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;
83 Cards in this Set
- Front
- Back
|
murmurs gen
|
-abnormal 1st and 2nd heart sounds or additional abnormal noises
-turbulent blood through: 1. altered valves 2. abnormal openings: septal defects, stenotic vessels 3. extracardial effects: fibrous pericarditis |
|
|
grade 1 murmur
|
nearly imperceptable: maybe in quiet room at PMI
|
|
|
grade 2 murmur
|
soft, but definite
-audible right over PMI |
|
|
grade 3 murmur
|
low to moderate
- audible also at some distance to PMI |
|
|
grade 4 murmur
|
loud
-audible all over chest, but not palpable |
|
|
grade 5 murmur
|
very loud
-audible throughout chest and palable |
|
|
grade 6 murmur
|
audible
-audible even when stethoscope not in contact with chest wall and palpable |
|
|
stenosis
|
-undersized valve of vessel
-murmurs created: 1. systole: semilunar valves 2. diastole: AV valves |
|
|
Insufficiency
|
-leakage of valve:
1. systole: AV valves 2. diastole: semilunar valves |
|
|
mitral insufficiency gen
|
-can be go to pathogenic bacteria that thickened and shortened valvular leaflets
-systolic murmur: due to valve not closing sufficiently and blood flow back into the atrium |
|
|
mitral insufficiency ECG
|
- murmur begins during QRS complex (systole) and ends during the T wave (end of systole)
-during diastole the AV valves should be open and murmur dies out |
|
|
machinery murmur
|
-timing: systolic + diastolic murmur
-causes: 1. combo of stenosis and insufficiency 2. patent ductus arteriosus |
|
|
fetal shunts
|
1. ductus arteriosus
2. foramen ovale 3. ductus venosus -high resistance through collapsed lung - low resistance though placenta and DA - BP of R heart is higher than L |
|
|
PDA
|
- at birth, inflation of lung reverses:
1. BP in L/ R heart 2. flow of oxygenated blood thru DA -duct is sensitive to O2 and closes within days-months -systolic-diastolic/ machinery murmur |
|
|
P foramen ovale
|
-normal close silmultaneously with rise of BP at birth
- hardly diagnosed b/c atrial pressure are too low to generate audible murmurs |
|
|
causes of conduction system failure
|
1.cardiac electrical abnormalities
2. cardiac structural abnormalities |
|
|
cardiac electrical abnormalities
|
1. excitation disturbances:
failure of SA node 2. conduction disorder: AV block |
|
|
cardiac structural abnormalities
|
1. morphological: hypertrophy of RV
2. functional: cardiac infarction |
|
|
Types of excitation disturbances
|
1. nontropic
2. heterotropic |
|
|
nomotropic excitation dysfunctions
|
1. sinus arrhythmia
2. sinus tachycardia 3. sinus bradycardia |
|
|
heterotropic excitation dysfunctions
|
-escape rhythm
- extra systoles - shifting pacemaker - supraventricular tachycardia - atrial flutter and fibrillation -ventricular tachycardia, flutter and fibrillation |
|
|
sinus arrhythmia
|
-normal P waves preceeding QRST indicate each sequence intiated by SA node
-normal in dogs: vagal tonus, increase HR during inspiration |
|
|
sinus tachy- and brady-cardia
|
-excitation and conduction are normal
- SA node is pacemaker but initiates APs at a rate lower/higher than normal |
|
|
escape rhythmn
|
-extreme sinus bradycardia: intrinsic rate of AV note exceeds the sinus rate and AV node takes over
- cause failing AV node: then one of the auxillary pacemakers takes over |
|
|
supraventricular systole
|
-premature stimulus generated by heterotropic atrial focus
- normal SA stimulus has no effect - next systole follows at an interval decided by sinus rhythmn |
|
|
supraventricular extra systole
|
-3rd depolarization originates from an ectopic supraventricular pacemaker (P wave precedes QRS)
-negative P wave in lead II and lead III indicates the ectopic initiation of the atrial depolarization |
|
|
shifting pacemaker
|
-If SA slows down or fails other pacemakers take over
- possible cause very high vagal tone - alters P wave and PQ segment - closer the pacemaker center is to AV node: shorter the PQ segment |
|
|
ventricular extra systole
|
-premature stimulus generated by heterotropic ventricular focus
- next systole follows at interval dedicated by sinus rhythmn |
|
|
supraventricular tachycardia
|
-high rate of APs generated in atrium: ectopic location
- different shapes of P waves indicated several ectopic atrial pacemakers |
|
|
atrial flutter and fibrillation
|
-ectopic (heterotopic) generation of APs cause a high atrial rate
-functional failure of both atria - myocardial infarction alters QRS - 50kg dog: 1. flutter: 200- 350 bpm 2. fibrillation: 350- 600 bpm |
|
|
ventricular tachycardia
|
-absence of regular preceeding P waves indicates R waves are generated by a ventricular pacemaker
|
|
|
sinus tachy- and brady-cardia
|
-excitation and conduction are normal
- SA node is pacemaker but initiates APs at a rate lower/higher than normal |
|
|
escape rhythmn
|
-extreme sinus bradycardia: intrinsic rate of AV note exceeds the sinus rate and AV node takes over
- cause failing AV node: then one of the auxillary pacemakers takes over |
|
|
supraventricular systole
|
-premature stimulus generated by heterotropic atrial focus
- normal SA stimulus has no effect - next systole follows at an interval decided by sinus rhythmn |
|
|
supraventricular extra systole
|
-3rd depolarization originates from an ectopic supraventricular pacemaker (P wave precedes QRS)
-negative P wave in lead II and lead III indicates the ectopic initiation of the atrial depolarization |
|
|
shifting pacemaker
|
-If SA slows down or fails other pacemakers take over
- possible cause very high vagal tone - alters P wave and PQ segment - closer the pacemaker center is to AV node: shorter the PQ segment |
|
|
ventricular extra systole
|
-premature stimulus generated by heterotropic ventricular focus
- next systole follows at interval dedicated by sinus rhythmn |
|
|
ventricular flutter and fibrillation
|
-multifocal excitation ceases pumping function
|
|
|
supraventricular tachycardia
|
-high rate of APs generated in atrium: ectopic location
- different shapes of P waves indicated several ectopic atrial pacemakers |
|
|
atrial flutter and fibrillation
|
-ectopic (heterotopic) generation of APs cause a high atrial rate
-functional failure of both atria - myocardial infarction alters QRS - 50kg dog: 1. flutter: 200- 350 bpm 2. fibrillation: 350- 600 bpm |
|
|
ventricular tachycardia
|
-absence of regular preceeding P waves indicates R waves are generated by a ventricular pacemaker
|
|
|
causes of conduction system failure
|
1. cardiac electrical abnormalities
2. cardiac structural abnormalities |
|
|
cardiac electrical abnormalities
|
1. excitation disturbances: eg failure of SA node
2. conduction disorder: eg AV block |
|
|
cardiac structural abnormalities
|
1. morphological: eg RV hypertrophy
2. functional: eg cardiac infarction |
|
|
AV block gen
|
- on means by an AP can ordinarily pass from atria into ventricle is AV node and bundle of His
- different conditions either decrease or increase the rate of conduction of the impulse through the AV node and bundle of His, or block impulse entirely |
|
|
AV block causes
|
1. ischemia
2. compression: scar tissue, calcification 3. inflammation: infection, rheumatic fever 4. extreme vagal tone |
|
|
degrees of AV blocks
|
1st: AV conduction abnormally slow
2nd: dropped beats 3rd: no propagation, total block |
|
|
1st degree AV block
|
-normally PQ interval decreases with increasing HR and vice versa
- pathologically decreased rate of conduction through AV node and bundle of His prolongs the PQ interval beyond physiological value |
|
|
2nd degree AV block
|
- if conduction from atrium to the ventricle fails intermittently then the atrium depolarizes and generates a P wave
- conduction failure creates absent QRST and ventricle doesn't contract =dropped beat -entire conduction system can fail intermittently |
|
|
3rd degree AV block
|
- connection between atrium and ventricle broken
-ventricle has to generate own APs: atrium and ventricle beat at different rate: 1. atrium: higher rate from SA 2. ventricle: auxillary pacemaker at lower rate, beats independent of atrial activities |
|
|
hypertrophy of RV
|
-more muscle= stronger signal= bigger R wave
- if only one side: timing of depolarization changes, increases depolarization time - shift of cardiac vector: hypertrophy causes shift to R |
|
|
myocardial infarction gen
|
-embolus that enters a coronary a will cause an occlusion due to minute anastomoses
- muscle supplied cannot sustain function= infarcted |
|
|
ECG of myocardial infarction
|
1. ischemia causes ST segment depression w or w/o T wave inversion as a result of altered repolarization
2. myocardial injury causes ST segment elevation w or w/o loss of R wave 3. infarction causes deep Q waves as a result of absence of depolarization current from dead tissue and receeding currents from opposite side of the heart |
|
|
electrical interference of ECG
|
- causes: poor contact of leads, dry skin, electric equipment nearby
- resembles atrial flutter or fibrillation |
|
|
trembling patient and ECG
|
-equipment doesn't distinguish between cardiac and skeletal m contraction= interference
- can be mistaken for atrial flutter |
|
|
manifestation of heart failure
|
-failure to pump blood adequately to meets bodily needs
-manifestations: 1. decrease of cardiac output 2. damming of blood behind the L or R heart 3. overloading of heart through increased cardiac output |
|
|
types of heart failure
|
1. low output
2. high output 2. high pressure |
|
|
types of low output heart failure
|
- total cardiac output falls below the required minimum:
1. compensated 2. decompensated 3. unilateral |
|
|
compensated heart failure
|
- type of low output failure
- minimum cardiac output is restored - cardiac reserve remains much reduced |
|
|
decompensated heart failure
|
- type of low output failure
- minimum cardiac output not restored - compensatory mechanisms continue -effects turn disasterous/ vicious cycle that is incompatible with life |
|
|
unilateral heart failure
|
-type of low output failure
- only one side fails |
|
|
high output failure
|
-heart forced to pump more blood than required because of some bypass of normal circulation
- continuous volume overload finally causes a final failure of the heart |
|
|
high pressure failure
|
-heart forced to develop more P than normally required due to unphysiologically high resistance in circulation
- consequences of increased workload cause final heart failure |
|
|
normal relationships btween cardiac output and atrial pressure (preload)
|
1. increased metabolism increased cardiac output
2. more blood returning to heart increases atrial P (preload) 3. better filling of ventricles= higher end diastolic volume - cardiac fibers: longer =stronger |
|
|
maximum cardiac output
|
-determined by limitations to heart:
1. max HR 2. max stroke volume |
|
|
minimum cardiac output
|
-determined by peripheral tissues: blood volume required to maintain metabolism without damage
-example 51 L/ min |
|
|
immediate countermeasures to heart failure
|
-CO drops below minimum:
1. blood returning from tissues backs up in atria: increased atrial P 2. sympathetic stimulation: stimulates cardiac m - increase CO but still deficient |
|
|
restoration of require cardiac output
|
1. heart recovers gradually and partially: more strength
2. not meeting required min CO, water and NaCl retention by kidney: increase in blood V= increase in atrial P - both result in increasing CO= compensation: kidney adaptation stops, cardiac dynamics are normal, but cardiac reserve remains reduced |
|
|
fluid retention in kidneys
|
-decrease in BP regarded as missing blood V (an in hemmorhage):
1. kidneys reduced urine production 2. begins after a few minutes of acute failure until normal BP is restored |
|
|
fluid retention after moderate heart damage
|
- pumping ability: 40-50% normal
1. better systemic filling: lower resistance, higher preload 2. CO may return to normal values |
|
|
fluid retention after severe heart damage
|
-pumping abiltiy: 25-45% normal:
fluid retention - effects 1. overstretching of heart: further weakening 2. perfusion of kidneys too low to balance salt and water intake/output: fluid/salt retention= severe edema (eg lungs) that can lead to death |
|
|
reparative process following myocardial infarction
|
-begins immediately:
1. new collateral blood supply begins to penetrate infarcted tissue: m at fringe areas may begin to function again 2. necrotic tissue replaced by CT 3. undamaged m hypertrophy 4. no hyperplasia of m (no new m) 5. scar remains 6. most of recovery in 5-7 weeks |
|
|
cardiac reserve in different compensated heart failures
|
-CO meets needs of tissues at expense of increased atrial P
- little cardiac reserve left: further increased of preload causes almost no change in CO ( graph horizontal) -heavy exercise usually causes immediate return of symptoms |
|
|
course of decompensated heart failure
|
-after initial failure:
1. heart doesn't recover sufficiently 2. cannot supply kidneys to meet normal function 3. kidneys retain salt and water 4. increased blood V 5. progressive edema: lung, etc 6. overstretching of heart m: dilation of ventricles 7. death |
|
|
course of decompensated heart failure
|
-neither sympathetic strengthening or fluid retention by kidney can restore minimum CO:
1. kidney doesn't stop retaining: increasingly higher blood volume 2. increase in preload overstretches m and dilates ventricles 3. cardiac edema 4. edema and increased preload further weaken heart and decrease CO 5. death due to lower CO followed by weakining in a cycle |
|
|
unilateral L heart failure
|
1. blood backs up into pulmonary veins and BP rises eg 18mm (normal 3)
2. to maintain lung perfusion: BP difference of 10 required 3. R heart increases P in pulmonary a to 28 4. mean lung P rises from 8 to 23, forcing more fluid into interstitium= pulmonary edema 5. if interstitial capacity exceeded, alveolar edema insues which is life-threatening |
|
|
unilateral heart failure summary
|
-L more likely because of higher workload
-most R failure occurs with L failure - R: peripheral edema - L: lung edema |
|
|
high output heart failure
|
-forced to pump more blood than demanded by tissues
- additional volume increases workload, which can result in overload and final heart failure -causes: 1. arterio-venous shunts 2. low blood flow resistance |
|
|
PDA
|
- fetus: lung small and compact, high resistance
- smaller PDA more unlikely to present -consequences: 1. to meet demands of tissues, L has to pump more blood= larger 2. large opening means that tissue don't get enough blood: reduced exercise ability, organ disfunction, death |
|
|
ventricular septal defect
|
-part of LV blood enters RV:
1. LV needs to pump more blood 2. increased LV workload 3. enlargement, thickening, and dilation of LV |
|
|
tetralogy of fallot
|
1. persistant R aortic arch
2. ventricular septal defect 3. pulmonary stenosis 4. ventricular dilation: forcing blood through VSD and stenosis |
|
|
low resistance to blood flow
|
-normally arterioles regulate blood flow in tissues: controlled by ANS
- beriberi: 1. vit B deficiency: decreased arteriolar tone 2. heart pumps more blood to maintain BP: inc CO 3. edema 4. leads to wobbling and trembling, sometimes death |
|
|
high P heart failure
|
-thickening of ventricular wall more on inside: smaller chamber volume
1. compensation by increased HR 2. eventually cannot eject sufficient blood volume 3. high pressure and high rate of contraction: high workload 4. can lead to final heart failure |
