1/64
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
Mitral (left) and tricuspid (right)
("LAB RAT" = left atrioventricular valve bicuspid/mitral, right atrioventricular valve tricuspid)
Which ones are the AV valves?
Atrial systole
This is the contraction of the atria causing the AV valves open so blood can enter the ventricles
Ventricular systole
This is contraction of the ventricles, forcing AV valves shut and semilunar open so blood leaves heart thru great arteries
Diastole
This is the relaxation of both atria and ventricles
Pressure difference (along with normal valves) ensures one way blood flow
Why is the pressure difference in the heart good?
Cardiac output
This is the volume of blood pumped over some unit of time
CO = heart rate x stroke volume
*stroke volume is the amount of blood leaving the heart per beat
How do you calculate cardiac output?
SV = end diastolic volume - end systolic volume
DETERMINED BY: preload, contractility, afterload
How do you calculate stroke volume? What things determine stroke volume?
Preload
This is the stretch of heart muscle fibers at the end of diastole just before contraction. Aka the "load" the heart has to work with BEFORE it contracts
Contractility
This is the intrinsic ability of the heart muscle to contract independent of preload. Stronger squeeze = stronger stroke volume
Afterload
This is the resistance the left ventricle must overcome to eject blood during systole. Aka the "load" or pressure the heart has to contract against
Increase it (which in turn increases stroke volume and blood pressure)
IV fluids do WHAT to preload?
Increases afterload (which in turn decreases stroke volume because resistance has increased)
Note: hypertension and aortic stenosis create high resistance to blood flow from the ventricles. because the left ventricle must generate more pressure to open the valve, the afterload, or forces it must contract against, increases.
Aortic stenosis or hypertension does WHAT to afterload?
4000 mL/minute or 4 L/min
The heart rate of a dog is 100 bpm. The volume of blood pumped is 4000 mL/min. The end systolic volume is 20 mLs. What is cardiac output?
CO/HR = SV
4000 mL/100 bpm = 40 mL/beat
The heart rate of a dog is 100 bpm. The volume of blood pumped is 4000 mL/min. The end systolic volume is 20 mLs. What is stroke volume?
Stroke volume + end systolic volume = end diastolic volume
40 mL + 20 mLs = 60 mLs
(remember the stroke volume was 4000 mL/100 bpm)
The heart rate of a dog is 100 bpm. The volume of blood pumped is 4000 mL/min. The end systolic volume is 20 mLs. What is end diastolic volume?
Stroke volume / end diastolic volume = ejection fraction
40/60 = 0.66 or 66%
(remember the stroke volume was 4000 mL/100 bpm)
The heart rate of a dog is 100 bpm. The volume of blood pumped is 4000 mL/min. The end systolic volume is 20 mLs. What is ejection fraction?
a. inotropy
Which is the contractile state of the heart:
a. inotropy
b. chronotropy
c. dromotropy
d. lusitropy
b. chronotropy
Which is the speed of the heart:
a. inotropy
b. chronotropy
c. dromotropy
d. lusitropy
c. dromotropy
Which is the speed of conduction of an electrical impulse of the heart:
a. inotropy
b. chronotropy
c. dromotropy
d. lusitropy
d. lusitropy
Which is the property relating to the speed of myocardial RELAXATION of the heart:
a. inotropy
b. chronotropy
c. dromotropy
d. lusitropy
a. SYMPATHETIC: increase heart rate
PARASYMPATHETIC: decrease heart rate
b. SYMPATHETIC: positive inotropy
PARASYMPATHETIC: negative inotropy
c. SYMPATHETIC: positive chronotropy
PARASYMPATHETIC: negative chronotropy
(remember inotrope is contractility, chronotropy is speed of heart)
What is the difference between sympathetic and parasympathetic in terms of what they do to:
a. the heart rate
b. inotropy
c. chronotropy
The more the heart muscle is stretching during filling (greater preload), the stronger the subsequent contraction, up to a physiologic limit (more stroke volume).
What does Starling's Law tell you about the heart?
Cardiac output x systemic vascular resistance
How do you calculate mean arterial pressure?
Increases MAP, because stroke volume increases which increases cardiac output
Exercise increases venous return (or preload). What does this do to MAP?
Decreases MAP because it decreases stroke volume which decreases cardiac output
Heart failure does what to MAP?
Increase MAP because they increase systemic vascular resistance thru vasoconstriction
Hypothermia and RAAS activation do what to MAP?
Decreases MAP
Decreased systemic vascular resistance because of something like septic shock does what to MAP?
Resistance
This is determined by blood viscosity, vessel length and vessel *radius*, usually altered by *arterial vasoconstriction*
Compliance
This is the volume of blood a vessel can hold at a given pressure, primarily altered by *venous capacity*
These two factors control cardiac output
Why do we care about compliance and vascular volume?
true
TRUE OR FALSE: much of the blood volume of circulation resides in systemic veins
FALSE: Most of the systemic vascular resistance is attributable to MICROCIRCULATION (like arterioles)
TRUE OR FALSE: Most of the systemic vascular resistance is attributable to macrocirculation.
FALSE: generalized vasoconstriction of arterioles CHANGE peripheral resistance, vasoconstriction of VEINS DON'T
TRUE OR FALSE: Generalized vasoconstriction of the veins change peripheral resistance, vasoconstriction of arterioles don't.
True
TRUE OR FALSE: the highest velocity of blood flow occurs in the vicinity of the heart (aorta, pulmonary artery), the lowest velocity of blood flow occurs in the capillaries.
Cardiac disease decreases cardiac output. This triggers SNS activation, which triggers RAAS, increasing ADH and endothelin. These mechanisms increase preload AND afterload which in turn puts more pressure on the heart which causes more cardiac injury.
What is the problem with cardiac disease and it's compensatory mechanisms?
Dec. renal perfusion -> angiotensinogen made in liver -> renin released by kidney -> renin acts on angiotensinogen to make Angiotensin I -> ACE enzyme acts on angiotensin I to make angiotensin II -> binds angiotensin type 1 and type 2 receptors and also increases aldosterone -> overall goal is to inc. Na retention, thirst, and ADH + fibrosis and remodeling
*note: angiotensin type I receptor and aldosterone seems more to inc. pathway (constriction, Na retention, thirst, inc. fibrosis) while angiotensin type II receptors seems more to stop the pathway (vasodilation, dec. fibrosis)
Briefly describe the RAAS pathway
Stop aldosterone uptake
Where do Mineralocorticoid receptor antagonists like spironolactone act to inhibit the RAAS system?
They stop angiotensin I from turning into angiotensin II
Bradykinin inactive fragments are used in the RAAS system. The ACE inhibitors act on these fragments to inhibit the RAAS system WHERE?
Salt and water homeostasis and blood pressure control (loss of sodium and water follows)
What are natriuretic peptides like ANP, BNP, and CNP for overall?
ANP = normally produced in atria after wall stress
BNP = more produced in ventricles after hypertrophy
Both ANP and BNP have the goal of vasodilation, natriuresis (pee out sodium) and blunting RAAS. So what is the difference between them?
Natriuretic peptides and angiotensin receptor type 2 both inhibit the RAAS system. So if these two things are inhibited, the mechanisms of RAAS continue.
What two pathways do you have to prevent to "stop the stoppage" of the RAAS system?
Wiggers Diagram
This comprehensive chart shows mechanical, electrical, and pressure events of the cardiac cycle as they occur over time
S1, S2, S3, S4
How many heart sounds are there?
S1
Which heart sound relates to the closure of the mitral and tricuspid valves?
S2
Which heart sound relates to the closure of aortic valve and then the pulmonary valve?
S3 (gallop sound)
Which heart sound relates to diastolic filling of the ventricle?
S4 (gallop sound)
Which heart sound relates to the atria contracting against a stiff ventricle (P wave on ECG)?
Gallop sounds
This type of extra heart sound occurs during diastole, created as blood rushes into non compliant, stiff left ventricle (such as with a cat with hypertrophic cardiomyopathy)
Mid systolic click
This type of heart sound occurs during systole, often signaling early chronic degenerative valve disease related to abnormal mitral valve
Splitting of S2
This type of heart sound is most frequently associated with delayed closure of the pulmonic valve (as the pulmonic valve is not closing when it should)
Congential, acquired, physiologic/innocent/functional
What are the 3 heart murmurs based on origin (when they start)?
a. congenital heart murmur
Patent ductus arteriosus, aortic stenosis, pulmonic stenosis, and ventricular septal defect are examples of:
a. congenital heart murmur
b. acquired heart murmur
c. physiologic/innocent heart murmur
b. acquired heart murmur
Degenerative valve disease, dilated cardiomyopathy, endocarditis, and tricuspid regurgitation are all examples of:
a. congenital heart murmur
b. acquired heart murmur
c. physiologic/innocent heart murmur
c. physiologic/innocent heart murmur
This type of murmur is commonly present in young, growing dogs:
a. congenital heart murmur
b. acquired heart murmur
c. physiologic/innocent heart murmur
Location, timing, loudness
What 3 things do you assess when listening to a heart murmur:
Ventral to the costochondral junction (typically AV valve regions, tricuspid and mitral)
What does "apical" mean when talking about location of a heart murmur
Dorsal to the costochondral junction (typically pulmonic and aortic semilunar valves)
What does "basilar" mean when talking about location of a heart murmur
Apical, basilar, and side of the chest
What 3 locations are there for murmurs?
Systolic, diastolic, and continuous
What 3 "times" are there for murmurs?
Systolic
This means a murmur occurs between S1 and S2 (closure of AV and semilunar valves)
Diastolic
This means a murmur occurs between S2 and the next S1 heart sound
Continuous
This means a murmur is present throughout both systole and diastole without a break
Grades 1-6
How many grades are there to assess "murmur loudness"?
1: "cardiologist murmur", heard in perfectly quiet conditions only at the point of max intensity
2: can easily be heard with stethoscope but is very soft, focal sound
3: heard easily with stethoscope, moderately loud. can hear is in region surrounding point of max intensity
4: loud and can be heard with a stethoscope in multiple areas on both sides of chest
5: can be heard throughout chest and you can feel precordial thrill. cannot be heard if stethoscope is off chest
6: can be heard throughout chest and even with stethoscope lifted off body, precordial thrill
Talk about the different murmur grades: