Cardiovascular Flashcards
Define Cardiac Output and Cardiac Index
CO = HR x SV CI = CO/BSA
Preload is estimated by LVEDV or LA pressure, less invasively we now use CVPs
How is contractility determined echocardiographically?
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%
Define Afterload
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)
Describe the compensatory response to inadequate preload
Improve preload by:
- Conserve salt and water in kidneys (RAAS + ADH)
- Inc HR and contractility (catecholamines)
- Selective vasoconstriction of peripheral circulation
Draw out a CVP tracing (waves and descent)
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)
Coronary Blood Flow is proportional to:
Q (flow) = P/R (aortic pressure /resistance)
Coronary blood flow depends on perfusion gradient btwn Ao diastolic pressure - RA pressure
Draw Frank-Starling curves (CO/SV vs preload) for
- normal ventricle
- Failing ventricle
- Inc inotropy
Figure 3.2 Lucking
Describe the muscle elements critical to myocardial contraction
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
What are the components affecting Stroke Volume?
Preload
Afterload
Contractility
Note: SV and CO inc with age, as HR dec
Draw pressure-volume loops for varying preload, afterload, contractility (Figure 3.6 Lucking)
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
Describe sinus arrhythmia
Inc HR to inc PBF during increasing alveolar ventilation
Where is pleural pressure most negative, apex or base?
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
Name 4 reasons why there is an overall decrease in CO during PPV?
- dec venous return
- inc RV afterload
- dec LV preload
- dec in ventricular contractility
Describe the venous return vs RA pressure curve
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
Describe the influence respiration has on systemic and splanchnic vascular beds
Downward movement of the diaphragm into a closed abdomen = inc intra-abdo pressure and forces blood into IVC
This is affected by volume status
- Hypervolemia (zone 3): IVC blood flow inc throughout diaphragm contraction/respiration
- 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
Describe PVR vs Lung Volume Curve
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
Describe 4 mechanisms by which LV filling (preload) may be decreased during respiration
- Dec RV output
- Leftward deviation of IVS due to inc RV volume
- Compression of fossa ovalis due to inc lung volumes
- 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
Describe the negative effect of intraventricular dependence in asthma and upper airway obstruction on CO
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
Why does PEEP aid the Left Ventricle?
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
Define pulsus and reverse pulsus paradoxus
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
How can myocardial contractility be compromised by PPV?
Direct compression of coronaries during inspiration
What 3 potential mechanisms support circulation during CPR?
- 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)
- 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
- 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
Describe the MOA of vasopressin
Protein acting on V1 and V2 receptors
1. V1 activates phospholipase C - phosphoinositol pathway = inc in cytosolic Ca = vascular SM contraction
- Blocks K-ATP channels which leads to inc in Ca entry into cytosol = vasoconstriction
- Vasodilation of cerebral and pulmonary circulation is due to induction of endothelial NO effect.
Describe key elements of effective compressions and ventilation according to 2018 PALS guideline
C-A-B
- Compression rate 100-120bpm
- Compression depth 1/3rd AP diameter (Infants = 4cm or 1.5in, children 5cm or 2in) w/ full chest recoil
- Compression:ventilation ratio is 30:2 for single rescuer, 15:2 for double rescuer –> Adult BLS when puberty hits (30:2)
- Ventilate at 8-10bpm if advanced airway and avoid excessive ventilation
- Rotate compressor q2min
When is epinephrine given during PALS pulseless algorithm?
After 2nd shock if shockable rhythm - q4min thereafter
After 2mins CPR if non-shockable rhythm - q4min thereafter
What is the energy dose for defibrillation? Cardioversion? (PALS)
Defibrillation: 1st shock = 2J/kg, 2nd shock = 4J/kg, max 10J/kg
Name 3 treatments for bradycardia with a pulse and poor perfusion (PALS)
- Epinephrine 1st line (0.01mg/kg IV)
- Atropine only for excessive vagal tone or 1o AV conduction block (0.02mg/kg IV; min dose 0.1mg, max 0.5mg)
- Transcutaneous pacing
Is amiodarone or lidocaine the preferred anti-arrhythmic according to PALS? What are their doses?
No preferred anti-arrhythmic
Lidocaine: 1mg/kg
Amio: 5mg/kg, may repeat twice
What are the Hs (7) and Ts (5)?
Hypovolemia Hypoxia H+ ions Hypoglycemia Hypothermia Hypo/Hypercalcemia Hypo/Hyperkalemia
Tension PTX Tamponade Toxins Thrombosis, pulmonary Thrombosis, cardiac
