Brainscape's Knowledge GenomeTM

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


See full index

PCCM Fellowship > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Define Cardiac Output and Cardiac Index

A 
CO = HR x SV
CI = CO/BSA

Preload is estimated by LVEDV or LA pressure, less invasively we now use CVPs

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

How is contractility determined echocardiographically?

A

Shortening fraction: % change in LV diameter which occurs with contraction (normal 30-40%)
SF = (LV diameter btwn diastole and systole) / LVEDV
*Value is influenced by state of volume loading

Ejection fraction normal 55-65%

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

Define Afterload

A

Force opposing contraction of LV myocytes during systole ~ estimated by Law of LaPlace

LV wall tension during contraction: T = (P x r) / 2w
aka (transmural LV pressure x radius of LV in end systole) / LV wall thickness

Note: Law of Laplace - Inc r = inc wall tension needed to balance a given transmural ventricular pressure)

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

Describe the compensatory response to inadequate preload

A

Improve preload by:

  1. Conserve salt and water in kidneys (RAAS + ADH)
  2. Inc HR and contractility (catecholamines)
  3. Selective vasoconstriction of peripheral circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Draw out a CVP tracing (waves and descent)

A

A wave - Atrial contraction
C wave - TV closes (onset of systole)
X descent - Valve annulus moves towards apex
V wave - Inc in RA volume/pressure in late systole due to RV ejection, driving blood through SVC/IVC
Y descent - TV opens (diastole begins)

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

Coronary Blood Flow is proportional to:

A

Q (flow) = P/R (aortic pressure /resistance)

Coronary blood flow depends on perfusion gradient btwn Ao diastolic pressure - RA pressure

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

Draw Frank-Starling curves (CO/SV vs preload) for

  1. normal ventricle
  2. Failing ventricle
  3. Inc inotropy
A

Figure 3.2 Lucking

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

Describe the muscle elements critical to myocardial contraction

A

Actin: thin filament attached to sarcomere at Z line (interdigitates with myosin); Actin-myosin contraction is ATP dependent

Troponin is a 3 subunit regulator protein and acts as on/off of contraction via influence of Ca (L-typed voltage gated channels):
1. TN-T: attaches acting and tropomyosin filaments
2. TN-C: Calcium binding site
3. TN-I: Inhibits ATPase responsible for actin/myosin interaction
Ca-TNc blocks TN-I inhibition –> conformational change in troponin/tropomyosin –> actin-myosin cross bridging

Contraction continues until Calcium decreases and no longer binds TN-C
(Calcium actively sequestered back into SR via an ATPase dependent pump; Ca is also extruded from cell by Na/Ca exchanger, and to some degree by an active Ca ATP-ase pump on cell membrane
Figure 3.4 Lucking

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

What are the components affecting Stroke Volume?

A

Preload
Afterload
Contractility
Note: SV and CO inc with age, as HR dec

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

Draw pressure-volume loops for varying preload, afterload, contractility (Figure 3.6 Lucking)

A

Inc preload: Inc SV but end-systolic volume (ESV) remains constant
Inc afterload: dec SV and inc ESV
Inc contractility: inc SV, dec ESV, shift ESPVR up and to left

Note: contractility is independent of preload and afterload
ESPVR: linear relationship of inc afterload and dec ESV

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

Describe sinus arrhythmia

A

Inc HR to inc PBF during increasing alveolar ventilation

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

Where is pleural pressure most negative, apex or base?

A

During spontaneous respiration and PPV in the upright position, the apex is more negative. However, high MAP abolishes this gravitational gradient and reduces regional differences in pleural pressure

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

Name 4 reasons why there is an overall decrease in CO during PPV?

A
  1. dec venous return
  2. inc RV afterload
  3. dec LV preload
  4. dec in ventricular contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the venous return vs RA pressure curve

A

Respiratory changes in intrathoracic pressure primarily alter venous return by changing RAp
Negative pressures dec RAp and inc pressure gradient btwn systemic veins and RA = inc venous return and PBF
– collapse of extra-thoracic BVs limits the effect of negative intrathoracic pressure on venous return, which bcms maximum when RAp is below 0mmHg (below this there is no inc in venous return (plateau - Figure 3.9 Lucking)

PPV decrease venous return by inc RAp and reducing gradient btwn systemic veins and RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the influence respiration has on systemic and splanchnic vascular beds

A

Downward movement of the diaphragm into a closed abdomen = inc intra-abdo pressure and forces blood into IVC

This is affected by volume status

  1. Hypervolemia (zone 3): IVC blood flow inc throughout diaphragm contraction/respiration
  2. Hypovolemia (abnormal zone 2): IVC blood flow is biphasic - original inc due to splanchnic BF, decreases then comes from resistance to infrahepatic, non-splanchnic BF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe PVR vs Lung Volume Curve

A

PVR is lowest at FRC
PVR inc at low lung volumes due to hypoxic vasoconstriction and collapse of extra-alveolar vessels (RV)
PVR inc at high lung volumes due to alveolar distension and compression of alveolar capillaries (TLC)

Figure 3.11 Lucking

17
Q

Describe 4 mechanisms by which LV filling (preload) may be decreased during respiration

A
  1. Dec RV output
  2. Leftward deviation of IVS due to inc RV volume
  3. Compression of fossa ovalis due to inc lung volumes
  4. Dec pulmonary venous return in hypovolemic states (zone 2 conditions)
    Note: in Zone 3 conditions, pulmonary venous return may increase as transpulmonary pressures are increased
18
Q

Describe the negative effect of intraventricular dependence in asthma and upper airway obstruction on CO

A

High lung volumes in asthma = inc RV afterload and inc RV diastolic volume
Inc venous return in UAO 2/2 negative intrathoracic pressure

Both combine to decrease LV compliance by shifting IVS to left = pulsus paradoxus

19
Q

Why does PEEP aid the Left Ventricle?

A

PPV decreases LV afterload by decreasing transmural wall pressure

LV afterload is proportional to transmural LV wall pressure (arterial pressure acting on internal ventricular wall - intrathoracic pressure acting on the external surface of ventricular wall during systole) OR
[P LV = P Ao (typically 90) - P It] ——- where P It can be -20 or +20 depending on spontaneous resp vs PPV

20
Q

Define pulsus and reverse pulsus paradoxus

A

Pulsus paradoxus: Dec BP during negative pressure breathing
Reverse pulsus paradoxus/systolic pressure variation: Transient inc in BP during PPV due to inc pulmonary venous return and decreased afterload –> secondary decrease in BP in early expiration 2/2 dec venous return to RV during PPV

21
Q

How can myocardial contractility be compromised by PPV?

A

Direct compression of coronaries during inspiration

22
Q

What 3 potential mechanisms support circulation during CPR?

A
  1. Cardiac Pump - direct squeeze of heart btwn sternum and spine or by direct cardiac massage. Predominates in young children with compliant thoracic wall (AoV open, MV closed)
  2. Thoracic Pump - Inc intrathoracic pressure creates gradient where blood flows to periphery. Predominates in older children. Heart is a conduit with both Ao and MVs open
  3. Abdominal Pump - Utilized in Interposed Abdominal Compression CPR (IAC-CPR) where compression of abdominal Ao forces blood to periphery and retrograde to heart and brain
23
Q

Describe the MOA of vasopressin

A

Protein acting on V1 and V2 receptors
1. V1 activates phospholipase C - phosphoinositol pathway = inc in cytosolic Ca = vascular SM contraction

  1. Blocks K-ATP channels which leads to inc in Ca entry into cytosol = vasoconstriction
  2. Vasodilation of cerebral and pulmonary circulation is due to induction of endothelial NO effect.
24
Q

Describe key elements of effective compressions and ventilation according to 2018 PALS guideline

A

C-A-B

  1. Compression rate 100-120bpm
  2. Compression depth 1/3rd AP diameter (Infants = 4cm or 1.5in, children 5cm or 2in) w/ full chest recoil
  3. Compression:ventilation ratio is 30:2 for single rescuer, 15:2 for double rescuer –> Adult BLS when puberty hits (30:2)
  4. Ventilate at 8-10bpm if advanced airway and avoid excessive ventilation
  5. Rotate compressor q2min
25
Q

When is epinephrine given during PALS pulseless algorithm?

A

After 2nd shock if shockable rhythm - q4min thereafter

After 2mins CPR if non-shockable rhythm - q4min thereafter

26
Q

What is the energy dose for defibrillation? Cardioversion? (PALS)

A

Defibrillation: 1st shock = 2J/kg, 2nd shock = 4J/kg, max 10J/kg

27
Q

Name 3 treatments for bradycardia with a pulse and poor perfusion (PALS)

A
  1. Epinephrine 1st line (0.01mg/kg IV)
  2. Atropine only for excessive vagal tone or 1o AV conduction block (0.02mg/kg IV; min dose 0.1mg, max 0.5mg)
  3. Transcutaneous pacing
28
Q

Is amiodarone or lidocaine the preferred anti-arrhythmic according to PALS? What are their doses?

A

No preferred anti-arrhythmic

Lidocaine: 1mg/kg
Amio: 5mg/kg, may repeat twice

29
Q

What are the Hs (7) and Ts (5)?

A 
Hypovolemia
Hypoxia
H+ ions
Hypoglycemia
Hypothermia
Hypo/Hypercalcemia
Hypo/Hyperkalemia
Tension PTX
Tamponade
Toxins
Thrombosis, pulmonary
Thrombosis, cardiac

PCCM Fellowship (18 decks)

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