Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
217 Cards in this Set
- Front
- Back
|
What is the function of the cardiovascular system?
|
to pump blood commensurate with metabolic needs and to do so with a pressure that is adequate to perfuse the vital organs
|
|
|
The heart functions as...
|
two separate pumps that are connected in series....over time cardiac output of left and right heart are equal
|
|
|
Pressure =
|
force/area
---generally measured in mmHg |
|
|
systemic circulation
|
high oxygen
high pressure |
|
|
pulmonary circulation
|
low oxygen
low pressure |
|
|
Functional Anatomy: right ventricle
|
pyramidal geometry
septomarginal trabeculation coarse trabeculae |
|
|
Functional Anatomy: left ventricle
|
smooth wall
fibrous continuity of aortic and mitral valves |
|
|
Stroke volume =
|
volume of blood that is ejected with each beat of the heart
|
|
|
Cardiac output
|
volume of blood pumped by the heart during one minute
conceptually important but not clinically measured (CO = SV x HR) |
|
|
CO=
|
CO = SV x HR
|
|
|
Heart Rate =
|
HR = number of cardiac cycles / minute
|
|
|
Heart Rate
|
DIRECT relationship with CO except when HR is so rapid that ventricular filling is impaired, decreasing stroke volume
species dependent |
|
|
Preload =
|
Preload = the force that stretches the myocardium prior to contraction
|
|
|
Preload
|
- the force that stretches the myocardium prior to contraction
- estimated by measuring the end-diastolic volume/pressure - larger preload -> greater force of ventricular contraction -> larger SV/increased CO (Frank-Starling, direct relationship) |
|
|
Afterload =
|
- the forces that oppose ventricular ejection
- related to aortic pressure/peripheral vascular resistance, but also to ventricular geometry -can be manipulated through the use of vasodilators -INVERSELY related to CO |
|
|
Contractility
|
-the intrinsic ability of the myocardium to shorten (the 'strength' of the myocardium)
-in healthy patients, is depndent on autonomic innervation (sympathetic + vagal activity) and concentration of circulating catecholamines - the level of contractility is called the inotropic state, so there are positive (increase CO/SV) and negative inotropic interventions (decrease CO/SV) - a DIRECT relationship with CO |
|
|
Positive inotropic intervention
|
increase CO/SV
|
|
|
Negative inotropic intervention
|
decrease CO/SV
|
|
|
Heart Failure
|
a SYNDROME of clinical signs that results from impaired emptying or filling of the heart (inadequate CO due to inefficiency of the heart)
-clinical signs result from venous congestion or inadequate perfusion |
|
|
Clinical signs of Heart Failure result from ____________ or ___________.
|
venous congestion or inadequate perfusion
|
|
|
Heart Disease is not _______________.
|
Heart disease is not HEART FAILURE.
|
|
|
Heart Disease
|
- is a structural or functional abnormality of the heart
-does not necessarily mean heart failure |
|
|
Heart failure: end result.....
|
-unless cause is eliminated, heart failure is terminal even with palliative therapy
|
|
|
Circulatory Failure
|
-When the CV system is unable to deliver adequate oxygen and metabolic substrate to body tissues
-can develop without cardiac disease (ex. shock after trauma) |
|
|
Forward (low output) Failure
|
when clinical presentation is dominated by signs resulting from poor perfusion: weakness, hypothermia, pre-renal azotemia
|
|
|
Backward (congestive) Heart Failure
|
-when clinical presentation is dominated by signs resulting from high venous pressures
-the most common manifestation of heart failure in veterinary patients -blood builds up behind the affected ventricle |
|
|
Left Ventricular Congestive Failure results in _________.
|
pulmonary edema
|
|
|
Right Ventricular Congestive Failure results in _______in dogs and __________ in cats.
|
- in dogs:
- usually results in ascites, sometimes concurrent pleural effusion, and rarely peripheral edema -pleural effusion w/out ascites is usu. due to extracardiac disease in cats: -pleural effusion in the absence of ascies can be a sign of left ventricular or biventricular failure -ascites is seldom related to heart disease |
|
|
left ventricular congestive failure
|
pulmonary edema
|
|
|
right ventricular congestive failure
|
ascites
|
|
|
Anatomical Classification of Heart Disease
|
-pericardial
-myocardial -endocardial/valvular -conduction system |
|
|
Pathophysiological Classification of Heart Disease
|
-useful b/c this classification dictates medical therapy
-volume overloads, contractile dysfunction, diastolic dysfunction, pressure overloads, arrhythmias, high cardiac output states |
|
|
Volume overloads
|
increase diastolic volume of the heart (valvular incompetence and shunts)
|
|
|
Contractile Dysfunction
|
functional or structural disorder of the sarcomeres, resulting in DILATED CARDIOMYOPATHY
|
|
|
Diastolic Dysfunction
|
impair ventricular filling
(hypertrophic cardiomyopathy, restrictive cardiomyopathy, pericardial disease) |
|
|
Pressure Overloads
|
increase systolic load, often due to an increased resistance
(aortic stenosis, pulmonary stenosis, pulmonary hypertension) |
|
|
Arrhythmias
|
abnormal cardiac rate or rhythm can result in syncope and sometimes, heart failure
|
|
|
High Cardiac Output States
|
certain states such as hyperthyroidism, chronic anemia, and the presence of an AV fistula may cause or precipitate heart failure
|
|
|
Heart Diseases in Dogs
|
-chronic degenerative valvular disease (CDVD)
-heartworm disease -dilated cardiomyopathy (DCM) -Arrhythmogenic Right Ventricular Cardiomyopathy -Pericardial Disease -Congenital Disease |
|
|
(1) Pathophysiology of Heart Disease and Heart Failure
|
(1)
|
|
|
(2) Diagnostic Approach to Heart Disease and Heart Failure
|
(2)
|
|
|
Heart Diseases in Dogs
|
-chronic degenerative valvular disease (CDVD)
-heartworm disease -dilated cardiomyopathy (DCM) -Arrhythmogenic Right Ventricular Cardiomyopathy -Pericardial Disease -Congenital Disease |
|
|
(1) Pathophysiology of Heart Disease and Heart Failure
|
(1)
|
|
|
(2) Diagnostic Approach to Heart Disease and Heart Failure
|
(2)
|
|
|
Heart Diseases in Dogs
|
-chronic degenerative valvular disease (CDVD)
-heartworm disease -dilated cardiomyopathy (DCM) -Arrhythmogenic Right Ventricular Cardiomyopathy -Pericardial Disease -Congenital Disease |
|
|
Chronic Degenerative Valvular Disease (CDVD)
|
-most common heart condition in dogs
-especially small dogs -geriatric -male > female |
|
|
What is the most common heart condition in dogs?
|
Chronic Degenerative Valvular Disease (CDVD)
|
|
|
Heartworm Disease
|
-preventative measures
- take into account signalment, history, geograph -test regularly and know how to interpret |
|
|
Dilated Cardiomyopathy (DCM)
|
-large or giant breeds
-middle age or younger -male > female -familial = doberman pinschers, boxers - other giant breeds = great danes, irish wolfhounds, scottish deerhounds, etc. |
|
|
Arrhythmogenic Right Ventricular Cardiomyopathy
|
Proclivity in boxers
- check for it if you hear an arrhythmia |
|
|
Pericardial Disease
|
-either tumors or fluids in the pericardium
-middle aged to geriatric -large breed dogs (idiopathic PE) - German Sherpherd and Golden Retrievers (hemangiosarcoma) -Brachycephalic (heart based tumors) |
|
|
Congenital Heart Disease
|
PDA= shetland sheepdogs, german shepherd, miniature poodle (female > male)
SAS = (subaortic stenosis) = golden retrievers, newfoundlands, boxers pulmonic stenosis = bulldogs, terriers, pomeranians |
|
|
American Cocker Spaniel is commonly affected by either _________ or ___________.
|
CDVD or DCM
|
|
|
Heart Disease in Cats
|
- Hypertrophic Cardiomyopathy (HCM)
- Restrictive Cardiomyopathy (RCM) - Heartworm Disease - Dilated Cardiomyopathy (DCM) - Congenital |
|
|
Hypertrophic Cardiomyopathy (HCM)
|
-Most common heart condition in cats
- young to middle aged - Male > female - familial in Maine Coon cats, Persians, others |
|
|
What is the most common heart condition in cats?
|
Hypertrophic Cardiomyopathy
|
|
|
Restrictive Cardiomyopathy (RCM)
|
-middle aged to geriatric
-male > female -might be end stage HCM |
|
|
Dilated Cardiomyopathy (DCM)
|
-middle aged to geriatric
- male > female -rare due to taurine supplementation |
|
|
Common history of cardiac disease/failure
|
exercise intolerance
anorexia weight loss dyspnea cough syncope nocturnal restlessness |
|
|
Exercise intolerance
|
hard to tell in cats
|
|
|
Anorexia
|
not unusual in dogs and cats with CHF but will continue to drink water
|
|
|
Weight Loss
|
significant weight loss is common in small dogs with CHF but is unusual in cats with CHF
|
|
|
Dyspnea
|
-typically the first clinical sign of heart disease in cats
-is the primary client complaint in dogs and cats with pulmonary edema (left ventricular CHF) |
|
|
Cough
|
-need to qualiffy: soft, productive, dry/honking, nocturnal
-small breed dogs may cough as a result of concomitant disease -is typically not a sign of heart disease in cats |
|
|
Syncope
|
-brief (seconds) - no post-ictus, no defecation, no tonic/clonic movements
- rear limb weakness -crying out may occur |
|
|
Nocturnal restlessness
|
may be combination of other clinical signs preventing sleep
|
|
|
Tests: Why is this patient coughing or dyspneic?
|
radiographs
brain natriuretic peptide |
|
|
Tests: Why does his patient have an irregular/fast/slow heart beat?
|
electrocardiogram
|
|
|
Tests: Why does this patient have a heart murmur or gallop sound?
|
Echocardiogram
|
|
|
Tests: Why does this patient have pleural effusion or ascites?
|
cytology/central venous pressure measurement/other lab tests
|
|
|
Thoracic Radiographs
|
- why is this patient dyspneic
-cardiogenic pulmonary edema could result in dyspnea and is visible on a radiograph -big heart, big pulmonary vein, big left atrium -pulmonary edema in interstitial tissues -should take radiographs before and after treatments to see if condition has improved ex. hypertrophic cardiomyopathy of left ventricle -> lung fluid noted in radiograph, gave loop diuretic (furosemide), took another x-ray |
|
|
Brain natriuretic peptide
|
-is released from the ventricle in response to increased wall tension (usually left ventricle)
-plasma BNP concentrations are elevated in dogs with CHF -plasma BNP is therefore a sensitive and specific test for dx of HF in dogs w/ cough/dyspnea -released as prohormone which is then cleaved into active hormone BNP and inactive NT-proBNP (more stable, easier to measure) - commercially available NT-proBNP assay for K9 and Fel. are available |
|
|
What is the best diagnostic test for evaluating heart rate and rhythm?
|
Electrocardiogram (ECG)
|
|
|
What is the best test for evaluating a heart murmur or gallop sound?
|
-Color-flow Doppler Echocardiogram
-more commonly done on cats as dogs are easier to dx |
|
|
What is the 'gold standard' diagnostic test for dx HCM, DCM, and most congenital heart diseases? (eg pericardial effusion)
|
Echocardiogram
|
|
|
Evaluating Hypotensive or Hypertensive Animals
|
-systemic blood pressure methods
1. direct *** 2. oscillometric 3. doppler |
|
|
What diagnostic test should you use when pleural effusion or ascites is present?
|
Central Venous Pressure
-occasionally performed on animals w/ unconfirmed right heart failure -minimally invasive -long jugular catheter is advanced into cranial vena cava and pressure measurement is obtained either by water manometer or electronic measurement |
|
|
If you suspect inflammation/infiltration of the myocardium...
|
measure Cardiac Troponin Levels
-levels increase when there is myocardial injury -establish normal range for dogs and cats using commonly available human analyzers |
|
|
Cardiac Troponin Levels are elevated in....?
|
-myocardial disease, valvular disease, and congenital heart disease
-pericardial effusion due to hemangiosarcoma -myocarditis (Babesia) -ischemic injury or trauma -high dose doxorubicin chemotherapy -oleander toxicity -increased age |
|
|
(3) The Cardiovascular System: History and Physical Exam
|
(3)
|
|
|
Reasons for examining the CV system
|
- recognition of cardiac disease
-cardiovascular consequences of non-cardiac disease (monitoring the critically ill) -anesthetic monitoring |
|
|
Heart disease definition
|
any structural/functional cardiac abnormality, either subclinical or clinical
|
|
|
Patient signalment: Age
|
-younger animals with clinical heart disease -> congenital
-older animals with clinical heart disease -> degenerative (although some congenital diseases can be tolerated for years prior to clinical signs) |
|
|
Patient signalment: Gender
|
occasionally helpful (HCM in cats is seen more in males)
|
|
|
Patient signalment: Breed
|
-canine DCM observed more in Doberman Pinschers and giant breed dogs
-Degenerative valvular disease more in small breed dogs -Tricuspid valve dysplasia - Labradors - HCM in Maine Coon cats |
|
|
Many clinical signs that result from heart disease/failure also result from __________ disease.
|
Respiratory Tract Disease
|
|
|
Exercise Tolerance
|
consider 'use' of patients (sedentary animals will not show exercise intolerance until disease is advanced, while it is apparent in athletes early on)
|
|
|
Cough
|
- in canine and equine patients (cats with heart disease rarely cough)
-a persistent cogh for months or years without treatment is more often due to respiratory disease, not cardiac |
|
|
Tachypnea/Hypernea/Respiratory Distress
|
-often sudden onset
-relatively consistent finding in patients with cardiogenic pulmonary edema |
|
|
Syncope (fainting)
|
-transient loss of consciousness
-when explained by cardiac disease, an arrhythmia is often responsible |
|
|
Failure to Thrive
|
uncommon
occurs with congenital malformations |
|
|
Consequences of Emboli
|
stasis in heart chambers as a result of cardiac disease -> clot -> embolize in periphery (ex. saddle thrombus)
|
|
|
Vital Signs
|
-Temperature rarely a big deal, maybe in severe cardiac disease
-pulse -Respiration |
|
|
Pulse Normals
|
Canine: 70-160
-----depends on breed and temperament -----30-40 when asleep Feline: 160-240 Equine: 24-50 Bovine: 60-110 |
|
|
Sinus Arrhythmias
|
normal arrhythmias associated with respiratory rate
- happens in dogs and cats - rarely observed in clinic as animal is stressed (too much SNS innervation) |
|
|
Arterial Pulse
|
during ventricular ejection, the kinetic wave delivered into the aorta is propagated as a pressure wave throughout the arterial system, resulting in palpable pulsations of peripheral arteries
|
|
|
The arterial pulse can be felt at...?
|
Femoral artery *** - (dog and cat) is felt on the cranial edge of femur (should feel both)
Dorsal pedal a., brachial a., coccygeal a., digital a., facial a. |
|
|
important characteristics of the arterial pulse that can be assessed by palpation
|
amplitude (strength)
quality/pulse character |
|
|
amplitude of arterial pulse
|
-strength of the arterial pulsation
-most closely related to pulse pressure (the difference between systolic and diastolic pressure) -the bump you feel is the difference between these two pressures -does not estimate absolute pressure |
|
|
pulse pressure =
|
the difference between systolic and diastolic pressure
|
|
|
pulse pressure depends on...
|
-stroke volume and the velocity it is ejected at
-physical characteristics of the proximal aorta (distensibility, elasticity) -peripheral resistance to flow -end-diastolic volume of arterial tree -heart rate |
|
|
Quality/Pulse Character
|
-a subtle property that refers t the shape of the arterial pressure pulse
-the shape of the contour is related to the rate at which the pressure rises and falls |
|
|
Weak (hypokinetic) arterial pulse
|
-reflects narrowing of the pulse width***
-usually caused by a decrease in stroke volume -associated with cardiac disease or hypovolemia (shock) -pulsus parvus et tardus |
|
|
Pulsus parvus et tardus
|
a special case of hypokinetic arterial pulse that involves aortic stenosis in which the amplitude is reduced and the rate of rise is slow
|
|
|
When do you have an Absent Arterial Pulse?
|
obstruction due to thromboembolism or an 'artifact'
|
|
|
Bounding (hyperkinetic) arterial pulse
|
-corresponds to an increase in pulse pressure
-can occur when the SV is large -can also occur due to PDA and aortic valve regurgitation |
|
|
What can cause the SV to be large (thus causing a bounding arterial pulse)?
|
sepsis
anemia hyperthyroidism- thyrotoxicosis obligatory bradycardia such as 3rd degree AV block or in athletic indiv. |
|
|
Why can a bounding arterial pulse be cause by PDA and/or aortic valve regurgitation?
|
-all about the difference between pressures
-in PDA, blood is leaking from the aorta to the pulmonary artery -in aortic valve regurgitation, blood is coming back into the left ventricle during diastole -either way it means there is increased systolic pressure in the periphery (since ventricle is bloated) -leaking aorta means blood leaks back into the ventricle, meaning a lowered diastolic pressure in the periphery -the gap b/w the two pressures is more than norm. and the result is increased arterial pressure |
|
|
Central Venous Pulse
|
-pulsation of the external jugular vein is physiologic (not pathologic)
-observing the jugular furrow located on either side of he trachea while patient is standing -the jug. pulse is biphasic and the peaks are assoc. w/ atrial and ventric. systole |
|
|
Central Venous Pulse in Healthy Animals
|
may pulse 5-8cm above the level of the right atrium (vertically, not horizontally), a point that is about one third of the way up the neck from he thoracic inlet
|
|
|
Central Venous Pulse: Unhealthy
|
if pulse is higher than 5-8 cm, elevation of the right ventricular diastolic pressure is likely (volume overload)
-tricuspid valve regurg., DCM, HW disease, cardiac tamponade resulting from pericardial effusion |
|
|
Mucous membranes
|
healthy animal: Pink (reflects presence of oxygenated emoglobin w/in the vasculature); rapid CRT after blanching (less than 2 sec.)
problem: CRT may be prolonged when peripheral perfusion is reduced - (CRT is not sensitive to acute decreases in CO) |
|
|
Mucous Membranes: Pallor
|
-a decrease in oxyhemoglobin due to anemia or vasoconsriction
-peripheral vasoconstriction can occur with pain, hypothermia, reduced CO |
|
|
Mucous Membranes: Cyanosis
|
-when the deoxygenated hemoglobin is visible w/in the vasculature of the membranes (visible when concentration exceeds 4g/dL)
-central cyanosis -peripheral cyanosis |
|
|
Mucous Membranes: Central cyanosis
|
-usually results from cardiopulmonary disease
----mismatch of ventilation and perfusion ----hypoventilation -rarely due to the presence of an anatomical shunt that causes venous admixture ----congenital malform. (ex. Tetralogy of Fallot) are uncommon (deoxy blood shunted to LV) -----cyanosis intensifies w/ exercise |
|
|
Mucous Membranes: Peripheral Cyanosis
|
-occurs when there is stasis of blood w/in the capillary beds
-hemoglobin desaturates -> increasing deoxyhemoglobin -> cyanosis - most often associated w/ reduced CO - if the canosis is localized - it could be due to a thrombosis (ex. saddle thrombosis) |
|
|
Where do you find the PMI (point of maximal intensity) of the precordial impulse
|
- felt over the left cardiac apex (apex beat)
|
|
|
Precordial Palpation
|
-PMI
-palpate prior to auscultation -right ventricular "heave" -precordial thrill |
|
|
Right ventricular "heave"
|
may be apparent when there is substantial right ventricular hypertrophy
|
|
|
Precordial thrill
|
a palpable vibration of the chest wall, may occur when kinetic energy from high intensit murmurs is communicated to the chest wall
---needs to be distinguished from the hyperdynamic apical impulse that results when cardiac enlargement is assoc. w/ preserved myocardial fxn. (mitral valve regurgitation) |
|
|
Auscultation
|
-auscultate both hemithoraces (use both the diaphragm and the bell of the stethoscope)
-check over a large area on both sides, should extend well into the axillary region -don't only listen to the heart's PMI -need to understand the relationship b/w normal and abnormal heart sounds and the mech. activity or the heart |
|
|
Mechanical steps of the cardiac cycle
|
early diastole
diastasis atrium contracts/ventricular filling AV valves snap shut systole- semilunar valves, ventricular ejection |
|
|
1. Early Diastole
|
AV valves open (mitral - left, tricuspid - right)
|
|
|
2. Diastasis
|
Filling
|
|
|
3. Atrium contracts
|
contributes to ventricular filling immediately prior to ventricular contraction
|
|
|
4. AV valves snap shut
|
- as pressure in the ventricle exceeds that of the atrium, the AV valves snap shut
|
|
|
5. Systole
|
Semilunar valves (pulmonary and aortic valves), ventricular ejection
|
|
|
6. myocardial relaxation
|
during myocardial relaxation - semilunar valves snap shut and the AV valves open again
|
|
|
___________pressures are low throughout the cycle.
|
Atrial
|
|
|
___________ are low during _________ to allow filling and rises during __________ (impetus for ventricular ejection).
|
(Ventricular pressures) are low during (diastole) to allow filling and rises during (systole) --- impetus for ventricular ejection
|
|
|
Pressures in _________ and ________ are the same as ventricles in systole, and their pressure is higher during diastole (if semilunar valves are functional)
|
Pressures in (aorta) and (pulmonary artery) are the same as ventricles in systole, and their pressure is higher during diastole (if semilunar valves are functional)
|
|
|
Transient Heart Sounds
|
first heart sound (S1)
Second Heart Sound (S2) Third Heart Sound (S3) Fourth Heart Sound (S4) |
|
|
First Heart Sound (S1)
|
-closure of the semilunar valves
-mitral valve slightly precedes tricuspid valve, but gen. imperceptible. (if both heard =splitting) -lower frequency than S2 -beginning of systole |
|
|
Second Heart Sound (S2)
|
-Closure of the semilunar valves
-occasionally can hear the two valves separately in normal animals (splitting) -higher freq. than S1 -end of systole |
|
|
The timing from S1 to S2 stays constant so when heart rate is elevated.....
|
it is the length of diastole that is altered
|
|
|
Third Heart Sound (S3)
|
-rapid ventricular filling during early diastole
-inaudible in normal dogs and cats, but is often heard in healthy horses -in SA, audible when atrial pressures are high and the ventricle is near its limit of distensibility -in canine, may be heard in patients w/ DCM or severe mitral valve regurg. (so S3 suggests presence of heart failure) |
|
|
Fourth Heart Sound (S4)
|
-Atrial contraction in late diastole
-inaudible in normal dogs and cats, but often heard in healthy horses -in SA, audible when ventricle has reduced compliance -generally assoc. w/ diseases that result in concentric left ventricular hypertrophy, such as HCM or aortic stenosis |
|
|
Splitting of heart sounds
|
-when there is a perceptible delay of valve closure of S1 or S2
|
|
|
S1 splitting
|
perceptible delay b/w mitral and tricuspid valve closure
causes: outflow tract stenosis, volume load, bundle branch block (intraventricular conduction delays), premature complexes (ventricle contracts too soon), physiologic and associated w/ respiration |
|
|
S2 splitting
|
perceptible delay b/w aortic and pulmonary valves
causes: bundle branch block (prolongation of right ventricular systole or shortening of left ventricular systole), pulmonary hypertension or stenosis, mitral regurgitation |
|
|
Systolic clicks
|
-high freq, mid-systolic sound assoc. w/ mitral valve prolapsed
-common in older, small-breed dogs -precursor or mitral valve regurgitation |
|
|
Gallop Sounds
|
-audibility of S3 and/or S4, resulting in a triple rhythm
-results from accentuation of physiologic event (not an arrhythmia) -summation gallop= S3 and S4 are temp. fused when HR is >150 (in cats and many dogs) -heard when atrial pressures are high and ventricle is close to its elastic limit -in SA, rarely heard in healthy animals, and is usu. a specific marker of heart disease -heard in healthy horses |
|
|
Murmurs
|
-prolonged series of vibrations that originate from the CV system and is audible w/ a stethoscope
-in gen. arise when laminar blood flow breaks down, resulting in turbulent blood flow |
|
|
The tendency for turbulence to develop is related to:
|
-Velocity: acceleration explains almost all murmurs
-viscosity - may explain murmurs when HCT <17 (anemia) -vessel diameter - rarely a cause |
|
|
Hemic Murmur
|
functional murmur of anemia
related to decrease in blood viscosity and sometimes, in chronic anemia, to an increase in flow velocity that occurs when SV is increased as a compensatory response |
|
|
Pathological Murmurs
|
assoc. w/ CV abnormalities (valvular or subvalvular stenosis, valvular regurgitation, shunting lesions)
|
|
|
Functional Murmurs
|
result from changes in blood flow velocity that are related to extracardiac factors
|
|
|
Murmurs are characterized based on...
|
Intensity
timing location (PMI) |
|
|
Intensity of Murmurs
|
Grade 1-6
|
|
|
Grade 1
|
very soft and focal; recognized only after careful auscultation
|
|
|
Grade 2
|
soft murmur
|
|
|
Grade 3
|
intermediate intensity
|
|
|
Grade 4
|
loud murmur w/out precordial thrill
|
|
|
Grade 5
|
loud murmur w/ an assoc. precordial thrill
|
|
|
Grade 6
|
loud murmur w/ precordial thrill that is audible when stethoscope is lifted off the chest
|
|
|
Timing of Murmurs
|
-systolic - start after S1, end before S2
-diastolic - start after S2, end before S1 (uncommon on its own) -continuous - begins during systole and persists into diastole - To-and-Fro/Bellows - separate systolic AND diastolic murmurs, but not continuous |
|
|
Location of murmurs (PMI)
|
-PMI may be described in terms of the valve areas of the precordium
|
|
|
Mitral valve murmurs
|
heard near sternum at left 6th ICS
|
|
|
Pulmonary valve murmurs
|
heard dorsally at left 4th ICS
|
|
|
Aortic valve murmurs
|
heard dorsally at left 5th ICS
|
|
|
Tricuspid valve murmurs
|
heard over right hemithorax
|
|
|
Usually easier to characterize murmurs as being heard...
|
on the left or right side, and at the heart apex (aortic, pulmonic) or heart base (tricuspid, mitral)
|
|
|
Configuration of Murmurs
|
refers to the phonocardiographic shape of the murmur
-regurgitant/ plateau-shaped: similar intensity throughout (mitral valve regurg) -Ejection/Diamond shaped: loudest at mid-systole (outflow tract obstruction) |
|
|
Innocent murmurs
|
murmurs that occur in absence of structural cardiac disease in healthy animals
-sometimes heard in puppies, kittens, and adult horses -soft (grade 1-2), mid-systolic murmurs heard over the left cardiac base -often labile w/ intensity changing in response to changes in loading condition and autonomic tone -usu. resolved by 6-8 months |
|
|
When SV increases __________ must also increase to maintain systole duration.
|
ejection volume
-occurs in 'high cardiac output states' --thyrotoxicosis, fever, athleticism, chronic anemia --can also result from shunts |
|
|
Quiescent/resting state
|
cardiomyocyte's interior has an electrical charge of -90mV that is negative relative to the exterior
---this rest period is diastole |
|
|
The resting membrane potential makes the cell _________ when provoked (same as in neurons)
|
excitable
|
|
|
Action Potential
|
a momentary reversal of trans-membrane potential (depolarization) that is sparked by a stimuli to the cell
|
|
|
How is the resting membrane potential maintained and depolarization controlled
|
through factors that include energy dependent ion pumps and the selective voltage-dependent permeability of the membrane
|
|
|
action potential propagation
|
occurs as a wave of depolarization through the conduction system and myocardium that is an electrical signal that triggers myocardial contraction
|
|
|
automacity
|
specialized cardiomyocytes that are structurally and functionally distinct from working cardiomycytes, spontaneously depolarize
|
|
|
working cardiomyocytes
|
don't normally depolarize unless a neighbor tells them to (they can in disease states ---> arrhythmia)
|
|
|
Sinoatrial (SA) Node
|
in RA wall, close to junction of RA and cranial vena cava
|
|
|
Atrioventricular (AV) node
|
in the atrial septum
-gives rise to the AV bundle which bifurcates producing the two bundle branches which give rise to a subendocardial network of purkinje fibers -the only electrical connection b/w atria and ventricles |
|
|
The _________ has a higher rate of spontaneous depolarization than __________ (the pacemaker)
|
SA Node----------AV Node
|
|
|
conduction through _______ is slower than conduction through the ___________.
|
AV node/bundle ---------owrking myocytes
|
|
|
Galvanometer
|
measures electrical potential difference (voltage)
|
|
|
Electrocardiogram
|
a graphic depiction of the electrical activity of the heart that provides information on: heart rate, heart rhythm, cardiac size, mean vector of ventricular or atrial activation
indirect: serum electrolytes and can thus indicate presence of myocardial ischemia |
|
|
What is the primary utility of the ECG?
|
to diagnose arrhythmias
-indicated when the HR is too fast, too slow, or inappropriately irregular |
|
|
What does the ECG measure?
|
-voltage is the electromotive force that causes charged particles to move between oppositely charged structures
-if all myocytes are in resting state or when completely depolarized, there is no potential diff. to be 'seen' -depolarization is propagated as a wave, so when one portion of the myocardium is depolarized and another is in resting state, there is a potential diff. that can be measured |
|
|
Bipolar lead
|
comprised of two electrodes (positive and negative)
- when a wave of depolarization is moving toward the positive electrode it is recorded as a positive deflection by the ECG |
|
|
For 6 commonly used leads, 3 electrodes are required - color coded
|
red - left hind
white- right fore black- left fore green - is an electrical ground |
|
|
Lead II links...
|
the right arm with the let leg, with the positive electrode on the left leg
|
|
|
Mean Electrical Axis
|
average direction taken by the wave of ventricular depolarization (should be toward the left hind limb)
|
|
|
What do the Electrocardiogram Axis stand for?
|
x-axis is time
y-axis is voltage ----paper speed is usu. 50 mm/sec (sometimes 25), specifies X-axis units -sensitivity is usu 1cm=1mV, specifies Y-axis units |
|
|
Normal ECG
|
in gen. the wave of depolarization travels cranial to caudal, rght to left, dorsal to ventral
---so Lead II ECG (right arm and left leg(+)) has deflections that are mainly positive |
|
|
P wave
|
a positive and small deflection, activation of atrial muscle (atrial depolarization)
|
|
|
QRS complex
|
mostly positive deflection, activation of the ventricles (ventricular depolarization)
=don't try to dissect diff. aspects of it out) -larger than p wave due to ventricle's larger mass |
|
|
T wave
|
positive/negative/even biphasic deflection, ventricular repolarization
|
|
|
RR interval
|
difference between ventricular depolarizations
|
|
|
Normal amplitudes and durations for waaves
|
values only apply when recorded in standard position - right lateral recumbency w/ the leads attached just below the olecranon and over the patellar ligament
|
|
|
ECG for cat
|
can be very variable
not uncommon for QRS to have very small deflections |
|
|
Normal Lead II QRS
|
should be rapid w/ a narrow and upright deflection
-looks like this when it goes through the specialized conduction system |
|
|
(5-6) Arrhythmias
|
(5-6)
|
|
|
arrhythmias
|
can be responsible for clinical signs including: syncope, Low CO, sudden cardiac death
-refers to any deviation from regular sinus rhythm |
|
|
Two main categories of arrhythmias
|
bradyarrhythmias and taccharrhythmias (includes single premature complexes as well as pathologic tachycardias such as supraventricular tachycardia, ventricular tachycardia, and atrial fibrillation)
|
|
|
arrhythmias develop when:
|
-disease of the conduction system prevents initiation or propagation of the AP wave -- explains bradyarrhythmias - AV block, SA node disease
-disease of the myocardium ccauses spontaneous depolarization of working myocytes 00 explains tachyarrhythmias - premature complexes, pathologic tachycardias |
|
|
Tachyarrhythmias
|
generally develop in association with structural cardiac disease or extra-cardiac disease (electrolyte, acid-base, ANS imbalances/disturbances)
|
|
|
Pathogenesis of Tachyarrhythmias
|
diseased hearts are often enlarged, meaning they require more oxygen, so they are subject to hypoxia and this interferes with maintainint the resting membrane potential (also compromised by dz processes like inflammation
|
|
|
Causes of Bradyarrhythmias
|
-often result when ribrosis (commonly idiopathic) of the conduction system prevents the initiation or propagation of the depolarizing wave
-also seen due to autonomic factors like high vagal tone |
|
|
What is your approach with electrocardiography rhythm analysis?
|
1. heart rate
2. rhythm (regular or irregular) ----are RR intervals the same (if not do they change abruptly) 3. what is the association b/w atrial and ventricular activity (is there a p wave before each QRS, and is there a normal complex to compare to) 4. mean electrical axis (MEA), amplitudes, etc. |
|
|
Sinus Arrhythmia
|
a P wave of normal morphology precedes every QRS by a consistent and believable PR interval
|
|
|
Sinus Tachycardia
|
rate exceeds:
160 bpm (dog) 240 b/m (cat) 50 b/m (horse) physiologic rhythm, expected with fear, anxiety, pain or exercise compensatory if cardiac perform. falls for any reason usu. present in CHF but is nonspecific finding that may also accompany hypovolemia |
|
|
sick sinus syndrome
|
older small breed dogs where sinus bradycardia and sinus arrest may be responsible for syncope
atropine will resolve physiologic sinus bradycardia |
|
|
Supraventricular Tachyarrhythmia (SVTA)
|
arise proximal to the bifurcation of the bundle of HIs
-therefore QRS is usually narrow (<.07 sec in k9) with normal configuration |
|
|
Supraventricular (atrial or junctional) premature complexes
|
occur early relative to previous RR interval
abrupt decrease in RR interval p wave may have abnormal morphology as it may be superimposed or even obscured by the t-wave of the previous complex -atrial bigeminy |
|
|
supraventricular tachycardia
|
a series of three or more ectopic (arising from abnormal location) supraventricular complexes
-usu begins and ends rapidly (extremely abrupt -> pathologic) -QRS usu. narrow -Rhythm is usu. regular and rapid (>240b/m) ----- in contrast atrial fibrillation is very irregular |
|
|
Atrial Fibrillation
|
-term used for disorganized electrical activity
-AV node is bombarded irregularl and rapidly by wavelets of atrial activity - rapid, irregular, with NO P waves -very abrupt changes in RR intervals -normal QRS |
|
|
Ventricular premature complexes
|
occur early
are wide and bizarre -can be assoc. w/ structural heart disease or extracardiac disease |
|
|
Ventricular Tacharrhythmias
|
when cardiac rhythm or electrocardiographic complex as an origin in the ventricles
-QRS usu. has an abnormal config. |
|
|
3rd degree AV block
|
no consistent relationship between the p wave and the QRS complexes
= more rapid atrial rhythm and slower ventricular rhythm |
|
|
Hyperkalemia
|
associated w/ urethral obstruction, oliguric renal failure and Addison's disease
-wide QRS -p waves of low amplitude or absent -peaked t-waves |
|
|
tachyarrhythmias are treated....
|
pharmacologically
|
|
|
symptomatic bradyarrhythmias are treated by ....
|
cardiac pacing
|
|
|
Indications for and echocardiogram
|
where is the murmur coming from
evaluates myocardial function detects: pericardial effusion tumors - heart base mass, RA/auricular mass, intracardiac mass thrombi/spontaneous echocontrast heartworms left atrial enlargement in cat |
|
|
lower frequencies
|
have better penetration
|
|
|
higher frequency
|
better detail (will tend to be a smaller probe as well)
|
