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ACVECC > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Cardiovascular Nerves

A
  • Reticular formationd of the medulla and lower 1/3 of pons
  • Afferent info: CN IX & X –> medulla –> integrated nucleus tract solitarus –> direct changes to CV centers
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2
Q

Cardiovascular brain centers

A

C1: vasoconstrictor center: upper medulla and lower pons
–> efferent neurons SNS

Cardiac accelerator center: SNS & synapse in the spinal cord and SNS ganglia –> increased firing rate of SA node, increases conduction velocity of AV node & increased contractility

Cardiac decelerator center: PSNS: vagus synapse on SA node –> decreased HR

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3
Q

PAOP

A

Normal = 5-12 mmHg

When mitral valve is open, LA pressure = LV end diastolic P = preload

** Therefore best indicator for fluid overload

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4
Q

DDX Sinus bradycardia

A

Hypothermia
hypothyroidism
Pre or POst CPA
Increased ICP
Brainstem disease
Metabolic (inc K, uremia)
Ocular Pressure
Carotid sinus pressure
Inc vagal tone
Sinus node disease
Normal varient (athletic dog)
Drugs (tranquilizer, GA, B blockers, Ca chanel blockers, digoxin)

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5
Q

DDX sinus tachycardia

A

Pain
Hyperthermia/fever
Anemia/hypoxia
CHF
Shock
Hypotension
Sepsis
Anxiety/fever
Excitement
Exercise
Electric Shock
Inc SNS tone
Toxins (chocolate)
Drugs (anticholinergics, sympathomimetics)

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6
Q

ACVIM Risk Categories Hypertension

A

AP0 : SBP<150, DBP <95
- minimal risk organ damage

AP1: SBP 150-159; DBP 95-99
-mild risk target organ damage

AP2: SBP 160-179; DBP 100-119
- moderate risk

AP3: SBP >/=180; DBP >/=120
- Severe risk

**Eyes and brai at biggest risk for damage

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7
Q

Bradykinin in vessels

A

With histamine

Arteriolar dilation & venular constriction –> increased cap hydrostatic pressure –> increased infiltration out of caps and local edema

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8
Q

Factors that increase CVP

A

-Decreased CO
-Increased blood flow
-Change standing to supine position
-Arterial dilation
-Muscle contraction (abdominal & limb)
- Forced expiration (valsalva)
- Venous costriction

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9
Q

2nd Degree AV block

A

Mobitz type I: progressive prolongation of PR interval before a nonconductive P wave
- common due to AV node disease or increased vagal tone

Type II: uniform PR interval preceding blocked impulse
- due to disease lower than AV conduction

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10
Q

What determines CVP

A
  1. Venous Return: blood flow, venous compliance, sympathetic tone
  2. R heart function: structural disease, preload, afterload, contractility, drugs
  3. Intrathoracic pressure: effusion, PEEP, pneumothorax, forced expiration
  4. Intra-abdominal P: effusion, hypertension, masses. post op, exp effort
  • Measure at end of expiration
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11
Q

Chronotropy

A

SA nodal conduction
HR

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12
Q

Lusitropy

A

rate of relaxation

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13
Q

What factors effect inotropy

A

-Preload
- Afterload
-HR
-Sympathetic stimulation

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14
Q

Pulmonary Arterial Catheter

(function, indication, complication)

A

Functions: CO, CVP, PAOP/PAWP, SvO2, ScvO2, pacing, angiog., research

Indications: Sepsis/SIRS, MODS, CHF, PHT

Complications: hemorrhage, thrombosis, arrhythmias (RBBB, vent), PA rupture, infection. valve damage, peumothorax

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15
Q

Pressure throughout the heart and Pulm Circulation

A
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16
Q

Hypertensive urgency vs emergency

A

Urgency:Sigificant increase in BP (ABP>160 mmHg) with no evidence of target organ damage
*Epistaxis can occur

Emergency: human recommendations dec ABP no more than 25% within 1 hr then to 110 within next 2-6 hrs
*Excessive drops –> organ ischemia

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17
Q

3 substances leading to cardiac remodeling

A

Angiotensin
Aldosterone
Norepinephrine

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18
Q

HCM breeds and diagnosis

A
  • Maine coon & ragdoll
  • Wall thickness >6 mm
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19
Q

Management CHF in cats

A
  1. Treat Congestion: diuretic, after load reducer (nitroglycerine), inodilator (pimobendan), +/ thoracocentesis
  2. Treat FATE: analgesia, antithrombotics (heparin, clopidogrel)
  3. Long Term management: beta blocker ( allow decreased filling due to increased chronotropy)
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20
Q

Secondary causes of cardiomyopathy

A
  1. Drugs: doxorubricin
  2. Nutrition: taurine, carnitine, vitamin E, grain free
  3. Muscular dystrophy
  4. Myocarditis (infection/inflammatory)
  5. Infiltrative (glycogen)
  6. Neoplastic
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21
Q

DCM treatment main stays

A
  1. Relieve Congestion ( diuretic)
  2. Inhibit RAAS: ACE inhibitor
  3. POsitive inotropy: Pimobendan
  4. Beta blocker: novel; no evidence CHF
  5. Diet: good protein and low Na
    6.Supplement: taurine & carnitine
  6. Digoxin: + inotropy and - chronotropy
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22
Q

ARVC (MC CS, ECG Findings, Treatment criteria)

A
  • Autosomal dominant
  • CS: 1/3 syncope. 1/3 CHF, 1/3 asymptomatic
  • ECG: R sided VPC (LBBB morphology), >100 VPC/24 hrs
  • Treatment Criteria: Couplets, runs, R on T, >500-1000 VPC/day
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23
Q

ECG changes assd with increased K+

A
  • Tall tented T waves
  • Prolonged QRS
  • Decreased P amplitudes
  • Sinusoidal appearance
  • ST Changes
  • atrial standstill
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24
Q

MC Myocarditis causes

A

Viral: parvo
Protozoal: Chagas Dz/Trypanasoma Cruzi

Noninfectious: doxorubricin

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25
Q

Pathophysiology of endocarditis

A
  • 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

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26
Q

Thermodilution technique

A
  • 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)

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27
Q

Atrial Natieuretic Peptides

A
  • Increase with increased atrial pressure, increased venous pressure and increased pulmonary hydrostatic pressure
  • causes fluids to shift from vascular space to interstitial space
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28
Q

Paroxysmal SVT

A
  • Not uncommon in large breeds of dog with no primary heart disease
  • Sustained tachycardia can cause tachycardia induced DCM

TX: diltiazem

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29
Q

Pulses Paradoxus

A
  • Stronger during expiration and weak/absent during inspiration

-pericardial effusion

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30
Q

Split S2 sound

A
  • only heard if there is disease
  • due to pulmomary hypertension
  • DDX: HW disease, obstructive pulm disease, congenital cardiac disease, or high altitude
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31
Q

1st Degree AV Block

A

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

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32
Q

Pulses alternans

A
  • Alternating weak and normal pulses with regular rhythm
  • MC due to decreased contractility, CHF & tachyarrhythmias
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33
Q

Factors that effect diffusion

A
  • Pore size of capillary
  • molecular size of diffusing substance
  • Concentration differences between 2 sides of membrane
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34
Q

Diseases assd with hypertension

A
  • Kidney Disease
  • Diabetes mellitis
  • Cushings
  • Hyperthyroid
  • Pheochromocytoma
  • Hyperaldosteronism
  • Hepatic Dz
  • polycythemia
  • chronic anemia
  • CHF
  • Neoplasia
  • Iatrogenic
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35
Q

Donnan Equilibrium Effect

A

~19 mmHg of colloid osmotic pressure is due to dissolved protein

An additional 9 mmHg is due to + charged cations ( mainly Na2+)

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36
Q

Preload is increased by:

A
  • 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
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37
Q

Preload

A

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

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38
Q

Afterload

A

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

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39
Q

Contractility

A
  • Intrinsic force of heart
  • Degree to which sarcomeres can shorten when activated independent of preload & afterload
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40
Q

Dromotropy

A

Conduction through AV node

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41
Q

Cardiac Innervation

A

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
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42
Q

Mediators of vasoconstruction

A
  • Catecholamines: NE/E
  • Angiotensin II
  • Endothelin
  • ADH/vasopressin
    -Ions (Ca2+)
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43
Q

Cardiogenic shock: define & causes

A

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
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44
Q

3 Components involved in pathophysiology of feline CHF

A
  • Diastolic Dysfunction
  • Systolic Anterior motion of mitral valve
  • Femoral arterial thromboemboli

** L auricle MC spot for clot formation

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45
Q

Mitral Valve Classes

A

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

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46
Q

CS Cardiogenic Shock

A

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

Metabolic Acidosis
Lactic Acidosis

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47
Q

Systolic Failure & mechanisms

A
  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
48
Q

Diastolic failure & mechanisms

A
  • INadequate filling: abnormal preload or relaxation

Ex: preicardial effusion or foibrosis
HCM
Tachyarrhythmias

49
Q

SVT

A

P wave for each QRS
Sustained tachycardia can induce DCM

**Diltiazem IV&raquo_space;esmolol in dogs
If refractory to diltiazem, second drug such as esmolol, procainamide, or lidocaine

50
Q

AIVR

A
  • 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
51
Q

Hypertensive Encephalopathy

A
  • 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
52
Q

Trigeminy

A

VPC every 3rd complex

53
Q

Sustained arrhythmia

A

Always

54
Q

Paroxysmal

A

Occasional

55
Q

Supraventricular

A

Above AV node
QRS normal shape

56
Q

Third degree AV block

A

No association with P wave rate (100-120 bpm) & normal regular ventricular escape rate (40-60 bpm)

**No meds work for this

57
Q

Atrial fibrillation

A

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
58
Q

Sick Sinus Syndrome

A

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

59
Q

Colloid osmotic pressure

A

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

60
Q

Interstitial solid structures

A
  1. Collagen fiber bundles–> gives tensile strength to tissue
  2. Proteoglycan filaments –> composed mainly of hyaluronic acid (fine reticular filaments)
61
Q

Unstressed volume

A

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

62
Q

Fluid creep

A
  • Fluids administer as vehicles for other meds (amount ‘creeps’ up on you)
63
Q

Frank Starling Law

A

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

64
Q

End Diastolic Pressure

A

Diastolic P immediately before contraction occurs

65
Q

Ejection Fraction

A
  • Fraction of end diastolic volume that is ejected during systole
  • Normal is 60% or 0.6?
66
Q

4 AFAST sites

A
  1. Subxiphoid or diaphragmatic hepatic
  2. L flank or splenorenal
  3. Midline bladder or cystocolic
  4. R flank or hepatorenal
67
Q

5 T fast Views

A
  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
68
Q

Parallell distribution of flow

A
  • 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
69
Q

Mean circulatory filling pressure

A
  • Average transmural pressure of circulatory system when blood flow has stopped
    -Determined by blood volume and autonomic control of vascular smooth muscle
70
Q

Hyperpolarization

A

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

71
Q

Depolarization

A

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

72
Q

Hypertensive therapy goals

A
  • 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
73
Q

Thromboxane A2 & vessels

A

Vasoconstriction

74
Q

Prostaglandin F & vessels

A

Vasoconstriction

75
Q

Angiotensin II & vessels

A

Vasoconstriction

76
Q

Laminar vs turbulent flow

A
  • 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)

77
Q

CO of different systems

A

Cerebral 15% CO
Coronary 5% CO
Renal 25% CO
GI 25% CO
Skeletal 25% CO
Skin 5% CO

** Not fixed

78
Q

Cardio changes with hypertension

A

Systolic murmurs
Cardiac gallops
LV Hypertrophy

79
Q

Glide sign

A

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

80
Q

A lines

A

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

81
Q

B Lines

A

-“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

82
Q

Lung Curtain

A

Movement of lung into and out of view

83
Q

Lung POint

A

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

84
Q

Torsades de pointes

A
  • Prefibrillatory rhythm
  • Sustained vtach
    -“twisting of peaks” around isoelectric line

TX: lidocaine

85
Q

Serotonin & vessels

A

released with blood vessel damage –> local vasoconstriction

86
Q

Prostacyclin & vessels

A

vasodilator

87
Q

Prostaglandin E & vessels

A

vasodilator

88
Q

V Wave

A

Atrial pressure wave
Caused by infilling of atria from venous return

89
Q

C wave

A

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

90
Q

A wave

A

Atrial pressure wave
- bump during atrial contraction

91
Q

Common sources infectious endocarditis

A
  • Prostatitis
  • UTI
  • Pneumonia
  • Diskospondylitis
  • Dental Disease
92
Q

Typical presentation of infectious endocarditis

A
  • middle age, large breed, male
  • Lab, golden, GSD, Boxer all over represented
  • MC CS: murmur, fever, lameness
  • Arrhythmia: SVT, AV block, Afib, Vent
93
Q

MSCRAMMS

A

microbial surface components recognizing adhesive matrix molecules

  • MC Staphylococcus and strep
94
Q

Echo findings with constrictive pericarditis

A
  • diastolic flattening
  • Abnormal septal motion
  • thick pericardium
95
Q

Cardiac tamponade definition

A

intrapericardial pressure> RA pressure
* Collapsed RA

96
Q

Define defibrillation

A

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
97
Q

Reliable criteria for Vtach

A
  • Wide bizarre QRS
  • No P waves ( AV dissociation)
  • Fusion beats present
  • Capture beats present

** MC assd with hypokalemia

98
Q

3 arrhythmagenic mechanisms

A
  1. Enhanced automaticity –> spontaneous depolarization
  2. Triggered activity –> small depolarization
  3. Re-entry –> circling non conductive tissue
99
Q

Indications for pacemaker

A
  • 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
100
Q

Ocular changes in hypertension

A

-“hypertensive retinopathy”
- retinal vessel totuosity
-edema
-retinal degeneration
- hyphema

** Increased risk >180 mmHg –> seen at pressures as low as 168

101
Q

5 phenotypes of feline cardomyopathies

A
  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
102
Q

Criteria of malignancy for ventricular arrhythmias

A
  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
103
Q

7 mechanisms of blunt cardiac injury

A
  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
104
Q

causes exudative pericardial effusion

A

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

105
Q

Hepatojugular reflex

A

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)

106
Q

Pericardiocentesis

A

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

107
Q

vasovagal syncope physiology

A

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
108
Q

Distinguishing sinus tachycardia from SVT

A
  • 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
109
Q

Distinguishing SVT from V tach

A
  • 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
110
Q

Narrow complex tachycardias

A

QRS <70ms dog
QRS <40 ms cats

111
Q

Characteristics suggestive of myocarditis

A
  • 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)
112
Q

Refractory periods

A

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

113
Q

CVP waves

A

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

114
Q

List modified duke criteria for endocarditis

A

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

115
Q

Neurohormonal effects of CHF

A
  • 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)
116
Q

indications for temporary pacemaker placement

A
  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)
  2. Medically refractory bradycardia in a patient that is in need of permanent pacemaker but requires hemodynamic stabilization first (systemic infection/endocarditis) –> transvenous preferred
  3. Medically refractory and potentially reversible bradycardia (usually drug OD) –> transvenous preferred
  4. 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

ACVECC (10 decks)

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