is specific but not sensitive Could be considered as an additional minor Duke criteria

Answer 263

Up to 80% on post-mortem can be sterile or septic and usually involve kidneys, spleen, myocardium, brain or limbs Risk factors: - mitral valve involvement - large vegetative lesion of >1-1.5cm - growing lesions despite antibiotic treatment

Answer 264

1) Three or four samples from different puncture sites should be clipped and aseptically prepared (e.g. cephalic vein, lateral saphenous vein, jugular vein) 2) The timing of sample collection should be **at trough if patient is already on antibiotics** 3)The person who performed venipuncture should wear sterile glove and the 5-10ml of blood should be collected from each site with 30 minutes to 1 hours apart. 4) The blood samples are aseptically put in the sealed vial for aerobic, anaerobic bacteria and Bartonella spp. (special medium BAPGM)

Answer 265

Major criteria 1) Positive echocardiogram - vegetative, oscillating lesion, erosive lesion, abscess 2) New valvular insufficiency 3) More than mild aortic insufficiency in the absence of subaortic stenosis 4) Positive blood culture ≤ 2 positive blood cultures ≥ 3 with common skin contaminant Minor criteria 1) Fever 2) Medium to large dog (> 15 kg) 3) Subaortic stenosis 4) Thromboembolic disease 5) Immune-mediated disease Polyarthritis Glomerulonephritis 6) Positive blood culture not meeting major criteria 7) Bartonella serology ≥1:1024

Answer 266

Definitive 1) Histopathology 2) Two major 3) One major + two minors Possible 1) One major + one minor 2) Three minors

Answer 267

Dog: +40 - +100 Cat: 0 - +160

Answer 268

Cardioversion: delivery the energy that is synchronized to the QRS complex Defibrillation: Asynchronously deliver the energy to terminate the life-threatening arrhythmias

Answer 269

The peak of R wave (absolute refractory period)

Answer 270

1-2 J/kg * much lower than emergency defibrillation in which 2-10J/Kg are delivered

Answer 271

Transvenous and transcutaneous are the most commonly used ones. Other ones: * Transesophageal * Transthoracic * Epicardial * Manual (thoracic thump)

Answer 272

This is a failure to capture pacemaker issue - pacemaker spike not followed by qrs. Adjust output (amplitude/time) to achieve threshold.

Answer 273

1) positive inotropic (by inhibiting Na-K ATPase → increased intracellular Na → increased intracellular Ca 2) Decreased AV conduction: vagomimic effect

Answer 274

Patients in AF with concurrent left ventricular dysfunction which makes them intolerant to beta-blockers and diltiazem Digoxin has significant inotropic effect which switches off RAAS (decreased after load)

Answer 275

- P-glycoprotein inhibitors: P-glycoprotein is an efflux pup that mediates secretion of digoxin in the kidneys, liver and gut. Amiodarone, quinidine, diltiazem, cyclosporine and itraconazole inhibit P-glycoprotein, therefore enhance digoxin toxicity risk and a dose reduction should be considered - hyperkalaemia reduces digoxin binding affinity with Na/K ATPase - hypermagnesemia and hypercalcaemia enhances calcium overload in the sarcoplasmic reticulum and increase the risk of spontaneous cardiac depolarization (VPCs)

Answer 276

digoxin binds at the K site of Na-K ATPase During hypokalemia, there are not that many potassiums competing with Dogoxin → increased toxicity

Answer 277

**cardiac**: early toxicity showing with VPCs, then any type of atrioventricular block, then supraventricular tachycardia and ventricular fibrillation **GI**: mesenteric ischemia due to excessive smooth muscle contraction

Answer 278

High serum digoxin levels have been associated with increased mortality even without overt signs of toxicity

Answer 279

- activated charcoals to reduce further GI absorption - atropine administration to reduce PNS-induced bradycardia - correct electrolyte abnormalities - digoxin-fab antibodies (ovine so possible anaphylaxis - use only in severe cases)

Answer 280

Cardiac troponin T: bind to tropomyosin and secure it to the thin filament Cardiac troponin I: inhibitory the hydrolysis of ATP → inhibit myosin and actin interaction Cardiac troponin C: binding site for calcium to remove the blockage of filament interaction

Answer 281

cTnT is tightly bound to actin, so its level should not be detectable in health vs cTnI < 0.05 ng/mL

Answer 282

Troponin C, because the skeletal and myocardium have very similar isoforms

Answer 283

Intracellular protein

Answer 284

2-3 hours after injury peak at 18-24 hours

Answer 285

Structural pool

Answer 286

Troponin I

Answer 287

Dying cells - Necrosis - Apoptosis - Cell turnover Viable cells - Increased permeability - Formation of vesicles - Increased proteolysis

Answer 288

Boxers Greyhounds

Answer 289

Reticulo-endothelial system Renal clearance It is advised to interpret increases in troponin very carefully in patients with renal impairment

Answer 290

True Non-cardiac myocardial injury > primary cardiac diseases

Answer 291

Yes for dogs and humans but not cats. In dogs critically ill patients have 4x the odds for poorer outcomes and longer hospitalisation stay if increased troponin. cTnI also increased APPLE score specificity without compromising sensitivity.

Answer 292

GDV, parvovirosis, sepsis and Babesiosis

Answer 293

1) acidic environment 2) increased extracellular K+ concentration 3) partial depolarized cells

Answer 294

renal excretion

Answer 295

IA (moderate): cause QT prolongation - Because it cause moderate blockade of the rapid component of the delayed rectifier K+ current IB (weak): cause QT shortening IC (strong): no effect on QT interval

Answer 296

𝜷-receptors are Gs-coupled protein receptors. Inhibition = drop CAMP = reduced activity of HCN (CAMP dependent) of funny current) and closing of L-type Ca channels --> Inhibit funny current --> drop HR

Answer 297

𝜷1, excreted by kidney

Answer 298

It is K channel blocker and also non-selective 𝜷 blocker

Answer 299

Sodium channel blocker, Slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, reduces conduction velocity.

Answer 300

Because sotalol is also a K channel blocker → AP prolongation allows more Ca to enter the cell

Answer 301

Class II (beta blockers) and IV (Ca channel blockers) --> work on AV node cells

Answer 302

1. **Phosphodiesterase III inhibitor** --> increased intracellular CAMP --> increased PKA activity --> increased phosphorylation of **phospholamban** --> inhibition of SERCA --> more Ca available (increased **lusitropy**) Also increased CAMP opensa **Ryanodine**-bound Ca channel and **L-type Ca channel** (increased **inotropy**) 2. Calcium sensitizing effect (increased **cTNc** affinity for Ca) 3. active metabolite inhibits **A1 adenosine receptor** (Gi coupled receptor) --> increased contractility 4. arterio-venous dilatory effect due to **phosphorilation (inactivation) MLCK**

Answer 303

In acidosis status troponin affinity for Ca++ is severely decreased. This is why pimobendan is a very good drug choice.

Answer 304

- no increase in oxygen demand - no increase in PAP - still effective in respiratory acidosis

Answer 305

- anti-inflammatory (inhibition of ngkB and less iNOs) - blunts sympathetic response - antithrombotic effect with decrease TXA release by platelets - insulinotropic effect via calcium sensitization

Answer 306

Yes mainly hepatic metabolism with <5% being excreted via renal route

Answer 307

stage B2 at day 35 decreased LVESd and LA/Ao also increased time to CHF development and cardiac-related death

Answer 308

1) Shunting defect 2) Perivalvular defect

Answer 309

Communication between Aorta and Pulmonary artery

Answer 310

Tetralogy of Fallot

Answer 311

Ventricular septal defect (VSD) Overriding aorta Pulmonary stenosis Right ventricular hypertrophy N.B. RV hypertrophy is secondary to "Eisenmenger physiology". Initially L to R shunt due to interventricular septal defect, but due to pulmonary stenosis and high pressure on R side the shunt reverts to R to L

Answer 312

True: tetralogy with R--> L shunt due to interventricular septal defect causes cianosis in the whole body vs PDA associated with pulmonary hypertension R--> L shunt distal to the origin of the left subclavian artery (after the major branches to the head and upper extremities have been given off) --> cianosis only in the caudal half of the body

Answer 313

Volume of the blood remove = body weight x blood volume x (Current PCV-Desired PCV)/Current PCV *Blood volume: 90 ml/kg (dog); 70 ml/kg (cat) Cut-off: 70% Target: 60%

Answer 314

1) Hypokalemia 2) Hypomagnesemia 3) Hypercalcemia 4) Hypothyroidism

Answer 315

25% prolongation of QRS complex

Answer 316

True * Hyperkalemia strongly enhances procainamide-induced conduction slowing by increasing the interaction between the drug and sodium channels during the rested phase of the cardiac cycle

Answer 317

FS (%) = (LV internal diameter at end-diastole - LV internal diameter at end-systole)/LV internal diameter at end-diastole Normal - Dog: 25-45% - Cat: 31-75%

Answer 318

Class III but mechanisms encompassing all classes of anti-arrhythmic

Answer 319

1) Hepatic toxicity 2) Thyroid dysfunction 3) Arrhythmias

Answer 320

Ulcerative facial dermatitis

Answer 321

True A rectal temperature of< 37.1C (98.9°F)has been shown to predict a < 50% survival probability (in ER textbook)

Answer 322

Right caudal lobe artery

Answer 323

Day 1: - Start on prednisone 0.5 mg/kg BID x 1 week, then 0.5 mg/kg SID x 1 week, then 0.5 mg/kg EOD x 2 weeks (if symptomatic) - Start Doxycycline 10 mg/kg BID x 4 weeks - Start macrocyclic lactone (i.e. ivermectin, milbemycin, moxidectin, and selamectin) to kill immature forms of heartworm Day 30: - Re-apply macrocyclic lactone (i.e. ivermectin, milbemycin, moxidectin, and selamectin) to kill immature forms of heartworm Day 31-60: - A one-month wait period following doxycycline before administering melarsomine is currently recommended as it is hypothesized to allow time for the Wolbachia surface proteins and other metabolites to dissipate before killing the adult worms. Day 61: - Apply macrocyclic lactone (i.e. ivermectin, milbemycin, moxidectin, and selamectin) to kill immature forms of heartworm - Melarsomine 2.5 mg/kg IM - Start on prednisone 0.5 mg/kg BID x 1 week, then 0.5 mg/kg SID x 1 week, then 0.5 mg/kg EOD x 2 weeks - STRICT cage rest Day 90: - Apply macrocyclic lactone (i.e. ivermectin, milbemycin, moxidectin, and selamectin) to kill immature forms of heartworm - Melarsomine 2.5 mg/kg IM - Start on prednisone 0.5 mg/kg BID x 1 week, then 0.5 mg/kg SID x 1 week, then 0.5 mg/kg EOD x 2 weeks - STRICT cage rest Day 91: - Melarsomine 2.5 mg/kg IM - Strict cage rest for 6-8 weeks Day 120: - Test for microfilaria Day 360: - Antigen test 9 months after last melarsomine injection - screen for MF - If still Ag positive, re-treat with doxycycline followed by two doses of melarsomine 24 hours apart This protocol has shown 100% negativization within 1y of diagnosis (vs only 2 doses of melarsomine or long term moxidectin without melarsomine)

Answer 324

Heartworm Associated Respiratory Disease - typical of cats - severe inflammatory response in the lungs mimicking asthma

Answer 325

To treat Wolbachia which is a symbiotic gram negative bacteria harboured by D. Immitis. It can significanlty worsen the inflammatory response triggered by D. Immitis.

Answer 326

Paradoxical rise in right atrial pressure (or right jugular venous pressure) during inspiration → decreased RV compliance for various reasons

Answer 327

Non-selective 𝜷 adrenergic agonist

Answer 328

Three letter system: V (chamber paced) V (chamber sensed) I (abiltiy to inhibit activity when intrinsic heart beat sensed) Permanent pacers also have a fourth letter indicating if the generator can change rate of firing according to patient's activity level

Answer 329

Atrial fibrillation: irregular atrial contraction Atrial flutter: regular but very rapid atrial contraction (atrial rate of 300 bpm with 'saw tooth' appearance and a atrial:qrs ratio of 2:1)

Answer 330

Fatty acid

Answer 331

Overdamping

Answer 332

D1 (post-synaptic): vasodilation D2 (pre-synaptic): inhibit NE release from sympathetic nerve ending → less vasoconstriction

Answer 333

G protein-coupled receptor

Answer 334

increase the release of NE from sympathetic nerve ending

Answer 335

Vascular resistance

Answer 336

1) Decreased blood viscosity → increased flow velocity —> increased shear stress → increased NO production → vasodilation 2) less Hb —> less NO scavenging

Answer 337

Both Preload: decreased sodium and water retension Afterload: vasodilaiton

Answer 338

Inhibit aldosterone

Answer 339

Competitive post-synaptic 𝜶1 receptor antagonist

Answer 340

True Aldosterone is considered proinflammatory and profibrotic and causes endothelial dysfunction secondary to vasoconstriction and vascular remodeling.

Answer 341

1) Increase aldosterone 2) Increase ADH 3) Cause vasoconstriction 4) Increase thirst drive within hypothalamus 5) Increase Na-H exchange at the proximal renal tubules

Answer 342

AT1 - mediates vasoconstriction AT2 - mediates vasodilation, antifibrotic, antiproliferative and natriuretic effects (counterbalance)

Answer 343

1. ACEi 2. ARBs 3. Aldosterone antagonist

Answer 344

Benazepril + spironolactone >>> benazepril alone

Answer 345

Cyanide toxicity Sodium nitroprusside oxidizes sulfhydryl groups present in erythrocytes and cell membranes or reacts with hemoglobin to produce methemoglobin. This reaction results in the production of nitric oxide (as well as five cyanide groups), which leads to direct vasodilation through the action on vascular smooth muscle. Free cyanide is converted to thiocyanate by either thiocyanate oxidase within erythrocytes or a transsulfuration reaction with thiosulfate by the rhodanese enzyme in the liver.

Answer 346

ESPVR (End-systolic pressure volume relationship) - ventricular compliance EDPVR (End-diastolic pressure volume relationship) - contractility

Answer 347

A1 - myocardial nodal tissue - Gi coupled (decreased HR) A2 - smooth muscle - Gs coupled (vasodilation) A3 - mast cell - inflammatory cytokines (important in lungs as they cause vasoconstriction and asthma)

Answer 348

1 second In a standard 25 mm/sec recording count QRS in 30 boxes = 6 seconds and multiply by 10 to obtain HR

Answer 349

Adrenal medulla and sympathetic nerve terminals From L-tyrosine --> L-dopa --> dopamine --> norepinephrine --> epinephrine

Answer 350

Thyrosine hydroxylase

Answer 351

Junctional (or post-synaptic) Pre-synaptic Extrajunctional (binds to circulating norepi synthesised by adrernal medulla)

Answer 352

Catecol-o-metyltransferase

Answer 353

negative feedback --> free norepi will bind to them and they will inhibit further norepi release

Answer 354

alpha 1 (a, b, d) alpha 2 (a/d, b, c) beta 1 beta 2 beta 3

Answer 355

alpha 1 Gq alpha 2 Gi beta Gs

Answer 356

junctional mainly mediate vasoconstrction with exception of alpha 1a which has inotropic effect on heart (NE>E) alpha 1a and 1d vasoconstriction large arteries alpha 1b vasoconstriction of smaller arteries and vascular hypertrophy (big role in development of systemic hypertension)

Answer 357

mainly extrajunctional mediate vasoconstriction (E>NE) exception for alpha 2 a/d vasodilation (located on epithelium and pre-synaptic membrane)

Answer 358

when norepi binds, Ca channel close, while K channel open --> hyperpolarization --> no more norepi release

Answer 359

located on endothelial cell and increase relase NO

Answer 360

alpha 1a vasoconstriction --> increase tone to counteract collapsibility due to increased HR and contractility beta 2 --> vasodilation Anyway overall the coronary perfusion is mainly under metabolic control not SNS

Answer 361

False beta 2 E>>>NE (this is why it is such a good bronchodilator) beta 1 E= NE

Answer 362

As a safety measure agains sympathetic overstimulation beta1 and beta 2 receptors are internalised after stimulation, however if excessive stimulation beta 3 are Gi and will inhibit further increase in chronotropy and inotropy

Answer 363

Both are Gs coupled --> PKA will phosphorylate beta-ARK protein which will uncople beta receptors and stimulate endocytosis. once recptor is in the vesicle it can either be recycled or degraded. Some internalised receptor bind to arrestin and start pathway that facilitate cardiac hypertrophy.

Answer 364

- increase BG (beta 3 on adipose tissue increase lipolysis, beta 2 on hepatocytes increase gluconeogenesis and glycogenolysis, alpha 2 in pancreas decrease insulin and increase glucagon secretion) - increase lactate - increase oxygen consumption decrease potassium increase plt activity (alpha 2 receptors with release of ADP, serotonin and TXA) - increased mitochondrial uncoupling and oxidative stress - immunoparalysis

Answer 365

act on noradrenergic neurons in the hypothalamus responsible for thermoregulation

Answer 366

PDI3 inhibitor used for vasodilation and decrease afterload in cardiac failure patients Renal elimination so very careful in CKD

Answer 367

dobutamine and vasopressin high risk of severe tissue necrosis all other vasopressor safe (if extravasation use phentolamine to reverse)

Answer 368

Sinus bradycardia, hypotension and vasodilation triggered by stimulation of baroreceptors and chemoreptors in the LV due to excitement, coughing, vomiting, serotonin, etc. Also known as vaso-vagal response.

Answer 369

1. sinus arrest 2. sinus block 3. sick sinus syndrome

Answer 370

Sinus arrest is the failure of generating impulse and involve P cells of the SA node vs sinus block is the failure of propagating the impulse and it is a dysfunction of T cells

Answer 371

Old Schnauzers and Terriers

Answer 372

LV wall stress = (LV pressure x LV radius) / LV thickness In order to reduce LV wall stress LV radius needs to be reduced or LV thickness needs to increase

Answer 373

Prazosin in selective alpha 1 antagonist while phenoxybenzamine is not and that's why phenoxybenzamine is preferred as a treatment for pheochromocytoma

Answer 374

It is both alpha and beta blocker, therefore there is vasodilation without compensatory tachycardia

Answer 375

non-selective PDEi

Answer 376

quaternary protein(each type has a signature AA sequence) with a central pore in the intracellular side and selectivity filter on the extracellular side

Answer 377

1. KATP (vasodilatory shock) 2. KCa (NO action) 3. Kv (voltage gated) 4. Kir (inward rectifying) 5. K2p (tandem pore domain - always open - 'leaky channels' - stabilise resting membrane potential)

Answer 378

open Katp channels --> allow K exit --> more negative intracellular environment --> ca channel close -- > no relase of insulin Used as part of insulinoma treatment

Answer 379

N-pro-BNP is produced in a 1:1 ratio with BNP and it is much more stable, so suitable for sampling and measurement ANP is only produced by atria vs BNP also by ventricle - they are both produced secondary to stretch stimulation

Answer 380

Dogs with MMVD and a N-pro-BNP >1500 pmol/L more likely to develop overt CHF in the following 3-6 months Dobermans >5y and N-pro-BNP >450 pmol/L high risk to develop DCM (even when still in occult phase)

Answer 381

- Infectious: viral (parvo, FIV, distemper), protozoal (Chagas disease by Tripanozoma cruzi), bacterial (Lyme disease, Bartonella, septicaemia), fungal and parasitic (Toxo and Neospora) - Toxic (doxorubicin with >250mg/m2 - irreversible damage) - Traumatic - Other (radiation, heat stroke, catecholamine toxicity)

Answer 382

Irreversible myocyte damage due to increased expression of autophagy receptors on myocytes membranes. Seen most often with doses of >250mg/m2

Answer 383

Jet lesion due to MMVD regurgitation (velocities up to 5m/s hitting the atrial tissue >100 times a minute)

Answer 384

Often clot seen in pericardial sac but also: - LA/Ao >1.6 - Mitral regurgitation jet occupying >50% LA - PE - cardiac tamponade

Answer 385

They are both non-selective alpha antagonists, but phenoxybenzamine binds to receptor irreversibly (changes shape) so it provides reliable long-term blockade vs phentolamine more rapid onset of action (more severe reflex tachycardia) and shorter duration as it a competititive reversible antagonist.

Answer 386

'A disorder affecting the heart or the kidney whereby acute or chronic disturbances of one organ cause detrimental effects on the other'

Answer 387

consensus in calling it cardiovascular-renal disorders (CVRDs) to highlight the role of vasculature in the pathogenesis of this complex disorder

Answer 388

CVRDh (primary heart) CVRDk (primary kidney) CVRDo (secondary to systemic disease i.e. sepsis or concurrent primary heart and primary renal conditions) these can be further differentiated into stable or unstable

Answer 389

- perform early investigations of the heart in patients with renal impairment and investigate kidney disease in instances of heart dysfunction - patients with heart disease should be treated with the lowest effective dose of diuretic to preserve renal health - prompt identification and treatment of SHT in renal patient - titrate drug dosage according to current ability of renal clearance (especially those with narrow therapeutic margin i.e. digoxin) - ensure adequate nutrition to avoid cardiac and renal cachexia

Answer 390

Successful resuscitation of both micro and macrocirculation

Answer 391

1. unstable macrocirculation but stable microcirculation --> continue fluid resuscitation and if not successful consider vasopressor 2. stable macrocirculation but unstable microcirculation --> more IVFT is not going to help and llikely detrimental Typical of sepsis/sirs

Answer 392

Severe inflammation leads to: - loss of glycocalix and endothelial integrity - induced rigidity of RBC and inability to release vasoactive ADP - increased iNOS. Consequences: - decreased O2 delivery to tissues due to tissue oedema and decreased microcirculatory flow - heterogeneous perfusion

Answer 393

- NIRS (near-infrared light to penetrate tissues and measures the absorption and scattering of these wavelengths by hemoglobin, myoglobin, and cytochromes, providing information on tissue oxygenation) - microcirculation visualisation with dark-field microscopy - thermography - cutaneous laser doppler - regional capnography - transcutaneous O2 and CO2 monitoring

Answer 394

Venous cannulation used to drain patient's blood into a reservoir --> heat and gas exchanger --> blood pumped back to patient via arterial cannulation Therapeutic hypothermia applied to decrease metabolic rate of tissues

Answer 395

It is a cold, pressure-controlled, hyperkalemic solution injection into the aortic root or coronary sinus which induces diastolic arrest

Answer 396

- often patients have negative IVF balance - manage hemostatic derangements - manage common lytes imbalances (hypokalemia, hypocalcemi, hypomagnesemia and hypernatremia) - avoid hyperglycaemia (insulin administration when BG >10mmol/L) - analgesia - 24h of antibiosis - continue heparin for 10 days post op and antiplatelet for 90 days - cardiac medications usually discontinued as issue surgically resolved but pimobendan could still be beneficial in supporting myocardiac recovery and reverse myocardia remodelling

Answer 397

- Thromboembolic events - Coronary spasm - Hypotension - Surgical site failure - Haemorrhage - ARDS - AKI - Arrhythmias - Immunocompromise

Answer 398

In the pH Stat approach, the high pH due to hypothermia (decreased metabolic rate and slower CO2 dissociation into H+ and HCO3-) is corrected by adding CO2 --> this leads to improved cerebral perfusion but higher risk of embolism. In Alpha Stat approach the pH is not corrected, this might lead to brain vasoconstriction but less risk of embolism. No difference in outcomes when body temp >28C. For temp <28 pH stat best during cooling while alpha stat best during rewarming.

Answer 399

These are two hemostatic techniques. Rummel tourniquet uses umbilical tape placed underneath a vessel while the two upper ends get through a piece of tubing. Pull the ends protruding from tubing and clamp them to occlude the vessel. Pringle manouver puts pressure on both hepatic artery and portal vein via the epiploic foramen

Answer 400

Higher risk of arrhythmias

Answer 401

State of **end-organ hypoperfusion** due to the heart's inability to deliver sufficient oxygen to tissues to meet metabolic demands in the presence of **adequate intravascular volume**.

Answer 402

1. Bioimpedance measures resistance to electric current to the thorax which is proportional to aortic flow 2. Bioreactance measure the phase shift (change in frequency of current applied to thorax) --> delay in phase shift = increase in CO Bioimpedance not reliable in dogs vs bioreactance accurate but no clinical applications in dogs so far

Answer 403

Yes, it Y descend on the CVP waveform is very prominent. In human a Y descend >4mm has been correlated to patients operating on the flat portion of the FS curve

Answer 404

A fluid-responsive patient should have a decrease in CVP during inspiration, if that doesn't occur it is an indication of possible fluid overload and it is called Kussmaul sign

Answer 405

Up to 40% Associated with poorer prognosis in the first 6months post diagnosis