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Complex Exam 2 Cheat Sheet (DRAFT) by

Hemodynamic monitoring

This is a draft cheat sheet. It is a work in progress and is not finished yet.


Hemody­namic Monito­ring:measur­ement of pressure, flow, and oxygen­ation within the cardio­vas­cular system. Monitoring is used to asses heart function, fluid balance, and the effects of fluids and drugs on cardiac output.
Indica­tions for hemody­namic monitoring include: shock, sepsis, anaphy­laxis, MI with right/left ventri­cular failure, Hypo/H­ype­rte­nsion, Cardiac tamponade, ARDS, Post open heart surgery, fluid resusc­ita­tion, and evaluation of cardiac output
Mean Arterial Pressure (MAP): the average pressure within the arterial system that is felt by organs in the body. Essent­ially how hard the blood is flowing when hitting the organs.
Calcul­ating MAP 2xDias­tolic + Systolic = #. # divided by 3. Example: BP:120/60: 2x60+1­20=240. 240/3= 80. MAP of 80.
Pulse Pressure: the difference between the systolic blood pressure (SBP) and diastolic blood pressure (DBP). Narrow­/de­cre­ased: shock state or HF- meaning insuff­icient preload leading to reduced cardiac output (CO). Wide/i­ncr­ease: occurs during exercise or in athero­scl­erosis- Increased ICP.
Calcul­ating Pulse Pressure: SBP-DB­P=Pulse Pressure
Stroke Volume: the amount of blood pumped by a ventricle with each beat.
Calcul­ating Stroke Volume: Cardiac Output/ HR= stroke volume
Cardiac Output: Amount of blood ejected from the heart into circul­ation each minute
Calcul­ating Cardiac Output: HRxSV= Cardiac Output
Cardiac Index: cardiac out that is adjusted for each individual based on the body surface area (BSA).
MAP: >60mm Hg. <65 needs to be addressed. <60 inadequate tissue and organ perfusion
Pulse Pressure: 40-60mm Hg
Stroke Volume: 60-150­mL/beat
Cardiac Output: 4-8L/min
Cardiac Index: 2.2-4L/min

Autonomic Nervous System

Autonomic Nervous System:ANS
ANS consists of the Sympat­hetic Nervous System (SNS) and the Parasy­mpa­thetic Nervous System (PNS)
SNS: this is the bodys' fight of flight. It controls blood flow by constr­icting the arteries throughout the body and increases blood pressure and blood flow.
How does SNS work?: The body senses a low arterial pressure. The SNS is then stimulated to maintain CO. Norepi and epi (catec­hol­amies) is released. The receptors respond the the norepi and epi by increasing the HR, contra­cti­lity, and conduction (chron­otr­opic, inotropic, dromot­ropic effects). This then increases myocardial oxygen demand.
SNS Effects: Chrono­tropic- increases the rate. Inotropic- increases the contra­cti­lity. Dromot­ropic- cardiac conduc­tivity time.
Chrono­tropic: responds to norepi­nep­hrine and epinep­hrine by increasing the HR.
Inotropic: responds to norepi­nep­hrine and epinep­hrine by increasing the contra­cti­lity.
Dromot­ropic: responds to norepi­nep­hrine and epinep­hrine by increasing the speed of conduc­tion.
PNS: this is the bodys' rest and digest. It controls blood flow by dilating the arteries which decrease blood pressure and blood flow.
How does PSN work? Happens after SNS response. It "­rev­ers­es" the SNS effects. Acetyl­choline is released which then decreases HR, conduction and irrita­bility. Stimulates the GI tract.


Four Parameters of Hemody­namics: Preload (think volume), Afterload (think resist­ance), Contra­ctility (thing ability to pump), and Cardiac Output (think perfusion status).
Contra­cti­lity: Hypoki­nesia: reduced movement or contra­ction of a segment of the heart muscle. Dyskin­esia: abnormal movement, myocardium bulges out in systole. Akinesia: lack of movement or contra­ction of a region of the heart muscle.
Preload:Amount the ventricles stretch at the end of diastole (the filling phase). Preload is once the ventricles are completely filled.
How to increase preload? (pt in hypovo­lemic shock) give fluids (incre­asing the amount of volume to fill the ventri­cle). Stimulate SNS - give vasopr­essors (causing vasoco­nst­ric­tion- making the area to fill "­sma­lle­r").
How to decrease preload? (pt is fluid overload) give diuretics (excreting excess fluids). Give vasodi­lators (creating more space for fluid to flow).
Afterload: the pressure the ventricles have to work against to get valves to open to pump blood out of the heart. Afterload is affected by vascular resistance.
Vascular Resistance in the right side of the heart: Right ventricle pumps blood to pulmonic valve. Pulmonic valve has to fight against pulmonary vascular resistance (PVR) to open and pump blood to the lungs.
Vascular Resistance in the left side of the heart: Left ventricle pumps blood to aortic valve. Aortic valve needs to fight against systemic vascular resistance to open and pump blood to the rest of the body (syste­mic­ally).
How to increase afterload? (pt is hypote­nsive) Can increase naturally by vasoco­nst­riction such as pulmonary HTN for left sided or HTN for right sided. This happens due to the increase vascular resist­ance. Valve problems cause an increase in after load (aortic stenosis)* due to the constr­iction of the valve increasing pressure on the ventri­cles.
How to decrease afterload? Give vasodi­lators. This will decrease vascular resistance resulting in a decrease of pressure to work against.
Effects on Cardiac Output: If HR, Preload, contra­ctility is increa­sed­/de­creased CO will follow suite