cardiology Flashcards
cardiac output =
Stroke volume: the amount of blood ejected with each heart beat
* Cardiac output is also termed cardiac performance
* Stroke volume times heart rate is equal to cardiac output (SV x HR=CO)
-determined by HR set by sinus node
determinants of Cardiac
Output: Preload
- The force of cardiac contraction is
dependent upon the level at which it is stretched prior to contraction (end diastolic volume) - Based upon Frank-Starling Law of the Heart
- Once the stretch exceeds a certain level, cardiac output falls (fibers are pulled too far apart
Determinants of Cardiac
Output: Afterload
- Determined by the resistance to ejection
- Increases in afterload lead to a drop in cardiac output
- Afterload is increased by increased chamber size
- Afterload is decreased by increasing wall thickness (normal response in failing hearts)
determinants of Cardiac
Output: Contractility
The intrinsic ability of the heart to
contract independent of preload
* Can be altered through outside factors:
– Catecholamines increase contractility
– Beta blockers decrease
– Few drugs increase
blood pressure
- Main determinants are cardiac output and systemic vascular resistance
- Increases in cardiac output can increase BP: ex hyperthyroidism
-Increases in SVR can increase BP: ex Cushings
forward (low output) cardiac failure
- Common in DCM, sometimes advanced CHF, arrhythmias, also with pericardial effusions
– Pulses poor, hypothermic, weak,
hypotensive, prolonged capillary refill time
– Can have syncope
– Progression to cardiogenic shock with organ dysfunction possible
backwards (congestive) heart failure
- Left sided (most common)
– Increased pressure in left atrium and pulmonary veins
– Left atrial enlargement and pulmonary edema (cough) - Right sided (tricuspid valve dx, heartworm)
– Right atrial pressure increases, jugular vein, CVC distended
– Pleural effusion or ascites result
compensation in cardiovascular medicine (normal bodies compensation methods)
-Frank-Starling Mechanism
* Ventricular hypertrophy
* Neurohumoral mechanisms:
– RAAS
– Adrenergic nervous system
– ADH
– ANP
* Combating neurohumoral activation prolongs lifespan!!!
frank starling mechanism
-Stroke volume decreased for
same preload
* Each beat pumps out less
blood
* This increases preload
* Next beat has better preload
* Eventually results in EDP
that is high enough to cause
edema
RAAS system compensation
-low BP/ decreased ardenergic stimulation or low salt-> renin is released by kidney
-renin transforms-> ang I -> ang II by ACE enzyme
-causes vasoconstriciton (increase BP)
-increase aldosterone (increase Na/H2O retention)
-increase thirst
-increase GFR
-myocardial hypertrophy
ardenergic nervous system compensation
-increase symph tone –> increases contractility, HR, vasoconstriction to increase BP
-increase afterload and O2 demand
-long term harmful to survival
classification of heart failure 4 types? + examples
-volume overload: eccentric hypertrophy (valvular insufficeincy, PDA, VSD)
-pressure overload: concentric hypertrophy (steontic lesions, pulmonary hypertension)
-myocardial failure: contractility decrease (idiopathic DCM, endstage heart failure, taurine deficiency)
-diastolic dysfunction: heart cannot relax (HCM, RCM<, tachycardias)
cardiovascular history
- Appetite, weight changes (loss)
- Activity level, exercise tolerance
- Weakness, syncope
- Previous history of a murmur
- Cough:
– Character: dry, productive, severity
– Timing, if during exersice more likley respiratory, if at times of rest cardiac
– Associated with weakness or syncope
cardiac physical exam
-observe first
-general physical
-retinal exam: hypertensive retinopathy
-mucous membranes: cyanosis, pale, icteric, ect.
-capillary refill time: prolonged with poor perfusion
-jugular vein: reflects status of right atrium (pulses and distension)
-palpate trachea: cough/ thyroid slip
-heart ascultation
heart exam for cardiac physical exam
Apex beat
– Location: shifts if heart shifts
– Strength: reduced with effusion, pneumothorax, obesity, DCM
- Pulses
– Palpate while ausculting
– Symmetry, strength, dorsal pedal - Auscultation
– Heart
– Lungs: sometimes after inducing cough
ascultation for cardiac exam
- Rhythm, dropped beats,
- Murmurs: Physiologic vs. Pathologic
– Physiologic: anemia, flow murmurs in athletes, young animals
– Pathologic: everything else - Murmur characterization
– Timing
– Intensity
– PMI - Lungs
what can an ECG do?
-Diagnose the rhythm
* Diagnose conduction defects
* Detect adverse effects of anesthesia on
cardiac impulse generation and
conduction
* Drug Monitoring (Digitalis, Beta-
Blocker) for meds that influence the
heart rhythm and conduction
* Detect cardiomegaly (better in cats)
* Combined with radiographs can offer
info on congenital defects (PS for
instance)
* Emergency test for suspected
hyperkalemia
* Helpful with pericardial effusion
what can ECG not do?
- Give a definitive diagnosis of heart size
- Determine the mechanical strength of the
contraction induced by the electrical
impulses - Determine if congestive heart failure is
present
indications for an ECG
- Arrhythmia on auscultation
- Heart disease present
- Dyspnea
- Cough
- Weakness, syncope
- Peri-operative especially with GDVs and
splenic disease
-Trauma patients - With certain meds (cardiac drugs, tri-
cyclics) - Monitoring during pericardiocentesis
- Shock
- Bradycardias
-screening tests
screening tests on ECG
Screening Tests
– Certain breeds: can find heart failure DCM 2 years before diagnosis and extend life with treatment. they will have arrythmias.
* Dobermans (highly likely to get DCM)
* Boxer
– Geriatric program
– Pre-operative
QRS complex on ECG waves
P-Wave = Atrial depolarization
* Q-Wave = Septum, first negative before
R
* R-Wave =First positive deflection after P
* S-Wave = First negative deflection after
R
* T-Wave = Repolarization
Indications for thoracic radiographs
- Cough (heart or lung?)
- Heart murmurs, abnormal lung sounds
- Exercise intolerance (heart or lung?)
- Neoplasia (met check)
- Dyspnea, tachypnea (edema, effusion,
tumor, fungus?) - Arrhythmias (heart, tumor?)
-Vital to determine cardiomegaly, vascular status, heart failure and lung changes
Echocardiography: Indications
- Cardiac disease in cats
-look at L atrium, if large =heart failure - Congenital disease
- Endocarditis suspects
- Early detection of DCM
- Pericardial effusion
- Arrhythmias without obvious cause
Factors That
Influence Cardiac Output
-Preload: increase preload, improve stroke
volume, up to a point and then get
congestion. when you reduce preload you reduce congestion with (diuretics)
* Afterload: reduce and improve CO
* Contractility: improve and improve CO
* Heart rate: increased HR improves CO,
up to a point
preload reduction
- Reduce preload to reduce congestion
- Can be achieved with diuretics,
venodilators or low salt diet
frucosemide
- Powerful loop diuretic: potassium
wasting - Potassium wasting can predispose to
arrhythmias and digoxin toxicity - Activates the RAAS by dropping volume
- Powerful enough to cause low output
failure, be cautious in those cases with
low output failure
spironolactone
- Potassium sparing diuretic, can result in
hyperkalemia - Not especially potent
- Usually an “add-on” diuretic
- The “in” drug right now, can prolong life
in humans with CHF - Probably blocks aldosterone escape
ace inhibitors
-as diaretic by cutting thirst,
aldosterone and ADH also reduces
preload
-enalapril, benazapril
reduce afterload:
-prolong life with refractory heart failure
* By decreasing ATII vasoconstriction is
counteracted
* Myocardial oxygen demand is reduced
* Compensatory cardiac hypertrophy is
counteracted
nitroglycerine
- Venodilator, proven efficacy in dogs
- Pools blood into the abdomen, away from the lungs
- Anti-thrombotic effect
- Ointment or patch, apply to skin
- Good for emergency work, tolerance
develops - Oral products: isosorbide dinitrate: not
effective
inotropic support (increasing contractility)
- Can be helpful in emergency situations
- Most agents are adrenergic agents
– Dobutamine: CRI only, preferred drug
– Dopamine: cheaper, can cause arrhythmias
and at higher doses vasoconstriction
-pimobinden
heart rate
- Increased heart rate increases cardiac output
- At high rates, ventricular filling is inadequate
and output drops - Sinus tachycardia is a normal response to
failure - Treating failure often reduces heart rate
- Becomes important with arrhythmias and
severe bradycardias
