Cardio Flashcards
What is the pericardium?
Fibroserous sac thay surrounds the heart
What is the pericardial cavity?
Located between pericardium and the heart
Normal: less than 1mL light yellow fluid
Atrioventricular values
Right AV valve - tricuspid valve
Left AV valve - mitral or bicuspid valve
Action potential
Rapid change in membrane potential or voltage - triggers muscle contractions
Resting membrane potential
Cardiac cell is not electrically charged (-90mV)
Threshold potential
Critical level that membrane potential must reach to initiate action potential
Phase 0
Depolarization (suddenly more +)
Rapid opening of NA channels –> Na ions flow into cell
Phase 2
Plateau phase
Cardiac ions into cell
Phase 1
K channels open –>K leaves cell (inactivated Na channels)
Negative state
(Repolarization)
Phase 3
Rapid repolarization
Cardiac channels close
K channels open = more Negative membrane potential
Phase 4
Diastole –> returns to resting membrane potential
Cardiac output
Stroke volume x heart rate
(Seesaw action)
Volume of blood being pumped by heart in each minute
Stroke volume
Cardiac preload
Cardiac contractility
Cardiac afterload
(Volume of blood being pumped from heart with each pump)
Blood pressure
Systemic vascular resistance x cardiac output
Failure to pump enough blood out into aorta or pulmonary artery, maintain SV, CO or ABP
Systolic failure, forward heart failure or low output heart failure (decreased CO and BP, hypotension, weakness, lethargy)
Preload
Force acting to stretch the ventricles at the end of diastole (end diastolic volume)
Increased in CHF, decreased in hypovolemia
Contractility
The ability or strength of the heart to contract
(Increased in SNS sympathetic stimulation, decreased in HF)
Afterload
Tension created within left ventricular just prior to aortic valve opening that the heart must overcome for blood to leave the heart
(Increased in vasoconstriction, decreased in vasodilation)
Frank starling law
SV increases with increases in preload and contractility and decreases in afterload
Inadequate ventricular filling
diastolic failure, backward heart failure (Heart unable to relax)
Heart unable to empty itself
Congestive heart failure (signs of congestion, pulmonary edema, pleural effusion, ascites)
Left sided heart failure
Signs of congestion, pulmonary edema, dyspnea (pleural effusion in cats)
Right sided heart failure
back op of systemic circulation, ascites, jugular vein distension and peripheral edema
Systolic Heart Failure
normal filling of ventricles, decrease in forward stroke volume –> decreased contractility (inotropy) or increased ventricular pressure (overload) or volume overload
DCM, MI, nutrition deficiency, doxorubicin toxicity
Volume Overload
valvular disease –> chronic mitral valve insufficiency, infectious endocarditis, ruptured chordae tenineae, PDA, atrial or ventral septal defect, hyper T4, chronic anemia
(Eccentric Ventricular hypertrophy)
Pressure Overload
Congential diseases such as pulmonic stenosis, subaortic stenosis, HCM, systemic hypertension, HWD, PTE, pulmonary hypertension
(Concentric hypertrophy)
Diastolic Heart Failure
Impairment to ventricle filling, normal systolic function
inability to relax heart, external constraint, abnormal cardiac compliance
(DCM, MI, ventricular filling obstruction, cardiac tamponade, neoplasia, ventricular hypertrophy
HF treatment
Oxygen therapy
Loop diuretic (furosemide) –> reduce preload, decrease hydrostatic pressure, remove pulmonary edema
Reduce afterload –> nitroglycerin paste, nitroprusside CRI (veno/arteriodilator)
Hydralazine - arterial dilator
Dobutamine –> BP
Pimo –> positive inotropy, reduce afterload
Chronic Valvular Heart Disease
Endocardiosis
AV Valves (mostly left)
Dilated cardiomyopathy
Cardiac enlargement and impaired systolic function
(Genetic, toxic, nutritional, viral)
Most common in dogs
Caval Syndrome of HWD
heavy worm burden >60 worms
Obstruct right heart inflow and tricuspid valve function
Reduce preload –> CO
Venotomy - local anesthesia, in left lateral to remove worms
Hypertrophic Cardiomyopathy
Thickening left ventricular wall and papillary muscles
(more common in cats)
Systemic Thromboembolism
Clot breaks free and becomes lodged in distal vasculature
(Virchows Triad)
Blood lactate from affected limb will be higher
Pericardial Effusion
Abnormal accumulation of fluid in the pericardial cavity
Fluid is significant and compresses heart –> cardiac tamponade
Decreased ventricular filling = decreased preload = decreased strove volume = decreased CO
Electical alternans –> unique ECG finding = swinging of heart once every other heart beat
Endocarditis
Destruction of valve and internal structures of heart (Left AV and aortic valve)
Blood cultures - gold standard
Trauma Associated Myocardial Injury (TAMI)
myocardial contusion 12-36 hours post thoracic trauma (arrythmias –> ventricular usually)
Arrhythmogenic Right Ventricular Cardiomyopathy
boxer cardiomyopathy - fibrous tissue replaced normal tissues
Dx with holter monitor
Sinus Bradycardia
HR abnormally low (parasympathetic nervous system)
sleep/athletes/drugs/severe hypertension/cushings reflex/ increased ICP/hyperkalemia/feline shock
Sinus Tachycardia
Abnormally fast HR (sympathetic nervous system)
vagal maneuver (carotid sinus massage, ocular pressure)
Pain/anxiety/shock/need to urinate/anemia/hyperthyroidism/pheochromocytoma/drugs/hypoxemia/hypercapnia
Sinus Arrythmia
Increase in rate during inspiration, decreased in rate during expiration
Normal in dogs- not normal in cats
Atrial Standstill
Total absence of atrial depolarization (no P wave)
severe hyperkalemia, atrial disease, ECG artifact)
Atrial Premature Contractions
Ectopic part of atrium –> structural or cardiac lesion, hyperT4, atrial tumors
Frank Starling Law
SV increases with increases in preload and contractility and decreases in afterload
Atrial Tachycardia
series of three or more APCs in rapid sequence at a rate greater than the sinus rhythm
(precede a fib)
Atrial fibrillation
Complete electrical disorganization at the atrial level
Can occur is structurally normal hearts under anesthesia –> w/hypoT4, pericardiocentesis, GI dz, volume overload, abdominal dz
Ventricular Premature Contractions
Premature, wide QRS complex
valvular heart dz, cardiomyopathies, congenital heart dz, anemia, hypoxia, GDV, abdominal masses, acidosis, hypokalema, sepsis, myocarditis, trauma, toxicities, anesthesic agents, excessive sympathetic stimulation, pain
Ventricular Tachycardia, flutter, accelerated idioventricular rhythm
3 or more rapid VPCs in rapid sequence that occur at HR at or above 160bpm
(when 3 or more occur at slower hr - AIVR)
Torsades de Pointes
Prolongation of QT interval
Hypokalemia, hypocalcemia, antiarrhythmia drug toxicity
First degree AV block
delay of conduction from atria to ventricles
* No treatment*
Second degree AV block
Complete but transient interruption of conduction from atria to ventricles
Mobitz type 1 - progressive lengthening of PR interval (P wave that occurs w/o QRS complex)
Mobitz type 2 - normal intervals but one or more P waves lacked QRS complexes
Third degree AV block
Complete failure of conductance and total dissociation of atria and ventricles
Sick sinus syndrome
electrical impulse out of sinus node
Junctional and ventricular escape rhythm
EB - wide and bizarre looking QRS complex - mimics VPCs
JEB - more narrow
PAM/345
Pulmonic valve, aortic valve, mitral valve
3rd intercostal space
4th intercostal space,
5th intercostal space,
Stages of heart failure
A - Healthy animals at risk for developing heart disease
B - Diagnostic evidence but no clinical signs
Class B1
Describes patients with low risk of developing CHF or ATE, mostly based on normal chamber sizes
Class B2
Describes patients WITH radiographic or echocardiographic evidence of cardiac remodeling that are at a higher risk of developing CHF- therapy is warranted
C - Cardiac remodeling and concurrent and historical signs of HF
D - CHF and respiratory signs not relieved by medications
Loop diuretics
Furosemide
Acts in loop of henle
Reduced NA, K and water reabsorption
Thiazide diuretics
Stage D
Interferes with sodium ion transport across renal tubular epithelium, resulting in increased excretion of sodium, chloride and water
Hydrochlorothiazide
Aldosterone antagonists
Competitively inhibits aldosterone in the kidney to increase excretion of sodium (and others)
Potassium-sparing
Spironolactone
Carbonic anhydrase inhibitors
Typically used in stage D MMVD
CA found in proximal tubule, reabsorbs sodium
Acetazolamide
Positive Inotropes
Pimobendan
Inodilator: positive inotropy and vasodilatory effects
Both occur through PDE-III inhibition (metabolizes cAMP)
Dobutamine
Beta-1 adrenergic agonist
Increases cAMP
Vasodilators
Arteriodilators
Work to decrease afterload
Amlodipine (dihydropyridine calcium channel blocker), hydralazine, telmisartan (angiotensin II antagonist)
Venodilators
Work to decrease pre- and afterload
Nitroglycerin
Prodrug that releases nitric oxide
Mixed dilators
ACE inhibitors (the “-aprils”)
Enalapril, benazepril
ARB
Angiotensin II receptor blocker
Ex.: telmisartan
Nitroprusside
Becks Triad
Jugular distension
Hypotension
Muffled Heart Sounds
