Cardiovascular system Flashcards
Cardiac Conduction system
SA Node → Atrial conduction → PAUSE -> AV node → Bundle of His → L/R bundle branches → Purkinje fibers → Ventricular conduction
Cardiac Circulation pathway
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
Difference between Pulmonary Artery and Pulmonary Veins
Pulmonary Artery = Carries Deoxygenated blood
Pulmonary Vein = Carries Oxygenated blood
Depolarization
Electrical Activation via loss of polarization with influx of Na+/Ca++ and eflux of K+
Repolarization
Electrical Inactivation; polarization restored via eflux of Na+/Ca++ and influx of K+
Preload
“End Diastolic filling volume” in ventricles or stretch force acting on ventriclular fibers
Afterload
What is its affect on cardiac workload?
force opposing LV immediately PRIOR to aortic valve ejecting blood to the body
resistance aortic valve has to overcome
increased afterload = increased cardiac workload
Contractility
Strength and ability of heart to contract
Refractory Period
state of recovery after neuron has fired an action potential
Absolute or Relative
protects nerve from rapid repetion
Absolute Refractory Period
period of time which 2nd action potential CANNOT occur despite strength of stimulus
Inactivates Na+ channels
Relative Refractory Period
channel activity
2nd action potential can only occur with stronger-than-normal stimulus
some Na+ channels return to resting state and can be reactivated
Inotropic effects
effects cardiac contractility
Positive Inotropes
strengthens cardiac contractility
Ex: Dobutamine
Negative Inotropes
weakens cardiac contractility
Ex: Diltiazem
CO =
CO = HR x SV
how fast the beat is x how strong
MAP =
CO x SVR
Systolic BP
Pressure within main arteries during systole
Ventricular contraction
Diastolic BP
Pressure within main arteries during diastole
Ventricular relaxation
Systole
Atrial/Ventricular contraction
Diastole
Atrial/Ventricular relaxation
“Lub-Dub”
Lub = closure of mitral/tricuspid valves
Dub = closure of aortic/pulmonic valves
silence on valve opening
Sinoatrial Node
Pacemaker of the heart, bundle of specialized muscle fibers that act like nerves, send stimulus to both atria
Atrioventricular Node
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
Printed ECG standard
25mm per second (25 small squares per second)
P wave
Atrial depolarization
(contraction)
Q wave
Depolarization of septum
first negative deflection in complex as it travels R to L
R wave
Depolarization of main ventricular walls
More voltage required due to thick ventricular wall = bigger wave
S wave
Depolarization of Purkinje fibers
T wave
Repolarization of ventricles
PR interval
Start of P-wave to start of Q-wave
time of impulse to travel from SA node → ventricular myocardium
ST interval
End of QRS to start of T-wave
Can shift ↑ or ↓ in position with different dz states
QT interval
Start of Q-wave to end of T-wave
time required for ventricular depolarization and repolarization to occur
may indicate electrolye abnormalities
Starlings Law
what is it in response to?
what relationship does this represent?
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
♡ Failure
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
Left sided ♡ failure
CS
Type of <3 dz that can cause LSHF
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)
Right sided ♡ failure
results from
CS
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
Systolic ♡ Failure
How does it affect SV/contractility?
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.
Diastolic ♡ Failure
results in
Examples
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)
Immediate physiological response to ♡ failure
which receptors involved?
↓ PANS and ↑ SANS = activation of alpha-1 and beta-1 adrenergic receptors = vasoconstriction, ↑ HR + contractility = improved CO and SVR
Delayed physiological response to ♡ failure
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.
Cycle of chronic activation of compensatory mechanisms of ♡ failure
effects on afterload; preload; CO
↓ CO → ↓ tissue perfusion → neuroendocrine response (SNS + RAAS) → ↑ afterload and Na+/H2o retention → ↑ preload/volume/pressure → Cardiac remodeling → decreased SV → ↓ CO
Chronic Valvular ♡ Disease
Breeds predisposed
Aka Endocardosis
degenerative dz of AV valves, Mitral specifically
LA enlargement +/- LV enlargement in progressive state
Life long dz
King Charles/Papillon
DCM
may be cause by =
characterized by =
May result from =
Tx
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
Caval Syndrome
how does it affect CO and preload?
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
Pathophysiology of HWD
CS in dogs vs cats
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)
HCM
–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
CHF manifestation from HCM in cats
in relation to pressure
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
Virchows Triad
3 contributions to thrombosis
1: Hypercoagulatbility
2: Endothelial damage
3: Stasis of blood flow
7
Disease processes at risk of Thromboembolism
PLN; PLE; Cushings; IMHA; ITP; Neoplasia; Trauma
-Also corticosteriod use
-HCM → LA thrombus → break off into abdominal terminal aorta
Endocarditis
what part of the heart does it infect?
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
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
EKG findings
Tx
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
LA:Ao Ratio
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
B-lines
definition
causes
= Pulmonary Edema
3+ in one site = CHF
caused by increased lung density i.a fluid/cells/fibrosis, Alveolar interstial syndrome (AIS/wet lung)
Occult DCM
Structural ♡ changes +/- arrhythmias with no outward CS
Clinical DCM
EKG, CS, TX
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
Type I, II, II ARVC
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
Congenital CV Disease
Shunting defects;
L→ R = CHF/Resp distress
R→ L = hypoxemia/cyanosis
Perivalvular defects; lesions associated with CHF/snycope/collapse
Tetralogy of Fallot
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
Myxomatous Valvular Disease
what specific structures does it affect
Physical changes seen
CS
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
HWD Treatment
Corticosteriods for Eosinophillic infiltrates
Bronchodilators
O2 therapy
Strict cage rest
Furosemide +/- Spironolactone
ACE inhibitors
Pulmonary Hypertension (PH)
Increase in pulmonary vascular BP
mPAP = > 25mmHg
severe > 75mmHg
imbalance between arteriole vasodilation + constriction, platelet activity and smooth muscle proliferation
Classifications of PH I-VI
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
Class I PH causes
causes/tx
HWD, congenital shunts (PDA)
shunts ↑ blood flow back and ↑ pulmonary blood flow
Eisenmengers syndrome
Tx: corticosteriods/bronchodilators for HWD, phlebotomy for polycythemia
Eisenmengers Syndrome
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
Class II PH causes
causes and tx
Chronic degenerative MVD → ↑ LA volume and pressure → ↑ pulmonary venous pressure = PH
Tx: MVD = pimobendan, diuretics/ACE inhibitors for CHF
Ex: MMVD
Class III PH causes
Tracheal collapse, chronic bronchitis, interstitial fibrosis
Tx: specific therapies for infection, bronchodilators and steroids
Class IV PH causes
Thromboembolytic causes;
HWD, IMHA, protein nephropathy/enteropathy, cushings dz, neoplasia, sepsis
Tx: antiplatelet therapy, fibrinolytics (controversial)
Cor Pulmonale
RV enlargement or hypertrophy due to pulmonary disease of arteries/lungs/upper airway
Sick Sinus Syndrome
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
Persistent Atrial Standstill
EKG findings; TX;
–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
Systemic Arterial Hypertension
determined by; Tx;
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
Conditions associated with Systemic Hypertension
“White coat” syndrome
AKD/CKD
DM
hyperadrenocorticism
polycythemia
hyperthyroidism (cats)
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
AV Block Poem
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
First Degree AV Block
Prolonged PR interval
increased vagal tone, AV node fibrosis, drugs that delay AV node conduction
“R is Far from P”
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
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
3rd Degree AV Block or Complete AV Block
CO drastically reduced
Ventricular activation reliant on escape rhythm
Ps and Qs DONT agree
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
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
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
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)
how does this affect systolic/diastolic BP?
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
Underdamped arterial waveform
May cause artificially high systolic and low diastolic
Myoxmatous Mitral Valve Disease (MMVD)
results in
Breed examples
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
Class I Antiarrhythmics
a, b, c
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
Class II Antiarrhythmics
What effect does it have?
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)
Propanolol vs Esmolol
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
cAMP levels
- Cyclic adenosine monophosphate: “second messenger” of beta-1 receptors
- Increase in levels causes increased chronotropy and inotropy
Class III Antiarrhythmics
How do they affect the refractory period?
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
Amiodarone MOA
blocks both currents and makes action potentials more uniform throughout the myocardium so it has the least reported proarrhythmic activity
Sotolol MOA
Combines nonselective beta blockade with rapid component potassium current inhibition
– Effective antiarrhythmic in both SVT and ventricular tachyarrhythmias
Class IV Antiarrhythmics
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
Diltiazem MOA
Used to immediately terminate a severe AV nodal- dependent tachyarrhytmia or slow the ventricular response rate to an atrial tachyarrhythmia (AFib)
Digoxin (digitalis glycosides)
– 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
Stage A of Heart Disease
Animals predisposed or at high risk for heart disease (no disease present at this stage)
Ex: Dobermans/Main Coons/Boxers
Stage B of Heart Disease
A murmur is heard but there are no clinical signs of heart failure
Stage B1 of Heart Disease
No radiographic evidence of heart enlargement or chang on x-ray
Cats: N - mildly lg LA, Low risk of CHF/ATE
Stage B2 of Heart Disease
Radiographic evidence of heart enlargement or changes on x-ray
Cats: moderate - severe lg LA, Higher risk of CHF/ATE
Stage C of Heart Disease
Cardiac remoldeling and/or evidence of heart failure is visible and treatment is necessary
Stage D of Heart Disease
Refractory CHF
Severe/debilitating signs of heart failure thats not responding to
standard treatment
Natriuretic Peptide System
Produced by
Induces =
response to =
Examples
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
Endothelin 1
what produces it
occurs in response to
efx
–Vasoconstrictor produced by vascular endothelial cells
–Response to sheer stress, angiotensin II, and other cytokines
–Alters Ca+ cycling in muscles
–Toxic to myocardiocytes
ACE Inhibitors
Efx on BP; Examples
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
Restrictive cardiomyopathy
definition
associated with
causes
–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
DLVOTO
Dynamic Left Ventricular Outflow Tract Obstruction
what is this commonly caused by?
–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
Systolic anterior motion of the mitral valve (SAM)
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
Feline Aortic Thromboembolism
Where does it typically occur?
caused by
example
Where does it typically occur?
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
Feline aortic thrombo-embolism (FATE) definition
– sudden migration of a left atrial thrombus into the systemic arteries
Feline aortic thrombo-embolism
Pathophys of FATE
– 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
Feline aortic thrombo-embolism
% of cardiomyopathic cats with spontaneous echocardiographic contrast (SEC aka smoke) with identifyable hypercoagulopathy
50%
Feline aortic thrombo-embolism
Diagnosis of FATE
5P rule, which comprises:
1. pallor (i.e., purple or pale toes),
1. polar (i.e., cold extremities),
1. pulselessness,
1. paralysis,
1. pain
Prognosis for FATE
– 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)
Pseudohypertrophy
Caused by dehydration
temporary thickening of cardiac walls due to low volume in chambers
Calcium ion effect on Myocardiocytes
systole vs daistole
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
Regularly Irregular Rhythm ex:
Distinct repeating pattern but not equally spaced
* Bigeminy/Trigeminy
* Sinus arrhythmia
A-flutter can have regular or irregular R-R interval
Irregularly Irregular Rhythm ex:
No distinct pattern with irregular spacing
A-fib
V-fib
Torsade de pointes
Definition; causes; concerns
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
Torsade de pointes
Cardiac remodeling with ♡ failure effects
#4
– Myocaridal/vascular remodeling
– Apoptosis
– Energy deficiency
– Abnormal Ca++ handling
Fursemide effects for ♡ failure treatment
Loop Diuretic
– ↓ cardiac preload, and pulmonary hydrostatic pressure
–removes pulmonary edema
–IV administration adds pulmonary vasodilation/bronchdilation
Nitroglyceride effects for ♡ failure treatment
Venodilator to reduce preload
Nitropruisside effects for ♡ failure treatment
Reduces afterload
– arterial/venous dilator
Dobutamine effects for ♡ failure treatment
Positive Inotrope
to improve contractility and systolic function
– increases cAMP
Pimobendan for ♡ failure treatment
PDE-III inhibitor (metabolizes cAMP)
Inodilator = positive inotrope + vasodilator
– ↑ SV and CO
–reduces afterload
–Does not increase myocardial O2 consumption or work
Why is Mannitol contraindication with Heart Failure?
–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
Hydrochlorothiazide
Thiazide diuretic
– Interferes with sodium ion transport across renal tubular epithelium, resulting in increased excretion of sodium, chloride and water
Spironolactone for heart failure treatment
Aldosterone antagonist by binding to its sites in DCT
–Na+/Ca++/H2o exretion without K+ loss
– Aldosterone blockage possibly slows myocardial remodeling/cardiac fibrosis
Sildenafil effects for PH treatment
PDE-V inhibitor
–PDE-V found in smooth muscle of pulmonary vasculature
–Inotrope and ateriolar dilator
–potentially delay adverse remodeling of pulmonary arteries
Digoxin effects for arrhythmia tx
Enhances ANS thru central and peripheral vagal tone
-slows SA node discharge
–prolongs AVN refractory period
Which disease process is predisposed to Digoxin toxicity?
Hypothyroidism
Magnesium Sulfate as antiarhythmia
Used for Torsades de pointes
–refractory VT or arrhythias arising from hypoMg++
Adverse efx; CN sdepression, bradycardia, hypotension, hypoCa++, QT prolongation
Pericardial Effusion causes
K9; neoplasia or idiopathic pericarditis
– HSA 61% of cases (Mets to lungs/liver/spleen)
–growth on RA
– Coagulopathy
–Trauma
–LA rupture
–HCM in cats
Chemodectomas
Heart base tumors
–Aortic body tumors
Breed predisposed: Boxes/bulldogs/bostons
Other types of heart based tumors:
Mesotheliomas
Lymphsarcoma
fibrosarcoma
thymomas
adenocarcinoma
Pathphys of Pericardial Effusion
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
What causes reperfusion injury with ATE?
Collacteral vasocontriction = toxic buildup of intracellular subtances in the blood
–lead to acidosis, hyperkalemia, renal dysfunction and arrhythmias
HARD definition
Heartworm associated respiratory disease - seen typically in cats
– anaphylaxis like reaction to HW death
–Rarely; RS-CHF and caval snydrome
Myocarditis
inflammation of myocardium as result of infection, infammatory process, toxin, trauma, or neoplasic causes
–DCM with arrhythmias typical consequence of MC
Myocarditis secondary to Lyme disease
Spirochetes produce toxins that damage myocardium
EKG= AVB possibly seen
Myocarditis secondary to Bartonella infection
flea/tick infestations
–infection travels to cardiac tissues causing arrhythmias/HM
Myocarditis secondary to Toxoplamsosis
most common cause of infectious MC in cats
–thickened ventricular walls
–pericaridal effusion
– nodular septum
Catecholamine definition
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)
Catecholamine effects on CVS
Increase ABP, myocardial contractility, and CO
B1-Receptor agonists
efx
Primarily responsible for HR/contractility
–ectopic pacemaker activity
Ex: Dobutamine
B2-receptor agonists
Efx
Primarily responsible for vasodilation/bronchodilation
Ex: terbutaline
Post + Presynaptic a1-a2 receptor agonists
Primarily responsible for vasoconstriction
Ex; norepi/epinephrine, phenylephrine
Precapillary PH
Hemodynamic classification
- No elevated LA pressure
- -Increased PVR
Ex: PH Classes I/III/IV/V
Post Capillary PH
Hemodynamic classification
- Increased LA pressure
- No increase in PVR
Ex: PH Class II LS-CHF
Combined post and pre capillary PH
- increased LA pressure with increased PVR
Ex: PH Class II with other underlying issue (class VI)
Action Potentional: Phase 0
- Rapid depolarization
- Opening of sodium channels, pours into cells
Action Potential: Phase 1
- Potassium channels open and sodium channels close
- Potassium leaves cell
Action Potential: Phase 2
- 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.
Action Potential: Phase 3
- Rapid Repolarization
- Calcium channels close and potassium channels still open
Actional Potential: Phase 4
- Resting membrane potential: diastole; state of rest
- Cell is freely permeable to potassium
Action Potential: Phase 0-3 known as
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
Purkinje fibers
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
Fusion beats
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.
Capture Beats
– 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
Fusion beats due to VT – the first of the narrower complexes is a fusion beat (the next two are capture beats)
Arrhythmogenic mechanisms
– 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
Ventricular premature contraction (VPCs)
– Cardiac contraction beginning in Purkinje fibers rather than
SA node
Multifocal VPCs
Originating from right or left ventricle
R-on-T phenomenon
The superimposition of an ectopic beat on the T wave of a preceding beat
What is R on T at risk for?
triggering V-fib
R-on-T phenomenon
Natriuretic peptide system
– counter balance for RAAS
Patent ductus arteriosus
Persistent opening between aorta and pulmonary artery
– Oxygen-rich and –poor blood mix and causes hypervolemia in the lungs, causes PAH
