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CSC Prep > Ch. 2 Hemodynamics > Flashcards

Ch. 2 Hemodynamics Flashcards

1
Q

+ Inotropy vs. - Inotropy Causes 3

A

+) SNS Stimulation
Sepsis
Hyperdynamic Ventricle
Drugs
-) Massive MI
Heart Failure
Increased resistance
Hypoxia, Beta blockers, CCBs
Hypercalcemia, Acidosis, Hypernapnia
Electrolyte Imbalances (hypercalcemia)

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2
Q

Preload
- Definition
- RA vs. CVP location
- PAOP measures what

A

The initial stretching of the myocardium/sarcomeres prior to contraction. Equated to volume status (with caution!)
RA: PA catheter in RA
CVP: Central line in SVC
PAOP: Left atrial pressure and LV end diastolic pressure

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3
Q
  1. When would preload be elevated
  2. When would preload decrease
  3. Causes of CVP elevation
  4. Causes of PAOP elevation
A
  1. This is vasoconstriction/fluid overload/high pressure.
    HF, Cardiogenic shock, pericardial tamponade, fluid overload, high PEEP
  2. This is vasodilation/hypovolemia/low pressure
    Hypovolemia, Bleeding, veno/vasodilation, decreased venous return, Drugs like morphine or beta blockers, diuresis, way too much PEEP
  3. Pressure backing up from RV failure, pulm HTN, tricuspid stenosis or regurg
  4. Mitral stenosis or regurg
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4
Q

Afterload
- Definition
- PVR vs SVR

A

The resistance/force the ventricles must overcome to eject blood
PVR: Afterload on the right side of the heart
SVR: Afterload on the left side of the heart

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5
Q

Normal Hemodynamic Values
*CO
*CI
SV
SVI
RVSWI
LVSWI
*SVO2
*ScVO2
PAP
*PAOP
*RAP/CVP
*SVR
*SVRI
*PVR

A

CO: 4-8 L/min
CI: 2.5-4 L/min/m^2
SV: 50-100 ml/beat
SVI: 35-60 ml/beat/m^2
RVSWI: 5-10 g/m^2/beat
LVSWI: 50-62 g/m^2/beat
SvO2: 60-75%
ScvO2: >70% (70%-85%)
PAP: 25/10 mmHg
PAOP: 8-12 mmHg
RAP/CVP: 2-6 mmHg
SVR: 900-1400 dynes/sec/cm^-5
SVRI: 1970-2370 d/sec/cm^-5/m^2
PVR: 90-250 d/sec/cm^-5

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6
Q

Hemodynamic Formulas
- CO
- SV
- CI

A
  • CO = HR x SV
    normal: 4-8 L/min
  • SV = EDV - ESV
    normal: ~70 ml
  • CI: 2.5 - 4.0
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7
Q
  1. When would afterload be elevated
  2. When would afterload decrease
A
  1. This is vasoconstriction
    HTN, Cardiogenic shock (heart is working harder against constricted vessels and increased water/salt retention), hypovolemia, bleeding, heart failure, cardiac tamponade, AV stenosis, vasoconstrictive drugs
  2. This is vasodilation
    Distributive shock (vasodilatory), vasoplegic shock, septic shock, anaphylactic shock, spinal/neurogenic shock, vasodilatory drugs
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8
Q

Vasoplegic syndrome
- Definition
- Cause

A
  • Low SVR<1600 & high CO>2.5 creating end-organ hypoperfusion d/t profoundly low SVR despite normal CO
  • Caused by endothelial injury, arginine-vasopressin system dysfunction, release of other vasodilatory inflammatory mediators and muscle hyperpolarization
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9
Q

PA Catheter
- Contraindications
- Zero where
- Dicrotic notch signifies

A
  • Tricuspid or pulmonic prosthetic valve, Right heart mass (tumor or thrombus), tricuspid or pulmonic valve endocarditis, left BBB if severe
  • Phlebostatic axis: level of left atrium is 4th ICS and 1/2 AP Diameter (anteroposterior)
  • Signifies closure of the pulmonic valve
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10
Q

PAOP Safety
- Stop inflating when
- Max inflate ml
- Max inflate time
- If waveform does not change
- Large waves =

A
  • Waveform changes or if resistance is met
  • 1.5 ml of air max
  • Inflate <15 seconds
  • Balloon may have ruptured or tip of PA is in the RV
  • Mitral stenosis
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11
Q

How much oxygen is extracted from PaO2 in SvO2/ScvO2

A

We extract about 25-30% oxygen to tissues

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12
Q

Norepinephrine
- Class and action
- Receptors
- Dosing
- Side effects 1

A
  • Vasopressor that stimulates α and some β1 resulting in increased BP & small amount of inotropy
  • Dose 0.5 - 100 mcg/min or 0.01 - 1 mcg/kg/min
  • Side effects include extravasation, bradycardia, dysrhythmias, HTN, renal artery vasoconstriction, digit and gut ischemia
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13
Q

Location of receptors
- α
- β1
- β2

A
  • Blood vessels (BP)
  • Heart (inotropy and chronotropy)
  • Bronchial and vascular smooth muscle (alveolar)
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14
Q

Norepinephrine (Levophed)
* Class
* Receptor activation
* Dosing
* Half life
* Side effects to watch for 1

A
  • Vasopressor which causes increased BP, SVR, and some CO
  • Alpha and β1
  • Dosing:
    1. 0.5 - 100 mcg/min (15-20 start thinking of a second drug)
    2. 0.01 - 1 mck/kg/min (sepsis)
  • Half life 2.5 mins
  • Watch out for extravasation, bradycardia, dysrhythmias, HTN, renal artery vasoconstriction, Digit and gut ischemia at high doses
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15
Q

Epinephrine (Adrenalin)
* Class
* Receptor activation
* Dosing mcg/min
* Half life
* Side effects to watch for 1

A
  • Vasopressor & Inotrope which causes increased BP, HR, CO, and SVR
  • α, β1, some β2
  • Dosing:
    1. 2 - 10 mcg/min
    2. 0.01 - 1 mcg/kg/min
    3. ACLS - 1 mg IV/IO
    4. Anaphylaxis 0.3 mg IM
  • Half life: 2-3 minutes
  • Watch for extravasation, tachycardia, dysrhythmias, chest pain, hyperglycemia, rise in lactate levels
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16
Q

Dopamine (Inotropin)
* Class
* Receptor activation
* Dosing mcg/min
* Half life
* Side effects to watch for 1

A
  • Vassopressor and inotrope which causes increased HR, BP. This is a precursor to NE and Epi
  • Stimulates β1 & small amount of β2 and alpha
  • Dosing:
    1. 0.5 - 5 mcg/kg/min - dopaminergic receptors (inc CO, inc UOP)
    2. 5 - 20 mcg/kg/min - β effects (inc CO, inc SVR)
    3. >20 mcg/kg/min - alpha effects (inc CO, inc SVR, inc HR)
    4. MAX 20-30 mcg/kg/min
  • Half life 2 min
  • Watch out for extravasation, tachycardia, arrhythmias
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17
Q

Phenylephrine (Neosynephrine)
* Class
* Receptor activation
* Dosing
* Half life
* Side effects to watch for

A
  • Vasopressor which increased BP and SVR
  • Pure alpha (alpha-1 agonist)
  • **Dosing: 0.05 - 3 mcg/kg/min **
    1. 0.05 - 3 mcg/kg/min
  • Watch for extravasation, reflex bradycardia - due to selective vasoconstriction and elevation of blood pressure, dysrhythmias, HTN, chest pain
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18
Q

Vasopressin (Pitressin)
* Class
* Receptor activation
* Indication
* Dosing
* Half life

A
  • Vasopressor which increases BP and SVR
  • Natural Antidiuretic hormone (ADH)
  • V1 agonist - vasoconstricts, inc SVR
    1. stimulates smooth muscle contraction of the vessels
  • V2 agonist - inc water reabsorption
    1. Works in the kidney as an anti-diuretic
  • 2nd line vasopressor in sepsis and CVS, also given for GI bleeding and DI
  • Dosing:
    1. 0.01 - 0.1 units/min
    2. Sepsis: 0.03 - 0.04 units/min
  • Half life 10 - 20 mins (why we dont actively titrate)
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19
Q

Phentolamine (Rigitine)
* Class and indication
* Receptor activation
* Dosing
* What can also be used

A
  • Alpha 1 blocker -> reverses alpha 1, used for vasopressor or dilantin extravasation. Prevents necrosis and sloughing of tissue
  • Phentolamine mesylate 5 - 10 mg
  • Topical nitroglycerin paste can also be used
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20
Q

Dobutamine (Dobutrex)
* Class
* Receptor activation
* indication
* Dosing
* Half life
* Side effects to watch for

A
  • Pressor medication that stimulates beta receptors, β1 (some alpha) inc contractility and CO.
  • Used in cardiac surgery and septic shock
  • Dosing:
    1. 2 - 20 mcg/kg/min IC (up to 50 mcg/kg/min)
    2. Onset 1 - 2 min up to 10 min
  • Half life 2 min
  • Monitor for tachycardia, hyper/hypotension/ ectopy, hypokalemia
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21
Q

Milrinone (Primacor)
* Class
* indication
* Dosing
* Half life

A
  • Phosphodiesterase (PDE) inhibitor which increases myocardial contractility and acts as a pulm vasodilator. Inc CI, dec PAOP, dec SVR, no change in HR (not only PA dilation)
  • Used as inotrope and as bridge to transplant
  • Dosing:
    1. Maintenance dose 0.375 - 0.75 mcg/kg/min
    2. Bolus 50 mcg/kg over 10 min not done often
  • Half life is long! 2.5 hours
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22
Q
  • Hypertensive crisis def
  • Damage associate with HTN
    1. kidney
    2. brain
    3. heart
    4. eyes
    5. vascular
A
  • BP >180/120 + target organ damage
  • Kidney: dec blood flor, hematuria, proteinuria
  • Brain: hypertensive encephalopathy
  • Heart: LVH, LVF, MI
  • Eyes: retinal hemorrhages
  • Vascular: vessel damage
23
Q
  • BP =
  • Arterial BP is controlled by what, where
  • what is activated
A
  • CO x SVR
  • Baroreceptors located in adrenal medulla and kidney (RASS system)
  • Baroreceptors in adrenal medulla signal catecholamine release leading to inc HR, BP, SVR
  • Baroreceptors in kidneys activated angiotensin 2
24
Q

4 first line agents in outpatient treatment of BP

A
  1. Ace inhibitor OR
  2. Angiotensin receptor blocker
  3. Calcium chyannel blocker
  4. Thiazide diuretic
25
Q

4 Second line agents in outpatient treatment of BP (and one example)

A
  1. Beta blocker: metoprolol
  2. Alpha 2 agonist: clonidine
  3. Alpha blockers “osin” : prazosin
  4. Renin inhibitors: Aliskiren
26
Q
  • Hypertensive crisis def
  • Damage assosiated with:
    1. Kidney
    2. brain
    3. heart
    4. eyes
    5. vascular system
A
  • Usually >180/120
  • Acute elevation associated with organ damage:
    1. Kidney: decreased blood flow, hematuria, proteinuria
    2. Brain: hypertensive encephalopathy
    3. Heart: LVH, LVF, MI
    4. Eyes: retinal hemorrhages
    5. Vascular: vessel damage
27
Q

4 steps treatment of hypertensive crisis

A
  1. Double check BP in both arms
  2. Consider 12 lead ECG
  3. Goal: decrease BP by 25% iin 1 - 2 hours
  4. IV Medications:
    * Nitroprusside (Nipride)
    * Nitroglycerin (tridil)
    * Labetalol (trandate)
    * Esmolol (brevibloc)
    * Nicardipine (cardene)
    * Clevidipine (cleviprex)
    * Hydralazine (Apreoline)
    * Fenoldopam (corlopam) **
28
Q

Nitroprusside (Nipride)
* Class
* Receptor activation
* Dosing
* Half life
* Side effects to watch for
* Unexplained drop in oxygenation –>

A
  • Nitrate antihypertensive which is a potent vasodilator decreasing BP and SVR. Reduces afterload and some preload which can create instability
  • So this would be an alpha agonist and beta 1
  • Dosing:
    1. 0.5 - 8 mcg/kg/min
  • Watch out for hypotension, can develop hypoxia from intrapulmonary shunt, may see increased HR
  • unexplained drop = shunt
29
Q

Nitroprusside/thiocyanate Toxicity
* When does this happen
* At risk group
* Signs/symptoms
* Monitor for

A
  • Happens infrequently but occurs if infusing >3 mcg/kg/min >72 hours
  • At risk: prolonged administration and renal/liver dysfunction. High doses for a prolonged period of time.
  • Clinical signs include vasodilation resulting in hypotension &/or dysrhythmias, ** tinitus, altered mental status**, delirium, coma, nausea, abdominal pain, muscle weakness
  • Monitor serum thiocyanate levels
29
Q

Notroprusside Toxicity treatment:
1. Administer what 3 treatments

A
  1. Administer sodium thiosulfate (150 mg/kg over 15 mins) or 3% sodium nitrate
  2. If hypoxic, mechanically ventilate with 100% oxygen to maximize oxygen availability
  3. Methemoglobinemia: admiinister methylene blue (1 - 2 mg/kg over 5 min)
30
Q

Nitroglycerin (Tridil)
* Class
* Receptor activation
* Indication
* Dosing
* Side effects to watch for
* Do not use in

A
  • Potent peripheral vasodilator which decreased BP and SVR. Dilates arterial and venous vasculature reduicing preload and afterload.
  • Alpha agonist
  • Used to treat angina, HF, HTN (not effective on some people)
  • Dosing:
    1. 5 mcg/min up to 200 mcg/min infusion
    2. Can titrate quickly every 5 to 10 minutes
  • Hypotension, bradycardia, dizziness, hypovolemia, headache, reflexive tachycardia, N/V,
  • Do not use in hypotension, hypovolemia, aortic stenosis, ICP issuies, constrictive pericarditits
30
Q

Calcium Channel blockers
* Action
* Effect

A
  • Blocks calcium channels in the heart and vessel wall
  • Causes relaxation of smooth muscle in vessel wall leading to decreased BP and resistance/afterload (SVR).
31
Q

Types of Calcium Channel Blockers
* DHP Dihydropyridines vs non-dihydropyridines
* Indication
* examples

A
  • Dihydropyridines: Used to treat HTN because they are vasoselective. Used for angina also
  • Examples include: All the “Pines,” Amlodipine (norvasc), Felodoipine (Plendil), Nifedipine (procardia), Nicardipine (Cardene), Clevidipoine (Cleviprex)
  • Non-dihydropyridines: Used to treat tachyarrhythmias, HCM, angina, and vasospasm because they are cardioselective and vasoselective
  • Examples include Verapimil (Calan, Isoptin), Diltiazem (Cardizem)
32
Q

Esmolol(Brevibloc)
* Action
* Initial dose
* Maintenance dose

A
  • Short acting beta blocker
  • Initial dose: 250 - 500 mcg/kg IV over 1 min
  • Maintenance dose: 0.05 - 0.3 mg/kg/min
33
Q

Labetalol (Trandate)
* Action
* Initial dose
* Maintenance dose

A
  • Blocks Beta 1 and Beta 2, slight alpha
  • Initial dose: 20 mg IV over 2 min; follow with 20-80 mg IV q10 - 15 min until BP is controlled
  • Maintenance dose: 2 mg/min IV continuous infusion; titrate up to 5-20 mg/min; not to exceed total dose of 300 mg
34
Q

Metoprolol
* Dose

A
  • 5mg IV q2 min up to 3 times
    *
35
Q

Fenoldopam (Corlopam)
* Mech. of action
* Continuous infusion dose
* Titrate by what dose
* onset, max effect time
* Side effects to monitor for

A
  • D1 dopamine receptor agonist: rapid-acting vasodilator which decreased peripheral vascular resistance and arterial resistance, increases renal blood flow. Also natural diuretic / natriuretic
  • Initiate dose at 0.01 - 0.3 mcg/kg/min IV
  • Titrate by 0.05 - 0.1 mcg/kg/min q 15 up to 1.6 mcg/kg/min used in clinical trials
  • Onset: 10 min, max effect 30-120 min
  • Monitor for Angina, dysrhythmias, dizziness, flushing, heart failure, hypotension, tachycardia, headache, N/V, increased creatinine
36
Q

Drugs for HTN emergency
* 4 options

A
  1. IV Nitrates (tridil or nitroiprusside)
  2. IV CCB (nicardipine/cardene, clevidipine/cleviprex)
  3. IV Hydralazine
  4. IV Fenoldopam
37
Q

Nitrates: Tridil or Nitroprusside
* Tridil vs Nipride

A
  • Tridil is mostly venodilation
  • Nipride decreases both afterload and preload
38
Q

Hemodynamics of Cardiogenic Shock (up or down)
CO
Preload
Afterload
SvO2

A

CO decreases
Preload increases
Afterload increases
SvO2 decreases

39
Q

Clinical Signs of Cardiogenic shock:
Name 5

A
  1. *Crackles
    • CI <2.0 L/min/m^2
  3. S3, Pulmonary edema
  4. Tachycardia
  5. Dysrhythmias
  6. Decreased perfusion
  7. Skin mottling
  8. Decreased UOP (oliguria <0.5 mg/kg/hr)
  9. Hypotension
40
Q

Hemodynamic profile of cardiogenic shock
CI
SVR
RA/CVP
SvO2
Treatment

A
  • CI < 2.0
  • Elevated SVR (afterload > 1200)
  • Elevated RA/CVP (preload >14)
  • Decreased SvO2 <65%
  • Inotropes, afterload reduction, pressors
41
Q

Cardiogenic shock picture:
What will these look like and why
* CXR
* Echo
* ABG

A
  • CXR: Pulmonary congestion
  • Echo: Decreased wall motion (hypokinesia: heart is not contracting like it should be)
  • ABG: Mixed respiratory acidosis from fluid build up, metabolic acidosis from lactic acid; hypoxemia, *Lactic acidosisis
42
Q

What is SAM?
Why is this harmful?

A
  • Systolic Anterior Motion: the dynamic movement of the mitral valve (MV) during systole anteriorly towards the left ventricular outflow tract (LVOT)
  • This can mean that the mitral valve is reopening and causing obstructed flow (d/t aortic valve closure) out of the left ventrible (LVOTO)
43
Q

Hymodynamic profile of Hypovolemic/hemorrhagic shock
CI
SVR
RA/CVP
SvO2
Treatment

A
  • CO/CI decreased
  • Preload CVP/PAOP decreased
  • Afterload SVR increased
  • SvO2 decreased
  • Treatment: Fluids or blood
44
Q

Hemodynamic profile of distributive/vasoplegic/septic shock
CI
SVR
RA/CVP
SvO2
Treatment

A
  • CO/CI increased
  • Preload CVP/PAOP decreased
  • Afterload SVR decreased
  • SvO2 decreased
  • Treatment: Fluids + pressors, inotropes, methylene blue
45
Q

Hemodynamic profile of Obstructive shock (Tamponade)
CI
SVR
RA/CVP
SvO2
Treatment

A
  • CO/CI decreased
  • Preload CVP/PAOP increased
  • Afterload SVR increased
  • SvO2 decreased
  • Treatment: Pericardiocentesis/re-sternotomy
46
Q

IABP inflation occurs at the onset of?
Deflates prior to?
Coronary arteries are perfused during?
Provides support equivalent to?
Benefits (4)

A
  • Diastole
  • Systole
  • Diastole
  • 250 cc bolus or 0.5 L/min support
    1. Decreased afterload
    2. Increased coronary artery perfusion
    3. Decreased O2 demand
    4. Increased O2 supply
47
Q

Dicrotic notch symbolizes:
Where should the balloon be on xray?
What symptoms do we monitor for and why?

A
  • Balloon inflation and closure of the aortic valve
  • Balloon should be 2nd to 3rd ICS
  • Monitor for decreased urine output and absent left radial pulse d/t catheter being superior to renal artery and inferior to subclavian artery
48
Q

Contraindications to IAMP therapy (3)
Complications (4)

A
  1. Aortic insufficiency/regurg
  2. Aortic aneurysm
  3. Aortic dissection
  4. Limb ischemia
  5. Incorrect timing
  6. Renal artery occlusion
  7. Infection
49
Q

Impella Device
* Where inserted and when
* Used to support which side of the heart

A
  • Inserted percutaneously via femoral or axillary artery. Prior to PCI, post MI or postop
  • Can support the left or the right ventricle (L up to 5 L/min Impella RP up to 4 L/min)
50
Q

VA ECMO supports:
VV Ecmo supports:
Complications to monitor for:

A
  • VA Heart and Lungs
  • VV just lungs
  • Monitor for limb ischemiaq
51
Q

LVAD
Fully supports what part of the heart
Monitor for what

A
  • Fully unloads the left ventricle
  • Monitor for right ventricular failure and rising CVP

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