Cardiology Flashcards
Cardiovascular Nerves
- Reticular formationd of the medulla and lower 1/3 of pons
- Afferent info: CN IX & X –> medulla –> integrated nucleus tract solitarus –> direct changes to CV centers
Cardiovascular brain centers
C1: vasoconstrictor center: upper medulla and lower pons
–> efferent neurons SNS
Cardiac accelerator center: SNS & synapse in the spinal cord and SNS ganglia –> increased firing rate of SA node, increases conduction velocity of AV node & increased contractility
Cardiac decelerator center: PSNS: vagus synapse on SA node –> decreased HR
PAOP
Normal = 5-12 mmHg
When mitral valve is open, LA pressure = LV end diastolic P = preload
** Therefore best indicator for fluid overload
DDX Sinus bradycardia
Hypothermia
hypothyroidism
Pre or POst CPA
Increased ICP
Brainstem disease
Metabolic (inc K, uremia)
Ocular Pressure
Carotid sinus pressure
Inc vagal tone
Sinus node disease
Normal varient (athletic dog)
Drugs (tranquilizer, GA, B blockers, Ca chanel blockers, digoxin)
DDX sinus tachycardia
Pain
Hyperthermia/fever
Anemia/hypoxia
CHF
Shock
Hypotension
Sepsis
Anxiety/fever
Excitement
Exercise
Electric Shock
Inc SNS tone
Toxins (chocolate)
Drugs (anticholinergics, sympathomimetics)
ACVIM Risk Categories Hypertension
AP0 : SBP<150, DBP <95
- minimal risk organ damage
AP1: SBP 150-159; DBP 95-99
-mild risk target organ damage
AP2: SBP 160-179; DBP 100-119
- moderate risk
AP3: SBP >/=180; DBP >/=120
- Severe risk
**Eyes and brai at biggest risk for damage
Bradykinin in vessels
With histamine
Arteriolar dilation & venular constriction –> increased cap hydrostatic pressure –> increased infiltration out of caps and local edema
Factors that increase CVP
-Decreased CO
-Increased blood flow
-Change standing to supine position
-Arterial dilation
-Muscle contraction (abdominal & limb)
- Forced expiration (valsalva)
- Venous costriction
2nd Degree AV block
Mobitz type I: progressive prolongation of PR interval before a nonconductive P wave
- common due to AV node disease or increased vagal tone
Type II: uniform PR interval preceding blocked impulse
- due to disease lower than AV conduction
What determines CVP
- Venous Return: blood flow, venous compliance, sympathetic tone
- R heart function: structural disease, preload, afterload, contractility, drugs
- Intrathoracic pressure: effusion, PEEP, pneumothorax, forced expiration
- Intra-abdominal P: effusion, hypertension, masses. post op, exp effort
- Measure at end of expiration
Chronotropy
SA nodal conduction
HR
Lusitropy
rate of relaxation
What factors effect inotropy
-Preload
- Afterload
-HR
-Sympathetic stimulation
Pulmonary Arterial Catheter
(function, indication, complication)
Functions: CO, CVP, PAOP/PAWP, SvO2, ScvO2, pacing, angiog., research
Indications: Sepsis/SIRS, MODS, CHF, PHT
Complications: hemorrhage, thrombosis, arrhythmias (RBBB, vent), PA rupture, infection. valve damage, peumothorax
Pressure throughout the heart and Pulm Circulation
Hypertensive urgency vs emergency
Urgency:Sigificant increase in BP (ABP>160 mmHg) with no evidence of target organ damage
*Epistaxis can occur
Emergency: human recommendations dec ABP no more than 25% within 1 hr then to 110 within next 2-6 hrs
*Excessive drops –> organ ischemia
3 substances leading to cardiac remodeling
Angiotensin
Aldosterone
Norepinephrine
HCM breeds and diagnosis
- Maine coon & ragdoll
- Wall thickness >6 mm
Management CHF in cats
- Treat Congestion: diuretic, after load reducer (nitroglycerine), inodilator (pimobendan), +/ thoracocentesis
- Treat FATE: analgesia, antithrombotics (heparin, clopidogrel)
- Long Term management: beta blocker ( allow decreased filling due to increased chronotropy)
Secondary causes of cardiomyopathy
- Drugs: doxorubricin
- Nutrition: taurine, carnitine, vitamin E, grain free
- Muscular dystrophy
- Myocarditis (infection/inflammatory)
- Infiltrative (glycogen)
- Neoplastic
DCM treatment main stays
- Relieve Congestion ( diuretic)
- Inhibit RAAS: ACE inhibitor
- POsitive inotropy: Pimobendan
- Beta blocker: novel; no evidence CHF
- Diet: good protein and low Na
6.Supplement: taurine & carnitine - Digoxin: + inotropy and - chronotropy
ARVC (MC CS, ECG Findings, Treatment criteria)
- Autosomal dominant
- CS: 1/3 syncope. 1/3 CHF, 1/3 asymptomatic
- ECG: R sided VPC (LBBB morphology), >100 VPC/24 hrs
- Treatment Criteria: Couplets, runs, R on T, >500-1000 VPC/day
ECG changes assd with increased K+
- Tall tented T waves
- Prolonged QRS
- Decreased P amplitudes
- Sinusoidal appearance
- ST Changes
- atrial standstill
MC Myocarditis causes
Viral: parvo
Protozoal: Chagas Dz/Trypanasoma Cruzi
Noninfectious: doxorubricin
Pathophysiology of endocarditis
- Inciting event: bacteria adhere to disrupted endothelial surface of valve
-Mechanical Lesion exposes EC matrix proteins –> bacteria seed –> coagulation triggered –> coagulum fibrin, fibrinogen, & fibronectin bind bacteria –> bacteria produce enzymes that build proliferative tissue
** Bacteria usually have MSCRAMMS
Thermodilution technique
- Know quantity & temp of either saline or 5% dextrose sol is injected rapidly at proximal port –> cool solution mixed with blood and cools it –> temp difference sensed by thermistor at distal site
- Change temp plotted on time -temp curve
- Area under the curve inversely proportional to CO
** Normal CO 125-200 ml/kg/min (canine) or 120 ml/kg/min (feline)
Atrial Natieuretic Peptides
- Increase with increased atrial pressure, increased venous pressure and increased pulmonary hydrostatic pressure
- causes fluids to shift from vascular space to interstitial space
Paroxysmal SVT
- Not uncommon in large breeds of dog with no primary heart disease
- Sustained tachycardia can cause tachycardia induced DCM
TX: diltiazem
Pulses Paradoxus
- Stronger during expiration and weak/absent during inspiration
-pericardial effusion
Split S2 sound
- only heard if there is disease
- due to pulmomary hypertension
- DDX: HW disease, obstructive pulm disease, congenital cardiac disease, or high altitude
1st Degree AV Block
Prolonged P-R interval, but all impulses conducted
(PR>130 msec in dog, >90 msec in cat)
Pulses alternans
- Alternating weak and normal pulses with regular rhythm
- MC due to decreased contractility, CHF & tachyarrhythmias
Factors that effect diffusion
- Pore size of capillary
- molecular size of diffusing substance
- Concentration differences between 2 sides of membrane
Diseases assd with hypertension
- Kidney Disease
- Diabetes mellitis
- Cushings
- Hyperthyroid
- Pheochromocytoma
- Hyperaldosteronism
- Hepatic Dz
- polycythemia
- chronic anemia
- CHF
- Neoplasia
- Iatrogenic
Donnan Equilibrium Effect
~19 mmHg of colloid osmotic pressure is due to dissolved protein
An additional 9 mmHg is due to + charged cations ( mainly Na2+)
Preload is increased by:
- Increased CVP (decreased venous compliance–> increased thoracic blood volume)
- Increased ventricular compliance (increased expansion of chamber)
- Increased atrial force of contraction
- decreased HR (increased filling tone)
- increased aortic pressure (increased afterload)–> decreased stroke volume (secondary increase in preload)
- Pathologic conditions: systolic failure, aortic insufficiency, subaortic stenosis
Preload
Degree of tension on muscle when it begins to contract
- End diastolic pressure (filled ventricle)
Afterload
Load at which cardiac muscle exert its force
- Pressure in aorta the ventricle pushes against
Contractility
- Intrinsic force of heart
- Degree to which sarcomeres can shorten when activated independent of preload & afterload
Dromotropy
Conduction through AV node
Cardiac Innervation
Automatic nervous system
- PSNS: increased K+ permeability –> hyperpolarize (decreased contractility, dromo, ino and chrono)
R vagus–> SA node
L Vagus - AV node
minimal innervation of ventricular tissue - SNS: beta agonist–> increased Ca2+ entry (inc ino & chrono)
Thoracolumbar N
Dense innervation ventricular tissue
Mediators of vasoconstruction
- Catecholamines: NE/E
- Angiotensin II
- Endothelin
- ADH/vasopressin
-Ions (Ca2+)
Cardiogenic shock: define & causes
Inadequate tissue O2 secondary to cardiac dysfunction
- Systolic dysfunction: failure of contractility, mechanical failure
- Diastolic dysfunction: decreased RV filling
- Bradycardia: decreased CO
3 Components involved in pathophysiology of feline CHF
- Diastolic Dysfunction
- Systolic Anterior motion of mitral valve
- Femoral arterial thromboemboli
** L auricle MC spot for clot formation
Mitral Valve Classes
A. at risk breeds: dobies Cavies
B. Asymptomatic disease
B1: murmur with with no cardiac remodeling
B2: murmur with remodeling (LA enlargement)
C. Historical/current evidence of cardiac failure
D. Severe/ detrimental cardiac failure
CS Cardiogenic Shock
Global Hypoperfusion
- Cold extremities
- Poor pulses
- Dull Mentation
- Prolonged CRT
- Decreased Temp
- Tachycardia
Metabolic Acidosis
Lactic Acidosis
Systolic Failure & mechanisms
- Poor Contractility
- Primary cardiac Dz (DCM)–> decreased contractility
- Extracardiac changes
- Sepsis
- Drug Induced: doxorubricin
- Drugs: CCB, digoxin, beta blockers
- Nutrition: taurine, carnitine, Vit E - Obstruction to Flow
- SAS
-HOCM
Diastolic failure & mechanisms
- INadequate filling: abnormal preload or relaxation
Ex: preicardial effusion or foibrosis
HCM
Tachyarrhythmias
SVT
P wave for each QRS
Sustained tachycardia can induce DCM
**Diltiazem IV»_space;esmolol in dogs
If refractory to diltiazem, second drug such as esmolol, procainamide, or lidocaine
AIVR
- Ventricular rhythm typically occurs during expiratory phase of resp sinus arrhythmia when sinus rate slows
- Sinus rate & ventricular rate similar
- Intervene if additional rapid ventricular rhythm occurs
Hypertensive Encephalopathy
- Common in a sudden rise of arterial BP
- Characterized by edema of white matter
- CS: altered mentation, disorientation, lethargy, seizures, balance disturbances, head tilt, nystagmus, behavior changes
Trigeminy
VPC every 3rd complex
Sustained arrhythmia
Always
Paroxysmal
Occasional
Supraventricular
Above AV node
QRS normal shape
Third degree AV block
No association with P wave rate (100-120 bpm) & normal regular ventricular escape rate (40-60 bpm)
**No meds work for this
Atrial fibrillation
irregularly irregular
increased HR
*Treatment = rate control + management underlying heart dz
- Diltiazem IV or orally
- If CHF or DCM → digoxin with diltiazem has more effective rate control
- If severe concurrent vent arrhythmias → sotalol or amiodarone could be used
- IV magnesium had synergistic effect when combined with other drugs that block the AV node resulting in improved rate control
- Target ventricular response rate for in hospital Afib management: 160-180 bpm
Sick Sinus Syndrome
Period sinus arrest
- some patients have episode of paroxysmal tachcyardia following bradycardic episode.
Colloid osmotic pressure
80% from albumin
20% from globulin
Tiny amount from fibrinogen
Interstitial solid structures
- Collagen fiber bundles–> gives tensile strength to tissue
- Proteoglycan filaments –> composed mainly of hyaluronic acid (fine reticular filaments)
Unstressed volume
Any blood volume that can be added to the venous system that does not contribute to pressure or stress being applied to vessel wall above transmural pressure of zero
**minimal blood volume to prevent collapse
Fluid creep
- Fluids administer as vehicles for other meds (amount ‘creeps’ up on you)
Frank Starling Law
Within physical limits, heart pumps all blood that returns to it by the way of the veins
End Diastolic Pressure
Diastolic P immediately before contraction occurs
Ejection Fraction
- Fraction of end diastolic volume that is ejected during systole
- Normal is 60% or 0.6?
4 AFAST sites
- Subxiphoid or diaphragmatic hepatic
- L flank or splenorenal
- Midline bladder or cystocolic
- R flank or hepatorenal
5 T fast Views
- Chest tube site: 1 on each side of chest btw intercostal spaces 7-9 (dorsal)
- Pericardial Chest site: 1 on each side of chest btw intercostal spaces 5-6 over heart (ventral)
- Subxiphoid AFAST site
Parallell distribution of flow
- Applies to major arteries of aorta
- Blood flow through each organ is a fraction of total blood flow, therefore no loss in pressure in major arteries & mean pressure of each artery will be approximately the same
Mean circulatory filling pressure
- Average transmural pressure of circulatory system when blood flow has stopped
-Determined by blood volume and autonomic control of vascular smooth muscle
Hyperpolarization
Membrane potential has become more negative and occurs when net movement of positive charge out of cell
Depolarization
Membrane potential becomes less negative
ie net movement of + charge into cell
Hypertensive therapy goals
- Decrease ABP to 110-150 mmHg
- Severely hypertensive patients (SBP >250) may exhibit signs of hypotension (syncope, weakness, exercise intolerance, prerenal azotemia)
- Reassess 3-5 days
Thromboxane A2 & vessels
Vasoconstriction
Prostaglandin F & vessels
Vasoconstriction
Angiotensin II & vessels
Vasoconstriction
Laminar vs turbulent flow
- Laminar: ideal- highest velocity in center and next to wall velocity = 0
-Turbulent: disruption interrupts flow and streams mix readily –> anemia, thrombi
Reynolds #: dimensionless number to decide if laminar or turbulent ( laminar if <2000; likely turbulent >2000; definitely turbulent >3000)
CO of different systems
Cerebral 15% CO
Coronary 5% CO
Renal 25% CO
GI 25% CO
Skeletal 25% CO
Skin 5% CO
** Not fixed
Cardio changes with hypertension
Systolic murmurs
Cardiac gallops
LV Hypertrophy
Glide sign
To and fro motion of visceral & parietal pleura as glide over one another with inspiration and expiration
A lines
Horizontal lines of decreased echogenicity visible in the far field similar to & equidistant to pleural line
*Artifact!
B Lines
-“Ring Downs” & “Comet tails”
- Hyper echoic vertical line extending from pleural line to edge of far field
- Occasional B lines = normal
- >3 = interstitial -alveolar abnormalities
Lung Curtain
Movement of lung into and out of view
Lung POint
In pneumo cases, point at which glide sign returns as move in dorsal to ventral position
Torsades de pointes
- Prefibrillatory rhythm
- Sustained vtach
-“twisting of peaks” around isoelectric line
TX: lidocaine
Serotonin & vessels
released with blood vessel damage –> local vasoconstriction
Prostacyclin & vessels
vasodilator
Prostaglandin E & vessels
vasodilator
V Wave
Atrial pressure wave
Caused by infilling of atria from venous return
C wave
Atrial pressure wave
- During ventricular contraction because of back flow of blood and bulge of AV valves toward atria
A wave
Atrial pressure wave
- bump during atrial contraction
Common sources infectious endocarditis
- Prostatitis
- UTI
- Pneumonia
- Diskospondylitis
- Dental Disease
Typical presentation of infectious endocarditis
- middle age, large breed, male
- Lab, golden, GSD, Boxer all over represented
- MC CS: murmur, fever, lameness
- Arrhythmia: SVT, AV block, Afib, Vent
MSCRAMMS
microbial surface components recognizing adhesive matrix molecules
- MC Staphylococcus and strep
Echo findings with constrictive pericarditis
- diastolic flattening
- Abnormal septal motion
- thick pericardium
Cardiac tamponade definition
intrapericardial pressure> RA pressure
* Collapsed RA
Define defibrillation
Shock delivered to critical mass of myocardium resulting in coordinated depolarization and refractory period
- Success depends on:
- Energy delivered
- pathway
- transthoracic impedance
- 4% energy reaches myocardium
- vector
Reliable criteria for Vtach
- Wide bizarre QRS
- No P waves ( AV dissociation)
- Fusion beats present
- Capture beats present
** MC assd with hypokalemia
3 arrhythmagenic mechanisms
- Enhanced automaticity –> spontaneous depolarization
- Triggered activity –> small depolarization
- Re-entry –> circling non conductive tissue
Indications for pacemaker
- CPA with asystole
- HIgh degree AV block
- Symptomatic sick sinus syndrome
- Decreased HR with evidence poor CO/hypotension–> unresponsive to cholinergic/sympathomimetics
- Drug toxicity: CCB, Beta blockers, digoxin
- Acute onset AV block causing frequent syncope
- severe bradyarrhythmia assd with hemodynamic instability during anesthesia
Ocular changes in hypertension
-“hypertensive retinopathy”
- retinal vessel totuosity
-edema
-retinal degeneration
- hyphema
** Increased risk >180 mmHg –> seen at pressures as low as 168
5 phenotypes of feline cardomyopathies
- HCM: LV wall thickening (diffuse or segmental)
- DCM: LV systolic dysfunction with normal or reduced LV thickness –> eventual LV and LA dilation
- Restrictive: either endopmycardial (LV septum) or myocardial (LA or biatrial) scar tissue infiltrate
- Arrhythmogenic RV: severe dilation r heart with RV systolic dysfunction andmyocardial thinning
- Unclassified: any that doesnt fit above 4
Criteria of malignancy for ventricular arrhythmias
- frequent paroxysmal or sustained V tach (HR>180 bpm)
- Evidence of complexity ( R on T phenomenon, triplets, couplets, bigeminy, trigeminy)
- Clinical signs of hemodynamic instability from arrhythmias
- Polymorphic ventricular premature complexes are often more concerning than monomorphic because they indicate multiple regions of disease within the ventricular myocardium
7 mechanisms of blunt cardiac injury
- Direct impact to chest in end diastole during which ventricles are at max capacity OR as end systole when atria are at max capacity
- Suddenly increased cardiac preload secondary to increased venous return due to impact applied to peripheral or abdominal veins
- Bidirectional forces that compress the heart within thoracic cage
- Forces of acceleration and deceleration that cause heart to move leading to myocardial samage/rupture and/or damage to great vessels or coronary arteries
- Blast force leading to cardiac contusion or rupture
- Concussive forces leading to development of arrhythmias
- Cardiac penetration by displaced fractures
causes exudative pericardial effusion
Migrating FB
FIP
Lepto, distemper
Chronic uremia
Idiopathic
Bacterial
Fungal - coccidio, asper, dissiminated tuberculosis
Hepatojugular reflex
Assessed by applying firm pressure to the cranial abdomen while the animal stands quietly with head in a normal position. This pressure transiently increases venous return. Normally there is little to no change in jugular vein appearance. Jugular distention that persists while abdominal pressure is applied constitutes a positive (abnormal) test result
(+result may indicate pericardial effusion)
Pericardiocentesis
Equiptment: Sterile extension tubing, 3 way stop cock, 3 ml syringe, small gauge need for local block, lidocaine, +/-scalpel), sterile gloves, surgical scrub, EDTA and red top tubes
ECG monitoring
Peripheral IVC with IVF before and during (while prepping, dont delay)
R pericardial window clipped (3rd -7th intercostal space) and cleaned
Patient in left lateral recumbency
0.5-1 ml 2% lidocaine instilled into puncture site
Large OTN angiocath (14G)
Advanced into the pericardial space toward the patients left shoulder and stylet removed
Extension tube attached
vasovagal syncope physiology
attributed to Bezold-jarish reflex: bradycardia, vasodilation and hypotension secondary to stimulation of intraventricular receptors (type C fibers) during tachycardia and hypercontractile ventricle
ECG tracing shows breif sinus tach before sudden drop in HE and long period of no or few beats
On occasion when rhythm returns may see paroxysmal atrial fib
Benign form of syncope
- common triggers intense activity/excitement, cough, vomiting
Distinguishing sinus tachycardia from SVT
- Sinus tachycardia: originates in SA node as appropriate response to increased need of CO or increased sympathetic tone
- Xtreme sinus tach can be seen with sympathomimetic toxicity such as chocolate or albuterol toxicity OR hyperT4 or pheochromocytoma
- Intermittent SVT more likely to abruptly start and stop unlike Sinus tach
- If intermittent, asses PR interval→ short with widening of initial QRS upstroke→ supports SVT
- P wave morphology is abnormal with SVT, normal with ST
- HR>220 bpm suggests SVT
- Responsive to vagal maneuver → suggests SVT
- If responds to fluid bolus → ST
- If suspect SVT and responds to diltiazem or esmolol→ SVT
Distinguishing SVT from V tach
- Most importantly QRS duration
- clearly discernible normal P wave independent of regular QRS is strongly suggestive of Vtach.
- ID P waves with a consistent relationship with QRS → SVT with aberration
- P’ waves can sometimes be seen in the ST or TP segments of ECG with some SVTs. These waves represent atrial depolarization initiated OUTSIDE the SA node. P’ waves look differents than normal P waves and have consistent relationship with QRS complex
- Fusion beats (Sinus beat with undetermined QRS) suggestive of Vtach
- Mean QRS axis is usually normal in SVT and abnormal in Vtach
**EXCEPTION: ARVC boxers→ normal qrs axis with wide/bizarre QRS
SVT HR often >240 bpm - Vtach → T wave often in opposite direction of QRS in Vtach. May be eitherway in SVT with more distinct junction btw QRS and ST segment
If tachyarrhythmia terminates in response to vagal maneuver = SVT. If not it may be either SVT or ventricular - If tachycardia terminates with administration of lidocaine IV → likely ventricular HOWEVER an atrial tachycardia will rarely convert with lidocaine and some accessory pathways are responsive to lidocaine
Narrow complex tachycardias
QRS <70ms dog
QRS <40 ms cats
Characteristics suggestive of myocarditis
- History suggests possible (Got doxo, dog lives in TX)
- Unusual signalment for heart disease
- Supportive ECG (conduction abnormalities or arrhythmias)
- Supportive echo (myocardial dysfunction +/- heart enlargement)
- Clin path support ( leukocytosis, eosinophilia, increased cTnI levels)
Refractory periods
Definition: normal AP cannot occur during this time (bc Na channels are closed and no inward depolarizing current possible)
Absolute Refractory Period (ARP): for most of duration of AP, the ventricular cell in incapable of firing another AP despite how large a stimulus bc most Na channels closed; includes upstroke, plateau and part of repolarization, until appx -50 mV
Effective Refractory Period (ERP): a conducted AP cannot be generated - not enough inward current to move to next site; is slightly longer than ARP; if trying to pace a patient with defibrillate - make sure not to do during T wave can throw into V fib
Relative Refractory Period (RRP): may generate a second AP but requires a greater than normal stimulus. If a second AP produced will have abnormal configuration and a shortened plateau phase, begins at end of ARP until cell membrane fully repolarized;
Supranormal period (SNP): follows RRP, begin when MP -70 continues until normal at -85mV, cell is more excitable than normal during this period so less inward current required to depolarize the cell to threshold potential; B/c Na inactivation gates are open and MP is closer to threshold potential than it is at rest so easier to fire an AP
CVP waves
a = atrial contraction
c= tricuspid bulging back into atrium after closure
v = filling of atria prior to tricuspid opening
x descent: decreased atrial pressure during ventricular ejection
y descent: rapid emptying RA after tricuspid opens
List modified duke criteria for endocarditis
Major criteria:
- Pathologic lesion noted on cardiac valve (Oscillating, Hyperechoic, or Shaggy lesion)
- New valvular insufficiency
- AI with no evidence of SAS
- Positive blood cultures
Greater than/equal to 2
Greater than 3 if common skin contaminant
Minor criteria:
- Medium-large breed dog
- Immune mediated disease
- SAS
- Fever
- Positive blood cultures with not common infection
- Thromboembolic disease
- Bartonella serology
Diagnosis
Definitive:
- Pathologic valve lesion
- and 2 major or 1 major, 2 minor
Possible:
3 minor
1 major, 1 minor
Neurohormonal effects of CHF
- RAAS activation : increased fluid retention, cardiac remodeling
- Chronic SNS stimulation: receptor down regulation, persistent tachycardia and myocardial O2 demand, & myocyte necrosis
- Overwhelming nateiuretic peptide system (normally counter regulates RAAS and SNS)
- Increased Endothelin-1 –> increases after load & directly toxic to cardiomyocytes
- Increased vasopressin: increased water retention –> may cause dilutional hyponatremia (poor prognostic indicator)
indications for temporary pacemaker placement
- Stabilization while permanent pacemaker is being placed (BP and HR support under GA)
2.BP & HR support during GA for dogs with clinically silent sinus nodal dysfunction (do not need perm) - Medically refractory bradycardia in a patient that is in need of permanent pacemaker but requires hemodynamic stabilization first (systemic infection/endocarditis) –> transvenous preferred
- Medically refractory and potentially reversible bradycardia (usually drug OD) –> transvenous preferred
- Cardiac arrest from medically refractory sinus arrest leading to asystole due to drug overdose OR natural sinus nodal or AV nodal disease in which meaningful recovery is possible –> transcutaneous preferred
