Cardiology Flashcards

Question

Pathophysiology of endocarditis

Answer 1

- Inciting event: bacteria adhere to disrupted endothelial surface of valve -Mechanical Lesion exposes EC matrix proteins --> bacteria seed --> coagulation triggered --> coagulum fibrin, fibrinogen, & fibronectin bind bacteria --> bacteria produce enzymes that build proliferative tissue ** Bacteria usually have MSCRAMMS

Answer 2

- Know quantity & temp of either saline or 5% dextrose sol is injected rapidly at proximal port --> cool solution mixed with blood and cools it --> temp difference sensed by thermistor at distal site - Change temp plotted on time -temp curve - Area under the curve inversely proportional to CO ** Normal CO 125-200 ml/kg/min (canine) or 120 ml/kg/min (feline)

Answer 3

- Increase with increased atrial pressure, increased venous pressure and increased pulmonary hydrostatic pressure - causes fluids to shift from vascular space to interstitial space

Answer 4

- Not uncommon in large breeds of dog with no primary heart disease - Sustained tachycardia can cause tachycardia induced DCM TX: diltiazem

Answer 5

- Stronger during expiration and weak/absent during inspiration -pericardial effusion

Answer 6

- only heard if there is disease - due to pulmomary hypertension - DDX: HW disease, obstructive pulm disease, congenital cardiac disease, or high altitude

Answer 7

Prolonged P-R interval, but all impulses conducted (PR>130 msec in dog, >90 msec in cat)

Answer 8

- Alternating weak and normal pulses with regular rhythm - MC due to decreased contractility, CHF & tachyarrhythmias

Answer 9

- Pore size of capillary - molecular size of diffusing substance - Concentration differences between 2 sides of membrane

Answer 10

- Kidney Disease - Diabetes mellitis - Cushings - Hyperthyroid - Pheochromocytoma - Hyperaldosteronism - Hepatic Dz - polycythemia - chronic anemia - CHF - Neoplasia - Iatrogenic

Answer 11

~19 mmHg of colloid osmotic pressure is due to dissolved protein An additional 9 mmHg is due to + charged cations ( mainly Na2+)

Answer 12

- Increased CVP (decreased venous compliance--> increased thoracic blood volume) - Increased ventricular compliance (increased expansion of chamber) - Increased atrial force of contraction - decreased HR (increased filling tone) - increased aortic pressure (increased afterload)--> decreased stroke volume (secondary increase in preload) - Pathologic conditions: systolic failure, aortic insufficiency, subaortic stenosis

Answer 13

Degree of tension on muscle when it begins to contract - End diastolic pressure (filled ventricle)

Answer 14

Load at which cardiac muscle exert its force - Pressure in aorta the ventricle pushes against

Answer 15

- Intrinsic force of heart - Degree to which sarcomeres can shorten when activated independent of preload & afterload

Answer 16

Conduction through AV node

Answer 17

Automatic nervous system - PSNS: increased K+ permeability --> hyperpolarize (decreased contractility, dromo, ino and chrono) R vagus--> SA node L Vagus - AV node minimal innervation of ventricular tissue - SNS: beta agonist--> increased Ca2+ entry (inc ino & chrono) Thoracolumbar N Dense innervation ventricular tissue

Answer 18

- Catecholamines: NE/E - Angiotensin II - Endothelin - ADH/vasopressin -Ions (Ca2+)

Answer 19

Inadequate tissue O2 secondary to cardiac dysfunction 1. Systolic dysfunction: failure of contractility, mechanical failure 2. Diastolic dysfunction: decreased RV filling 3. Bradycardia: decreased CO

Answer 20

- Diastolic Dysfunction - Systolic Anterior motion of mitral valve - Femoral arterial thromboemboli ** L auricle MC spot for clot formation

Answer 21

A. at risk breeds: dobies Cavies B. Asymptomatic disease B1: murmur with with no cardiac remodeling B2: murmur with remodeling (LA enlargement) C. Historical/current evidence of cardiac failure D. Severe/ detrimental cardiac failure

Answer 22

Global Hypoperfusion - Cold extremities - Poor pulses - Dull Mentation - Prolonged CRT - Decreased Temp - Tachycardia Metabolic Acidosis Lactic Acidosis

Answer 23

1. Poor Contractility - Primary cardiac Dz (DCM)--> decreased contractility - Extracardiac changes - Sepsis - Drug Induced: doxorubricin - Drugs: CCB, digoxin, beta blockers - Nutrition: taurine, carnitine, Vit E 2. Obstruction to Flow - SAS -HOCM

Answer 24

- INadequate filling: abnormal preload or relaxation Ex: preicardial effusion or foibrosis HCM Tachyarrhythmias

Answer 25

P wave for each QRS Sustained tachycardia can induce DCM **Diltiazem IV >>esmolol in dogs If refractory to diltiazem, second drug such as esmolol, procainamide, or lidocaine

Answer 26

- Ventricular rhythm typically occurs during expiratory phase of resp sinus arrhythmia when sinus rate slows - Sinus rate & ventricular rate similar - Intervene if additional rapid ventricular rhythm occurs

Answer 27

- Common in a sudden rise of arterial BP - Characterized by edema of white matter - CS: altered mentation, disorientation, lethargy, seizures, balance disturbances, head tilt, nystagmus, behavior changes

Answer 28

VPC every 3rd complex

Answer 29

Occasional

Answer 30

Above AV node QRS normal shape

Answer 31

No association with P wave rate (100-120 bpm) & normal regular ventricular escape rate (40-60 bpm) **No meds work for this

Answer 32

irregularly irregular increased HR *Treatment = rate control + management underlying heart dz - Diltiazem IV or orally - If CHF or DCM → digoxin with diltiazem has more effective rate control - If severe concurrent vent arrhythmias → sotalol or amiodarone could be used - IV magnesium had synergistic effect when combined with other drugs that block the AV node resulting in improved rate control - Target ventricular response rate for in hospital Afib management: 160-180 bpm

Answer 33

Period sinus arrest - some patients have episode of paroxysmal tachcyardia following bradycardic episode.

Answer 34

80% from albumin 20% from globulin Tiny amount from fibrinogen

Answer 35

1. Collagen fiber bundles--> gives tensile strength to tissue 2. Proteoglycan filaments --> composed mainly of hyaluronic acid (fine reticular filaments)

Answer 36

Any blood volume that can be added to the venous system that does not contribute to pressure or stress being applied to vessel wall above transmural pressure of zero **minimal blood volume to prevent collapse

Answer 37

- Fluids administer as vehicles for other meds (amount 'creeps' up on you)

Answer 38

Within physical limits, heart pumps all blood that returns to it by the way of the veins

Answer 39

Diastolic P immediately before contraction occurs

Answer 40

- Fraction of end diastolic volume that is ejected during systole - Normal is 60% or 0.6?

Answer 41

1. Subxiphoid or diaphragmatic hepatic 2. L flank or splenorenal 3. Midline bladder or cystocolic 4. R flank or hepatorenal

Answer 42

1. Chest tube site: 1 on each side of chest btw intercostal spaces 7-9 (dorsal) 2. Pericardial Chest site: 1 on each side of chest btw intercostal spaces 5-6 over heart (ventral) 3. Subxiphoid AFAST site

Answer 43

- Applies to major arteries of aorta - Blood flow through each organ is a fraction of total blood flow, therefore no loss in pressure in major arteries & mean pressure of each artery will be approximately the same

Answer 44

- Average transmural pressure of circulatory system when blood flow has stopped -Determined by blood volume and autonomic control of vascular smooth muscle

Answer 45

Membrane potential has become more negative and occurs when net movement of positive charge out of cell

Answer 46

Membrane potential becomes less negative ie net movement of + charge into cell

Answer 47

- Decrease ABP to 110-150 mmHg - Severely hypertensive patients (SBP >250) may exhibit signs of hypotension (syncope, weakness, exercise intolerance, prerenal azotemia) - Reassess 3-5 days

Answer 48

Vasoconstriction

Answer 49

Vasoconstriction

Answer 50

Vasoconstriction

Answer 51

- Laminar: ideal- highest velocity in center and next to wall velocity = 0 -Turbulent: disruption interrupts flow and streams mix readily --> anemia, thrombi Reynolds #: dimensionless number to decide if laminar or turbulent ( laminar if <2000; likely turbulent >2000; definitely turbulent >3000)

Answer 52

Cerebral 15% CO Coronary 5% CO Renal 25% CO GI 25% CO Skeletal 25% CO Skin 5% CO ** Not fixed

Answer 53

Systolic murmurs Cardiac gallops LV Hypertrophy

Answer 54

To and fro motion of visceral & parietal pleura as glide over one another with inspiration and expiration

Answer 55

Horizontal lines of decreased echogenicity visible in the far field similar to & equidistant to pleural line *Artifact!

Answer 56

-"Ring Downs" & "Comet tails" - Hyper echoic vertical line extending from pleural line to edge of far field - Occasional B lines = normal - >3 = interstitial -alveolar abnormalities

Answer 57

Movement of lung into and out of view

Answer 58

In pneumo cases, point at which glide sign returns as move in dorsal to ventral position

Answer 59

- Prefibrillatory rhythm - Sustained vtach -"twisting of peaks" around isoelectric line TX: lidocaine

Answer 60

released with blood vessel damage --> local vasoconstriction

Answer 61

vasodilator

Answer 62

vasodilator

Answer 63

Atrial pressure wave Caused by infilling of atria from venous return

Answer 64

Atrial pressure wave - During ventricular contraction because of back flow of blood and bulge of AV valves toward atria

Answer 65

Atrial pressure wave - bump during atrial contraction

Answer 66

- Prostatitis - UTI - Pneumonia - Diskospondylitis - Dental Disease

Answer 67

- middle age, large breed, male - Lab, golden, GSD, Boxer all over represented - MC CS: murmur, fever, lameness - Arrhythmia: SVT, AV block, Afib, Vent

Answer 68

microbial surface components recognizing adhesive matrix molecules - MC Staphylococcus and strep

Answer 69

- diastolic flattening - Abnormal septal motion - thick pericardium

Answer 70

intrapericardial pressure> RA pressure * Collapsed RA

Answer 71

Shock delivered to critical mass of myocardium resulting in coordinated depolarization and refractory period * Success depends on: - Energy delivered - pathway - transthoracic impedance - 4% energy reaches myocardium - vector

Answer 72

- Wide bizarre QRS - No P waves ( AV dissociation) - Fusion beats present - Capture beats present ** MC assd with hypokalemia

Answer 73

1. Enhanced automaticity --> spontaneous depolarization 2. Triggered activity --> small depolarization 3. Re-entry --> circling non conductive tissue

Answer 74

- CPA with asystole - HIgh degree AV block - Symptomatic sick sinus syndrome - Decreased HR with evidence poor CO/hypotension--> unresponsive to cholinergic/sympathomimetics - Drug toxicity: CCB, Beta blockers, digoxin 1. Acute onset AV block causing frequent syncope 2. severe bradyarrhythmia assd with hemodynamic instability during anesthesia

Answer 75

-"hypertensive retinopathy" - retinal vessel totuosity -edema -retinal degeneration - hyphema ** Increased risk >180 mmHg --> seen at pressures as low as 168

Answer 76

1. HCM: LV wall thickening (diffuse or segmental) 2. DCM: LV systolic dysfunction with normal or reduced LV thickness --> eventual LV and LA dilation 3. Restrictive: either endopmycardial (LV septum) or myocardial (LA or biatrial) scar tissue infiltrate 4. Arrhythmogenic RV: severe dilation r heart with RV systolic dysfunction andmyocardial thinning 5. Unclassified: any that doesnt fit above 4

Answer 77

1. frequent paroxysmal or sustained V tach (HR>180 bpm) 2. Evidence of complexity ( R on T phenomenon, triplets, couplets, bigeminy, trigeminy) 3. Clinical signs of hemodynamic instability from arrhythmias 4. Polymorphic ventricular premature complexes are often more concerning than monomorphic because they indicate multiple regions of disease within the ventricular myocardium

Answer 78

1. Direct impact to chest in end diastole during which ventricles are at max capacity OR as end systole when atria are at max capacity 2. Suddenly increased cardiac preload secondary to increased venous return due to impact applied to peripheral or abdominal veins 3. Bidirectional forces that compress the heart within thoracic cage 4. Forces of acceleration and deceleration that cause heart to move leading to myocardial samage/rupture and/or damage to great vessels or coronary arteries 5. Blast force leading to cardiac contusion or rupture 6. Concussive forces leading to development of arrhythmias 7. Cardiac penetration by displaced fractures

Answer 79

Migrating FB FIP Lepto, distemper Chronic uremia Idiopathic Bacterial Fungal - coccidio, asper, dissiminated tuberculosis

Answer 80

Assessed by applying firm pressure to the cranial abdomen while the animal stands quietly with head in a normal position. This pressure transiently increases venous return. Normally there is little to no change in jugular vein appearance. Jugular distention that persists while abdominal pressure is applied constitutes a positive (abnormal) test result (+result may indicate pericardial effusion)

Answer 81

Equiptment: Sterile extension tubing, 3 way stop cock, 3 ml syringe, small gauge need for local block, lidocaine, +/-scalpel), sterile gloves, surgical scrub, EDTA and red top tubes ECG monitoring Peripheral IVC with IVF before and during (while prepping, dont delay) R pericardial window clipped (3rd -7th intercostal space) and cleaned Patient in left lateral recumbency 0.5-1 ml 2% lidocaine instilled into puncture site Large OTN angiocath (14G) Advanced into the pericardial space toward the patients left shoulder and stylet removed Extension tube attached

Answer 82

attributed to Bezold-jarish reflex: bradycardia, vasodilation and hypotension secondary to stimulation of intraventricular receptors (type C fibers) during tachycardia and hypercontractile ventricle ECG tracing shows breif sinus tach before sudden drop in HE and long period of no or few beats On occasion when rhythm returns may see paroxysmal atrial fib **Benign form of syncope** * common triggers intense activity/excitement, cough, vomiting

Answer 83

- Sinus tachycardia: originates in SA node as appropriate response to increased need of CO or increased sympathetic tone - Xtreme sinus tach can be seen with sympathomimetic toxicity such as chocolate or albuterol toxicity OR hyperT4 or pheochromocytoma - Intermittent SVT more likely to abruptly start and stop unlike Sinus tach - If intermittent, asses PR interval→ short with widening of initial QRS upstroke→ supports SVT - P wave morphology is abnormal with SVT, normal with ST - HR>220 bpm suggests SVT - Responsive to vagal maneuver → suggests SVT - If responds to fluid bolus → ST - If suspect SVT and responds to diltiazem or esmolol→ SVT

Answer 84

- Most importantly QRS duration - clearly discernible normal P wave independent of regular QRS is strongly suggestive of Vtach. - ID P waves with a consistent relationship with QRS → SVT with aberration - P’ waves can sometimes be seen in the ST or TP segments of ECG with some SVTs. These waves represent atrial depolarization initiated OUTSIDE the SA node. P’ waves look differents than normal P waves and have consistent relationship with QRS complex - Fusion beats (Sinus beat with undetermined QRS) suggestive of Vtach - Mean QRS axis is usually normal in SVT and abnormal in Vtach **EXCEPTION: ARVC boxers→ normal qrs axis with wide/bizarre QRS SVT HR often >240 bpm - Vtach → T wave often in opposite direction of QRS in Vtach. May be eitherway in SVT with more distinct junction btw QRS and ST segment If tachyarrhythmia terminates in response to vagal maneuver = SVT. If not it may be either SVT or ventricular - If tachycardia terminates with administration of lidocaine IV → likely ventricular HOWEVER an atrial tachycardia will rarely convert with lidocaine and some accessory pathways are responsive to lidocaine

Answer 85

QRS <70ms dog QRS <40 ms cats

Answer 86

- History suggests possible (Got doxo, dog lives in TX) - Unusual signalment for heart disease - Supportive ECG (conduction abnormalities or arrhythmias) - Supportive echo (myocardial dysfunction +/- heart enlargement) - Clin path support ( leukocytosis, eosinophilia, increased cTnI levels)

Answer 87

Definition: normal AP cannot occur during this time (bc Na channels are closed and no inward depolarizing current possible) Absolute Refractory Period (ARP): for most of duration of AP, the ventricular cell in incapable of firing another AP despite how large a stimulus bc most Na channels closed; includes upstroke, plateau and part of repolarization, until appx -50 mV Effective Refractory Period (ERP): a conducted AP cannot be generated - not enough inward current to move to next site; is slightly longer than ARP; if trying to pace a patient with defibrillate - make sure not to do during T wave can throw into V fib Relative Refractory Period (RRP): may generate a second AP but requires a greater than normal stimulus. If a second AP produced will have abnormal configuration and a shortened plateau phase, begins at end of ARP until cell membrane fully repolarized; Supranormal period (SNP): follows RRP, begin when MP -70 continues until normal at -85mV, cell is more excitable than normal during this period so less inward current required to depolarize the cell to threshold potential; B/c Na inactivation gates are open and MP is closer to threshold potential than it is at rest so easier to fire an AP

Answer 88

a = atrial contraction c= tricuspid bulging back into atrium after closure v = filling of atria prior to tricuspid opening x descent: decreased atrial pressure during ventricular ejection y descent: rapid emptying RA after tricuspid opens

Answer 89

Major criteria: - Pathologic lesion noted on cardiac valve (Oscillating, Hyperechoic, or Shaggy lesion) - New valvular insufficiency - AI with no evidence of SAS - Positive blood cultures Greater than/equal to 2 Greater than 3 if common skin contaminant Minor criteria: - Medium-large breed dog - Immune mediated disease - SAS - Fever - Positive blood cultures with not common infection - Thromboembolic disease - Bartonella serology Diagnosis Definitive: - Pathologic valve lesion - and 2 major or 1 major, 2 minor Possible: 3 minor 1 major, 1 minor

Answer 90

- RAAS activation : increased fluid retention, cardiac remodeling - Chronic SNS stimulation: receptor down regulation, persistent tachycardia and myocardial O2 demand, & myocyte necrosis - Overwhelming nateiuretic peptide system (normally counter regulates RAAS and SNS) - Increased Endothelin-1 --> increases after load & directly toxic to cardiomyocytes - Increased vasopressin: increased water retention --> may cause dilutional hyponatremia (poor prognostic indicator)

Answer 91

1. Stabilization while permanent pacemaker is being placed (BP and HR support under GA) 2.BP & HR support during GA for dogs with clinically silent sinus nodal dysfunction (do not need perm) 3. Medically refractory bradycardia in a patient that is in need of permanent pacemaker but requires hemodynamic stabilization first (systemic infection/endocarditis) --> transvenous preferred 4. Medically refractory and potentially reversible bradycardia (usually drug OD) --> transvenous preferred 5. Cardiac arrest from medically refractory sinus arrest leading to asystole due to drug overdose OR natural sinus nodal or AV nodal disease in which meaningful recovery is possible --> transcutaneous preferred

Cardiology Flashcards

(116 cards)