Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards Review > Cardiology Recap > Flashcards

Cardiology Recap Flashcards

1
Q

Draw and label the functional unit of the cardiac myocyte.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Explain the action of Troponin C

A

Binds to C++ to remove the inhibition of Tnl.
When TnC is not bound to Ca, troponin complexes are “relaxed” so actin and myosin cannot interact.
When TnC is bount to Ca, removed Tnl inhibition and actin and myosin can interact.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain the actions of Troponin I

A

Inhibits actin unless it is bound to TnC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the actions of Tropomyosin

A

Supports actin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the actions of Troponin T

A

Distributes TNI effects across the sarcomere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the actions of CERCA (sarcoendoplasmic reticulum ATPase) and Phospholamban.

A

SERCA is an intracellular pump that moves calcium back into the sarcoplasmic reticulum following contraction (leading to myocardial cell relaxation).
Normally phospholamban depresses the effect of SERCA. When phosphorylated, Phospholamban is inhibited so SERCA can be more active.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the effects of stimulation Beta receptors on the heart?

A

increased chronotropy (rate)
inotropy (contractility)
dromotropy (conduction)
lusitropy (relaxation)
bathmotropy (excitability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the effects of stimulation of Muscarinic receptors (Ach) on the heart?

A

depressed heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the effects of stimulation of Alpha receptors on the heart?

A

minimal effects, may have a positive ionotropic effect in some species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the main determinants of blood pressure?

A

Cardiac output (contractility, preload, afterload)
Systemic vascular resistance
Plasma volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Poiseulle’s law of laminar steady flow?

A

deltaP = (8uLQ)/(pieR^4)
delta P= the pressure difference between the two ends
L is the length of pipe
u is the dynamic viscosity
Q is the volumetric flow rate
R is the pipe radius

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is the largest pressure drop in the vascular bed (main site of SVR control)?

A

Arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where is the highest resistance in the vascular bed?

A

Capillaries (however they are in parallel, not in series, so they can still accommodate a large volume of blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What sensors are involved in BP regulation?

A
  • Stretch receptors: aortic and carotid sinuses, ventricular myocardium
  • Low pressure/volume receptors: atrium, peripheral vasculature
  • Osmoreceptors: hypothalamus
  • Chemoreceptors: aortic and carotid bodies (pH)
  • JG apparatus in the kidney: pressure and [Na]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What hormones/outputs are involved in BP regulation?

A

Autonomic nerve signals (sympathetic)
ANP and BNP
Angiotensin II
ADH (Vasopressin)
Aldosterone
Endothelin
NO
Prostaglandins
Thromboxane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the effect of autonomic nerve signals on BP regulation?

A

Sympathetic -> catecholamine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the effect of ANP & BNP on BP regulation?

A

Na/water loss in the kidneys, vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the effect of Angiotensin II on BP regulation?

A

Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the effect of ADH (Vasopressin) on BP regulation?

A

Vasoconstriction, Na/water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the effect of Aldosterone on BP regulation?

A

Na/water retention, K excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the effect of Endothelin on BP regulation?

A

Local vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the effect of NO on BP regulation?

A

Local vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the effect of Prostaglandins on BP regulation?

A

Local vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the effect of Thromboxane on BP regulation?

A

Local vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Draw and label a Wigger’s Diagram.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Define Preload.

A

The force on the cardiac myocytes prior to contraction, length of a sarcomere prior to contraction (stretch, volume in ventricle).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Define Ventricular Compliance.

A

Pressure generated at a given volume of blood.
Change in volume/change in pressure (how stiff the ventricle is)

28
Q

Define Afterload.

A

The “load” against which the heart must contract to eject blood (the stress applied to the ventricle during ejection of blood). = aortic pressure for the left ventricle, pulmonary artery pressure for the right ventricle

29
Q

Define Inotropy

A

The contractility of the heart, strength of interaction between actin and myosin INDEPENDENT of changes in sarcomere length.

30
Q

Draw a cardiac pressure volume loop.

A
31
Q

How would increased venous return affect a cardiac pressure volume loop. (Draw)

A
32
Q

How would increased/decreased aortic pressure (afterload) affect a cardiac pressure volume loop. (Draw)

A
33
Q

How would increased/decreased inotropy affect a cardiac pressure volume loop. (Draw)

A
34
Q

List 5 compensatory mechanisms in heart failure.

A
  1. Frank-Starling Mechanism: increase in preload enhances cardiac performance
  2. RAAS: reduced renal perfusion 🡪 Renin 🡪 AT I 🡪 AT II 🡪 vasoconstriction & aldosterone 🡪 Increase in BP
  3. Sympathetic Nervous System Activation: SNS 🡪 increased HR, peripheral vasoconstriction, increased inotropy
  4. Myocardial Hypertrophy
  5. Natriuretic peptides
35
Q

Is the Frank-Starling compensatory mechanism in heart failure helpful or harmful.

A

(increase in preload enhances cardiac performance)
In a failing heart if ventricular end-diastolic pressures and preload are chronically elevated to maintain CO, exercise drives the ventricle along the flat portion of the performance curve and increases in ventricular volume or pressure do not increase ventricular performance.

36
Q

Is the RAAS compensatory mechanism in heart failure helpful or harmful.

A

(reduced renal perfusion 🡪 Renin 🡪 AT I 🡪 AT II 🡪 vasoconstriction & aldosterone 🡪 Increase in BP)
Angiotensin II stimulates the release of growth factors that promote remodeling of the myocardium & causes pathologic ventricular hypertrophy, myocardial necrosis (from cytotoxic effects), and loss of myocardial contractile mass 🡪 cardiac dysfunction.

37
Q

Is the Sympathetic nervous system activation compensatory mechanism in heart failure helpful or harmful.

A

(SNS 🡪 increased HR, peripheral vasoconstriction, increased inotropy)
Chronic activation of the SNS causes cardiac NorEpi depletion, down-regulation and desensitization of B1 receptors, and overloads the heart by increasing venous return, increased myocardial oxygen consumption, and damaging the myocardium.

38
Q

Is the myocardial hypertrophy compensatory mechanism in heart failure helpful or harmful.

A
  • Eccentric hypertrophy (volume-overload): allows the ventricle to pump a relatively normal amount of blood despite abnormal systolic function
    • > Characterized by chamber dilation
  • Concentric hypertrophy (pressure-overload): normalizes systolic wall tension by increasing myocardium thickness
  • -> Characterized by thickening of ventricular walls
39
Q

Is the natriuretic peptides compensatory mechanism in heart failure helpful or harmful.

A

Increased atrial stretch 🡪 ANP release 🡪 Na and H20 excretion by kidneys (counteracts RAAS), actually helpful!

40
Q

Briefly explain the action potential/depolarization in a general ventricular cell.

A

“Fast response” depolarization, has to be triggered by a stimulus. Action potential is primarily generated by rapid entry of Na (fast sodium channels).

41
Q

Briefly explain the action potential/depolarization in a pacemaker cell.

A

“Slow response action potential”. Automatic/rhythmic contraction, without a stimulus. Some are slower than others to depolarize. Resting membrane potential is not constant (like a wave), depolarization is due to slow calcium channel activation (not Na).

42
Q

Draw Einthoven’s Triangle.
Use this to explain the 6 leads of an EKG.

A
  • Lead I: RF is negative compared to LF
  • Lead II: RF is negative compared to LH
  • Lead III: LF is negative compared to LH
  • aVR: RF (+) compared to point b/w LF and LH
  • aVL: LF (+) compared to point b/w RF and LH
  • aVF: LH (+) compared to pt b/w LF and RF
43
Q

Draw an MEA diagram.
Use this to explain the 6 leads of an EKG.

A
  • Right side of image is LEFT
  • Top of image is CRANIAL
  • Because the heart is angled in the chest, the left ventricular apex is actually oriented toward the positive pole of lead 2 (+ 60°)
  • Leads I, II, III are bipolar leads- positive and negative poles
  • Leads aVr (augmented voltage right arm), aVL (left arm) and aVf (left foot) are unipolar leads- only have a positive pole, activity of the positive pole is compared with the average of the other 2 leads
  • The label for each lead is placed at the position of the positive pole on the EKG diagram
44
Q

What is the Mean Electrical axis?

A

Principal vector of ventricular depolarization- represents the sum of all waves of depolarization occurring simultaneously
Normally points toward the left ventricle (because it is the larger one)

45
Q

Torsemide:
Class/Effect
MOA
Side effects

A

C/E: loop diuretic, increases H2O excretion.

MOA: Binds to Na/K/2Cl co-transporter in loop of henle 🡪 loss of Na, Cl, K, Ca, Mg (and thus water)

SE: Dehydration
Electrolyte changes: (hyponatremia, hypokalemia)
Hypotension
Decreased GFR

46
Q

Spironolactone
Class/Effect
MOA
Side effects

A

C/E: K-sparing diuretic. Increases H20 excretion (weak alone).

MOA: Inhibits aldosterone in the distal tubules by competitive binding.

SE: Hyperkalemia

47
Q

Diltiazem
Class/Effect
MOA
Side effects

A

C/E: Calcium channel blocker, Class IV Anti-arrhythmic (SVT’s)

MOA: Inhibits Ca entry 🡪 inhibit smooth muscle in heart and inhibits pacemaker cell automaticity.

SE: GI upset, hypotension, bradycardia, AV block

48
Q

Amlodipine
Class/Effect
MOA
Side effects

A

C/E: Calcium channel blocker 🡪 only vascular effects (vasodilation), not cardiac. “Nifedipine” sub-class.

MOA: Inhibits Ca entry 🡪 inhibit smooth muscle in arteries -> Vasodilation.

SE: Generally rare. Hypotension, gingival hyperplasia.

49
Q

Benazepril
Class/Effect
MOA
Side effects

A

C/E: ACE inhibitor 🡪 afterload reducer (primarily arteriodilator, small amount of venodilation)

MOA: Inhibits conversion of AT 1 🡪 AT II 🡪 natriuresis, inhibition of aldosterone release 🡪 vasodilation, Na loss in urine, inhibition of ADH. Also controls glomerular capillary hypertention 🡪 decreased proteinuria and renal protection by decreasing inflammatory mediator release.

SE: Hypertension, decreased GFR/renal perfusion, hyperkalemia

50
Q

Pimobendan
Class/Effect
MOA
Side effects

A

C/E: Phosphodiesterase inhibitor

MOA:

SE:

51
Q

Procainamide
Class/Effect
MOA
Side effects

A

C/E: Class IA anti-arrhythmic, best for ventricular arrhythmias

MOA: Intermediate blocker of fast Na channels 🡪 slower conduction.

SE: GI upset, bradycardia, hypotension, depression/sedation

52
Q

Carvedilol
Class/Effect
MOA
Side effects

A

C/E: Class II Anti-arrhythmic, B-blocker. 3rd generation.

MOA: Reduce sympathetic activity of B-agonists (block B-receptor) 🡪 slowed pacemaker activity and repolarization, decreased contractility

S/E: Impaired contractility -> worsened CHF, bradycardia, lethargy

53
Q

Mexiletine
Class/Effect
MOA
Side effects

A

C/E: Class 1B anti-arrhythmic, best for ventricular arrhythmias

MOA: Rapid blocker of fast Na channels 🡪 slower conduction.

SE: Oral only form, GI signs, brardycardia depression/sedation

54
Q

Amiodarone
Class/Effect
MOA
Side effects

A

C/E: Class III anti-arrhythmic, Selective K channel blocker

MOA: Blocks K (Phase 3) -> prolonged action potential/refractory period

SE: Pulmonary fibrosis, hepatic dysfunction, arrhythmias

55
Q

Discuss Stage A for DVD and general recommendations.

A

At risk but currently normal.

Auscult regularly for murmur, no treatment, avoid breeding

56
Q

Discuss Stage B for DVD and general recommendations.

A

Structural heart disease (murmur, regurg), but asymptomatic.

Recommend CXR, BP, and ideally echo

B1: no cardiac enlargement. Monitor, no treatment.

B2: cardiac enlargement on rads or echo (La:A0 > 1.6, VHS > 10.5), typically murmur >/= 3/6. Definitely pimo, mild Na restriction.
Consider ACEI, cough suppressants. SX??
NO B-blockers, NO spironolactone.

57
Q

Discuss Stage C for DVD and general recommendations.

A

Clinical signs.
CXR, BW, Echo.
Treat as usual, recommend Lasix, pimo, ace inhibitor for chronic therapy. +/- other drugs

58
Q

Discuss Stage D for DVD and general recommendations.

A

Refractory CHF.
Need to start adding drugs, higher doses.

59
Q

Explain things a NON cardiologist using focused ECHO could be expected to assess:

A
  • Detect pleural or pericardial effusion (estimate amount, location, best centesis site, assess for recurrence.
  • Assess for tamponade with PE and if obvious cardiac mass present.
  • If evidence of severe LA enlargement (left sided failure).
  • If mitral or tricuspid valve obviously thickened or if chordae rupture occurred.
  • If there is severe RA and RV enlargement (right sided failure , cor pulmonale with pulmonary hypertension).
  • Assess LV contractility (either “eyeball” it or measure fractional shortening).
  • Assess if there is severe LV concentric hypertrophy (HCM in cats).
  • Evidence of LA thrombus or “smoke” (spontaneous contrast) in RA or ventricle.
  • Severe hypovolemia by looking at serial chamber sizes.
60
Q

Name and interpret the following echo image:

A

M-mode of R-parasternal short axis view of LV (“mushroom view”). Poor contractility/FS (ie DCM, sepsis induced systolic dysfunction).

61
Q

Name and interpret the following echo image:

A

R parasternal short-axis view of heart base. Severe LA dilation (La/Ao >2:1)

62
Q

Name and interpret the following echo image:

A

R-parasternal short axis view of LV. RV dilation (ie right sided CHF, pulmonary hypertension)

63
Q

Name and interpret the following echo image:

A

R parasternal long-axis view (“4-chamber view”). Pericardial effusion with cardiac tamponade (RA collapse) and RA mass.

64
Q

What are the 2 main biomarker classes used for cardiac disease?

A

Troponins
Natriuretic Peptides

65
Q

Discuss Troponins. What do they help to assess?

A
  • Proteins that bind actin/myosin.
  • TNI, TnT, TnC. cTnI and cTnT = cardiac isoforms.
  • cTnI used most often.
  • Elevation indicates injury to cardiac myocytes- MVD, DCM, SIRS states.
66
Q

Discuss Natriuretic peptides. What do they help to assess?

A
  • ANP: released due to atrial stretch.
    Not very stable in circulation, so harder to measure
  • BNP: released in response to ventricular (and small amount from atrial) stretch – indicate volume overload.
    Pro-form is most stable to measure (NT-proBNP).
    Best used to assess impending or current failure (Ie compared to other primary respiratory diseases) when echo is not available.

Boards Review (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions