edema, congestion and shock

pulmonary edema due to congestive left heart failure

These pressures in left heart failure can cause rupture. Bleeding in alveolar space. Almost diagnostic of congestive heart failure-get heart failure cells

blood pressure mean arterial pressure

Pa = CO x TPR Pa = mean arterial pressure (mm Hg) CO = cardiac output (mL/min) TPR = total peripheral resistance (mm Hg/mL/min) **Ohms law TPR = govenrend by tone of precapillary arterioles Decrease CO then mean pressure drops Decrease tpr bp will drop Decrease? CO and tpr it aint good. Bp will plummet. Develop shock

edem

-accumulation of fluid in the interstitium causing swelling Intracellular edema is a shift of water from the interstitial space into the intracellular space as a result of cell injury most often by alterations in altered Na+ homeostasis (e.g., during early ischemia, direct toxicity) However unless otherwise specified, edema will be referred to as a shift of fluid from the intravascular space into the interstitial space or transcellular into body cavities (hydrothorax, hydropericardium, ascites). *Ascites- accumulation of fluid in peritoneal cavity *Transcellular fluid is fluid within epithelial lined spaces. Ocular fluid, joint fluid, cerebrospinal fluid, bladder urine

_____passive _______ of the lung, PRECEDES _______

ACUTE passive CONGESTION (HYPEREMIA) of the lung, PRECEDES ACUTE PULMONARY EDEMA

impared venous return (increased microvascular pressure )

Congestion. For a variety of reason if the outflow of venule side is decreased, the blood cannot get back to heart as fast as it should. Normally you would extend microcirculation due to backpressure of non oxygenated blood. This in itself can cause edema and hypoxic response and secondarily would cause increase in vascular permeability increasing edema Congestion (inflammatory, blood clot, congestive heart failure). Impared venous returrn. Intravascular pressure increases and build up. Similar to other forms of edema. Add up pressures going out and reduced coming in, hydrostatic will increase because backup of fluid you clinincaly will see in deep vein Thrombotic Edema (Thrombophlebitis) *in this case the other leg is normal, you assume its DVT. If both legs swell youre in congestive heart failure.

what is a fluid wave

Due to liver cirrhosis. They stick needles into abdominal cavity, can drain 6-8L How many gallons is in 3.5 liters?

septic shock : inflammatory players

Endotoxins (LPS, PAMPs) Vascular Endothelium Inflammatory Cells Polymorphonuclear Leukocytes, Platelets Lymphocytes, Monocytes Plasma Protein Mediators Complement, Kallikrein-Kinin, Blood Coagulation and Fibrinolytic Cell-Derived Inflammatory Mediators Cytokines (TNF, IL-1, IL-6, IL-8, IL-17), PAF, NO, Prostaglandins, Leukotrienes, ROS **Microorganism causing shock= septic shock Gram negative microorganisms which have PAMPs (LPS or endotoxin) and can interact with toll like receptors throughout body. When they interact (thinking TLR 4) these reeceptors can activate a variety of systems and inflammatory cells Vascular endothelium involved and all the other stuff Ultimately cell derived mediators that take over and lead to irreversible development shock and multiple organ failure and death

Decreased plasma protein concentrations (lowered oncotic pressure)

Everything else can be the same with normal pressure Something happens to decrease plasma protein conc Oncotic pressure drops less than 22 Then net pressure decreases preventing resorption of water on venular side of microcirculation throughout the body clinical situation-Edema (Anasarca) of Protein Deficiency(Kwashiorkor) Deficiency of protein. Decreased plasma protein concentration lead to lowered osmotic pressure led to edema in venule Essential amino acids that we cannot synthesize. Good caloric intake but not protein intake. Plasma Decreases colloid oncotic pressure, edema makes them look fat Anasarca = edema throughout the body.

impaired lymphatic drainage

Everything totally normal. Except you have lymphatic destruction Over time the drain will build up and one will develop edema clinical= filariasis caused by roundworms. Love to grow in lymph node. Develop horrible elephantiasis. Common in 3rd world countries Post masectomy- surgeons would normally remove as many axial lymph nodes as possible in area. By removing lymph nodes they destroy lymphatic drain in that side of body. They have it for the rest of their lives. Requires intense therapy to prevent. Today what happens for the most part you do a centinal node procedure. Inject die into lymph nodes that were part of cancer, then leave the others alone. Lymphatic drain important. Palpable lymph nodes there is a good chance for edema proximal to lymph nodes that you are feeling

Edema Due To Liver Disease

Hypoalbuminemia Increased pressure in splanchnic circulation Lymphatic compression & overload in splanchnic circulation ***If you have a sick liver, it is responsible for generating proteins. For coagulation etc. Hypoalbuminemia - Effects plasma oncotic pressure Liverr cirrhosis gets strangulation of livver. Get build up in hepatic portal vein from splanchic region. Congestion in lvier and causes some necrosis. With back pressure you get edema in pancreas spleen and down into intestines (large intestion esp). All splanchic circulation has to go thru liver. Liver cirrosis can get. Can get so severe of ascites (inflammation in belly) Because of edema and swelling you get lymph compression draining splanchic. Worsens the entire situation Low protein Circulation blocked due to pressure constriction Lymphatic constriction as well due to pressure constriction

clinical features of shock

Hypotension Tachycardia Tachypnea Warm skin cool skin cyanosis Renal insufficiency Loss of mental faculties Death *Please note that this is generally a LINEAR sequence of events, with not too much overlap, and does not usually progress in any other ORDER, except this one. This is how most people die, who do not die acutely.

causes of shock

Hypovolemic- decrease in blood volume Cardiogenic- something wrong with the heart, infarction, myopathy, l or r failure, Neurogenic- neurological cns problems or nerves severed

Pathophysiologic Sequellae of Shock

Inadequate tissue perfusion Tissue hypoxia If uncorrected - fatal outcome

artriole dilation in microcirculation (increased microvascular pressure)

Pressure increased well above 40mmHg. Can get to 60-65 so net outflow relative to oncotic pressure (conssitant at 22), a hell of a lot more water goes out(transudate not exudate). Even on venular side we see incrases in hydrostatic pressure.. Amount of pressure pushing back is reduced. We get accumulatoon of fluid in tissue. Absorption not proper and lymphatics have limited capacity (can happen with primary pulmonary hypertension)

nephrotic syndrome

Protein normally prevented we pee with low protein. Protein goes thru glomerular capillaries and is peed out 5-6 g per day bc of disease. Pee protein. These people pee out a lot of protein presenting antioedema. Steroid treatment can help it go away. Once protein ceases to be filtered out she will go back to normal once oncotic pressure is reestablsihed.

primary pulmonary hypertension

Pulmonary edema occurs only when the pulmonary capillary pressure rises to values exceeding the plasma colloid osmotic pressure, which is approximately 28 mm Hg in the human. Because the normal pulmonary capillary pressure is 8 to 12 mm Hg, there is a substantial margin of safety in the development of pulmonary edema. At pressures of 12 to 18 mm Hg, the vessel borders become progressively hazier because of increasing extravasation of fluid into the interstitium. This effect is sometimes evident as Kerley B lines, which are horizontal, pleural-based, peripheral linear densities. As PCWP increases above 18 to 20 mm Hg, pulmonary edema occurs, with interstitial fluid present in sufficient amounts to cause a perihilar "bat wing" appearance. One gets hypertension respons Hydrostatic pressur in septa increase pushes huge amount of lfuids into alveolar space itself

stages in shock

Stage 1: in response to initial hypotension, vasoconstriction in non-essential organs and renal shut down Stage 2: lactic acidosis, vasodilation, endothelial injury, anasarca, decreasing blood volume, decreasing cardiac output Stage 3: irreversible anoxic damage Stage 4: > 80% fatal outcome *Anasarca - edema throuhgout body Stage 2 is probably close to point of no return

left venticual co vs right co

The CO comoing out of RV better be same as LV. If there is imbalance between 2 you have pressure build up in lungs Left heart failure- left heart is not pumping out enough that right is. Another way to get pulmonary edema. Icnrease of pulmonary hypertension. Huge increase in hydrostatic pressure. Drives fluid out into alveoli. LV failure they gurlgle if you auscultate. Right heart failure- right heart not pumping enough, what happens is pressure of returning blood thru vena cavas increases because it can only distend/compliant. Point where intravascular pressure on venous side increases brings down to microcitculatory causing legs to swell

microcirculation pressure

VERY LOW 40 arterioles Venules 5 Then you see increase in hydrostatic pressure

Vasodilation/Increased Vascular Permeability mediators

Vasoactive amines (histamine, serotonin) Leukocyte cationic proteins Kinins (bradykinin, Kallidin, C2-kinin) C3a and C5a anaphylatoxins (mast cell & platelet dependent) Leukotriene E4 (LTE4) Platelet-activating factor (PAF) Substance P Note: PGE2 synergizes with above mediators

Interstitial Edema(Underlying Settings)

When there is increases microvascular hydrostatic pressures (arteriolar dilation, impaired venous return) When there are decreases in plasma protein (albumin) concentrations (lowered colloid oncotic pressures) When there are increases vascular permeability (inflammation, endothelial cell injury) When there is Impaired lymphatic drainage When there is an impairment in sodium/water homeostasis

shock

clinincal features that arise because of a decrease in blood pressure due to cardiovascular collapse Definition: cardiovascular collapse with severe systemic hypotension and the clinical features of shock Pathophysiology: inadequate cardiac output, decreased TPR, inadequate blood volume

conjestion

disruption in blood flow particullarly in the micro circulation and the blood vessels will become distended not because of hydrostatic pressur necessarily but because blood cells will just get packed nd cannot empty (gets pluged up) Congestion. For a variety of reason if the outflow of venule side is decreased, the blood cannot get back to heart as fast as it should. Normally you would extend microcirculation due to backpressure of non oxygenated blood. This in itself can cause edema and hypoxic response and secondarily would cause increase in vascular permeability increasing edema

hydrostatic vs oncotic pressure normal and abnormal

hydrostatic pressure pussing out of the vessles high in arterioles, oncotis pressure pushing back in is high in venules Normal occurs because arteriolar side hydrostatic pressure exceeds oncotic pressure. Net outflow pushes transudation water into tissue. Most of the fluid low in protein will be reabsorbed at venule ned where hydrostatic has decreased less than oncotic. What water is not reabsorbed is drained thru lymphatics. Normal. abnormal-Huge increases in blood flow is huge dilation. Blood vessels can dilate to certain point, often due to hypertension, increases intravascular pressure and increases transudation and can cause edema

most events of edema occur where

in the microcirculation , blood vessels are eithe rgunna get leaky or plugged up and there will be a backup of circultion

water distribution in body

plasma- 7% transcellular-2% interstitial-31% intracellular - 60% extracellular total=40% intracellular=60% *Transcellular =body cavities, peritoneal cavity joint spaces csf

Lower Extremity Pitting Edema (Congestive _____Sided Heart Failure)

right Gravity pushes down. Huge bilateral edema, so severe you get 'pitting edema' diagnostic of congestive heart failure

Increased vascular permeability (inflammation, endothelial cell injury)

talked about this before Hydrostatic increases and decreases oncotic pressure on venule side (decreased plasma protein, went into interstitium by migration etc) Vasodilation can increase pressure One can get development of severe edema that lymphatics cant carry away clincal case-angioedema (type 1 hypersensitivity)

In normal people if you take in 2.5 L you better __________or it accumulates in one of the compartnmetns probably interstitital

you better pee or sweat it out,