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