Cardiac Diseases/Pathophysiology Flashcards
Cardiac Disease
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
ANP, BNP, NT-proBNP (precursor of BNP)
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
cTnI
troponin c = marker of cardiac injury
o NT-proBNP + cardiac troponin 1 (CTn1) probably most useful for detecting occult CM in cats
Vertebral Heart Score
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
L CHF
Enlarged LA
Enlarged pulmonary veins
Interstitial/alveolar pattern DT pulmonary edema
Pleural effusion in cats (obscuring of heart margins)
R CHF
Enlarged RA/RV
Distended CdVC - larger than aorta
Pleural effusion
Ascites
Ejection Fraction
50-60% in dog, 50-80% cats
* Decent measure of contractility
* (EDV-ESV)/EDV x 100
* Long axis view (4 chamber view)
LV Fractional Shortening
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
Long-Axis Four Chambered Each View
RV/Ra at top
LV/LA on bottom - bigger
Short Axis View
Mushroom = LV
Above the mushroom RV
5 MOA Arrhythmias
- Automaticity
- Excitability
- Ectopic PM
- Re-entry
- Triggered Activity
Automaticity
Ability of heart to spontaneously generate electrical impulse to generate ctx
If SA node not working, other cells take over
Excitability
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
Ectopic PM
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
Re-Entry
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
Triggered Activity
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
Sinus Bradycardia
Normal sinus rhythm with lower expected HR
* Cardiac dz (SSS), hypothyroidism, hypothermia, hyperkalemia
Sinus tachycardia
- 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
Wandering Pacemarker
- 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
Arrhythmias with Disturbances of Supraventricular Impulse Formation
Immediate Tx: Esmolol, Ca channel blockers
Chronic Tx: oral digoxin, diltiazem, +/- beta blockers, occasionally sotalol
APCS
Atrial tachycardia
Atrial flutter - F waves
Atrial fibrillation
Atrial Fibrailltion
“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
Tx Afib
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
APCS
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
Atrial Flutter
Marco-reentry circuit within RA
Atrial enlargement, HCM or restrictive CM
* HR 250-400bpm
Conduction to ventricles variable, may see AV block
Typical Atrial Flutter
regular “saw tooth” appearance (f or flutter waves)
Atypical Atrial Flutter
flutter mimics very fast p waves
Atrioventricular Reciprocating Tachycardia
Congenital AV accessory pathways – muscular tracts that connect atria, ventricle –> bypass AV node
* Accessory pathways usually concealed
Circus movement tachycardia = macro-reentrant tachycardia
orthodromic AV reciprocating tachycardia (OAVRT)
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
Focal Atrial Tachycardia
- 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
Atrioventricular Junctional Rhythm
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
SVT
Used to describe tachycardia from anywhere ABOVE the ventricle including atrial tachycardia, AV junctional rhythm
Avoid drugs that increase AV nodal conductance
Arrhythmias with Disturbances to Ventricular Impulse Conduction
Immediate Tx: lidocaine, procainamide, short-acting beta blockers
Long term therapy: sotalol, mexiletine, amiodarone
VPCS
Vtach
VF
AIVR
BBB
Bigeminy, Trigeminy
Escape complexes
TdP
VPCs
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
Univocal vs multifocal VPCs:
- Unifocal VPCs: same morphology = same foci of depol
- Multifocal VPCs: differing morphologies = different foci of depol
Interpolated VPC
Single VPC occurs without disturbing sinus rhythm
Ddx VPC
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
GSDs and paroxysmal VT
inherited ventricular arrhythmias, affects dogs btw 3-24mo of age
due to myocardial repolarization defect
o Sudden death btw 5-9mo most common
Ventricular tachycardia
> 4 VPCs in a row, HR >160-180bpm
o Decreased diastolic filling time = decreased CO
Reduced pulses, become weaker with increased HR
Paroxysmal VT
Very short duration
Sustained VT
> 30s
Non-sustained VT
<30s
DDX VT
hypoxia, cardiac disease (myocarditis, ARVC), neoplasia, trauma, structural cardiac disease, splenic/hepatic neoplasia, GDV, acidosis, pain, increased catecholamines/sympathomimetic therapy
VF
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
Accelerated Idioventricular Rhythm
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
BBB
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
RBBB
Deep/negatiive QRS with slurred s - think eighth note appearance
RVH, in assoc with VSD, heart dz, RV conduction abnormalities
LBBB
Tall positive QR with negative S/T
DDx: CM, degenerative conduction system dz, ischemia, aortic stenosis, drug tox, secondary to LVH
Ventricular Bigeminy
one normal complex to one ectopic complex
THIOPENTAL
Ventricular Trigeminy
two sinus complexes to one ectopic
Ventricular Escape Complexes
- When dominant pacemaker fails to discharge for long time, “escapes” control of SA node
- <60bpm, usually <30-40bpm
- Multiple = ventricular escape rhythm
TdP
- 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
Ventricular Standstill
P waves with no QRS complexes
SA Block
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
SA Arrest
Failure of SA node to produce depolarization, failure of subsequent P QRS T complex DT severely depressed automaticity of SA node
Persistent Atrial Standstill
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)
First Degree AV Block
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
Second Degree AV Block
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
Mobitz Type I (Wenckebach)
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!
Mobilize type II
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
Third Degree AV Blick
Complete, sustained interruption of AV conduction
Ventricles depolarize according to slow, regular, independent rhythm = escape rhythm
Reentry Circuits
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
Sick Sinus Syndrome
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
Heart Failure
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
*
CHF
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)
MOA HF
o Primary or secondary myocardial failure
o Pressure Overload
o Volume Overload
o Decreased ventricular filling DT poor venous return or abnormal ventricular compliance
Myocardial Failure
loss of cardiac contractile strength
Pressure Overload
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
Volume Overload
increase end diastolic chamber size with normal end-systolic chamber size (contractility N, SV increase)
o Valvular insufficiency, DCM, anatomic shunts
o Eccentric hypertrophy
decreased ventricular filling
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)
Pulmonic Stenosis
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
Pathophys of PS
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
How quantify PS Obstruction
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
Types of PS
Subvalvular
Valvular - A, B
Mixed
Valvular Type A PS
- 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
Valvular Type B PS
- 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
Valvular Type B PS
- 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
Exam Findings of PS
- ECG: often RBBB DT RVH
- PE: L basilar systolic murmur
Associated pathology of PS
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
Anesthetic Goals/Considerations of PS
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
Other Considerations of PS
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
SAS
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)
Fixed SAS
anatomic abnormality creating stenotic lesion
o Severity of obstruction does not change with rate or velocity of flow through area
Dynamic SAS
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
Anesthetic Goals of SAS
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
Mitral Valve Dz
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
Anesthetic Goals of MiVD
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
V-Clamp Procedure
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
Considerations with V Clamp Procedure
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
MiV Stenosis
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
TrV Stenosis
independent finding = rare in SA, valve incompetence much more often DT TrV dysplasia or underlying cardiac disease
Anesthetic Goals of TrV, MiV Stenois
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
Arrhythmogenic Cardiomyopathy
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
DCM
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
Anesthetic Goals
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
VSD
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
Anesthetic Management: VSD
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
PDA
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
Normal DA Physiology
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
CS PDA
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
Ax Goals PDA
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
Branham’s Reflex with PDA
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
Reverse PDA
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
Anesthetic Goals: Reverse PDA
Avoid decreased SVR, avoid increased PVR (hypoventilation, hypoxemia, high PIP, PEEP)
Check lines for air bubbles: air embolus risk
ToF
Overriding aorta,, PS, RVH, VSD
Chronic hypoxemia, polycythemia – up to 70-75% - want PCV at or below 65%, decreased beta2-mediated VD: propranolol
Ax Goals TOF
Avoid decreased SVR, avoid increased PVR (hypoventilation, hypoxemia, excessive ventilation), avoid tachycardia, embolus risk
Consider phlebotomy if needed before go
HCM
Idiopathic concentric thickening of cardiac m = stiffening of myocardium, failure of relaxation
Diastolic dysfunction with concentric LVH
Pathophysiology of HCM
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
HOCM
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
Anesthetic Goals HCM
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
Pulmonary Hypertension
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
Type I PH
Primary PH
Type II PH
PH DT L heart disease
Type III PH
PH DT pulmonary hypoxia, other lung disease
Type IV PH
PH DT thromboembolic dz
Type V PH
miscellaneous
Dx/Eval PH
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
Treatment of PH
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
Ax Goals for PH
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
Pericardial Effusion
Pericardial fluid = cardiac compression = diastolic dysfunction
Cardiac tamponade: effusion causes decreased filling, decreased CO
* Electrical alternans
Anesthetic management Pericardial Effusion
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
Caval Syndrome
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
Hypertension
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
Hypertension - causes
Primary
Secondary
Causes of Secondary Hypertension: endocrine dz
pheo, primary aldosteronism, hyperadrenocorticism, hyperparathyroidism, hypo/hyperthyroidism
How does endocrine dz cause hypertension?
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
Secondary Causes of Hypertension: Renal Dz
Chronic renal dz: renal parenchymal dz, renal artery stenosis
increased neurohormonal activation: increased SNS, direct effects on AngII/RAAS
Secondary Causes of Hypertension
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
Consequences of Hypertension
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
Tx Hypertension
- Thiazide diuretic
- Dihydropyridine Ca channel blocker: amlodipine
Direct vasodilator effect without salt restriction - ACE-I: RAAS = block angiotensin II production: no VC, no H2O/Na retention
- ARB (angiotensin II R blocker, telmisartan) – RAAS – AngII cannot bind to R, no VC, no H2O/Na retention
