Lecture 3 - hemodynamics Flashcards
purpose of hemodynamic monitoring (3)
1) monitor for potential alterations in tissue perfusion
- HR
- BP
- MAP
- CVP
- SVR
- PVR
- SV
2) meet oxygen demands of tissues
- may require supplemental O2 (increased O2 demands for perfusion)
3) titrate medications that promote tissue perfusion
- PO/IV
TIP:
- vasoactive substances
- monitor for desired affects
components of hemodynamic monitoring (5)
BP
HR
RR (increased = metabolic imbalance)
CVC (measures pressure in heart and veins)
Labs:
- lactic acid, ABGs, central venous oxygenation (ScvO2)
- other labs that are surrogate for impending failure (trop/BNP)
- chem panels (BUN/Cr/GFR, AST/ALT)
CO
determinants of CO
formula: Stroke volume x Heart rate
volume x rate/min = vol/min
- sv: volume of blood ejected from the LV
- hr: how fast the heart is beating per minute
ie. stroke volume of 70 mL x 60 BPM = 4200 ml/min
preload(what, measurement (3))
vol of the ventricle at end of diastole (amount of ventricular stretch or amount of pressure in the heart at the end of diastole in the LV)
- starlings law of the heart/starlings curve
- volume measured by left ventricular end diastole pressure (LVEDP) -> impossible to measure
- if there is an increase in stretch -> there is an increase in volume the ventricle can hold
tip:
- end diastole (relax) -> look at LV
afterload
pressure that the heart must overcome to open the aortic valve (amount of resistance the LV has to work against to eject blood during systole)
- ventricular wall tension or stress during systolic ejection
- atherosclerosis INcreases afterload, vasoDILATION DEcreases afterload
contractility
strength of the “squeeze” of each beat
- positive or negative inotropic
- epi, dobutamine, milrinone, dopamine
- squeeze gets stronger
in response to a stressor, activation of the ________ will result in? (4)
SNS
- increased contractility
- increased HR
- vasoconstriction
- increased RR/gas exchange
review: the cardiac cycle (3)
1) cardiac diastole: both atria/ventricle are relaxed and filling with blood
2) atrial systole/vent diastole: atria contracts blood into the ventricle
3) vent systole/atrial diastole: ventricle contracts blood into aorta
note:
- ventricles passively fill with blood, atrial systole allows for max vent filling (atrial kick)
- higher pressure in the SVC than atria, allow for passive filling
review: cardiac action potential and electrical conduction pathway (3)
1) SA node is the primary pacemaker of the heart
- spontaneously fires
- pacemaker cells generate action potentials that spread through myocytes of the atria (aka neighbor cell coupling)
2) pacemaker cells are located in the SA node
- function: initiate electrical impulse that triggers heart beat
- make up 1% of cardiac cells
3) pacemaker cells action potential spreads through gap junctions to the contractile cells, creating their action potentials
tip:
- review notes
blood pressure
BP = cardiac output x peripheral vascular resistance
- PVR is the amt of resistance to blood flow in the circulatory system
key: SVR affects will affect BP
cardiac output
1) the volume of blood ejected from the heart over 1 minute
- SV x HR
what is the frank starling curve
as we increase in volume, we increased in CO
- however, theres a point where too much volume can cause a decrease in CO
key: want to optimize fluid balance
regulation of volume status: in patients with CHF, low perfusion at the lvl of the kidneys will cause sodium resorption and exacerbation of an already elevated preload -> volume overload
- what class of drug can we give to alter this process in a diseases heart?
ace inhibitors -> artificially inhibits RAAS to decrease BP
conditions that alter preload (5)
1) intravascular volume gain/loss
- IV fluids too fast/too slow (major GI/CABG)
- bleeding
- diuresis
- diarrhea
- overuse of diuretics
- “third spacing” -> low preload will third space fluid but eventually remobilize
2) low HR/loss of atrial kick
- symptomatic bradycardia
- afib
3) low EF
- lead to volume overload d/t stimulation of RAAS (resorption of Na+/H2O at kidneys)
4) decreased LV compliance
- dilated cardiomyopathy
5) aortic stenosis
- as a result of increase in afterload, results in vol overload (increased artificial preload)
- beware of over diuresis and nitrates as it can lead to vascular collapse
- key: blood will back up soo much, fluid will leak -> revasculature -> third spacing -> eventually affecting parenchyma of lungs -> patient will be crackly
what increases afterload (4)
increase in SVR (blockages)
- HTN (vasoconstriction/atherosclerosis)
- aortic stenosis (narrowing of bv)
- constriction of the bv d/t neurohormonal effects as response to RAAS (overactivation)
- ACE/ARBs remedy this by vasodilation
what increases SVR (5)
arterial vasoconstriction
- hypothermia
- LV failure (compensatory via RAAS activation)
- shock: hypovolemic/cardiogenic
- stress/anxiety
- atherosclerosis
what decreases SVR
arterial vasodilation
- shock: distributive (septic,anaphylactic,neurogenic)
- hyperthermia: TOO hot
pharmacologic treatments of alterations in SVR: too low SVR
alpha vasopressors:
- high dose dopamine
- levophed (first line)
- requires large bore IV bc it can cause tissue necrosis by extraversion
pharmacologic treatments of alterations in SVR: too high SVR
vasodilators:
- nitrates including nipride
- hydralazine
pharmacologic treatments of alterations in SVR: too high SVR r/t contractility
some inotropes:
- dobutamine (in conjunction with ACE-I to reduce constriction)
pharmacologic treatments of alterations in SVR: too high svr (rate/rhythm control)
alpha/calcium channels blockers
- cardura
- amlodipine, procardia
pharmacologic treatments of alterations in SVR: aortic valve stenosis
structurally elevated SVR
- valvuplasty
- AVR
- TAVR
right vs left cardiac chambers (atria vs. vent)
atria: thin walled, low pressure chambers
- contribute 30% of ventricular filling
- “atrial kick” or atrial systole
ventricles: primary pumping force of the heart
- thicker, stronger left vent is the “power pump”
- thinner RV is the low pressure chamber
right side of heart -> increased in _____
a: pressure
- can see increase in R heart vol. d/t excessive volume overloaded from L side of the heart
- atrial and ventricular septal defects (shunting of blood to right side)
- pulmonary vascular HTN
- severe chronic lung disease
central venous pressure (4)
1) volume that is measures on the right side of the heart
2) can be independent (hyper/hypovolemia) or dependent (backing up) on left side of heart
- LV failure -> increased R pressure
3) dependent on venous return (SVC)
- impedance of venous return will drop CVP
- blood clots, laying on back
4) AKA: method of measurement of volume
RANGE: 0-10
conditions that alter CVP (increase) (3)
- intravascular volume
- increased systemic return - mobile 3rd spacing
- increase in piulmonary vascular resistance (pulmonary HTN, pulmonary stenosis, tricuspid regurgitation/lung disease)
conditions that alter CVP (decrease) (3)
- intravascular vol. loss
- systemic venous dilation (neurogenic, early septic shock)
- third spacing of volume (liver failure, burns)
conditions that alter afterload: right sided (Pulmonary vascular resistance) INcrease (5)
- hypoxia
- obstruction
- decrease pulmonary compliance (pulmonary edema, ARDS, fluid overload)
- vasoconstriction (acidemia, hypoxia)
- pulmonary HTN
conditions that alter afterload: right sided (Pulmonary vascular resistance) DEcrease (3)
- vasodilators (nitric oxide, sildenafil, remodulin)
- correction of hypoxemia or acidosis
- normal response in exercise (physiological response to increase O2 demands to tissues -> dilation of vascular bed efficiently to provide O2)
contractility (refers to Left side of the heart): affected by (4)
1) myocardial oxygenation (hypoxia, MI)
2) electrolyte balance:
- hypo-ca
- hypo-mg
- hyper-K
- Ph balance (too acid/too alk = myocardium will be depressed)
3) positive/negative inotropic drugs
- digoxin (PO), epi, dobutamine, dopamine
4) amt functional myocardium
- dilated cardiomyopathy
conditions that INcrease contractility (3)
1) hyperdynamic states
- early septic shock (tachy -> O2 supply/demand mismatch)
- hyperthyroidism
2) positive inotropes:
- beta andrenergic stimulants such as epi, dobutamine
3) endogenous catecholamine release
- SNS (part of ANS)
- metabolic rate, exercise, stress, pain, anxiety
conditions that DEcrease contractility (7)
1) HYPOdynamic states
- late sepsis
- cardiogenic shock
- MI
- hypercarbia (acidosis)
2) increased preload (starling curve)
3) negative inotropes:
- beta blockers, CCB
4) electrolyte imbalance:
- Low Na, Ca, Mg
- High K
5) decreased O2 supply: anaerobic metabolism
6) loss of functional myocardium
7) severe metabolic acidosis, <7.0
- key: treat with SODIUM BICARB (basic)
parameters that increase CO (3)
optimal HR: between 50 - 150/min
optimal filling time
optimal preload (frank starling law)
- ideal amount of myocardial stretch
parameters that reduce CO (5)
HR <50 or >150
lack of atrial kick with new onset AFIB
frank starling law (less myocardial stretch)
significant REduction in preload
significant INcrease in afterload
bedside hemodynamic monitoring (3)
physical assessment
1) good BP/HR
2) LOC/mentation
3) color/temp of skin (peripheral circulation, decreased CO reflects in skin)
- pink/war or cold/mottled
invasive monitoring:
- arterial lines
- pulmonary catheters
types of invasive monitoring equipment (3)
arterial lines
pulmonary catheters
central venous catheters
4 components of hemodyaminc monitoring system (6)
- invasive catheter
- high pressure tubing with flush system
- transducer to convert information to electrical energy signal
- bedside monitoring
- flush system: maintains patency
- calibration of equipment: “stop cock” opened to atmospheric pressure @ phlebostatic axis
Bedside Hemodynamic Monitoring (where, levels with, patient position) (3)
1) Phlebostatic axis
- Physical reference point
- 4th intercostal space, midaxillary line
2) Leveling the transducer
- Aligning transducer with level of LEFT atrium
3) Patient position
- Supine, head-of-bed 0 to 60 degrees
- Landmarks change if patient in lateral position
- Raising the transducer will drop pressures
Intra-arterial Blood Pressure Monitoring (inducation, catheters and site, maintain)
Indications:
- Need for multiple vasopressors to maintain BP (ex: Levophed, Epi, Vasopressin, Dopamine)
- Labile BP (ie. head injuries, pre-e)
- IV Vasodilators (ex: Nipride/Nitroprusside)
Catheters and sites:
- Location dictates size of catheter used (radial vs. femoral)
- Allen’s test for collateral circulation in the hand with radial access - use pulse ox for confirmation
- how: occlude radial artery + ulnar, then let go of ulnar and should turn back to pink
Maintain perfusion pressure:
- Use mean arterial pressure (MAP)
- MAP goal is based on disease states (cardiac (wide pp) vs. neuro (narrow pp)) 60-65
- (MAP =systolic blood pressure + 2 diastolic blood pressure / 3)
Intraarterial Blood Pressure Monitoring: nurse monitoring (3)
1) Titrate medications to maintain MAP
2) Monitor Pulse pressure
- Affected by the patients rhythm
- You can see variation with abnormal rhythms (PVCs, afib)
3) Compare to cuff blood pressure
- Normovolemic pressure little difference exists between cuff and arterial pressure
- Cuff pressures help to determine if there is “under dampening” or “over dampening” - clot over tip
closure of arterial line (2)
Femoral: Direct pressure, time dependent on Fr. Size ie. 7, 10, etc
- 20 minute w/ increase Q5min per 10 Fr increase
Radial: Hemoband for procedures, direct pressure for arterial waveform measurement
Venous Catheters (3 locations, ____ via AC, types (3))
1) Need a central venous line
- Jugular (BEST)
- Brachial
- Femoral
2) PICC via AC
3) Types of Catheters
- Central venous system
- Right atrial catheters
- Pulmonary Catheters (ie. Swan-Ganz catheters)
Central Venous Pressure Monitoring (inserted, indication (3), complications (3)
1) Inserted into central venous system.
- Procedure performed at bedside under sterile technique
- Internal Jugular or Subclavian vein
- Can use indwelling “cordis” catheter
2) Indication
- Volume loss
- Volume overload
- Need for fluid resuscitation without hemodynamic response.
3) Complications
- Air embolism if lines are open
- Thrombus formation at end of catheter
- Infection
normal CVP
0-10
what will increase CVP
PEEP
Pulmonary Artery Pressure Monitoring (indications (3) - ___ and ___ of (4), difficult to determine if ____ or ____, referred to as ___ in cath lab, used for diagnosis of ___, can determine, used for (3))
1) Indications:
- Diagnosis and evaluation of heart disease, shock states, acute respiratory distress syndrome and conditions that compromise cardiac output
- Difficult to determine if central venous issue or left side of heart issue
- In cardiac cath lab referred as right heart cath, used for diagnosis severity of valve disease and intra cardiac shunts
2) Can determine Cardiac output
3) Hemodynamic monitoring is used for Oxygen supply and demand evaluation (mismatch)
- Preload
- Afterload
- Contractility
Pulmonary Artery Catheters- Lumens (5)
1) Right atrial (proximal) lumen or CVP lumen
2) Pulmonary artery (distal) lumen
3) Balloon lumen
4) Thermo lumen to determine CO and monitor core temp
5) Additional features: continuous Svo2, cardiac pacing, continuous cardiac output measurement, right ventricular ejection fraction measurement
Basics of Hemodynamics:Normal Values (KNOW CO, CI, RAP, PASP, PAMP, PDP, PCWP, MW)
Cardiac output: 4 to 6 liters per minute
Cardiac index: 2.5 to 4.0 liters per minute per square meter (of body surface area)
- Right atrial pressure: 2 to 5 mmHg
- Pulmonary artery systolic pressure: 20 to 30 millimeters of mercury (mmHg)
- Pulmonary artery mean pressure: 10 to 15 mmHg
- Pulmonary diastolic pressure: 5 to 10 mmHg
- Pulmonary capillary wedge pressure: 5 to 12 mmHg
- Mean wedge is same as the pulmonary diastolic pressure - also same as the Left Atrial pressure
Pulmonary Artery Catheters - insertion/waveform
1) Insertion-Similar to Venous line
Site- Femoral, Subclavian or Internal Jugular Veins
2) Waveform interpretation-
Clinician is able to determine location type of waveform
- Right atrial waveform
- Right ventricular waveform
- Pulmonary artery waveform
- Pulmonary artery occlusion waveform (wedge pressure
tip: pulmonary HTN and CHF may cause elevations in diastolic pressure
pressures in the heart (4)
RA: 2-5
RV: 0-25
LA: 3-12
LV: 120/70
Complication PA Monitoring (8)
Bleeding
Air Embolism
Pulmonary Artery Rupture with balloon inflation
Pulmonary ischemia
Catheter Knotting
Clot formation
Ventricular Dysrhythmias
Infection
Cardiac Output Measurement (_____ method, influenced by (4)
1) Thermodilution method
- Most common method used in the ICU when a swan is present
- Assumes all blood is traveling uni-directionally through the heart
2) Influenced by:
- Cardiac output curve
- Injectate temperature
- Patient position and cardiac output
- Clinical conditions that alter cardiac output (Early sepsis will show hyper-dynamic state with high CO numbers)
Continuous Monitoring of Venous Oxygen Saturation (Scvo2) (what, 3)
1) Central Venous Catheter
2) Scvo2 port is present on PA catheter to allow for additional monitoring
- Monitoring balance between oxygen supply and demand as a function of arterial oxygen saturation, cardiac output (via Fick), hemoglobin, and venous oxygen saturation
- Is a good indicator of documenting response to therapy, whether oxygen or improving circulation to tissues
Clinical Conditions that Alter ScvO2: INcrease (2)
- O2 supply exceeds O2 demand
- Alteration in O2 delivery: Cardiac Output elevated, See with early septic shock
Clinical Conditions that Alter ScvO2: DEcrease (4)
- O2 demand exceeds O2 supply
- Decrease CO
- Decrease Hgb
- Decrease pulse ox (SaO2)
normal SCVO2
70%
EV1000 Monitor (4)
Combines data from arterial lines with a specialized ScvO2 catheter
Requires nurse to input patient data: height, weight, age & sex
Measures Cardiac Output (CO), Stroke Volume (SV), Systemic vascular resistance (SVR)
In ventilated patients, measures SVV (Stroke Volume Variation)
ELWI (Extravascular Lung Water Index) and PVPI (Pulmonary Vascular Permeability Index)
guide fluid resuscitation
Stroke Volume Variation (SVV): (measuring the ____…, has been proven to be highly sensitive and specific indicator for ________ responsiveness, predicting whether a patient will benefit from?, greater svv =? (4)
Measuring the variation in stroke volume in patients undergoing mechanical positive pressure inhalation and exhalation (Ventilated)
SVV has been proven to be a highly sensitive and specific indicator for preload responsiveness.
In nursing context: predicting whether a patient will benefit from volume before the fluid is given
Greater SVV=better response to fluid (variations per inhale/exhale -> give fluid to decrease variation), preload responsive
tip: Breathing compresses vasculature, Preload changes.
Stroke Volume Variation (SVV) and Volume (what has been proven to clinically act like a self volume challenge to indicate status on the frank starling curve, situations where its not possible to use svv (3))
Passive Leg Raising: Passive raising of the legs has been proven clinically to
act like a “self volume challenge” to indicate status on the Frank-Starling curve (Augmenting Stroke Volume by increasing preload), increases SVV
Situations where it is not possible to use SVV:
- During arrhythmias
- Patients not on control-mode of ventilation
- Patients at risk of complications from fluid loading
Cooling Protocol Post Cardiac Arrest (2)
- Therapeutic Hypothermia (TH)
- Targeted Temperature Management (TTM)
Preserving brain function and maximizing meaningful recovery in the event of an arrest
- Hypoxic encephalopathy and loss of neuro function
Post Cardiac Arrest Guidelines - 2015
Unconscious adult patients with return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest should be cooled to 32 (89.5F) -36 (96.8)ºC for at least 24 hours when initial rhythm was ventricular fibrillation (VF)
Similar therapy may be beneficial for patients with non-VF arrest out-of-hospital or with in-hospital arrest
Cooling Guidelines (9)
- Don’t re-warm mildly hypothermic patients
- Cool early in the emergency department.
- Used to use any cooling method possible.
- Patients can continue to be cooled during percutaneous coronary intervention (PCI) while we look for precipitating factors
- Use any pharmacologic agent necessary for primary cardiac condition (eg, aspirin, antiplatelet compounds, thrombolytics)
- Treat patients as you would any critical care patient (tight glycemic control, vigilance for signs of infection, maintain perfusion, and use pressors if necessary).
- Practice standard neuroprotective strategies such as placing the head of the bed at 30º and use seizure precautions.
- Predict and be proactive regarding management of complications from return of spontaneous circulation and hypothermia, including:
shivering,
fever,
hypotension or hypertension,
hyperglycemia,
hypokalemia or hyperkalemia,
bradycardia and ongoing ischemia. - Cooling reduces cerebral metabolism (approximately 6-8% per 1ºC)
-> Reduces excitatory amino acid neurotransmitters (Specifically Glutamate)
key: MAP <65, 30 degree promotes Venous drainage and improves cerebral perfusion.
- Norcuron and nimbex
- Hypokalemia during cooling, hyperkalemia during re-warming.
Inclusion criteria for hypothermia (3)
Intubated patients with treatment initiated within a 6-hour post cardiac arrest
Consistent Systolic blood pressure >90 mm Hg, with or without pressors/bolus, after cardiopulmonary resuscitation (CPR)
Those not following commands
- Brainstem reflexes and pathological/posturing movements are permissible. Patients with a Glasgow Coma Score (GCS) of 3 are eligible for hypothermia.
Exclusion criteria (4)
- Recent major surgery within 14 days - - Hypothermia may increase the risk of:
infection, bleeding.
Systemic infection/sepsis – not done
Hypothermia may inhibit immune function and is associated with a small increase in risk of infection
- Patients comatose from other causes (drug intoxication, preexisting coma prior to arrest)
- Patients with a known bleeding disorders or with active ongoing bleeding – (Hypothermia may impair the clotting system).
-> Check prothrombin time/partial thromboplastin time - Patients with a valid do not resuscitate order (DNR)
Arctic Sun Automated Cooling/Rewarming Device
Provides consistency which follows guidelines- but also captures data for further research and extrapolation.
Re-warming (6)
Arctic sun and other systems do this for you!
- Maintain the paralytic agent and sedation until the patient’s temperature reaches 35°C (d/t shivering).
- Discontinue paralytic agent first. Then sedation may be discontinued at the practitioner’s discretion.
- Monitor the patient for hypotension secondary to vasodilatation related to re-warming.
- Discontinue potassium infusions.
- The goal after re-warming is normothermia (ie, avoidance of hyperthermia).
- Await 72 hours for metabolism of sedatives before determining neurological status
tip: hypothermia decreases potassium, increase in temperature will increase potassium
Nursing Care of cooling/rewarming (11)
- Head of the bed at 30º
- Tight glycemic control
- PCO2 should be normal (35-45 mm Hg)
- Skin care should be checked every 2-6 hours for thermal injury
- Do not provide enteral nutrition during cooling and rewarming
- MAP >80
- Paralytics to prevent shiver
- Watch for arrhythmias->Bradycardia can lead to lethal arrhythmias
- Monitor K+, PT/PTT & CBC during cooling & rewarm every 6 hours
- Support family
- Provide information of Protocol
ACCORDING TO THE AHA: cardiac arrest outcomes (2)
1) Cardiac Arrest has extremely poor outcomes
Poor prognosis:
- Only 14-40% achieve ROSC
- Only 20% will survive through hospital admission
- Few Proven interventions: #1 CPR
2) Difficult to research:
- Complex, Heterogeneity, High acuity
– Impossible to blind to Temp Treatment
SHORT TERM MECHANICAL CIRCULATORY SUPPORT (4, types (3))
1) Restore Cardiac output to preserve the end organ perfusion
2) Off-Load the Left Ventricle
3) Optimize balance of supply and demand
4) Allow time for recovery of injured myocardium
types:
- Intra-Aortic Balloon Pump (IABP),
- Extra-Corporeal Membrane Oxygenation (ECMO)
- Impella
Intra-Aortic Balloon Pumps (6)
- Pneumatic, pulsatile
- Inserted retrograde via femoral artery
- KEY: NOT USED TO PROVIDE CARDIAC OUTPUT-
- But still may augment flow by 0.5L/min
- Not much hemolysis or bleeding
- Can be inserted at bedside
IABP function (4)
1) Inflates during diastole
- Increases/Augments coronary blood flow
- Increases Diastolic BP
2) Deflates in Pre-systole
- Reduces afterload
- Reduces SBP
- MAP stays the same, sometimes improves
3) Used for STEMI, not the most effective for cardiogenic shock
4) need Daily CXR
VA ECMO (3)
Venous/Arterial
Extracorporeal Membrane
Oxygenation
Femoral Vein from right atrium ->
centrifugal pump (cardiac) ->
oxygenator (lungs) ->
Femoral Artery for systemic circulation
- Provides full cardiac and pulmonary support
- Late stage support (Survival rate relatively low)
- In Babies, survival rate is much better
Impella Device 8)
- Non-pulsatile, similar placement as the IABP
- Retrograde through fem artery -> aorta
- Pulls blood from left ventricle, uses impellor-contained catheter to pull blood into the aorta
- Can improve CO by 5L (new approach- Axillary/Subclavian)
- Used for V-tach ablation
- Lots of hemolysis in the past, requires anticoagulation
- Requires functional Aortic Valve
- Impella runs at 33,000RPM to generate 4-5L/min
