Ch. 2 Hemodynamics Flashcards
+ Inotropy vs. - Inotropy Causes 3
+) SNS Stimulation
Sepsis
Hyperdynamic Ventricle
Drugs
-) Massive MI
Heart Failure
Increased resistance
Hypoxia, Beta blockers, CCBs
Hypercalcemia, Acidosis, Hypernapnia
Electrolyte Imbalances (hypercalcemia)
Preload
- Definition
- RA vs. CVP location
- PAOP measures what
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
- When would preload be elevated
- When would preload decrease
- Causes of CVP elevation
- Causes of PAOP elevation
- This is vasoconstriction/fluid overload/high pressure.
HF, Cardiogenic shock, pericardial tamponade, fluid overload, high PEEP - This is vasodilation/hypovolemia/low pressure
Hypovolemia, Bleeding, veno/vasodilation, decreased venous return, Drugs like morphine or beta blockers, diuresis, way too much PEEP - Pressure backing up from RV failure, pulm HTN, tricuspid stenosis or regurg
- Mitral stenosis or regurg
Afterload
- Definition
- PVR vs SVR
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
Normal Hemodynamic Values
*CO
*CI
SV
SVI
RVSWI
LVSWI
*SVO2
*ScVO2
PAP
*PAOP
*RAP/CVP
*SVR
*SVRI
*PVR
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
Hemodynamic Formulas
- CO
- SV
- CI
- CO = HR x SV
normal: 4-8 L/min - SV = EDV - ESV
normal: ~70 ml - CI: 2.5 - 4.0
- When would afterload be elevated
- When would afterload decrease
- 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 - This is vasodilation
Distributive shock (vasodilatory), vasoplegic shock, septic shock, anaphylactic shock, spinal/neurogenic shock, vasodilatory drugs
Vasoplegic syndrome
- Definition
- Cause
- 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
PA Catheter
- Contraindications
- Zero where
- Dicrotic notch signifies
- 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
PAOP Safety
- Stop inflating when
- Max inflate ml
- Max inflate time
- If waveform does not change
- Large waves =
- 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
How much oxygen is extracted from PaO2 in SvO2/ScvO2
We extract about 25-30% oxygen to tissues
Norepinephrine
- Class and action
- Receptors
- Dosing
- Side effects 1
- 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
Location of receptors
- α
- β1
- β2
- Blood vessels (BP)
- Heart (inotropy and chronotropy)
- Bronchial and vascular smooth muscle (alveolar)
Norepinephrine (Levophed)
* Class
* Receptor activation
* Dosing
* Half life
* Side effects to watch for 1
- 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
Epinephrine (Adrenalin)
* Class
* Receptor activation
* Dosing mcg/min
* Half life
* Side effects to watch for 1
- 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
Dopamine (Inotropin)
* Class
* Receptor activation
* Dosing mcg/min
* Half life
* Side effects to watch for 1
- 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
Phenylephrine (Neosynephrine)
* Class
* Receptor activation
* Dosing
* Half life
* Side effects to watch for
- 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
Vasopressin (Pitressin)
* Class
* Receptor activation
* Indication
* Dosing
* Half life
- 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)
Phentolamine (Rigitine)
* Class and indication
* Receptor activation
* Dosing
* What can also be used
- 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
Dobutamine (Dobutrex)
* Class
* Receptor activation
* indication
* Dosing
* Half life
* Side effects to watch for
- 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
Milrinone (Primacor)
* Class
* indication
* Dosing
* Half life
- 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
- Hypertensive crisis def
- Damage associate with HTN
1. kidney
2. brain
3. heart
4. eyes
5. vascular
- 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
- BP =
- Arterial BP is controlled by what, where
- what is activated
- 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
4 first line agents in outpatient treatment of BP
- Ace inhibitor OR
- Angiotensin receptor blocker
- Calcium chyannel blocker
- Thiazide diuretic
4 Second line agents in outpatient treatment of BP (and one example)
- Beta blocker: metoprolol
- Alpha 2 agonist: clonidine
- Alpha blockers “osin” : prazosin
- Renin inhibitors: Aliskiren
- Hypertensive crisis def
- Damage assosiated with:
1. Kidney
2. brain
3. heart
4. eyes
5. vascular system
- 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
4 steps treatment of hypertensive crisis
- Double check BP in both arms
- Consider 12 lead ECG
- Goal: decrease BP by 25% iin 1 - 2 hours
- IV Medications:
* Nitroprusside (Nipride)
* Nitroglycerin (tridil)
* Labetalol (trandate)
* Esmolol (brevibloc)
* Nicardipine (cardene)
* Clevidipine (cleviprex)
* Hydralazine (Apreoline)
* Fenoldopam (corlopam) **
Nitroprusside (Nipride)
* Class
* Receptor activation
* Dosing
* Half life
* Side effects to watch for
* Unexplained drop in oxygenation –>
- 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
Nitroprusside/thiocyanate Toxicity
* When does this happen
* At risk group
* Signs/symptoms
* Monitor for
- 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
Notroprusside Toxicity treatment:
1. Administer what 3 treatments
- Administer sodium thiosulfate (150 mg/kg over 15 mins) or 3% sodium nitrate
- If hypoxic, mechanically ventilate with 100% oxygen to maximize oxygen availability
- Methemoglobinemia: admiinister methylene blue (1 - 2 mg/kg over 5 min)
Nitroglycerin (Tridil)
* Class
* Receptor activation
* Indication
* Dosing
* Side effects to watch for
* Do not use in
- 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
Calcium Channel blockers
* Action
* Effect
- 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).
Types of Calcium Channel Blockers
* DHP Dihydropyridines vs non-dihydropyridines
* Indication
* examples
- 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)
Esmolol(Brevibloc)
* Action
* Initial dose
* Maintenance dose
- Short acting beta blocker
- Initial dose: 250 - 500 mcg/kg IV over 1 min
- Maintenance dose: 0.05 - 0.3 mg/kg/min
Labetalol (Trandate)
* Action
* Initial dose
* Maintenance dose
- 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
Metoprolol
* Dose
- 5mg IV q2 min up to 3 times
*
Fenoldopam (Corlopam)
* Mech. of action
* Continuous infusion dose
* Titrate by what dose
* onset, max effect time
* Side effects to monitor for
- 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
Drugs for HTN emergency
* 4 options
- IV Nitrates (tridil or nitroiprusside)
- IV CCB (nicardipine/cardene, clevidipine/cleviprex)
- IV Hydralazine
- IV Fenoldopam
Nitrates: Tridil or Nitroprusside
* Tridil vs Nipride
- Tridil is mostly venodilation
- Nipride decreases both afterload and preload
Hemodynamics of Cardiogenic Shock (up or down)
CO
Preload
Afterload
SvO2
CO decreases
Preload increases
Afterload increases
SvO2 decreases
Clinical Signs of Cardiogenic shock:
Name 5
- *Crackles
- CI <2.0 L/min/m^2
- S3, Pulmonary edema
- Tachycardia
- Dysrhythmias
- Decreased perfusion
- Skin mottling
- Decreased UOP (oliguria <0.5 mg/kg/hr)
- Hypotension
Hemodynamic profile of cardiogenic shock
CI
SVR
RA/CVP
SvO2
Treatment
- CI < 2.0
- Elevated SVR (afterload > 1200)
- Elevated RA/CVP (preload >14)
- Decreased SvO2 <65%
- Inotropes, afterload reduction, pressors
Cardiogenic shock picture:
What will these look like and why
* CXR
* Echo
* ABG
- 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
What is SAM?
Why is this harmful?
- 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)
Hymodynamic profile of Hypovolemic/hemorrhagic shock
CI
SVR
RA/CVP
SvO2
Treatment
- CO/CI decreased
- Preload CVP/PAOP decreased
- Afterload SVR increased
- SvO2 decreased
- Treatment: Fluids or blood
Hemodynamic profile of distributive/vasoplegic/septic shock
CI
SVR
RA/CVP
SvO2
Treatment
- CO/CI increased
- Preload CVP/PAOP decreased
- Afterload SVR decreased
- SvO2 decreased
- Treatment: Fluids + pressors, inotropes, methylene blue
Hemodynamic profile of Obstructive shock (Tamponade)
CI
SVR
RA/CVP
SvO2
Treatment
- CO/CI decreased
- Preload CVP/PAOP increased
- Afterload SVR increased
- SvO2 decreased
- Treatment: Pericardiocentesis/re-sternotomy
IABP inflation occurs at the onset of?
Deflates prior to?
Coronary arteries are perfused during?
Provides support equivalent to?
Benefits (4)
- 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
Dicrotic notch symbolizes:
Where should the balloon be on xray?
What symptoms do we monitor for and why?
- 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
Contraindications to IAMP therapy (3)
Complications (4)
- Aortic insufficiency/regurg
- Aortic aneurysm
- Aortic dissection
- Limb ischemia
- Incorrect timing
- Renal artery occlusion
- Infection
Impella Device
* Where inserted and when
* Used to support which side of the heart
- 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)
VA ECMO supports:
VV Ecmo supports:
Complications to monitor for:
- VA Heart and Lungs
- VV just lungs
- Monitor for limb ischemiaq
LVAD
Fully supports what part of the heart
Monitor for what
- Fully unloads the left ventricle
- Monitor for right ventricular failure and rising CVP
