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APA I > Group Presentations > Flashcards

Group Presentations Flashcards

1
Q

Stroke volume

A

SV = EDV - ESV

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2
Q

Cardiac output

A

CO = Stoke volume x HR

Changes in HR will greater effect CO.

  • HR may increase 100-200% with exercise
  • stroke volume may increase <50%

Normal CO of adult at rest = 5-6 L/min

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3
Q

Cardiac index

A

-normalizes CO to individuals of different sizes

CI = CO/BSA

Normal CI = 2.6 - 4.2 L/min/m2

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4
Q

How does increasing HR affect CO?

A

-stroke volume falls as HR increases due to decrease ventricular filling

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5
Q

What are some mechanisms that cause stroke volume to increase despite increased HR and decreased filling time?

A
  • Anrep effect: abrupt increase in afterload can cause a modest increase in inotropy
  • Treppe (Bowditch effect): when HR is elevated Ca++ doesn’t have time to completely leave cell. The increase of Ca++ sitting on actin and myosin causes a stronger squeeze, increasing contractility with high HR
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6
Q

Preload

A
  • initial stretching of the cardiac myocytes prior to contraction; therefore is related to sarcomere length at the end of diastole
  • sarcomere length difficult to determine, indirect indices are used
    • EDV and EDP
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7
Q

How does ventricular compliance affect preload?

A

Decreased compliance: decreased volume at higher pressure

Increased compliance: higher volumes at lower pressure

-compliance is the ratio of change in volume/change in pressure

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8
Q

Frank-Starling mechanism

A

-stretched fibers recoil harder

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9
Q

What determines ventricular preload?

A

—increases preload—

  • increased venous pressure
  • ventricular compliance: greater compliance = greater filling and greater preload
  • increased outflow resistance (pulmonary valve stenosis, pulmonary HTN) impairs ventricular emptying and increases preload
  • decreased ventricular inotropy (ventricular failure)

-atrial contraction: normally small contribution. Sympathetic innervation enhances force of contraction at higher heart rates enhancing ventricular filling

—decreases preload—
-heart rate: HR and ventricular filling are inversely related

-inflow resistance: increase in this decreases preload

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10
Q

Afterload

A
  • the “load” against which the heart must contract
  • mainly aortic pressure
    • aortic valve stenosis
    • ventricular dilation
  • the greater the pressure the greater the afterload and the less CO
  • afterload decreases velocity of fiber shortening

-increased afterload = increased cardiac workload

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11
Q

Inotropy

A
  • length-independent activation of contractile proteins
  • an inotrope is any mechanism that alter myocin ATPase activity at a given sarcomere length alters force generation
  • most inotropes involve Ca++
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12
Q

What increases contractility?

A
  • catecholamines
  • HR (bowditch/treppe effect)
  • afterload (anrep effect)
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13
Q

What decreases contractility?

A
  • parasympathetic innervation

- systolic failure

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14
Q

Systemic vascular resistance (SVR)

A
  • resistance to blood flow offered by all systemic vasculature
  • associated with LV afterload, but not synonymous

SVR = (MAP-CVP)
—————- x80
CO

Normal SVR = 900-1200 dynes/sec/cm5

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15
Q

Determinants of SVR

A
  • arteriolar tone is primary determinant of SVR

- vessels in the systemic system are more compliant than in the pulmonary vascular system

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16
Q

What causes elevated SVR?

A

-mechanisms that cause vasoconstriction increase SVR

  • sympathetic activation
  • hypovolemia
  • hemorrhagic or cardiogenic shock
  • vasoconstricting drugs
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17
Q

What reduces SVR?

A

-mechanisms that cause vasodilation decrease SVR

  • septic shock
  • vasodilation medications
  • parasympathetic stimulus
  • hypercarbia
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18
Q

Systemic vascular resistance index

A

SVRI = (MAP - CVP)
______________ x80
CI

Commonly used to offer guidance in the use of vasoconstrictors or vasodilators

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19
Q

Pulmonary vascular resistance

A
  • reflects blood flow through the pulmonary circulation. Resistance is influence by pulmonary capillaries and arteries
  • if PVR high, right ventricle must work harder to move blood past pulmonic valve. Will lead to dilation of RV

PVR = (MPAP - PAWP)
———————- x80
CO
Normal PVR = 100 - 200 dynes/sec/cm5

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20
Q

Factors that increase PVR

A
  • vasoconsticting drugs
  • hypoxemia
  • acidemia
  • hypercapnia
  • atelectasis
  • hypovolemia
  • hyperinflation (increased PEEP, increases PIP)
  • sympathetic stimulation
  • high Hct
  • alpha-adrenergic agonists
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21
Q

Factors that decrease PVR

A
  • vasodilating drugs
  • alkalemia
  • hypocapnia
  • strenuous exercise
  • block sympathetic stimulation (narcotics)
  • low Hct
  • alpha adrenergic antagonists
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22
Q

Pulmonary vascular resistance index

A

-PVRI = (MPAP-PAWP)
—————— x80
CI

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23
Q

SVO2

A
  • O2 saturation of the blood returning to the right side of the heart.
  • it is the measurement of the relationship between O2 consumption and O2 delivery in the body
  • normal = 60-80%
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24
Q

What causes low SVO2?

A
  • <60%. O2 supply is insufficient or the O2 demand has increased
  • decreased Hgb
  • decreased SaO2 (hypoxemia)
  • any form of shock or arrhythmia
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25
Q

What causes high SVO2?

A
  • > 80%. O2 demand has declined or the O2 supply had increased
  • increased O2 delivery
  • decreased O2 demand (hypothermia, anesthesia, neuromuscular blockade)
  • high flow states: sepsis, hyperthyroidism, severe liver disease
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26
Q

Einthoven’s law

A
  • if the ECGs are recorded simultaneously with the 3 limb leads, the sum of the potentials recorded in leads I and III will equal the potential in lead II
  • Lead I potential + Lead III potential = Lead II potential
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27
Q

What is most useful lead in detecting cardiac arrhythmia?

A

Lead II as it lies close to cardiac axis

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28
Q

Benefit to lead V1?

A
  • distinguish between LV ectopy and RV ectopy
  • can tell right BB from left BB
  • p waves are more easily seen in right sided monitoring leads
  • differentiation of SVT and vtach
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29
Q

Wilson’s Central Terminal Theory

A

-serves as a reference point for each of the 6 electrodes in 12 lead EKG

30
Q

How could you look at posterior heart with EKG?

A

V6—>V9
V5—>V8
V4—>V7

31
Q

What are 2 main coronary arteries that supply the heart?

A

Left and right coronary arteries

  • originate in the aorta, immediately superior to the aortic valve
  • perfused during diastole
32
Q

Left coronary artery supplies what?

A
  • Anterior left ventricle
  • Left lateral portion of left ventricle

Divides into:

  • Left anterior descending: supplies anterior and septal regions of the heart
    • including LV, interventricular septum, and parts of RV
  • Left circumflex: supplies lateral portions of the heart
    • including left atrium and LV
33
Q

Right coronary artery supplies what?

A
  • Right atrium
  • Most of the right ventricle
  • Posterior part of left ventricle (in 80-90% of population)

Divides into:

  • Right martial artery: supplies right atrium and RV
  • posterior descending artery: supplies the bottom portion of LV and back of septum (in conjunction with left circumflex)
34
Q

ST elevation

A

-elevation >0.5-1mm in 2 or more contiguous precordial leads, or 2 mor more adjacent limb leads

35
Q

What is seen with posterior wall ischemia/infarct?

A
  • ECG changes will be reversed as will be looking at the endocardial surface of the posterior heart wall
  • initially ST segments V1 and V2 are depressed
  • ST elevation in leads V7, V8, and V9
  • RCA (PDA) and/or LCX involved
  • rarely seen by itself
36
Q

Contraindications to fibrinolytic therapy

A
  • SBP>180
  • DBP>110
  • right arm vs left arm BP difference >15
  • stoke >3 hours or < 3 months
  • Hx of structural CNS disease
  • head/facial trauma within 3 weeks
  • major trauma (GI bleeding/surgery within 4 weeks)
  • taking blood thinners
  • pregnancy
  • Hx intercranial hemorrhage
  • advanced cancer, sever liver/renal disease
37
Q

Time goals for reperfussion therapies

A
  • balloon inflation PCI: door to inflation goal 90 min

- fibrinolysis: door to needle goal 30 min

38
Q

What do you do if ST elevation during surgery?

A

*mange causes of decreased O2

  • tachycardia
  • hypotension
  • decreased O2
  • anemia
  • manage causes of increased O2 demand
  • tachycardia
  • increase preload
  • increased contractility
  • increased afterload
39
Q

What is CVP?

A

Central venous pressure

  • direct measurement of the blood pressure in the right atrium and vena cava
  • tip of the catheter rests in the lower third of the superior vena cava
40
Q

What are the 3 ports of a pulmonary artery catheter?

A
  1. Proximal: (CVP) port measures right atrial and central venous pressures
  2. Distal port measures pulmonary artery pressure and wedge pressure when a balloon is inflated
  3. Thermistor port is connected to the monitor to give continuous temp readings
41
Q

CVP measurement

A
  • normal 1-10 mmHg
  • measured at the end of expiration, this is when pleural pressure are approximately equal to atmospheric pressure (unless using PEEP)
42
Q

Waveform of CVP

A
  • a wave: contraction of RA
  • c wave: closure of tricuspid valve and contraction of ventricles
  • v wave: passive filling of RA
  • x descent: drop in atrial pressure during ventricular systole caused by atrial relaxation
  • y descent: atrial pressure drop as blood enters the ventricle during diastole (early ventricular filling)
43
Q

What can cause abnormal CVP waveforms?

A
  • malpositioning of catheter
  • dysrhythmias
    • atrial fibrillation
    • junctional rhythms
    • premature ventricular contractions

-valvular defects also produce dramatic changes in CVP, causing increase in amplitude of the v wave

44
Q

What causes “cannon” a waves or giant a waves?

A
  • junctional rhythms
  • complete AV block
  • PVCs
  • ventricular pacing
  • tricuspid or mitral stenosis
  • diastolic dysfunction
  • myocardial ischemia
  • ventricular hypertophy
45
Q

What causes loss of a waves or only v waves on CVP?

A
  • a-fib

- v-pacing in the setting of asystole

46
Q

What causes large v waves on CVP?

A
  • tricuspid or mitral regurgitation

- acute increase in intravascular volume

47
Q

Causes of low CVP?

A

-hypovolemia

48
Q

Causes of higher CVP

A
  • higher PEEP settings
    • PEEP of 10 cm H2O usually results in increase of CVP by 3 cmH2O
  • RV failure
  • tricuspid stenosis or regurgitation
  • cardiac tamponade
  • constrictive pericarditis
  • volume overload
  • pulmonary HTN
  • LV failure (chronic)
49
Q

Where is proper placement of PA cath?

A
  • 2cm left of mediastinal border
  • zone 3 of lungs is the optimal location
  • tip of the cath sits in the pulmonary artery
50
Q

Pulmonary artery pressures

A
  • normal PAP = 15-25/5-15
  • dicrotic notch is the usual feature of the PA waveform and represents aortic valve closure

MPAP: is the average pressure in the pulmonary vasculature throughout the cardiac cycle

51
Q

Mean arterial pressure

A 
MAP = SVR x CO
MAP = DBP + (SV/3)
52
Q

Korotkoff sounds

A

-these sounds appear and disappear as the BP cuff is inflated and deflated

53
Q

Auscultation vs oscillometric BP reading

A
  • both can be taken manually
  • either by listening or by watching oscillometric variation of on sphygmomanometer

-automatic machines use oscillometric variation to read pressures

54
Q

Contraindications of a-lines

A

-pt with compromised arterial supply such as pts with Reynolds or thromboangitis obliterans (Buerger’s disease)

55
Q

What are signs of possible hypovolemia in vented pt with a-line?

A

-the more hypovolemc a pt is, the greater the inspiratory decrease of SBP and stroke volume

56
Q

What do the different colors of color Doppler represent?

A
  • blue: away from transducer
  • red: towards transducer
  • green/mosaic: turbulent flow
57
Q

What are the main recommended cuts for TEE?

A
  • 20 cuts/views determined by The American Society of Echocardiography (ASE) and The Society of Cardiovascular Anesthesiologists (SCA)
  • est a systemiztion of TEE
58
Q

Uses of TEE during cardiac and thoracic surgery

A
  • confirm and refine pre-op diagnosis
  • detect more or unsuspected pathology
  • adjust the anesthetic and surgical plan accordingly
  • assess the results of surgical intervention
59
Q

What are some things that intro-op TEE can assess for?

A
  • assessment of hemodynamic instability
  • valvular assessment
  • monitoring myocardial ischemia
  • detention of aortic atheromatous plaques
  • aortic dissection
  • congenital cardiopathy
  • detection intracardiac air
60
Q

Contraindications of TEE

A
  • esophageal stenosis
  • large esophageal diverticuli
  • recent esophageal surgery/sutures
  • know esophageal interruptions
61
Q

What are the 3 fundamental processes of thermoregulation?

A
  1. Afferent sensing: receptors throughout body send info to hypothalamus
  2. Central control: hypothalamus primary center for them control. Calculated response is made from eh afferent signal
  3. Efferent response: sends calculated response to targeted functions systems within the body
62
Q

What are actions that can help with temperature control of pt?

A
  • prewarming pt
  • room conditions
  • warming IV fluids
  • warming blanket
63
Q

What are some effects of hypothermia?

A
  • cardiac arrhythmias and ischemia
  • increased peripheral vascular resistance
  • left-shift of the hemoglobin-oxygen saturation curve
  • reversible coagulopathy
  • altered mental status
  • impaired renal function
  • delayed drug metabolism
  • impaired wound healing
  • increased risk of infection
64
Q

How do anesthetics interfere with central thermoregulation?

A
  • all inhaled agents cause vasodilation
  • spinal/epidural: vasodilation and altered perception of temp
  • general: vasodilation and redistribution
  • opioids: depress sympathetic outflow
65
Q

What are the 3 phases of intra-op hypothermia?

A
  • Phase 1: core temp decreases 1-2 degrees C during 1st hour of general anesthesia
    • anesthetic induced vasodilation
    • heat shifts from central compartments
    • little heat loss from pt to environment
  • Phase 2; gradual decline in core temp (hours 3-4 of surgery)
    • continuous heat loss from pt to environment
    • heat loss = metabolic heat production ???
  • Phase 3: when core temp reaches a point of steady state
66
Q

What is malignant hyperthermia (MH)?

A

-rare hyperametabolic disease following exposure to inhaled General anesthetics or succinylcholine
-presents within minutes up to 1 hour after triggering anesthetic
Causes:
-mutation of Ryr1 receptor located on chromosome 19
-mutations involving sodium channel of chromosome 17
-autosomal recessive form of MH has been associated with king-Denborough syndrome

67
Q

What are signs and symptoms of MH?

A
  • increased CO2
  • increased sympathetic activity
  • markedly increased metabolism
  • hyperthermia
68
Q

What drugs are known to trigger MH?

A
  • inhaled anethetics
  • ether
  • halothane
  • methoxyflurane
  • enflurane
  • isoflurane
  • desflurane
  • sevoflurane
  • depolarizing muscle relaxant
  • succinylcholine
69
Q

What other conditions to consider if pt exhibiting some symptoms of MH?

A
  • NMS
  • thyroid storm
  • pheochromocytoma
  • drugs-induced hyperthermia
  • environmental hyperthermia
  • brain injury
  • sepsis
  • transfusion reaction
70
Q

What is the treatment of MH?

A
  • stop triggering agents
  • hyperventilate/100% O2
  • Dantrolene (2.5mg/kg)
  • bicarbonate
  • glucose and insulin
  • IVF and cooling blanket
  • fluid output monitoring and furosemide
  • fast heart (tachycardia)

APA I (9 decks)

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