Group Presentations Flashcards
1
Q
Stroke volume
A
SV = EDV - ESV
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
3
Q
Cardiac index
A
-normalizes CO to individuals of different sizes
CI = CO/BSA
Normal CI = 2.6 - 4.2 L/min/m2
4
Q
How does increasing HR affect CO?
A
-stroke volume falls as HR increases due to decrease ventricular filling
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
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
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
8
Q
Frank-Starling mechanism
A
-stretched fibers recoil harder
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
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
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++
12
Q
What increases contractility?
A
- catecholamines
- HR (bowditch/treppe effect)
- afterload (anrep effect)
13
Q
What decreases contractility?
A
- parasympathetic innervation
- systolic failure
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
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
16
Q
What causes elevated SVR?
A
-mechanisms that cause vasoconstriction increase SVR
- sympathetic activation
- hypovolemia
- hemorrhagic or cardiogenic shock
- vasoconstricting drugs
17
Q
What reduces SVR?
A
-mechanisms that cause vasodilation decrease SVR
- septic shock
- vasodilation medications
- parasympathetic stimulus
- hypercarbia
18
Q
Systemic vascular resistance index
A
SVRI = (MAP - CVP)
______________ x80
CI
Commonly used to offer guidance in the use of vasoconstrictors or vasodilators
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
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
21
Q
Factors that decrease PVR
A
- vasodilating drugs
- alkalemia
- hypocapnia
- strenuous exercise
- block sympathetic stimulation (narcotics)
- low Hct
- alpha adrenergic antagonists
22
Q
Pulmonary vascular resistance index
A
-PVRI = (MPAP-PAWP)
—————— x80
CI
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%
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
25
What causes high SVO2?
* >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
26
Einthoven’s law
- 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
27
What is most useful lead in detecting cardiac arrhythmia?
Lead II as it lies close to cardiac axis
28
Benefit to lead V1?
- 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
29
Wilson’s Central Terminal Theory
-serves as a reference point for each of the 6 electrodes in 12 lead EKG
30
How could you look at posterior heart with EKG?
V6—>V9
V5—>V8
V4—>V7
31
What are 2 main coronary arteries that supply the heart?
Left and right coronary arteries
- originate in the aorta, immediately superior to the aortic valve
- perfused during diastole
32
Left coronary artery supplies what?
- 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
Right coronary artery supplies what?
- 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
ST elevation
-elevation >0.5-1mm in 2 or more contiguous precordial leads, or 2 mor more adjacent limb leads
35
What is seen with posterior wall ischemia/infarct?
- 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
Contraindications to fibrinolytic therapy
- 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
Time goals for reperfussion therapies
- balloon inflation PCI: door to inflation goal 90 min
| - fibrinolysis: door to needle goal 30 min
38
What do you do if ST elevation during surgery?
*mange causes of decreased O2
- tachycardia
- hypotension
- decreased O2
- anemia
* manage causes of increased O2 demand
- tachycardia
- increase preload
- increased contractility
- increased afterload
39
What is CVP?
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
What are the 3 ports of a pulmonary artery catheter?
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
CVP measurement
- 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
Waveform of CVP
- 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
What can cause abnormal CVP waveforms?
- 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
What causes “cannon” a waves or giant a waves?
- junctional rhythms
- complete AV block
- PVCs
- ventricular pacing
- tricuspid or mitral stenosis
- diastolic dysfunction
- myocardial ischemia
- ventricular hypertophy
45
What causes loss of a waves or only v waves on CVP?
- a-fib
| - v-pacing in the setting of asystole
46
What causes large v waves on CVP?
- tricuspid or mitral regurgitation
| - acute increase in intravascular volume
47
Causes of low CVP?
-hypovolemia
48
Causes of higher CVP
- 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
Where is proper placement of PA cath?
- 2cm left of mediastinal border
- zone 3 of lungs is the optimal location
- tip of the cath sits in the pulmonary artery
50
Pulmonary artery pressures
- 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
Mean arterial pressure
```
MAP = SVR x CO
MAP = DBP + (SV/3)
```
52
Korotkoff sounds
-these sounds appear and disappear as the BP cuff is inflated and deflated
53
Auscultation vs oscillometric BP reading
- 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
Contraindications of a-lines
-pt with compromised arterial supply such as pts with Reynolds or thromboangitis obliterans (Buerger’s disease)
55
What are signs of possible hypovolemia in vented pt with a-line?
-the more hypovolemc a pt is, the greater the inspiratory decrease of SBP and stroke volume
56
What do the different colors of color Doppler represent?
- blue: away from transducer
- red: towards transducer
- green/mosaic: turbulent flow
57
What are the main recommended cuts for TEE?
- 20 cuts/views determined by The American Society of Echocardiography (ASE) and The Society of Cardiovascular Anesthesiologists (SCA)
- est a systemiztion of TEE
58
Uses of TEE during cardiac and thoracic surgery
- 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
What are some things that intro-op TEE can assess for?
- assessment of hemodynamic instability
- valvular assessment
- monitoring myocardial ischemia
- detention of aortic atheromatous plaques
- aortic dissection
- congenital cardiopathy
- detection intracardiac air
60
Contraindications of TEE
- esophageal stenosis
- large esophageal diverticuli
- recent esophageal surgery/sutures
- know esophageal interruptions
61
What are the 3 fundamental processes of thermoregulation?
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
What are actions that can help with temperature control of pt?
- prewarming pt
- room conditions
- warming IV fluids
- warming blanket
63
What are some effects of hypothermia?
- 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
How do anesthetics interfere with central thermoregulation?
- all inhaled agents cause vasodilation
- spinal/epidural: vasodilation and altered perception of temp
- general: vasodilation and redistribution
- opioids: depress sympathetic outflow
65
What are the 3 phases of intra-op hypothermia?
- 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
What is malignant hyperthermia (MH)?
-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
What are signs and symptoms of MH?
- increased CO2
- increased sympathetic activity
- markedly increased metabolism
- hyperthermia
68
What drugs are known to trigger MH?
* inhaled anethetics
- ether
- halothane
- methoxyflurane
- enflurane
- isoflurane
- desflurane
- sevoflurane
* depolarizing muscle relaxant
- succinylcholine
69
What other conditions to consider if pt exhibiting some symptoms of MH?
- NMS
- thyroid storm
- pheochromocytoma
- drugs-induced hyperthermia
- environmental hyperthermia
- brain injury
- sepsis
- transfusion reaction
70
What is the treatment of MH?
- 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)
