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Boards: Cardiovascular > Cardiac Diseases/Pathophysiology > Flashcards

Cardiac Diseases/Pathophysiology Flashcards

1
Q

Cardiac Disease

A

decreased ability of CV system to ensure adequate oxygen delivery for day to day survival
* Goal: preserve oxygen delivery, esp important in patients with less than optimal cardiac function

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2
Q

ANP, BNP, NT-proBNP (precursor of BNP)

A

Differentiate cardiac vs pulmonary dz

Detection of occult CM

NT-proBNP moderately specific, sensitive for cardiac dz in adult cats with murmur, gallop or other arrhythmia

False positive in healthy populations: not recommended for routine pre-ax eval

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3
Q

cTnI

A

troponin c = marker of cardiac injury

o NT-proBNP + cardiac troponin 1 (CTn1) probably most useful for detecting occult CM in cats

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4
Q

Vertebral Heart Score

A

R lat: Measuring from ventral portion of carina to apex of heart, across widest part of heart

Count # of vertebral bodies beginning at cranial aspect of T4

Cats: 6.9-8.1, dogs 8.5-10.5

Other things to look for for LA: more pronounced angle at intersection of trachea, heart

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5
Q

L CHF

A

Enlarged LA
Enlarged pulmonary veins
Interstitial/alveolar pattern DT pulmonary edema
Pleural effusion in cats (obscuring of heart margins)

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6
Q

R CHF

A

Enlarged RA/RV
Distended CdVC - larger than aorta
Pleural effusion
Ascites

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7
Q

Ejection Fraction

A

50-60% in dog, 50-80% cats
* Decent measure of contractility
* (EDV-ESV)/EDV x 100
* Long axis view (4 chamber view)

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8
Q

LV Fractional Shortening

A

 LV fractional shortening: 20-50% in dog, 40-50% in cat
* (LVDd-LVDs)/LVDd x 100
* Short axis view (mushroom)
* Influenced by vol overload, how well LV contracting

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9
Q

Long-Axis Four Chambered Each View

A

RV/Ra at top
LV/LA on bottom - bigger

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10
Q

Short Axis View

A

Mushroom = LV
Above the mushroom RV

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11
Q

5 MOA Arrhythmias

A
  1. Automaticity
  2. Excitability
  3. Ectopic PM
  4. Re-entry
  5. Triggered Activity
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12
Q

Automaticity

A

Ability of heart to spontaneously generate electrical impulse to generate ctx

If SA node not working, other cells take over

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13
Q

Excitability

A

Ability of cardiac cell to respond to stimulus by depolarizing

Measure of excitability = difference btw RMP, threshold potential
 Smaller the difference, more excitable the cell
 Enhanced automaticity occurs if TP becomes more negative, or RMP becomes less negative

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14
Q

Ectopic PM

A

Abnormal foci: manifests as premature contraction of heart btw normal beats

Depolarization wave spreads from ectopic PM –> initiates premature ctx
o Most commonly AV node, Bundle of His
o Impulses generated outside SA node follow different (usually slower) conduction pathway, generates changes in configuration of QRS wave on ECG

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15
Q

Re-Entry

A

Unidirectional block in conduction pathway + critical timing + length of refractory period in normal tissue

Propagated electrical signal not completing normal circuit, alterative loop upon itself
 Develops self-perpetuating rapid, abnormal activation (“circus movement”)
o SVT, atrial flutter, atrial fibrillation, VPCs, WPW syndrome, VT, V flutter, V fib

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16
Q

Triggered Activity

A

o Early, late afterdepolarizations
o Occur in assoc with normal electrical activation of CaM cells
o Torsades des Pointes, ventricular bigeminy, catecholamine-dependent atrial tach/VT

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17
Q

Sinus Bradycardia

A

Normal sinus rhythm with lower expected HR
* Cardiac dz (SSS), hypothyroidism, hypothermia, hyperkalemia

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18
Q

Sinus tachycardia

A
  • HR >160bpm in dogs, >200-220bpm in cats
  • Normal physiologic response to pain, stress, anxiety
  • Drug overdoses of anticholinergics, catecholamines/derivatives
  • Pain, hyperthermia, fever, shock, CHF, early stages of hypoxia
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19
Q

Wandering Pacemarker

A
  • Sinus rhythm with variation in origin of P wave within SA node
  • Likely DT variable vagal tone within SA node
  • Cyclic variation in P wave conformation amid normal sinus rhythm
  • If P wave isoelectric, will not see on ECG
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20
Q

Arrhythmias with Disturbances of Supraventricular Impulse Formation

A

Immediate Tx: Esmolol, Ca channel blockers
Chronic Tx: oral digoxin, diltiazem, +/- beta blockers, occasionally sotalol

APCS
Atrial tachycardia
Atrial flutter - F waves
Atrial fibrillation

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21
Q

Atrial Fibrailltion

A

“Irregularly irregular”
Complete loss of p waves, complete lack of coordinated atrial activity
o Prevents atrial kick in most if not all cardiac cycles, significant decrease in CO

DCM in large breed dogs (lone AF), severe atrial enlargement of any cause, cases with severe MvR

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22
Q

Tx Afib

A

Tx: digoxin, beta blockers, Ca channel blockers
o Prevent development of heart failure, extend diastolic filling time to improve CO
* Long-term conversion warranted if heart otherwise structurally normal

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23
Q

APCS

A

Ectopic foci of depolarization within atria

Loss of coordination, timing of atrial contraction (atrial kick) prevents increase in EDV: decrease CO if sufficiently frequent

Cardiac dz – most commonly atrial enlargement secondary of AV valvular dz, valvular dysplasia, PDA
o Also seen with metabolic, neoplastic +/- inflammatory conditions that affect atria

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24
Q

Atrial Flutter

A

Marco-reentry circuit within RA

Atrial enlargement, HCM or restrictive CM
* HR 250-400bpm

Conduction to ventricles variable, may see AV block

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25
Q

Typical Atrial Flutter

A

regular “saw tooth” appearance (f or flutter waves)

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26
Q

Atypical Atrial Flutter

A

flutter mimics very fast p waves

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27
Q

Atrioventricular Reciprocating Tachycardia

A

Congenital AV accessory pathways – muscular tracts that connect atria, ventricle –> bypass AV node
* Accessory pathways usually concealed

Circus movement tachycardia = macro-reentrant tachycardia

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28
Q

orthodromic AV reciprocating tachycardia (OAVRT)

A

Electrical depol travels down AV node in normal direction, depolarization of ventricles occurs

When depol reaches bypass tract, conducted retrograde back up to atra
o Always 1:1 AV conduction
o Labradors, boxers
o Acute start, stop of SVT without warming up or cooling down; pulse rate ~300-400bpm, often terminated by APC or VPC

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29
Q

Focal Atrial Tachycardia

A
  • Rhythmic, atrial focus that activates atrial depol
  • Abnormal automaticity or micro re-entry
  • Can trigger tachycardia-induced myocardial failure, onset of atrial fibrillation
  • Slower SVT 160-300bpm, starts slower then speeds up, cools down before ends
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30
Q

Atrioventricular Junctional Rhythm

A

Re-entry circuit, DT ectopic focus of depolarization of AV node

Narrow, tall QRS complex with inverted p waves before, during, after QRS complex

Tx: breaking reentry circuit with Ca channel blocker decrease Ca entry into myocyte, decrease HR

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31
Q

SVT

A

Used to describe tachycardia from anywhere ABOVE the ventricle including atrial tachycardia, AV junctional rhythm

Avoid drugs that increase AV nodal conductance

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32
Q

Arrhythmias with Disturbances to Ventricular Impulse Conduction

A

Immediate Tx: lidocaine, procainamide, short-acting beta blockers
Long term therapy: sotalol, mexiletine, amiodarone

VPCS
Vtach
VF
AIVR
BBB
Bigeminy, Trigeminy
Escape complexes
TdP

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33
Q

VPCs

A

Ectopic depol foci located in ventricular myocardium, occur before next expected QRS complex
o Depol spreads cell to cell: wide QRS complex

EARLY

Tx: When treat: affect BP, R on T, sustained, polymorphic
–R on T: VPC so premature that superimposed on T wave of preceding complex so ventricles depolarized before repolarized

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34
Q

Univocal vs multifocal VPCs:

A
  • Unifocal VPCs: same morphology = same foci of depol
  • Multifocal VPCs: differing morphologies = different foci of depol
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35
Q

Interpolated VPC

A

Single VPC occurs without disturbing sinus rhythm

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36
Q

Ddx VPC

A

o Degenerative: degenerative valve dz
o Developmental: HCM
o Infectious: sepsis
o Iatrogenic: digitalis, barbiturates
o Nutritional: DCM
o Trauma: myocardial injury
o Vascular: hypoxemia, shock/hypovolemia, hypotension, GDV, acute myocardial infarction, high catecholamine state
o Other: electrolyte abnormalities (hypoK, hypoMg, hyperCa); acid base disturbances

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37
Q

GSDs and paroxysmal VT

A

inherited ventricular arrhythmias, affects dogs btw 3-24mo of age

due to myocardial repolarization defect
o Sudden death btw 5-9mo most common

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38
Q

Ventricular tachycardia

A

> 4 VPCs in a row, HR >160-180bpm
o Decreased diastolic filling time = decreased CO

Reduced pulses, become weaker with increased HR

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39
Q

Paroxysmal VT

A

Very short duration

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40
Q

Sustained VT

A

> 30s

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41
Q

Non-sustained VT

A

<30s

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42
Q

DDX VT

A

hypoxia, cardiac disease (myocarditis, ARVC), neoplasia, trauma, structural cardiac disease, splenic/hepatic neoplasia, GDV, acidosis, pain, increased catecholamines/sympathomimetic therapy

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43
Q

VF

A

Chaotic organization of coarsely wandering electrical potentials of variable duration, amplitude with no PQRST organization

Nonperfusing rhythm, no mechanical activity: CO near zero

Consequence of severe VT/TdP, severe systemic/cardiac dz, cardiac sx

Tx: electrical defibrillation

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44
Q

Accelerated Idioventricular Rhythm

A

Ventricular ectopic rhythm >30-50bpm, <180bpm in dogs and >90-100bpm, <180 in cats
* Occurs when focus that should normally be suppressed increases at rate faster than that of the sinus node or AV node

Enhanced automaticity of His-Purkinje +/- myocardium (vagal excess, decreased SNS activity)
* Well tolerated, rarely causes hemodynamic compromise or hypotension

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45
Q

BBB

A

Abnormal depolarization patterns DT delay in depolarization of ventricles supplied by “blocked” conduction tissue
o Blocked tissue: cell to cell communication of depolar, results in wide/slow QRS
o Normal conduction through portion of ventricle NOT blocked
o Aberrant ventricular conduction
o Ventricular aberrancy

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46
Q

RBBB

A

Deep/negatiive QRS with slurred s - think eighth note appearance

RVH, in assoc with VSD, heart dz, RV conduction abnormalities

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47
Q

LBBB

A

Tall positive QR with negative S/T

DDx: CM, degenerative conduction system dz, ischemia, aortic stenosis, drug tox, secondary to LVH

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48
Q

Ventricular Bigeminy

A

one normal complex to one ectopic complex
THIOPENTAL

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49
Q

Ventricular Trigeminy

A

two sinus complexes to one ectopic

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50
Q

Ventricular Escape Complexes

A
  • When dominant pacemaker fails to discharge for long time, “escapes” control of SA node
  • <60bpm, usually <30-40bpm
  • Multiple = ventricular escape rhythm
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51
Q

TdP

A
  • Think twisted sin wave
  • Polymorphic ventricular tachycardia
  • Always follows long Q-T intervals
    o QT interval: duration of ventricular depolarization, repolarization; impacts recovery times of cells (rate-dependent)
  • Can progress to vfib
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52
Q

Ventricular Standstill

A

P waves with no QRS complexes

53
Q

SA Block

A

Failure of conduction

Ddx: carotid sinus or ocular stimulation, SA nodal fibrosis, digoxin, beta adrenergic blockers, hyperexcitability of Vagus N (vagotonia) with intrathoracic or cervical mass manipulation

54
Q

SA Arrest

A

Failure of SA node to produce depolarization, failure of subsequent P QRS T complex DT severely depressed automaticity of SA node

55
Q

Persistent Atrial Standstill

A

Failure of normally generated SA nodal potentials to depolarize atria
* ECG: flat line, no P waves

DDx: dz atrial myocardium unable to depolarize normally or electrolyte imbalances (hyperkalemia)

56
Q

First Degree AV Block

A

Prolongation of PR interval DT slowed conduction through AV node - R away from P

o DDx: AV nodal dz (fibrosis, ischemia, CM), vagal stimulation, electrolyte imbalances (hypo/hyperkalemia, drug SE (propranolol, digitals)
o Not usually clinically significant, not usually visible on ECG

57
Q

Second Degree AV Block

A

Intermittent failure/delay in assoc of atrial depol through AV node to bundle of His, subsequent ventricular depol

One or more isolated P waves not followed by QRS complexes

58
Q

Mobitz Type I (Wenckebach)

A

increase in duration of P to R interval in successive sinus beats until P wave completely blocked, not conducted through AV node
 DT altered AV nodal physiology, AV nodal dz, drug SE
 May be normal in high vagal tone species

Longer, longer, longer, drop!

59
Q

Mobilize type II

A

acute, intermittent failure of conduction of P wave through AV node
 PR intervals of successfully conducted P waves normal duration
 Many P waves not conducted so that PR interval cannot be assessed, termed high grade

60
Q

Third Degree AV Blick

A

Complete, sustained interruption of AV conduction

Ventricles depolarize according to slow, regular, independent rhythm = escape rhythm

61
Q

Reentry Circuits

A

Ventricular pre-excitation (VPE): atrial bypass tract outside AV junction connects atrium to ventricle around AV node

ECG findings:
 Short P-R interval
 If bypass tract circumvents both AV node and bundle of His, early activation of ventricles causes slurring of QRS upstroke = delta wave
o Retrograde conduction may result in supraventricular paroxysmal tachycardia DT reentry mechanism = WPW
o AKA accessory pathway mediated SVT in Labradors, WPW

62
Q

Sick Sinus Syndrome

A

Abnormally functioning SA node, fails to trigger normal sinus complexes
o Sinus node dysfunction
o No escape rhythm triggered during long periods of sinus arrest

Often no escape rhythm +/- variety of bradyarrhythmias

Female miniature Schnauzers >6yo, WHWT, Cairn terriers

63
Q

Heart Failure

A

Def: inability of heart to function as a pump, create forward flow

Activation of multiple neurohormonal, vascular mechanisms that compensate for lack of forward flow
o Initially mechanisms beneficial: improve BP, perfusion
*

64
Q

CHF

A

failure of LV or RV, subsequent mechanisms that lead to fluid accumulation in lungs (pulmonary edema with L CHF) or abdomen (ascites with R CHF)

65
Q

MOA HF

A

o Primary or secondary myocardial failure
o Pressure Overload
o Volume Overload
o Decreased ventricular filling DT poor venous return or abnormal ventricular compliance

66
Q

Myocardial Failure

A

loss of cardiac contractile strength

67
Q

Pressure Overload

A

DT increase in myocardial wall stress after increases in ventricular systolic pressure

Valvular stenosis: SAS, PS; increases in SVR/PVR from systemic or PH

Concentric hypertrophy
 Inner layers of hypertrophied m may be underperfused: ischemia, ventricular arrhythmias, fibrillation, sudden death

68
Q

Volume Overload

A

increase end diastolic chamber size with normal end-systolic chamber size (contractility N, SV increase)
o Valvular insufficiency, DCM, anatomic shunts
o Eccentric hypertrophy

69
Q

decreased ventricular filling

A

when physical obstruction to blood flow, blood vol decreased or impaired relaxation/impaired ventricular filling

–Physical obstruction: enlarged abdominal organs, surgical manipulation of vasculature responsible for venous return, PPV
–decreased preload: acute or chronic
–decreased ventricular compliance: HCM, constrictive pericarditis

Poor compliance = abnormally high filling pressures, relatively normal filling volumes (tall PV loop)

70
Q

Pulmonic Stenosis

A

Obstruction to right ventricular outflow increased resistance to systolic ejection, proportional increased in ventricular systolic pressure
* Concentric hypertrophy of RV = Attempt to normalize wall stress

71
Q

Pathophys of PS

A

During systole, the blood ejected from the RV accelerates as it traverses the obstructive orifice
o Blood flow velocity increases, becomes turbulent distal to the obstruction
o Poststenotic dilation develops in the main pulmonary artery as the turbulent jet flow decelerates and expends some of kinetic energy against the vessel wall

Concentric hypertrophy reduces right ventricular diastolic compliance, impairs ventricular filling, and often results in elevated right atrial pressure

72
Q

How quantify PS Obstruction

A

peak velocity of blood flow jet must be recorded on a spectral Doppler tracing acquired with the continuous wave Doppler beam in parallel alignment with the direction of flow

Modified Bernoulli equation: change in P = 4V2: relates instantaneous pressure gradient across obstruction to peak velocity of jet distal to obstruction
Mild <50
Moderate 50-80
Severe >80

73
Q

Types of PS

A

Subvalvular
Valvular - A, B
Mixed

74
Q

Valvular Type A PS

A
  • Normal annular size with various degrees of valve leaflet thickening, incomplete separation of valve commissures to almost complete fusion
  • Causes systolic doming of the valve

Post-stenotic dilatation of pulmonary truck present with various degrees of severity

75
Q

Valvular Type B PS

A
  • Hypoplastic ostium with various degrees of valvular leaflet thickening,m immobility but little commissural fusion
  • Main pulmonary trunk often hypoplastic: rarely presents post-stenotic dilatation
76
Q

Valvular Type B PS

A
  • Hypoplastic ostium with various degrees of valvular leaflet thickening,m immobility but little commissural fusion
  • Main pulmonary trunk often hypoplastic: rarely presents post-stenotic dilatation
77
Q

Exam Findings of PS

A
  • ECG: often RBBB DT RVH
  • PE: L basilar systolic murmur
78
Q

Associated pathology of PS

A

Associated pathology: PFO (membrane)/ ASD (hole)
o ~30%

Bulldogs: aberrant coronary artery
o If balloon, will rapidly bleed out from ruptured artery
o Aortic root injection of contrast

79
Q

Anesthetic Goals/Considerations of PS

A

Maintain preload: noncompliant ventricles, poor diastolic function
 Fluid therapy, avoid overload
 Conservative IPPV with low PIP

Avoid decreased PVR: will increase pressure gradient, increase myocardial work

Avoid hypocapnia, alkalosis

Avoid increased HR, maintain NSR

80
Q

Other Considerations of PS

A

o If have PFO: can have shunting of blood from R to L (hypoxemia), can use alpha agonist to increase pressure on aorta which increases LV pressure: support shunt going L –> R

81
Q

SAS

A

LV pressure overload, (concentric hypertrophy) outflow tract usually fixed
* Most common congenital cardiac dz in large breed dogs

Can be fixed (anatomic abnormality critic stenotic lesion) or dynamic (HCM)

82
Q

Fixed SAS

A

anatomic abnormality creating stenotic lesion
o Severity of obstruction does not change with rate or velocity of flow through area

83
Q

Dynamic SAS

A

obstruction of LVOT that changes based on flow rate through subaortic outflow tract
o Increases in HR, cardiac contractility = decrease in intraluminal pressure (based on modified Bernoulli equation), increase in degree of LVOT

84
Q

Anesthetic Goals of SAS

A

Maintain preload: noncompliant ventricles, poor diastolic function
 Fluid therapy, avoid overload
 Conservative IPPV with low PIP

Avoid decreased SVR: will increase pressure gradient, increases myocardial work
Predisposed to myocardial ischemia

85
Q

Mitral Valve Dz

A

Volume overload= eccentric hypertrophy, annular dilation –> MR
o MR causes excess blood to go back into LA
o Further dilation of valve, worsening of MR, worsening of enlargement/MR

Vol of regurg dictated by size of space btw valve leaflets, pressure gradient btw ventricles and atria, duration of systole

86
Q

Anesthetic Goals of MiVD

A

Maintain high to normal HR to minimize ventricular volume, decrease time for retrograde flow

Avoid increases in SVR: worsen regurgitation to increased pressure gradient
Support systolic function: inhalant sparing techniques, etomidate, dobutamine

87
Q

V-Clamp Procedure

A

 L thoracotomy incision near apex of heart, +/- verify with fluoro
 Lungs packed off, PEEP not always possible
 Purse string in apex of heart  most commonly when see VPCs
 Heparin 50IU/kg IV after purse string placement
 Guide wire, introducer through purse-string into apex, across MitV into LA
 Time spent getting valve, device lined up before deploying clamp

88
Q

Considerations with V Clamp Procedure

A

Possible complications: hemorrhage

Once device deployed, can see development of bradycardia that sometimes requires anticholinergic admin
 +/- adjust chamber vol with fluid therapy bc have vol-expanded ventricle now receiving less volume
o Closure: chest tube placement, chest evacuated once closed plus IC/intrapleural LA

89
Q

MiV Stenosis

A

Murmur: mid diastolic, low frequency with possible split second heart sound

Stenotic lesion creates pressure gradient across valve –> increase LA pressure, transmitted to pulmonary vasculature = pulmonary edema with severe stenosis

90
Q

TrV Stenosis

A

independent finding = rare in SA, valve incompetence much more often DT TrV dysplasia or underlying cardiac disease

91
Q

Anesthetic Goals of TrV, MiV Stenois

A

preserve CO

As MVS worsens in severity, ventricular filling depends on diastolic filling time, RAP

Loss of assoc btw atrial depolarization/atrial kick further decreases EDV, can be exacerbated by SVT, atrial fib
o Acute VD, decreased atrial preload will also worsen
o Pressure overload to pulmonary vasculature from MVS can precipitate pulmonary edema

92
Q

Arrhythmogenic Cardiomyopathy

A

AKA boxer CM

Syncope, EI, sudden death

Ax management similar to DCM
o Avoid increase SNS tone DT pain, stress, excitement to decrease arrhythmogenic effects of catecholamine release

93
Q

DCM

A

Idiopathic primary loss of cardiac contractility or DT secondary causes

Loss of contractility = systolic dysfunction, decreased SV (decreased ejection fraction, fractional shortening, rate of injection) = eccentric dilation, vol overload –> annular dilation, MR = further vol overload

94
Q

Anesthetic Goals

A

maintain forward flow, minimize regurgitant flow, maintenance of systolic function, minimize arrhythmias, prevent CHF

Maintain high-normal HR
Avoid increased SVR
Support systolic function
BP: dobutamine - hypotension may be refractory DT down regulation of beta R
Have arrhythmogenics on hand

95
Q

VSD

A

Left to right shunt: vol overload of pulmonary circulation, left heart

If increase pulmonary, RV pressures, can decrease shunt flow or shunt reversal = RAPID DETERIORATION

96
Q

Anesthetic Management: VSD

A

minimize shunt flow, prevent shunt reversal

Avoid increased SVR (and large decreases)
Avoid decreased SVR (and large increases)
Conservative fluid administration DT risk of volume overload

97
Q

PDA

A

Defect btw aorta, pulmonary artery: creates left to right shunt
o Vol overload of pulmonary circulation, left heart

Direction of shunt flow balance btw SVR, PVR

98
Q

Normal DA Physiology

A

DA: fetal structure, 6th embryonic arch: 80-90% RV output/total blood flow from PA to aorta necessary to avoid blood flow through high vascular resistance of fetal lungs
 Increases in oxygen tension in ductus with neonatal ventilation = closure of DA

Normally: following parturition/onset of breathing, PVR decreases so flow through ductus reverses
o Resulting increase in arterial oxygen leads to inhibition of local PGE release = constriction of vascular smooth muscle within vessel wall, closure of ductus
o Usually closed within 7-10d after birth

99
Q

CS PDA

A

loud, continuous murmur dorsal/cranial to heart base

Most will develop L CHF by 1yo

Degree of LV eccentric hypertrophy, LAE reflect magnitude of shunt

If increase pulmonary or RV pressures, can decrease shunt flow or cause shunt reversal = RAPID DETERIORATION

100
Q

Ax Goals PDA

A

minimize shunt flow, prevent shunt reversal, maintain CO

Avoid increasing SVR, significant decreases
Avoid decreasing PVR, large increases

If PH: decreased SVR/increased PVR will risk reverse shunt flow

Conservative fluids DT risk of volume overload

101
Q

Branham’s Reflex with PDA

A

decreased HR secondary to PDA ligation
 Mediated by carotid sinus/aortic arch: increased DAP/MAP stimulates BR causing decreased HR, VD
 3-7% of cases, more likely if larger PDA bc greater change in pressure

102
Q

Reverse PDA

A

R to L shunt, uncommon, usually DT PH
Hypoxemia, polycythemia – up to 70-75%
* CHF rare

o Decrease PCV (phlebotomy to maintain <65%)
o Decrease B2-mediated VD during exercise: propranolol

103
Q

Anesthetic Goals: Reverse PDA

A

Avoid decreased SVR, avoid increased PVR (hypoventilation, hypoxemia, high PIP, PEEP)

Check lines for air bubbles: air embolus risk

104
Q

ToF

A

Overriding aorta,, PS, RVH, VSD

Chronic hypoxemia, polycythemia – up to 70-75% - want PCV at or below 65%, decreased beta2-mediated VD: propranolol

105
Q

Ax Goals TOF

A

Avoid decreased SVR, avoid increased PVR (hypoventilation, hypoxemia, excessive ventilation), avoid tachycardia, embolus risk

Consider phlebotomy if needed before go

106
Q

HCM

A

Idiopathic concentric thickening of cardiac m = stiffening of myocardium, failure of relaxation

Diastolic dysfunction with concentric LVH

107
Q

Pathophysiology of HCM

A

Primarily affects LV free wall, IVS/papillary m

Thickening: decreased internal vol of ventricle when relaxed (EDV), inability to accept venous return –> eventual increase in LA pressure, MiR, pulmonary edema, L heart fail

Poor blood flow DT poor ventricular diastolic compliance, blood stasis = thrombus formation (ATE)
o Poor diastolic ventricular filling also leads to poor CO, BP

108
Q

HOCM

A

muscular hypertrophy pulls anterior mitral valve leaflet into LVOT, dynamic obstruction of ventricular outflow

Increases in HR, velocity of blood flow through LVOT can predispose to systolic anterior motion (SAM) of MV leaflet = worsening of LV CO

109
Q

Anesthetic Goals HCM

A

optimize diastolic filling/function, avoid increases in contractility – prevention of myocardial ischemia, secondary arrhythmias

Avoid decreased SVR - general recommended is VPs if HOCM bc concerns for worsening SAM/LVOT with positive inotropes (dopamine)

Avoid increases in myocardial work

Low to normal HRs

110
Q

Pulmonary Hypertension

A

Abnormally high pressure in blood vessels of pulmonary circulation
o DT increases in: blood flow, blood viscosity, PVR

Normal PVR: systolic 15-25mmHg, diastolic 5-10mm Hg
o >25-35mm Hg = abnormally high

111
Q

Type I PH

A

Primary PH

112
Q

Type II PH

A

PH DT L heart disease

113
Q

Type III PH

A

PH DT pulmonary hypoxia, other lung disease

114
Q

Type IV PH

A

PH DT thromboembolic dz

115
Q

Type V PH

A

miscellaneous

116
Q

Dx/Eval PH

A

determining magnitude of pulmonary hypertension
o TXR: underlying cardioresp dz that predispose to PH

Echo: allows for grading of severity of PAH via measurement of velocity across TrV, surrogate for PA systolic pressure

117
Q

Treatment of PH

A

often fails unless underlying cause identified/addressed before pulmonary vascular remodeling becomes fixed
– vessel intimal proliferation, medial hypertrophy, decreased d compliance

Sildenafil: direct pulmonary VD via PDE-I

118
Q

Ax Goals for PH

A

Prevent hypoxemia
 Pre-oxyg: 100% oxygen = potent pulmonary VD via stimulation of NO (ALU)

Maintain normocapnia
 Mechanical ventilation with conservative PIP
 Maintain normothermia
 Monitor ABGs

Avoid increases in PVR: avoid acidosis, hypoxia, hypercapnia, hypothermia, pain, agitation

119
Q

Pericardial Effusion

A

Pericardial fluid = cardiac compression = diastolic dysfunction

Cardiac tamponade: effusion causes decreased filling, decreased CO
* Electrical alternans

120
Q

Anesthetic management Pericardial Effusion

A

preserve compensatory mechanisms for decreased SV

Optimize preload
 Small fluid bolus PRN
 Conservative IPPV – low PIP, I:E ratio

Maintain normal-high HR
 Anticholinergic PRN
 Ketamine useful

Increase Contractility +/- SVR
 Dopamine, dobutamine, NE

121
Q

Caval Syndrome

A

Retrograde migration of heartworm from PA to RV, RA and VC

Severe tricuspid insufficiency, decreased CO

Hemolysis (marked hemoglobinuria/hemogloinemia, anemia = decreased DO2

Histamine release: increased PVR, DIC, vasculitis

122
Q

Hypertension

A

Risk factor for CV dz: atherosclerosis, CHF, stroke, renal dz, decreased survival

Definition of hypertension: persistently elevated BP
o Systolic >160-180 mmHg, diastolic >90-100

123
Q

Hypertension - causes

A

Primary

Secondary

124
Q

Causes of Secondary Hypertension: endocrine dz

A

pheo, primary aldosteronism, hyperadrenocorticism, hyperparathyroidism, hypo/hyperthyroidism

125
Q

How does endocrine dz cause hypertension?

A

Thyroid hormone: increased HR, increased ctx/peripheral VD - sinus tach with hypertension DT increased in CO

Hyperadrenocorticism, increased circulating glucocorticoids: salt/water retention

Increased circulating catecholamines: hypertension, tachyarrhythmias

126
Q

Secondary Causes of Hypertension: Renal Dz

A

Chronic renal dz: renal parenchymal dz, renal artery stenosis

increased neurohormonal activation: increased SNS, direct effects on AngII/RAAS

127
Q

Secondary Causes of Hypertension

A

 Medication use: chronic NSAIDS, antidepressants, steroids, cylosporin, phenylpronaolamine, EPO
 Aortic coarctation: narrowing of aorta, birth defect
 Polycythemia, DM, increases in ICP, hypercholesterolemia
 Toxicities: salt, lead, nicotine, vitamin D, a1/b1 agonist admin

128
Q

Consequences of Hypertension

A

o Ophthalmic: retinal hemorrhage, acute blindness, retinal detachment, hyphema, retinal atrophy
o Renal: pressure diuresis, glomerulonephritis, renal failure
o CV: gallop rhythms, HM, arrhythmias, hemorrhage (epistaxis, hyphema, etc)
o Neuro: stroke, infarction, hemorrhage  head tilt, sz, paraesis, other neuro signs

129
Q

Tx Hypertension

A
  1. Thiazide diuretic
  2. Dihydropyridine Ca channel blocker: amlodipine
     Direct vasodilator effect without salt restriction
  3. ACE-I: RAAS = block angiotensin II production: no VC, no H2O/Na retention
  4. ARB (angiotensin II R blocker, telmisartan) – RAAS – AngII cannot bind to R, no VC, no H2O/Na retention

Boards: Cardiovascular (11 decks)

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