synovial, intestinal and cerebrospinal fluid, sweat, intraocular fluids are                        fluids

the fluid located outside the blood vessels between the cells of tissue is                    fluid

synovial, intestinal and cerebrospinal fluid, sweat, intraocular fluids are transcellular fluids

the fluid located outside the blood vessels between the cells of tissue is interstitial fluid

body fluid compartments:

               and               = 40% of b.w.

               = 20% of b.w.

body fluid compartments:

 ECF and solid matter  = 40% of b.w.

ICF = 20% of b.w.

hydrostatic pressure vs. oncotic pressure:

where are they highest in the capillary?

how does this effect the flow of water?

hydrostatic pressure is higher at the arteriole side

"pushes" water from the vessel to the interstitium

oncotic pressure is higher at the venous side due to higher [proteins] in the blood vs. interstitium due to water loss on the arteriole end

"pulls" water from the interstitium into the vessel

Alterations in Starling's law of the capillaries leads to                . 

What is Starling's Law?

Alterations in Starling's law of the capillaries leads to edema. 

Starling's Law:  state of equilibrium at the arterial and venous ends of the capillary in which filtered fluid and absorbed fluid + lymphatic fluid are nearly equal

obstruction distally in a vein will result in high               pressure                 to the blockage.

Fluid will move from what to what?

obstruction distally in a vein will result in high hydrostatic pressure proximal to the blockage.

Fluid will move from the vessel to the interstitium

malnutrition and cirrhosis cause decreased capillary                 pressure.

cirrhosis will result in what specifically?

oncotic

chirrhosis will result in peripheral edema and ascites

burns and allergic rxns

↓

increased capillary membrane permeability

↓

loss of plasma proteins

↓

increased tissue oncotic pressure

↓

edema

cirrhosis and malnutrition

↓

decreased production of plasma proteins

↓

decreased capillary oncotic pressure

↓

edema

venous obstruction

↓

fluid movement into tissues

↓

edema

lymph obstruction or removal

↓

decreased absorbtion of interstital fluid

↓

edema

RAAS system:

what increases hydrostatic pressure?

what is the endocrine role?

what is reabsorbed in the proximal tubule?

RAAS system:

Angiotensin II stimulates vasoconstriction to increase hydrostatic pressure

Angiotensin II stimulates the release of endocrine hormones aldosterone and ADH to regulate Na+/H20 retention and thirst

Angiotensin II stimulates Na+ reabsorption in the proximal tubule

compensatory mechanisms in CHF that result in increased capillary hyrdostatic pressure and edema are

1.

2.

1.  higher cardiac filling pressures, which are transmitted to the capillary circulation, increased hydrostatic pressure

2.  renal sodium retention, causing reexpansion of the plamsa volume, increasing hydostatic pressure

pulmonary edema is associated with what type of heart failure?

Why?

left-sided heart failure

due to Na+ and H2O retention of the pulmonary vessels

A 87 year-old man presents with fatigue, dyspnea after climbing one flight of stairs, orthopnea, and RUQ abdominal discomfort. Physical examination reveals tachypnea, pulmonary rales, lateral displacement of apical impulse, hepatomegaly and lower extremity edema.

What is the underlying disease causing edema?

A 56 year-old female with a past medical history significant for alcohol abuse presents with anorexia, nausea, and vomiting. Physical examination reveals ascites, peripheral edema and pleural effusions.

what is the underlying disease causing edema?

                     syndrome are disorders that result in structural alteration of the glomerulus.

what will be in the urine?  

what will blood tests show?

nephrotic syndrome

urine:  hematuria, proteinuria

blood:  hyperlipidemia, hypoproteinema, ↑ serum creatinine

deep vein thrombophlebitis, venous insufficiency, and Baker's cyst will cause....due to...

CHF

renal failure

corticosteroid or estrogen use

pregnancy

venous insufficiency

causes of what?

bilateral leg edema due to decreased oncotic pressure

name 3 causes

malnutrition

hepatocellular failure

nephrotic syndrome

bilateral leg edema due to increased capillary permeability

name 2 causes

systemic vasculitis

allergic reactions

low protein

sodium restriction

fluid restriction

Physical examination reveals peripheral edema and ascites. Diagnostic studies reveals serum albumin concentration < 3 g/dL (normal 3.5-5.5 g/dL) and 24-hour urine collection protein loss of >3.5 g/24 hr.

what is the likely underlying disease?

tx?

nephrotic syndrome

tx:  diuretics, Na+ restriction

82 y/o women comes to your office with complaint of fatigue and DOE for 3 weeks. PE reveals BP- 98/66, P-116 & irregular, +JVD, bibasilar rales, irregularly-irregular rhythm & +S3 gallop, +2 pitting bilateral ankle edema.

What is her diagnosis?

Heart failure

and

A-fib (or PVC, but likely A-fib)

what is defined as the percentage of blood in the end of diastole ejected with each beat?

what ratio/fraction is this also expressed as?

what ratio or percentage should this be?

Ejection fraction

EF = EDV/ESV

should be 2/3 or 67%

MUGA (nuclear medicine)

Echo

cardiac cath

chronotropic =

inotropic =

chronotropic = HR

inotropic = contractility

preload

contractility

afterload

determine what?

heart rate and venous return determine what?

increasing this will increase what else? (2 factors)

preload

increase preload = increase force of contraction = increased SV

actin and myosin

LV can strech effectively up to 2.4 um (and will increase force of contraction up to that point).  After that, optimal actin-myosin overlap is lost.

increased arterial BP

ventricular dilation

affect what?

what decreases this?

afterload

decreased by increased wall thickness

venticular wall thickness and afterload are inversely proportional

State in which heart is unable meet metabolic demands of the tissues for blood.

definition of what?

due to what 2 factors?

heart failure

due to increased metabolic demand or diminished pump function

heart failure

6 million people with symptomatic HF, >500,000 new cases per year

increased preload

decreased afterload

decreased contractility

compensatory mechanisms

pathophys for what disease?

define congestive heart failure

what are the types...

output: (2)

anatomical: (3)

mechanical: (3)

state of circulatory congestion secondary to HF

types...

output: high (forward) and low (backward)

anatomical: L-sided, R-sided, and biventricular

mechanical: systolic, diastolic, and combined

what type of HF is due to increased metabolic demands and too much venous return with decreased PVR and increased RA pressure?

what type of HF is due to diminshed pump function?

increased metabolic demands and too much venous return with decreased PVR and increased RA pressure = high output HF

diminshed pump function = low output HF

Beriberi**(what is this?)

AV Fistula or shunt
Hyperthyroidism
Anemia

cause what type of HF?

high output HF

Beriberi: Thiamine deficiency with marked peripheral vasodilation

contractility, preload, and afterload are increased or decreased with...(match one to each of the following)

Aortic regurgitation, Hypervolemia, VSD?

Hypertension and Aortic stenosis (AS)?

Myocardial infarction and Cardiomyopathies?

all of these cause what type of HF?

Aortic regurgitation, Hypervolemia, VSD = inc. preload

Hypertension and Aortic stenosis (AS) = inc. afterload

Myocardial infarction and Cardiomyopathies = dec. contractility

all are causes of low output HF

hypertension and CAD

increased afterload

HTN

AS

MR

MI

ednocarditis

HCOM

dilated & restricted cardiomyopathy

causes of what type of HF?

R-sided HF

liver

**L-sided HF is most common cause of R-sided HF

pulmonary edema

rhales

pulmonary effusion

S3

associated w/ what type of HF?

L-sided HF

HF with reduced ejection fraction is called what?

name 4 causes

systolic HF

4 causes:

MI/ischemia

AS

dilated cardiomyopathies

HTN

women, older pts, DM, inc. BMI, A. fib

associated with what type of HF?

diastolic HF

HF with preserved EF

beta blocker

CCBs

obesity

glucose intolerane

obstructive sleep apnea

List the compensation associated with the initial response to HF.

1. Humoral responses:
2. Sympathetic responses:
3. Hypertrophy:  what will you see?
4. 2,3-DPG:  what is this and what does it mean?!

humoral responses:  RAAS initially to increase preload (plasma volume)...eventually decompensation from hypervolemia and increased afterload from vasoconstriction

sympathetic responses:  initially Epi and NE response...eventually decompensation from inc. O2 demand of SNS nerves, dysrrhythmia, and inc. afterload.

Hypertrophy:  inc. wall thickness/sarcomeres...eventually maladaptive due to inc. O2 demand, diastolic dysfunction, dilation, and remodeling (will see vavlular regurg due to vent. dilation)

2,3-DPG:  2,3-DPG decreases affinity of Hgb for O2, shifts oxy-hemoglobin dissociation curve to the right, more O2 released in tissues

what 2 peptides can be measured in the blood to test for HF?

what is their function?

ANP and BNP

naturetic effect (oppose RAAS system effects)

antifibrotic, anti-Aldost., SNS-inhib, and vasodilatory effects

Sx:  fatigue, anorexia, nausea, RUQ discomfort, ankle edems

Signs:  JVD, hepatomegaly & hepatojugular reflex from portal HTN, edema/ascites

disease?

Sx:  fatigue, dyspnea, orthopnea, PND, cough, hemoptysis, wheezing

Signs:  tachypea, rales, wheezes, Laterally displaced PMI, S3, paradoxical split S2, pleural effustion, murmurs

disease?

CXR findings with HF

there are 6 key ones

thinks fluid...where will it end up?

1. Cardiomegaly
2. Cephalization of flow (fluid in the upper vessels)
3. Pleural effusions (blunted costo-phrenic angles)
4. Kerley's B Lines
5. Increased pulmonary vascular markings
6. Butterfly pattern with pulmonary edema (see below)[image]

1.  what Dx study would you use to examine structural changes associated w/ HF?

what are some common findings?

2.  what would a MUGA scan result likely be?

1.  Echo

common findings:

Wall chamber hypertrophy or dilatation
Wall akinetic or dyskinetic areas
Decreased LVEF (in systolic HF)
Valvular lesions

2.  decreased LVEF (left vent. ejection fraction)

Of the 4 stages of HF and tx standards, how many are asymptomatic?

At what stage is the pt consider to "have HF"?

2 (stage A, B)

Stage A: Patients at high risk
Stage B: Patients with structural abnormalities but asymptomatic (LVH, ↓ LVEF, VHD)
Stage C: Patients with current or prior symptoms ("Have HF")
Stage D: Patients with refractory end-stage disease. Symptoms at rest on Rx

ACC/AHA Tx of HF Stages

Stage A: Patients at high risk

what are the risk factors? (6)

Stage B: Patients with structural abnormalities but asymptomatic (LVH, ↓ LVEF, VHD)

what 2 Dx would show LVH?

Stage C: Patients with current or prior symptoms
Stage D: Patients with refractory end-stage disease. Symptoms at rest on Rx

Stage A: Patients at high risk

what are the risk factors? obese, HTN, smoker, DM, elderly, obstructive sleep apnea

Stage B: Patients with structural abnormalities but asymptomatic (LVH, ↓ LVEF, VHD)

what 2 Dx would show LVH? 

EKG:  left-axis deviation

Echo:  chamber size

HF Stage A: Patients at high risk

Tx?

Treat underlying disease--HTN, DM, dysarrhythmias, obesity, etc

Decrease atherosclerosis risk--ASA, statin

ACE-I or ARB in HTN, vascular disease, DM

HF Stage B: Patients with structural abnormalities but asymptomatic (LVH, ↓ LVEF, VHD)

Tx?

Same as group A

ACE-I or ARBs

Beta-blockers in some pts

revascularization if appropriate (CAD, consider stent or CABG)

valve repair when indicated

HF Stage C: Patients with current or prior symptoms

Tx?

dec. preload: modify what? use what?  avoid what?

dec. afterload:  what for AA populations?

inc. contractility: use only w/ what comorbidity?  What do you avoid?  what is ok?

dec. preload:  Na+ restriction (1.6-2.0 g Na or 4-5g NaCl), diuretic (loop first...Furosemide), nitrates, avoid NSAIDS

dec. afterload:  ACE-I (Captoril, etc.) or ARB (Candersartan, Valsartan), Hydralazine and isosorbide dinitrate in AA populations

inc. contractility: digoxin (use only w/ A-fib), avoid CCB's and antiarrhythmics except amiordorone

carvedilol

metoprolol succinate XL

Diuretics, ACE-I, CCBs and beta blockers are used but
ARBs not shown to be helpful with what type of HF?

what medication should be avoided as well?

HF with preserved EF

avoid digoxin

what type of HF has the worst prognosis?

Left venticular dysfunction with low EF and symptomatic

[image]

ABG measures:

what is the normal value?

Pulse Ox measures:

what is the normal value?

ABG measures: PaO2 and PaCO2

what is the normal value?  PaO2 80-100mmHg at sea level

Pulse Ox measures: O2 saturation

what is the normal value? 98% on room air

O2 sat of 92% = 70 mmHg

shifts the oxy-hemoglobin dissociation curve to the right, pH = 7.6

see slide[image]

normal venous blood is           % saturated w/ O2

tissues use up to about            % of O2 in the blood

shock or sickness will have higher or lower demand?

75% venous blood O2 sat.

25% tissue demand of O2

shock or sickness, demand increases, body must compensate

first:  increase CO via inc. HR  (delivery of O2= CO x CaO2)  CaO2 is O2 content

second:  extract more O2 from hemoglobin

what is SmvO2?

what does this represent?

when will this be lower?

what is SmvO2? oxygen saturation in the pulmonary artery

what does this represent? how much O2 has been extracted from the tissues

when will this be lower?  when exercising...extracting more O2

what would lab work show to indicate lactic acidosis?

what is lactic acidosis a marker of?

what lactate level is a reason for concern?

lactic acidosis = low bicarb in blood

lactic acidosis is a marker of poor perfusion and shock

lactate levels around 4 or 5 are reason for concern

shock is associated with what SBP?

what population uses the equation:  70 + 2x age for adequate SBP?

MAP = ? (equation)

shock = SBP <80-90mmHg

adequate SBP in children = 70 +2x age

MAP = CO x SVR (systemic vascular resistance)

what is the best numerical indicator of shock?

how is this related to cerebral perfusion pressure?

MAP is the best numerical indicator of shock

need 65-75 MAP for cerebral perfusion pressure

which organs are the most sensitive to hypoperfusion? (3)

how can you tell if a pt has hypoperfusion to one of these?

Brain:  mental status, talking ok?, etc.

Heart:  chest pain, SOB

Kidneys (especially the tubule):  no urine output, acute tubular necrosis

cellular response to hypoperfusion:

no ATP for what ion pump?

influx of what ion and efflux of what ion?

cell death due to release of what enzymes?

no ATP for Na-ATPase pump

influx of Na+ and efflux of K+

cell death due to release of lysosomal enzymes

catecholamines

glucocorticoids

bradykinin

histamine

beta endophins

what are these all part of?

what are the signs of shock that you should look for?

Temp...

HR...what would cause this to be blunted?

BP...

MAP...do you know how to calculate?

temp:  elevated (>101) or depressed (<96)** worse sign, means not mounting a response

HR:  >90bpm (blunted by BBs, cardiac disease, hypoglycemia)

BP: SBP <80-90mmHg, DBP will fall late in shock

MAP:  65-75 needed for cerebral perfusion pressure

(note:  MAP = 2/3 DBP + 1/3 SBP)

minute ventilation =          x       

What are some signs of shock that involve the GI?

what would you look for on the abdominal exam?

GI bleed

Ischemic bowel

abdominal pain

Signs on abdominal exam:

decreased bowel sounds

high pitched bowel sounds

signs of shock

pupils:

breathing:

skin:

pulse:

signs of shock

pupils: dilated

breathing: shallow, labored, rapid

skin: pale to bluish, cold, clammy, profuse sweating

pulse: weak, rapid

increased BUN:Cr

oliguria

anuria

hematuria

signs of what?

in early shock, do you see acidosis or alkalosis and is it respiratory or metabolic? 

what about late shock?

early shock:  respiratory alkalosis (due to inc. minute ventilation and blowing off more CO2)

late shock:  metabolic acidosis (due to lactic acidosis)

1. solid organ injuries and internal bleeding (i.e. liver laceration)
2. AAA rupture or aortic aneurysm
3. refractory gastroenteritis
4. burns
5. big GI bleeds
6. general trauma, pelvic and femur fractures

what 2 types of IV fluids are given w/ shock tx?

isotonic crystalloid solution is typically used in volume replacement for the management of shock. The two most common fluids are normal saline (NSS) and lactated ringer's. crystalloid is a substance which in solution passes readily through animal membranes, can be crystallized, and lowers the freezing point of the solvent

Colloid fluids contain albumin, FFP, or hetastarch and increase the oncotic pressue to keep the fluid in the vessel and not just diffuse in the tissue.

what is cardiogenic shock?

how much of the myocardium is damaged most likely?

What is the most common cause?

cardiogenic shock: decreased pumping ability of the heart that causes a shock like state.

probably at least 40% of the myocardium is damaged

most common cause is acute MI

acute myocarditis (cocksackie)

beta or CCBs

drug doxicity (what drug?)

tamponade

falty valves

cardiomyopathy

all are causes of...

cardiogenic shock

drug toxicity = adriamycin (chemo/lymphoma drug)

florid pulmonary edema = coughing up frothy fluid

associated with cardiogenic shock

JVD

peripheral edema

marker tachycardia

florid pulmonary edema

poor peripheral pulses and cool extremities

SBP <80mmHG

PCWP >18 ??

PE findings for what?

cardiogenic shock

not sure what PCWP is...

just remember florid pulmonary edema = frothy business = cardiogenic shock

What do you want to avoid in tx of cardiogenic shock?

what are the keys to tx?

cardiogenic shock

AVOID:  nitrates, morphine, beta blockers (all decrease BP)

Tx:  High flow O2, intubate if necessary, large bore IVs, ABCs

pharm review...

the 'pressors' (used in cardiogenic shock)

NE would cause...

dopamine would cause...

dobutamine would cause...why is it a 'pseudo-pressor'?

NE = vasoconstricion

dopamine = a lot of HR, some inc. BP

dobutamine = inc. CO, peripheral vasodilation

pseudo-pressor b/c can have no effect, increased, or decreased BP w/ dobutamine

• high venous pressure (JVD)
• low arterial pressure (low SBP and narrow pulse pressure)
• muffled heart tones and tachycardia

what are these 3 Sx called?

what are the characteristic of?

Beck's Triad

• high venous pressure (JVD)
• low arterial pressure (low SBP and narrow pulse pressure)
• muffled heart tones and tachycardia

cx of cardiac compression (tamponade)

what 'pressor' can you give w/ cardiac tamponade?

what do you not do or do minimally?

Norepinephrine

do not load up with fluids, give some, but monitor

                 is a state of alteration of tissue perfusion resulting in end organ dysfunction

Distributive shock is severe                     due to a reduction in SVR or systemic vascular resistance.  Most of the time, patients here have an elevated                        .

Shock is a state of alteration of tissue perfusion resulting in end organ dysfunction

Distributive shock is severe hypotension due to a reduction in SVR or systemic vascular resistance.  Most of the time, patients here have an elevated cardiac output

most common cause of peripheral/distributive shock is...

3 other causes

most common cause of peripheral/distributive shock is septic shock due to infection

other causes...

Systemic inflammatory response (SIRS)

Toxic Shock Syndrome (TSS)

Anaphylaxis

diffuse wheexing

diffuse urticaria (raised rash)

angioedema

respiratory distress

hypotension

signs of what?

key tx?

anaphylactic shock

key tx:  Sub Cutaneous epinephrine**

Epi reverses anaphylaxis by causing the mast cells and basophils to stop releasing histamine

additional tx:

Wheezing:  B2 agonist/anticholinergic

IV steroids, antihistamine, H2 blockers

milky urine and flank pain

low O2 saturations

CXR evidence of pneumonia

cellulitis

meningitis

these are all evidence               and are assoicated w/                   .

infection

septic shock

what type of ABX are indicated for septic shock?

what do you do immediately for management?

do you use NE, Epi, or dopamine?

septic shock ABX = broad spectrum

high flow O2 by mask immediately

NE is the best choice (inc. PR and does not inc. HR)

spinal cord shock

manage w/ a lot of fluid and dopamine (inc. HR)

MAP

Brain

urine output

skin