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VTS ECC 2024 > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

1
Q

Cardiac Conduction system

A

SA Node → Atrial conduction → PAUSE -> AV node → Bundle of His → L/R bundle branches → Purkinje fibers → Ventricular conduction

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2
Q

Cardiac Circulation pathway

A

Venous circulation → Superior/Inferior Vena Cava → RA → Tricuspid valve → RV → Pulmonic valve →Pulmonary Artery →Lungs → Pulmonary Veins → LA → Mitral valve → LV → Aortic valve → Aorta → Systemic arterial circulation

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3
Q

Difference between Pulmonary Artery and Pulmonary Veins

A

Pulmonary Artery = Carries Deoxygenated blood
Pulmonary Vein = Carries Oxygenated blood

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4
Q

Depolarization

A

Electrical Activation via loss of polarization with influx of Na+/Ca++ and eflux of K+

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5
Q

Repolarization

A

Electrical Inactivation; polarization restored via eflux of Na+/Ca++ and influx of K+

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6
Q

Preload

A

“End Diastolic filling volume” in ventricles or stretch force acting on ventriclular fibers

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7
Q

Afterload

What is its affect on cardiac workload?

A

force opposing LV immediately PRIOR to aortic valve ejecting blood to the body

resistance aortic valve has to overcome

increased afterload = increased cardiac workload

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8
Q

Contractility

A

Strength and ability of heart to contract

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9
Q

Refractory Period

A

state of recovery after neuron has fired an action potential

Absolute or Relative

protects nerve from rapid repetion

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10
Q

Absolute Refractory Period

A

period of time which 2nd action potential CANNOT occur despite strength of stimulus

Inactivates Na+ channels

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11
Q

Relative Refractory Period

channel activity

A

2nd action potential can only occur with stronger-than-normal stimulus

some Na+ channels return to resting state and can be reactivated

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12
Q

Inotropic effects

A

effects cardiac contractility

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13
Q

Positive Inotropes

A

strengthens cardiac contractility

Ex: Dobutamine

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14
Q

Negative Inotropes

A

weakens cardiac contractility

Ex: Diltiazem

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15
Q

CO =

A

CO = HR x SV

how fast the beat is x how strong

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16
Q

MAP =

A

CO x SVR

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17
Q

Systolic BP

A

Pressure within main arteries during systole

Ventricular contraction

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18
Q

Diastolic BP

A

Pressure within main arteries during diastole

Ventricular relaxation

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19
Q

Systole

A

Atrial/Ventricular contraction

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20
Q

Diastole

A

Atrial/Ventricular relaxation

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21
Q

“Lub-Dub”

A

Lub = closure of mitral/tricuspid valves
Dub = closure of aortic/pulmonic valves

silence on valve opening

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22
Q

Sinoatrial Node

A

Pacemaker of the heart, bundle of specialized muscle fibers that act like nerves, send stimulus to both atria

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23
Q

Atrioventricular Node

A

Controls heart rate, slows electrical current via decremental conduction (faster the signal, slower the conduction)

prevents rapid ventricular conduction in cases of a-fib, and a-flutter

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24
Q

Printed ECG standard

A

25mm per second (25 small squares per second)

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25
Q

P wave

A

Atrial depolarization

(contraction)

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26
Q

Q wave

A

Depolarization of septum

first negative deflection in complex as it travels R to L

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27
Q

R wave

A

Depolarization of main ventricular walls

More voltage required due to thick ventricular wall = bigger wave

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28
Q

S wave

A

Depolarization of Purkinje fibers

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29
Q

T wave

A

Repolarization of ventricles

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30
Q

PR interval

A

Start of P-wave to start of Q-wave
time of impulse to travel from SA node → ventricular myocardium

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31
Q

ST interval

A

End of QRS to start of T-wave
Can shift ↑ or ↓ in position with different dz states

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32
Q

QT interval

A

Start of Q-wave to end of T-wave
time required for ventricular depolarization and repolarization to occur

may indicate electrolye abnormalities

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33
Q

Starlings Law

what is it in response to?
what relationship does this represent?

A

Stroke Volume will ↑ in response to an ↑ in Preload (filling volume) and contractility and ↓ in afterload (resistance prior to blood ejection)

represents relationship between stroke volume and end diastolic volume

stronger preload = stronger contraction

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34
Q

♡ Failure

A

Impaired cardiac pumping = ↓ CO and venous return to ♡ = ↓ O2 delivery to the body
–Baroreceptors sense ↓ ABP in aortic arch and corotid sinus
–mechanoreceptors in ♡ and Kidneys sense change in volume/BP → neuroendocrine response

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35
Q

Left sided ♡ failure

CS
Type of <3 dz that can cause LSHF

A

Failure to pump blood from ♡ to the body
CS: Pulmonary Edema (seen exclussively due to congestion) coughing, collapse, orthopnea and dyspnea. Pleural effusion in cats (due to vasculature)

seen with: DCM, MVD, PDA (K9) HCM (cats)

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36
Q

Right sided ♡ failure

results from
CS

A

Faliure of forward flow results in back up to systemic circulation → ascites, jugular distension, peripheral edema
CS: weakness, syncope, pallor, tachypnea

Typically results from Left sided heart failure causing fluid back up into lungs and then back to Right side

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37
Q

Systolic ♡ Failure

How does it affect SV/contractility?

A

Ventricles fill normally but forward stroke volume is ↓ = ↓ contractility or ↑ ventricular pressure or volume overload

1° causes - DCM, myocardial infarction, nutrition deficiency, doxorubicin toxicity
2° causes - STEM via chronic volume/pressure overload.

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38
Q

Diastolic ♡ Failure

results in
Examples

A

Abnormal cardiac relaxation/compliance resulting in impairment of ventricular filling

Ex: Ventricular hypertrophy; HCM, subaortic stenosis, pulmonic stenosis, systemic hypertension.
DCM; infarction; filling obstruction (neoplasia). Pericardial dz (cardiac tamponade)

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39
Q

Immediate physiological response to ♡ failure

which receptors involved?

A

↓ PANS and ↑ SANS = activation of alpha-1 and beta-1 adrenergic receptors = vasoconstriction, ↑ HR + contractility = improved CO and SVR

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40
Q

Delayed physiological response to ♡ failure

A

RAAS activation due to ↓ firing at mechanoreceptors/volume receptors in Kidneys from ↓ renal blood flow.
↑ retention of Na+/H2o to ↑ circulating volume

causes vasoconstriction, Na+/H20 retention to increase circulating volume.

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41
Q

Cycle of chronic activation of compensatory mechanisms of ♡ failure

effects on afterload; preload; CO

A

↓ CO → ↓ tissue perfusion → neuroendocrine response (SNS + RAAS) → ↑ afterload and Na+/H2o retention → ↑ preload/volume/pressure → Cardiac remodeling → decreased SV → ↓ CO

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42
Q

Chronic Valvular ♡ Disease

Breeds predisposed

A

Aka Endocardosis
degenerative dz of AV valves, Mitral specifically
LA enlargement +/- LV enlargement in progressive state
Life long dz

King Charles/Papillon

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43
Q

DCM

may be cause by =

characterized by =
May result from =
Tx

A

1° myocaridal dz in dogs
characterized ♡ enlargement
imparied systolic function - soft systolic HM from mitral regurgitation
Can result from - doxorubicin, grain free, and myocarditis

Dobermans, Giant breed dogs

Taurine deficiency in cats
Dobutamine used to improve systolic funstion

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44
Q

Caval Syndrome

how does it affect CO and preload?

A

Life threatening complication of HWD
Lg worm burden
Parasites obstruct flow to R side of ♡
interfere → ↑ pul. artery pressures → tricuspid regurgitation → R-side CHF
↓ Preload and CO
Trauma to RBCs → intravascular hemolysis → hemoglodinemia/uria
can lead to DIC
Parasite extraction via jugular venotomy

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45
Q

Pathophysiology of HWD

CS in dogs vs cats

A

K9/Fel/Ferrets susceptible
Parasites carried to pulmonary vasculature between 2-6months
settles in distal portion of pul. artery
K9s; resp. distress 2° to pneumonitis +/- PTE, pul. hypertension → R-side CHF
Fel; asthma like symptoms 2° to HW resp. dz, anaphylaxis due to worm death. Typically low adult burden (clears immature stage)

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46
Q

HCM

A

–Common ♡ dz in Cats
–Thickening of LV wall = small chamber size → large LA
–↓ diastolic function
Hypercontractility →hypertrophy
–Systolic HM, gallop rhythm
2° to systemic hypertension; hyperthyroidism; dehydration
stasis of blood flow/endothelial damage → ATE

Main Coons, Ragdolls, Norwegian Forrest cats, Sphynx

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47
Q

CHF manifestation from HCM in cats

in relation to pressure

A

Hydrostatic pressure within the venous capillaries exceeds the oncotic pressure
–holds fluid within vasculature → fluid leaks out of the capillaries → manifests as pulmonary edema and/or pleural/pericardial effusions

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48
Q

Virchows Triad

A

3 contributions to thrombosis
1: Hypercoagulatbility
2: Endothelial damage
3: Stasis of blood flow

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49
Q

7

Disease processes at risk of Thromboembolism

A

PLN; PLE; Cushings; IMHA; ITP; Neoplasia; Trauma
-Also corticosteriod use
-HCM → LA thrombus → break off into abdominal terminal aorta

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50
Q

Endocarditis

what part of the heart does it infect?

A

Colonization of micro-organisms in smooth muscle lining heart chambers/valve surfaces → destruction of valve/internal structures
Arrhythmias, ECHO → vegetative valve growth
mild non-regen anemia, inflammatory leukogram

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51
Q

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

EKG findings
Tx

A

Boxer Cardiomyopathy
fribrous tissue replaces normal myocardial tissue → alterin normal electical conduction → arrhythmia
ECG = VPCs, V-Tach
Syncope, weakness

Type I, II, III

Tx: : Lidocaine, defib for pulses V-Tach. Long term = Mexiletine, atenolol, sotalol

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52
Q

LA:Ao Ratio

A

LA to Aorta ratio @ the end of systole (contraction) just before mitral valve opens when LA is the largest
LA diameter ÷ Aortic diameter

Normal = < 1.6mm

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53
Q

B-lines

definition
causes

A

= Pulmonary Edema
3+ in one site = CHF

caused by increased lung density i.a fluid/cells/fibrosis, Alveolar interstial syndrome (AIS/wet lung)

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54
Q

Occult DCM

A

Structural ♡ changes +/- arrhythmias with no outward CS

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55
Q

Clinical DCM

EKG, CS, TX

A

VT or SVT, A-fib, L-side CHF
Lethargy, inappetence ↑ RR/RE, C+, exercise intolerance, syncope
Crackles, pul. edema, pleural effusion

Tx: ACE inhibitors, inodialator, beta-blocker

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56
Q

Type I, II, II ARVC

A

Type I: subclinical ventricular arrhythmias
Type II: arrhythmias + syncope
Type III: structural ♡ changes on echo with CHF
Typically L-side CHF seen
Dx: Holter monitor sees 300+ VPCs within 24 hr period

Tx: Sotalol, Mexiletine to reduce ventricular arrhythmias

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57
Q

Congenital CV Disease

A

Shunting defects;
L→ R = CHF/Resp distress
R→ L = hypoxemia/cyanosis
Perivalvular defects; lesions associated with CHF/snycope/collapse

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58
Q

Tetralogy of Fallot

A

R → L shunting defect = central cyanosis
– Ventricular septal defect, overriding aorta, pulmonary
stenosis, and right ventricular hypertrophy
– Causes oxygen-poor blood to circulate to the rest of the body

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59
Q

Myxomatous Valvular Disease

what specific structures does it affect
Physical changes seen
CS

A

Degeneration of cardiac valves (mitral/tricuspid)
Changes in collagen of affected valves → becomes progressively thicker with curled edges
+ chorda tendonae → thick/stiff, loses elasticity
= LA/LV enlargement
Results in Pulmonary Hypertension 2° to L-sided ♡ dz or
Ascites from R-sided CHF

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60
Q

HWD Treatment

A

Corticosteriods for Eosinophillic infiltrates
Bronchodilators
O2 therapy
Strict cage rest
Furosemide +/- Spironolactone
ACE inhibitors

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61
Q

Pulmonary Hypertension (PH)

A

Increase in pulmonary vascular BP
mPAP = > 25mmHg
severe > 75mmHg
imbalance between arteriole vasodilation + constriction, platelet activity and smooth muscle proliferation

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62
Q

Classifications of PH I-VI

A

I: congenital/hereditary/ idiopathetic arterial hypertension
II: due to L-side ♡ dz
III: due to pulmonary dz
IV: due to thromboembolic dz
V: due to Parasities
VI: due to uncertain multifactorial mechs

CHIHuahuas Love Running Then Passing Out

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63
Q

Class I PH causes

causes/tx

A

HWD, congenital shunts (PDA)
shunts ↑ blood flow back and ↑ pulmonary blood flow
Eisenmengers syndrome
Tx: corticosteriods/bronchodilators for HWD, phlebotomy for polycythemia

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64
Q

Eisenmengers Syndrome

A

Irregular blood flow with in the <3
chronic or large L → R shunt allowing large amount of blood flow to R side
= causes pulmonary vascular changes and ↑ pulmonary pressure/resistance
= ↑ R side cardiac pressure to exceed L-side pressure
= shunt back flow R → L
= deoxygenated blood entering circulation
= cyanosis and polycythemia

Congenital <3 dz

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65
Q

Class II PH causes

causes and tx

A

Chronic degenerative MVD → ↑ LA volume and pressure → ↑ pulmonary venous pressure = PH
Tx: MVD = pimobendan, diuretics/ACE inhibitors for CHF

Ex: MMVD

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66
Q

Class III PH causes

A

Tracheal collapse, chronic bronchitis, interstitial fibrosis
Tx: specific therapies for infection, bronchodilators and steroids

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67
Q

Class IV PH causes

A

Thromboembolytic causes;
HWD, IMHA, protein nephropathy/enteropathy, cushings dz, neoplasia, sepsis
Tx: antiplatelet therapy, fibrinolytics (controversial)

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68
Q

Cor Pulmonale

A

RV enlargement or hypertrophy due to pulmonary disease of arteries/lungs/upper airway

69
Q

Sick Sinus Syndrome

A

intermittent failure of the SA node to fire, resulting in sinus bradycardia or sinus arrest
CS: weakness, collapse, syncope
prolonged sinus pauses > 6-7seconds
SVT may precede sinus pauses

Atropine response test
Tx: Pacemaker

small/toy breeds, schnauzers, westies, dashunds

70
Q

Persistent Atrial Standstill

EKG findings; TX;

A

–Atria fail to depolarize despite SA node firing
–Missing P-wave on ECG
→ AV node junctional or ventricular escape beat
–possible to become A-fib
–Standstill due to hyperk+, SA nodal discharge occurs, but atrial depolarization is blocked by the effects of hyperkalemia

Tx: hyperkalemia tx, Pacemaker

71
Q

Systemic Arterial Hypertension

determined by; Tx;

A

Systemic increase in arterial blood pressure
MAP → determined by CO, SVR and peripheral arterial resistance

slow antihypertensive therapy, no more than 25% reduction at a time
Nitroprusside CRI

72
Q

Conditions associated with Systemic Hypertension

A

“White coat” syndrome
AKD/CKD
DM
hyperadrenocorticism
polycythemia
hyperthyroidism (cats)

73
Q
A

A: anacrotic limb → systolic upstroke, ventricular ejection of blood to system
B: 1st decent, peak/max systolic BP during ejection
C: Rapid decline (dicrotic limb) = ventricular contraction ends
D: final descent = lowest point = diastolic BP

74
Q

AV Block Poem

A

If R is Far from P then you have First Degree
Long long longer DROP then you have WENKENBACH (2nd degree)
If some P’s dont get through then you have Mobitz II (2nd degree)
If P’s and Q’s Don’t Agree then you have 3rd Degree

75
Q
A

First Degree AV Block
Prolonged PR interval
increased vagal tone, AV node fibrosis, drugs that delay AV node conduction

“R is Far from P”

76
Q
A

Second Degree AV Block Wenckenbach (Type I)
progressive delay in AV conduction - PR interval gradual prolongation

“Longer Longer Longer DROP”

Progressive vagal tone
typically benign, no tx needed

77
Q
A

Second Degree AV Block Mobitz II
unexpected block of P-waves, not every P has QRS.
“some Ps don’t get through”

No change to PR interval. QRS complexes can appear wide due to block bel

Can worsen
Atropine test - Type II worses or remains unchanged

78
Q
A

3rd Degree AV Block or Complete AV Block
CO drastically reduced
Ventricular activation reliant on escape rhythm

Ps and Qs DONT agree

79
Q
A

Atrial Fibrillation
No Pwaves - “F waves” - fibrillation
Irregularly irregular
Fast ventricular rate >160 K9 >220 feline

Seen with advanced DCM and valvular Dz

Tx: control rate with mgmt of underlying dz
Diltiazem +/- Digoxin if concurrent CHF

80
Q
A

Atrial Flutter
No Pwaves “saw tooth atrial appearance”
RR interval can be regular or irregular

structural <3 dz -> atrial enlargement
Possible to evolve into A-fib

81
Q
A

Sinus tachycardia with electrical alternans

Electrical alternans (variation in R-R height) can be caused by effusions damping complexes i.e pericardial/pleural effusion or diagphragmatic hernias

82
Q
A

SVT
tachycardia that arises from atria or AV nodal tissue for initiation and maintenance
Rapid narrow QRS complexes, regular R-R intervals

associated with underlying structural heart dz or noncardiac dz (sepsis/panc/splenic torsion/GDV)

83
Q

how does this affect systolic/diastolic BP?

A

Overdamped arterial waveform
Can be cause by air bubble present in the tubing
Microclot within the catheter
or connection tubing TOO compliant (not stiff enough)
Systolic may be artificially lowered and diastolic higher

84
Q
A

Underdamped arterial waveform
May cause artificially high systolic and low diastolic

85
Q

Myoxmatous Mitral Valve Disease (MMVD)

results in
Breed examples

A

Most common cause of ♡ failure in K9s
Variable degrees of valve thickening/prolapse/abnormal confirmation
Leads to systolic mitral valve regurgitation
Can affect all valves
Progressive chamber dilation/decrease in stroke volume activates neurohormonal activation (RAAS)

Cavalier King Charles, Dachshunds, Mini Poodles, Yorkies

86
Q

Class I Antiarrhythmics

a, b, c

A

Na+ channel inhibitors
Ia: fast Na+ channel blocker → prolongs refractory time in both atria and ventricles, depresses automaticity and conduction velocity, used for SVT
Ib: Shortens action potential duration, inhibits recovery after repolarization; no efx on atrial myocytes; suppresses automaticity/velocity in ventricular myocardium
Ic: greater efx as depolarization increases; prolongs refractory periods in atrial and ventricular tissues

Ex: Ia; Procainamide Ib; Lidocaine/ Mexiletine Ic; propadfenone

TX: Ventricular arrhythmia or SVT

87
Q

Class II Antiarrhythmics

What effect does it have?

A

Beta-Blockers; Slow AVN conduction in SVT
antagonizes beta-adrenergic receptors → lowers HR, AV conduction, myocardial O2 demand
– inhibits the inward calcium current indirectly by decreasing cAMP levels
– suppresses Vtach thought to work by increasing sympathetic tone

TX: SVT (AV node conduct) Ventricular arrhythmias

Ex: Propanolol, Esmolol, Atenolol, Sotalol (LOL Group)

88
Q

Propanolol vs Esmolol

A

Propranolol: blocks both beta-1- and beta-2-adrenergic receptors in the myocardium, bronchi, and vascular smooth muscle
Esmolol: primarily blocks beta-1 adrenergic receptors in the myocardium.
– Both have No intrinsic sympathomimetic activity

89
Q

cAMP levels

A
  • Cyclic adenosine monophosphate: “second messenger” of beta-1 receptors
  • Increase in levels causes increased chronotropy and inotropy
90
Q

Class III Antiarrhythmics

How do they affect the refractory period?

A

K+ channel blockers
Results in prolongs repolarization and refractory period = myocardial repolarization
– Sotolol: also non-selective beta blocker
– Amiodarone: also blocks Na+ and Ca++ channels and β-adrenergic receptors

TX: Supra Ventricular and ventricular arrhthymias

Ex: Sotolol, Amiodarone

91
Q

Amiodarone MOA

A

blocks both currents and makes action potentials more uniform throughout the myocardium so it has the least reported proarrhythmic activity

92
Q

Sotolol MOA

A

Combines nonselective beta blockade with rapid component potassium current inhibition
– Effective antiarrhythmic in both SVT and ventricular tachyarrhythmias

93
Q

Class IV Antiarrhythmics

A

Ca++ channel blockers
lowers SA and AV node conduction
slows conduction and HR
– Effective in slowing the ventricular response rate to atrial tachyarrhythmias and can prolong AV nodal ERP to the point that an AV-node dependent tachyarrhythmia is terminated

TX: Supraventricular arrhythmias

Ex: Diltiazem

94
Q

Diltiazem MOA

A

Used to immediately terminate a severe AV nodal- dependent tachyarrhytmia or slow the ventricular response rate to an atrial tachyarrhythmia (AFib)

95
Q

Digoxin (digitalis glycosides)

A

– low therapeutic index
– Effects occur indirectly through the autonomic nervous system by enhancing central and peripheral vagal tone
– Results in slowing of the sinus node discharge rate, prolongation of AV nodal refractoriness, and shortening of atrial refractoriness

96
Q

Stage A of Heart Disease

A

Animals predisposed or at high risk for heart disease (no disease present at this stage)
Ex: Dobermans/Main Coons/Boxers

97
Q

Stage B of Heart Disease

A

A murmur is heard but there are no clinical signs of heart failure

98
Q

Stage B1 of Heart Disease

A

No radiographic evidence of heart enlargement or chang on x-ray
Cats: N - mildly lg LA, Low risk of CHF/ATE

99
Q

Stage B2 of Heart Disease

A

Radiographic evidence of heart enlargement or changes on x-ray
Cats: moderate - severe lg LA, Higher risk of CHF/ATE

100
Q

Stage C of Heart Disease

A

Cardiac remoldeling and/or evidence of heart failure is visible and treatment is necessary

101
Q

Stage D of Heart Disease

A

Refractory CHF
Severe/debilitating signs of heart failure thats not responding to
standard treatment

102
Q

Natriuretic Peptide System

Produced by
Induces =
response to =
Examples

A

Two hormones produced by myocardial tissue → induce natriuresis, diuresis, and vasodilation
Atrial natriuretic peptide and
B-type natriuretic peptide (ANP & BNP)
Produced in response to stretch or stress of myocardial tissue
Counter regulatory system to RAAS and SNS

103
Q

Endothelin 1

what produces it
occurs in response to
efx

A

–Vasoconstrictor produced by vascular endothelial cells
–Response to sheer stress, angiotensin II, and other cytokines
–Alters Ca+ cycling in muscles
–Toxic to myocardiocytes

104
Q

ACE Inhibitors

Efx on BP; Examples

A

block the conversion of angiotensin I → angiotensin II =
Lowers arteriolar resistance → reduces Preload
Increases venous capacity, increases natriuresis
Decreases BP
Decreased ventricular remodeling and ventricular hypertrophy

cardiac disease, proteinuria, and hypertension

_PRIL Enalapril, Benazapril

105
Q

Restrictive cardiomyopathy

definition
associated with
causes

A

–Ventricular stiffening/noncomplient causing filing impairment
–↑ diastolic pressures
–Absence of myocardial hypertrophy (HCM) or pericardial disease
–Atrial enlargement associated

2nd most common cardiomyopathy in cats

scarring or fibrosis of myocardium

106
Q

DLVOTO

Dynamic Left Ventricular Outflow Tract Obstruction

what is this commonly caused by?

A

–Form of subaortic stenosis that progressively worsens throughout systole
–Commonly caused by Systolic anterior motion of the mitral valve (SAM)

Common in cats with HCM, rare in dogs

107
Q

Systolic anterior motion of the mitral valve (SAM)

A

Due to the hypertrophied/displaced anterior leaflet of the anmitral valve into a normal or narrowed left ventricular outflow tract (LVOT)
–typically cause of HM in cats with HCM
–Murmur often dynamic → louder with stress/excitment

108
Q

Feline Aortic Thromboembolism

Where does it typically occur?
caused by
example
Where does it typically occur?

A

ischemic injury from vasoactive substances released from thrombis, activated platelets,
i.e serotonin, → decreases blood flow/collateral artery constriction contributes to ischemic injury

not the result of the primary arterial occlusion

Thromboembolism typically lodges in Aortic trifurcation

109
Q

Feline aortic thrombo-embolism (FATE) definition

A

– sudden migration of a left atrial thrombus into the systemic arteries

110
Q

Feline aortic thrombo-embolism

Pathophys of FATE

A

– presence of one or more of the factors described by Virchow’s triad:
– Blood stasis can be caused by reduced blood velocity or turbulent blood flow, often caused by vascular or heart valve or chamber anomalies
– left atrial (LA) size, decreased LA function, LA to aorta ratio (LA:Ao), and the presence of SEC in cats

111
Q

Feline aortic thrombo-embolism

% of cardiomyopathic cats with spontaneous echocardiographic contrast (SEC aka smoke) with identifyable hypercoagulopathy

A

50%

112
Q

Feline aortic thrombo-embolism

Diagnosis of FATE

A

5P rule, which comprises:
1. pallor (i.e., purple or pale toes),
1. polar (i.e., cold extremities),
1. pulselessness,
1. paralysis,
1. pain

113
Q

Prognosis for FATE

A

– considered poor,
– When treated, survival is between 27% and 45%, with no real identifiable trends
– Cats with motor function at admission or one limb affected have a better prognosis (70% survival to discharge)

114
Q

Pseudohypertrophy

A

Caused by dehydration
temporary thickening of cardiac walls due to low volume in chambers

115
Q

Calcium ion effect on Myocardiocytes

systole vs daistole

A

Systole;Ca++ enters cell → triggers release of Ca++ from sarcoplasmic reticulum (SR) → binds to troponin C → causes contraction
Diastole: Release of Ca++ from troponin initiates relaxation → Ca++ ion move back to SR

Abnormalities → Electrical distruptions/apoptosis/necrosis

116
Q

Regularly Irregular Rhythm ex:

A

Distinct repeating pattern but not equally spaced
* Bigeminy/Trigeminy
* Sinus arrhythmia

A-flutter can have regular or irregular R-R interval

117
Q

Irregularly Irregular Rhythm ex:

A

No distinct pattern with irregular spacing
A-fib
V-fib

118
Q

Torsade de pointes

Definition; causes; concerns

A

Specific form of Polymorphic ventricular tachycardia (PVT): when the ventricles beat faster than the atria
– prolonged QT = prolonged myocyte repolarisation due to ion channel malfunction
– QRS complexes “twist” around
–Causes: hypoxemia; 2nd to multiple drug effects; antiarrhthymics that prolong QT interval; lyte abnormalities; HypOK+, HypOMg+
–can lead to V-Fib, bradycardia, sudden death

must have evidence of both PVT and QT prolongation

Tx; magneium sulfate +/- lidocaine

119
Q
A

Torsade de pointes

120
Q

Cardiac remodeling with ♡ failure effects

#4

A

– Myocaridal/vascular remodeling
– Apoptosis
– Energy deficiency
– Abnormal Ca++ handling

121
Q

Fursemide effects for ♡ failure treatment

A

Loop Diuretic
– ↓ cardiac preload, and pulmonary hydrostatic pressure
–removes pulmonary edema
–IV administration adds pulmonary vasodilation/bronchdilation

122
Q

Nitroglyceride effects for ♡ failure treatment

A

Venodilator to reduce preload

123
Q

Nitropruisside effects for ♡ failure treatment

A

Reduces afterload
– arterial/venous dilator

124
Q

Dobutamine effects for ♡ failure treatment

A

Positive Inotrope
to improve contractility and systolic function
– increases cAMP

125
Q

Pimobendan for ♡ failure treatment

A

PDE-III inhibitor (metabolizes cAMP)
Inodilator = positive inotrope + vasodilator
– ↑ SV and CO
–reduces afterload
–Does not increase myocardial O2 consumption or work

126
Q

Why is Mannitol contraindication with Heart Failure?

A

–Sugar alcohol that creates hyperosmolarity to shift fluid from interstitial/intracelluar space to intravascular space
–Increases intravascular volume which puts more stress on the heart

127
Q

Hydrochlorothiazide

A

Thiazide diuretic
– Interferes with sodium ion transport across renal tubular epithelium, resulting in increased excretion of sodium, chloride and water

128
Q

Spironolactone for heart failure treatment

A

Aldosterone antagonist by binding to its sites in DCT
–Na+/Ca++/H2o exretion without K+ loss
– Aldosterone blockage possibly slows myocardial remodeling/cardiac fibrosis

129
Q

Sildenafil effects for PH treatment

A

PDE-V inhibitor
–PDE-V found in smooth muscle of pulmonary vasculature
–Inotrope and ateriolar dilator
–potentially delay adverse remodeling of pulmonary arteries

130
Q

Digoxin effects for arrhythmia tx

A

Enhances ANS thru central and peripheral vagal tone
-slows SA node discharge
–prolongs AVN refractory period

131
Q

Which disease process is predisposed to Digoxin toxicity?

A

Hypothyroidism

132
Q

Magnesium Sulfate as antiarhythmia

A

Used for Torsades de pointes
–refractory VT or arrhythias arising from hypoMg++

Adverse efx; CN sdepression, bradycardia, hypotension, hypoCa++, QT prolongation

133
Q

Pericardial Effusion causes

A

K9; neoplasia or idiopathic pericarditis
– HSA 61% of cases (Mets to lungs/liver/spleen)
–growth on RA
– Coagulopathy
–Trauma
–LA rupture
–HCM in cats

134
Q

Chemodectomas

A

Heart base tumors
–Aortic body tumors

Breed predisposed: Boxes/bulldogs/bostons

135
Q

Other types of heart based tumors:

A

Mesotheliomas
Lymphsarcoma
fibrosarcoma
thymomas
adenocarcinoma

136
Q

Pathphys of Pericardial Effusion

A

Fluid in pericardial space = ↑ intrapericaridal pressure that exceeds normal diastolic pressures
–Compression collapses RA
–diastole/ventricular filling (Preload) becomes imparied = ↓ SV/CO and ↑ systemic venous congestion
–chronic PE will activate RAAS and accumulation fluid to ↑ preload

137
Q

What causes reperfusion injury with ATE?

A

Collacteral vasocontriction = toxic buildup of intracellular subtances in the blood
–lead to acidosis, hyperkalemia, renal dysfunction and arrhythmias

138
Q

HARD definition

A

Heartworm associated respiratory disease - seen typically in cats
– anaphylaxis like reaction to HW death
–Rarely; RS-CHF and caval snydrome

139
Q

Myocarditis

A

inflammation of myocardium as result of infection, infammatory process, toxin, trauma, or neoplasic causes
–DCM with arrhythmias typical consequence of MC

140
Q

Myocarditis secondary to Lyme disease

A

Spirochetes produce toxins that damage myocardium
EKG= AVB possibly seen

141
Q

Myocarditis secondary to Bartonella infection

A

flea/tick infestations
–infection travels to cardiac tissues causing arrhythmias/HM

142
Q

Myocarditis secondary to Toxoplamsosis

A

most common cause of infectious MC in cats
–thickened ventricular walls
–pericaridal effusion
– nodular septum

143
Q

Catecholamine definition

A

A type of neurohormone (a chemical that is made by nerve cells and used to send signals to other cells)
– released by adrenal glands
–important in stress responses
–Examples include dopamine, epinephrine (adrenaline), and norepinephrine (noradrenaline)

144
Q

Catecholamine effects on CVS

A

Increase ABP, myocardial contractility, and CO

145
Q

B1-Receptor agonists

efx

A

Primarily responsible for HR/contractility
–ectopic pacemaker activity

Ex: Dobutamine

146
Q

B2-receptor agonists

Efx

A

Primarily responsible for vasodilation/bronchodilation

Ex: terbutaline

147
Q

Post + Presynaptic a1-a2 receptor agonists

A

Primarily responsible for vasoconstriction

Ex; norepi/epinephrine, phenylephrine

148
Q

Precapillary PH

Hemodynamic classification

A
  • No elevated LA pressure
  • -Increased PVR

Ex: PH Classes I/III/IV/V

149
Q

Post Capillary PH

Hemodynamic classification

A
  • Increased LA pressure
  • No increase in PVR

Ex: PH Class II LS-CHF

150
Q

Combined post and pre capillary PH

A
  • increased LA pressure with increased PVR

Ex: PH Class II with other underlying issue (class VI)

151
Q

Action Potentional: Phase 0

A
  • Rapid depolarization
  • Opening of sodium channels, pours into cells
152
Q

Action Potential: Phase 1

A
  • Potassium channels open and sodium channels close
  • Potassium leaves cell
153
Q

Action Potential: Phase 2

A
  • Calcium channels open while potassium channels are still open
  • Calcium is entering cell and potassium leaves cell, charges balance
    eachother out
  • it is responsible for contraction of the heart via ryanodine receptors located within the sarcoplasmic reticulum of the cardiac cell.
154
Q

Action Potential: Phase 3

A
  • Rapid Repolarization
  • Calcium channels close and potassium channels still open
155
Q

Actional Potential: Phase 4

A
  • Resting membrane potential: diastole; state of rest
  • Cell is freely permeable to potassium
156
Q

Action Potential: Phase 0-3 known as

A

Effective refractory period
* Window of time when you can’t trigger another phase 0 action potential
* Built in mechanism to prevent cell from overfiring
* Prolonged ERP causes decreased HR

157
Q
A
158
Q

Purkinje fibers

A

Specialized ventricular cells that may work as a pacemaker when the SA and AV nodes fail to function
– can show up as ventricular escape rhythm or idioventricular rhythm at a rate of 30- 40 bpm in dogs and 60-130 bpm in cats

159
Q

Fusion beats

A

result from the summation of a ventricular impulse and a simultaneous supraventricular impulse, resulting in a QRS complex of mixed morphology and preceded by a P wave
– occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.

160
Q

Capture Beats

A

– occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
– supraventricular impulse conducting through the normal conduction pathways to the ventricle during an episode of VTach or AIVR

161
Q
A

Fusion beats due to VT – the first of the narrower complexes is a fusion beat (the next two are capture beats)

162
Q

Arrhythmogenic mechanisms

A

– Enhanced automaticity
§ membrane potential becomes less negative, which gives it the ability to generate an action potential similar to that of the sinus node
– Triggered activity
– Reentry
§ Requires an impulse to leave a point of departure and return to its starting point with a sufficient delay that the cardiac tissue has recovered its excitability
§ Atrial fibrillation

163
Q

Ventricular premature contraction (VPCs)

A

– Cardiac contraction beginning in Purkinje fibers rather than
SA node

164
Q

Multifocal VPCs

A

Originating from right or left ventricle

165
Q

R-on-T phenomenon

A

The superimposition of an ectopic beat on the T wave of a preceding beat

166
Q

What is R on T at risk for?

A

triggering V-fib

167
Q
A

R-on-T phenomenon

168
Q
A

Natriuretic peptide system
– counter balance for RAAS

169
Q

Patent ductus arteriosus

A

Persistent opening between aorta and pulmonary artery
– Oxygen-rich and –poor blood mix and causes hypervolemia in the lungs, causes PAH

VTS ECC 2024 (17 decks)

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