Test 2 Flashcards by Sydney Coopland

CWCM stands for

Colour
Warmth
Circulation
Movement

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taken w meals and then w vitamin c

Pyrosulfate supplement

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can stain teeth - rinse mouth out after

Oral liquid iron

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When taking supplements iron will be checked, ________ will be checked
When things are back to normal continue therapy for at least 2 months after normalized

hemoglobin

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-B12 deficiency, folic acid deficiency
Cobalamin deficiency is the most common
Neurological, nerve, muscle problems
Can have upset stomach, nausea, abdominal discomfort, vomiting
High alcohol intake – absorption of B12 (substance use consideration)
Wounds that don’t heal, changes in neuro, muscle weakness, thinking process impaired

Megaloblastic anemia

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Rare, autoimmune
Can lead to cobalamin deficiency
Middle age
Ethnic groups - African, northern European ancestry ++ impacted
Women more than men
Can often be more severe
Lack of intrinsic factor (IF) - protein needed for cobalamin absorption **

Pernicious anemia

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People w ____ have increased risk of gastric cancer

anemia

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need to be on supplements parenteral, intranasal because they can’t absorb it. Won’t cure will help w blood levels. As long as they use supplement - symptoms can be reversed. Neuro problems won’t be reversed if symptoms left untreated

Pernicious anemia

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part of megaloblastic anemia, some links to other diseases and deformities - deficiency could be related to diet, absorption, alcohol use, medications

Folic acid

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Normal ______ levels 11-57

folate

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Some anti-seizure medications in particular affect absorption - Dilantin

Folic acid

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Under production of RBC
Possible underlying conditions: Chronic renal problems, chronic liver disease - on going inflammation
Thyroid problems, chronic endocrine disease
Looking for: Serum folate, iron store, cobalamin levels
Best thing to do is treat the underlying cause

Anemia related to disease

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Decrease in all blood cell types - RBC, WBC, and platelets
Potential cause: malfunctioning bone marrow - stem cell transplants, repressive therapy, bone marry transplants
Lots of things cause this - even radiation, chemical stuff, chromosomal problems
Can be abrupt or gradual development

Aplastic anemia

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Identify and treat ____________: Important to do for all forms anemia

Underlying cause

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Gradual development is often missed until symptoms are really pronounced
Symptoms will manifest as general symptoms of anemia (fatigue, heart has to work harder, SOB, WBC decrease, neutropenia, thrombocytopenia (platelets are really decreased)

Aplastic anemia (Gradual Development)

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Low neutrophil count is at risk for infection
Low platelet count is at risk for bleeding
Watch for signs / symptoms of infection (fever, chills, decreased LOC)
Thrombocytopenia - red spot rash, easy bruising, bleeding gum & nose

Aplastic anemia

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can be acute or chronic

Blood loss

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Trauma, cuts, heavy periods
Anything where there is a lot of blood loss - loss of RBC - decreased available oxygen

Decreased RBC will not be reflected in labs right away - reflection of actual blood loss will happen with 2-3 days, because of volume
Volume of blood has also decreased - so it will be proportionate

Acute Blood Loss

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Goal: prevent shock
Replace blood volume - stop the bleeding

Acute Blood Loss

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Clinical signs are key - we need to pick up clinical signs quicker than 2-3 days in order to prevent bleeding out

Acute Blood Loss

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HR increase
BP decrease
As we lose more blood LOC will change, pallor/grey (noticeable)

Clinical signs of shock (in acute blood loss)

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Symptoms
Pain - volume of blood pushing organs with internal bleeding, pressing on nerves

Acute blood loss

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Major complication of acute blood loss is ____

shock

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Need to do some kind of volume replacement
May get packed red blood cells, may need supplemental iron
As soon as we notice increase HR and decrease BP - pt heading toward shock

Shock prevention (blood loss)

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Lab work will reflect blood loss Symptoms very similar to iron deficiency Treated w iron supplements

Chronic blood loss

Hemorrhoids, menstrual bleeding, epistaxis - identify the source Effects are related to iron stores

Chronic blood loss

Vitamin C helps w absorption Changes stools - not like Malena Liquid - rinse mouth out, take w a straw Metallic taste in mouth Foods high in - beans, lentils, spinach, red meat

Iron Supplements - pt teaching

Destruction of erythrocytes greater than production can be caused by:

Hereditary problem External factors

Destruction of hemoglobin or RBC is the spleen - primary site of destruction

Splenomegaly

Inherited Abnormal form of hemoglobin Prevent organ damage from happening Since hereditary found in early childhood Predominantly African descent, east Indian, Arabian

Sickle cell disorder

Antibodies are destroying RBCs

Acquired hemolytic

Iron overload Jaundice, abdominal pain

Hemochromatosis

Goal to get rid of iron Donate blood

Hemochromatosis

Increased production increase amount of RBC, increases thickness/viscosity of blood Causes an Increase hyper viscosity Thicker blood Need to decrease thickness - increase volume and decrease thickness, look at bone marrow activity Circulation is impaired

Polycythemia

_________ changes associated with blood disorders: Pallor (decreased hemoglobin, blood flow to the skin) Jaundice (increase concentration of serum bilirubin) Bilirubin can cause skin itching as a symptom Eyes often show jaundice, bottom of feet, palms of hands - darker skin people Pruritus' (increase serum and skin bile salt concentrations)

Integumentary changes

_________ changes associated with blood disorders: Can eventually result in heart failure Edema Manifesting cardiopulmonary change

Cardiopulmonary

Anemia is not a normal finding in _________: Person will have symptoms, be exhausted Nutritional deficiencies - fixed income Worsening cardiovascular & pulmonary problems w anemia Pallor, confusion, fatigue, trouble walking - increase risk of falls

older adults

Organs enlarge w organs not getting enough blood

sickle cell

Changes in ________: Eyes can be very sensitive Erectile dysfunction

circulation

Includes RBC, WBC and platelets Follows what is being formed in that bone marrow

CBC

Size & volume of blood cells

MCV

Ratio between CBC and MCV

MCH

A decrease in _____ can increase risk of infection. Neutrophils are important to look at to look at

WBC

Combined amount of iron w proteins in serum Looking at status of what is being used and what is being stored

Serum Iron

One of the largest proteins that bonds w iron With this one you will see a decrease in iron deficiency anemia and increase in megaloblastic

Transferrin

Platelets can be low do to virus, chronic disease The lower this number is, the risk of bleeding Pregnancy Can be inherited, acquired, autoimmune, splenomegaly

Thrombocytopenia

low platelets

Thrombocytopenia

_____ disorders can be caused be cause production impaired, destruction, abnormal amount

Platelet

most common, destruction of circulating platelets

ITP (Immune thrombocytopenic purpura)

Platelets function normally till they get to spleen then the spleen mistakes them as foreign & destroys Big goal: prevent bleeding

ITP (Immune thrombocytopenic purpura)

Platelets normally live 10 days, in _____ they live 3 days

ITP (Immune thrombocytopenic purpura)

Splenectomy is treatment, steroids in high dosages More common

ITP (Immune thrombocytopenic purpura)

When platelet count is <____ × 109/L increase in internal bleeding Headaches, stroke symptoms, eye sight changes, pain

150

Related to certain drugs Not common but very serious Increased agglutination - clotting is out of wack Hemolytic anemia, neurological changes happening Body will react - fever but no infection

TTP (Thrombotic thrombocytopenic purpura)

IS a medical emergency

TTP (Thrombotic thrombocytopenic purpura)

What classifies any thrombocytopenia is when platelet count drops below 150 × ____/L

109

Can start within a couple of days when someone starts on heparin As early as 5 days Person has a clot - shouldn't have that with heparin

Heparin-Induced Thrombocytopenia

Pressuring about a clot, pulmonary problem Should be zero Measures fibrin We would see an increase in this value w a pulmonary emboli

D-dimer

comparison of prothrombin time

INR

Genetic disorder Defective/deficient in coagulation factor Chronic illness Symptoms can be mild/severe

Hemophilia

factor 8 has a problem

Hemophilia A

factor 9 has a problem

Hemophilia B

a bleeding disorder caused by the qualitative or quantitative deficiency of the pro-von Willebrand factor.

Von Willebrand's disease

Pt needs to be educated Preventing situations where it can be a problem Symptoms can be mild/severe

Von Willebrand's disease

Affected people may complain of excessive bruising, prolonged bleeding from mucosal surfaces, and prolonged bleeding after minor trauma. Pallor, melena, hemoptysis, changes in Mental Status, headaches, joint pain, abdominal pains Coagulation part - clots form - inhibits circulation

Von Willebrand's disease

Bad thing to have, serious bleeding, serious clotting changes that can lead to severe hemorrhage Always caused by something underlying - If cause is not identified - person will die Has to be diagnosed quickly Bleeding, clotting (thrombotic manifestations) Clots forming anywhere

Disseminated intravascular coagulation (DIC)

Decrease in WBC Cancer of the blood (malignant) Accumulation of dysfunctional cells Bone marrow is being replaced w leukocytes that are not functional (proliferating leukocytes) Fatal if untreated

Leukemia

Causes: chemicals, radiation, genetics, viral impact, chromosomal changes Incidence increased in radiologists, or work in radiology People who previously had chemo increased risk

Leukemia

Myelocytes, along with metamyelocytes and promyelocytes, are the precursors of neutrophils High percentage of adult leukemia Abnormal bleeding, lots of infection Onset is abrupt Mostly adults

AML - acute myelogenous leukemia

Most common in KIDS 20% adults Abrupt onset of symptoms: fever, feeling sick, bleeding gums (more blood than usual - usually first sign)

ALL - Acute lymphocytic leukemia

Excess development of neoplastic granulocytes Move into blood system, infiltrate liver, spleen Start off more chronic then become more acute

CML - chronic misogynist leukemia

Associated w changes in genetic materials in chromosome 9 and 22

CML - chronic misogynist leukemia

Chronic phase can last for years and usually treated and well controlled - can sometimes go into remission Often eventually progress to accelerated phase where it rapidly changes and needs aggressive treatment

CML - chronic misogynist leukemia

Mature appearing lymphocytes but functionally inactive Common in adults Increased risk of infection Often disease of older people Symptoms often related to bone marrow failure - everything is changes - thrombocytopenia, anemia, changes in WBC in production & functioning, organ enlargement, lymphopenia (enlarged lymph nodes), brain symptoms, bone pain

CLL - chronic lymphocytic leukemia

decrease in neutrophil counts

Neutropenia

lots of diff symptoms related to anemia, neutropenia, thrombocytopenia; diagnosed through bone marrow biopsy; seen in older peoples (over the age of 80); risk increases w age

Myelodysplastic syndrome (MDS)

Symptoms of bleeding, infection Labs: # of platelets are not functioning the way they should Often diagnosed when someone is doing tests for anemia, then they do the bone marrow biopsy - more complicated at >80 yrs

Myelodysplastic syndrome (MDS)

Aggressiveness of treatment will match aggressiveness of disease _______ prone to more side effects / complications for aggressive treatments

Older ppl

________ - cancer of the lymphocytes - Starts in bone marrow - Hodgkin's lymphoma and Non-Hodgkin's

Lymphomas

Increase in Reed Sternberg Cells - located in lymph nodes Connection w Epstein bar virus, genetic predisposition, toxics (HIV) Chemotherapy is done w this one Nursing is based on management of problems that come up - like pain

Hodgkin's

Originates outside the lymph nodes People with this will have a progressive disease by the time it's diagnosed meaning treatment has to be aggressive (chemo, biotherapy, radiation)

Non-Hodgkin's

A type of non-Hodgkin's lymphoma (NHL) that grows and spreads slowly. Treatment is better

Indolent lymphoma

Slow and insidious Seldom cured, remission can occur w not trace of illness Life can be extended Chemo is treatment Involves bones Bone breakdown

Multiple Myeloma

Increased filtering and capacity of circulating blood cells, which decreases amount of circulating blood cells (lol what) Can palpate when it's large Sometimes you have abdominal pain / sometimes you don't When enlarged there is a risk of pain

Enlarged Spleen (splenomegaly)

Problems that occur w/ _______ problems: Teaching signs and symptoms to the family as well when someone is in isolation Impaired oral mucous membrane integrity - soft bristle toothbrush Possible Nursing Diagnoses: Knowledge deficit Risk of bleeding

hematological

on an EKG is the top of the QRS

on an EKG is the little T wave

with this condition the U wave will be opposite direction on an EKG

Hypokalemia

baroreceptors, autonomic NS, ANS impact on heart & blood vessels, chemoreceptors, blood pressure

What regulates your cardiovascular system? ***

Kyphosis can affect placement of everything, making pumping action hard & breathing hard Heart can enlarge, increased vascular rigidity due to this our heart's ability to pump will increase/decrease Ability to adapt to exercise not the same Blood vessels - arterial stiffening Age related - impacts blood vessels, heart Dyspnea - is this respiratory or cardiac? Can be hard to tell w/ out diagnostics Dizziness Postural blood pressure changes (orthostatic hypertension/hypo?) Claudication, erectile dysfunction is often present when there is a change in a males body, any vascular change - it is impacted QRS can become widened - heart arrythmia problem, medications - need to be watched - regular EKG

Older adults

Objective data: vitals, chest exam, trunk-al obesity, cardiovascular system can impact way a person is thinking, Mental Status changes, confusion/fogginess

Older adults - important info

troponin, CK-MB, myoglobin

Cardiac biomarkers

big one, if MI occurs it is released, can be detected 4-6 hrs and lasts 14 hrs. Anyone who has chest pain they check this level

Troponin

creatine kinase, specific to the heart MB, elevated with any kind of injury, starts to rise anywhere between 3-6 hours, peaks 12-24 hours then goes down to baseline - has to be caught in that other time frame. Returns to baseline anywhere between 12-48 hours after MI

CK-MB

protein, comes from skeletal muscle, released whenever any kind of problem, cardiac marker but it is not specific to that

Myoglobin

released from atrium & ventricles, and released in endothelial cells (renal), used to distinguish SOB is respiratory / cardiac *

Cardiac natriuretic peptide markers

HDL, LVL, triglycerides, cholesterol is a lipid panel, often bound to proteins so sometimes call lipoproteins. Increased LDL and something risk of cardiovascular disease increased, increased HDL (protective cholesterol - gets rid of that cholesterol) the risk is lower

Serum lipids

another one that is done, inflammation in general, history of MI / chest pain they probably will have this elevated - but this alone is not enough to say it's cardiac, but goes along w the package to support it, CRP increase can indicate further risk of cardiac problems in people w cardiac history

C reactive proteins

portion that is released w protein breakdown, at increased risk of Cardiovascular/peripheral vascular disease & stroke, can be monitored w history/family history of cardiac stuff. Tell tale sign

Homocysteine

associated phospholipase A2 - is an enzyme that is elevated when plaque in blood vessels

Lipoprotein

Chest pain for _______ - some of these biomarkers might be back to normal. CK-MB could possibly still be elevated, other ones could be back to normal - that is why we try to catch them early on also to prevent damage

24 hours

silent killer **

Hypertension

+ hypertension (BP) = + risk of ____ = + risk of heart failure = + risk of stroke = + risk of renal disease

Hugely modifiable - medication, exercise, diet Things we can do to try and prevent that As we age high BP go up, women who have high BP are at increased risk of cardiovascular disease, Indigenous peoples, older women are at a higher risk than older men

Hypertension

_______ need lower BP Why? High sugars already damage the vessels High BP on top of diabetes = + risk for stroke and any other kind of cardio disease Which is why we try and maintain that lower - important to do this Some ppl w diabetes on medication for hypertension right away because of this

Diabetes

Blood pressure = cardiac output + systemic vascular resistance Any one of these parts is off, + BP

Hypertension

the volume of blood ejected from the heart per minute

Cardiac output

another term they look at, amount of normal blood volume, 60-100 ml. At rest heart pump 5-6 L per minute, increase w exercise

Stroke volume

renal fluid volume control (salt impact) (Renin Angiotensin S system, naturetic peptide); cardiac wise (HR, contraction, conductivity - affect CO) - Renal & cardiac

Factors influencing cardiac output

neurohormonal stuff (vasoconstrictors (angiotensin & norepinephrine)); sympathetic nervous system; local regulation - When one or more of these not working = + BP

Systemic vascular resistance

androgenic receptors (vasoconstrictors; α1 and α2); B2 - adrenergic receptor (opens it) medications work in these specific areas *

Sympathetic NS

α1- and α2- adrenergic: Vasoconstriction β1-adrenergic: Increased HR and conduction β2-adrenergic: Vasodilation and increased renin secretion Dopaminergic: Vasodilation Sympathetic nervous system (SNS) Baroreceptors Vascular endothelium Renal system Renin–angiotensin–aldosterone system (RAAS) Endocrine system

Normal Regulation of BP

α1- and α2- adrenergic: _________

Vasoconstriction

β1-adrenergic: Increased _______ and conduction

β2-adrenergic: __________ and increased renin secretion

Vasodilation

If our BP drops then we have automatic protection (________); increase CO & vascular resistance

renin

_________ tell our brain what is going on "our BP is too high, we need to decrease" then we have communication & decrease HR by stimulating Vagus nerve to decrease CO

Baroreceptors

"our BP is too high, we need to decrease" then we have communication & decrease HR by stimulating __________ to decrease CO Neurotransmitters that are released & we have them in SA node, myocardium & vascular smooth muscle has these receptors (a1 and a2; b1 & b2; the adrenergic receptors) B1 adrenergic receptor responds by + HR; prototrophic effect Increases inotropic effect (when force of contraction is +) Increase conduction - dromotropic effect

Vagus nerve

__________ that are released & we have them in SA node, myocardium & vascular smooth muscle has these receptors (a1 and a2; b1 & b2; the adrenergic receptors)

Neurotransmitters

______________ responds by + HR; prototrophic effect - Increases inotropic effect (when force of contraction is +) Increase conduction - dromotropic effect

B1 adrenergic receptor

___________ work on protropin, inotropic, dromotropic

Medications

β1-Adrenergic receptors in the heart respond to NE with increased HR (___________ effect), increased force of contraction (____________ effect), and increased speed of conduction (_____________ effect).

chronotropic; inotropic; dromotropic

B2 receptor activated by NE; causes _____

dilation

pressure receptors; sensitive to stretching in blood vessels

Baroreceptors

Carotid arteries, aortic areas Stretching - activation of Sympathetic NS, ____________ will occur A fall in BP, sensed by the baroreceptors, leads to activation of the SNS. The result is constriction of the peripheral arterioles, increased HR, and increased contractility of the heart.

vasodilation

Stimulation of vagus nerve can ________ HR

decrease

has an impact of BP control (sodium increased; water retained; all increase heart stroke volume & others CO) RAS system - pg 775 Angiotensin converting enzyme Decrease BP we need ACE inhibitor to block that effect

Renal system

HF is a progressive disease Salt restricted Maximize heart functioning, get rid of fluids

Acute interventions

- Automatic (start impulse and continue) - Excitability (heart responds to the impulse by contracting) - Conductivity (transmission of impulse) - Contractility (electrically stimulated)

Properties of Conduction System

_______ nervous system controls rate of impulse, speed of conduction and strength

Autonomic

Impulse starts in _______ ** - Make atrium and ventricle contract PR interval - purkinje fibres

SA node

__________ control of Heart - Autonomic controls rate of impulse, speed of conduction & strength - Parasympathetic - decreases force, rate - Sympathetic - opposite; increases

Nervous System

- Most commonly used diagnostic tool - Hearts electrical activity - Each beat is seen thru one wave

Electrocardiogram

- Drug toxicity - Diagnostic tool Electrical forces in the horizontal plane

12 Lead EKG

_____ - isoelectric flatline ** Important when looking at EKG Time period where there is no electrical activity in the heart

QT line

Evaluation of _______ - Stress testing - Treadmill - Holter monitoring Feel like heart is skipping beats - person will wear monitor, keep a diary and say how they feel at diff times - Take strip and see if the information matches their symptom

Dysrhythmias

- Sinus nodes fires <60 beats - Normal rhythm in aerobically trained athletes and during sleep - Starting at sinus nodes - Hypothyroidism can cause - Outside problem, not a heart problem

Sinus Bradycardia

Clinical associations, responds to: - Can get when we have carotid sinus massage - Valsalva maneuver (pooping) - that is why sometimes people faint - Increased intraocular pressure

Sinus Bradycardia

Clinical associations, occurs in disease: - Inferior wall MI - Head injury/intercranial pressure - Hypothyroidism - Obstructive jaundice Meds that bring this up - beta, calcium channel blockers

Sinus Bradycardia

Clinically significant Symptoms - Hypotension - Pale, cool skin - Confusion - Disorientation - Do delirium workup to differentiate

Sinus Bradycardia

Treatment - Atropine (when serious and person is symptomatic) - Pacemaker may be required - Epinephrine/dopamine infusions

Sinus Bradycardia

Can be normal related to stress, exercise, fever, anxiety, pain Conduction pathway same as bradycardia; starting at SA Greater than 100 BPM

Sinus Tachycardia (too fast)

Hypotension ** Hypovolemia Anemia Hypoxia MI Heart failure Hyperthyroidism ** she said test question lol

Associated w physiological & psychological stressors (Sinus Tach)

Clinical significance Is person symptomatic Dizziness; hypotension due to decreased CO Increased myocardial oxygen consumption may lead to angina

Sinus tach

Stress, alcohol, tobacco, hyperthyroidism, heart disease, stress, caffeine, hypoxia, electrolyte imbalance, COPD Originating from ECTOPIC (outside) focus in atrium location other than SA node Travels across atria by abnormal pathway creating distorted P wave May be stopped, delayed, or conducted normally at the atrioventricular node (AV)

Premature Atrial Contraction (PAC)

ventricle movement, atrial working MORE than the rest Can get into a saw like pattern Not getting full ventricular conduction w it Not normal

Atrial flutter

Can lead to decreased CO, heart failure because of that, stroke Recurring and regular Atria is moving fast 250-350

Atrial flutter

Caused by CAD Severe hypertension Mitral valve disorders Pulmonary emolus Have to figure out WHY this is happening; could be many diff underlying conditions

Atrial flutter

When happening for >48 hours can cause a stroke due to thrombus formation in the atria Often people put on blood thinner High ventricular rate >100 and loss of atrial "kick" can decrease CO and precipitate Heart Failure (HF), angina Could have chest pain, really decreasing CO Need to convert atrial flutter BACK to sinus rhythm Calcium channel blockers Adrenergic blockers To try and control

Atrial flutter

Disorganized Telling you that there are different areas stimulated to produce that rhythm Most common dysrhythmia Increases w age 1-2% of pop live w this Decrease consciousness Can be intermittent Increase risk of stroke Ventricular rate can be from normal to abnormal - increase risk for clots (thrombus) Not recommend doing radial pulse; do apical (manually) Not as accurate to use automatic BP machine; doesn't pick it up the same

Atrial Fibrillation

What is a common dysrhythmia that occurs as we age? ____________ Disorganized - that is how we would identify (abnormal pattern) QRS could be a normal pattern; but irregular pattern

Atrial fibrillation

Clinical associations - usually occurs w underlying heart disease Rheumatic heart disease Cardiomyopathy - diseased heart Heart failure (HF) Pericarditis CAD Acute onset: caffeine use, stimulants, stress, alcohol, electrolyte disturbances - main things you look at right away

Atrial fib

Clinical significance Decrease CO (due to ineffective atrial contractions/loss of atrial kick) Risk of stroke 3-5 x higher w _______

atrial fib

Treatment Goals Decrease ventricular rate (improve the control) Prevent cerebral embolic events Long term anticoagulation therapy

Atrial fib

Originates in AV node (weird because should start in SA node - this isn't working proper; skipping this part) SA node fails to fire; has been blocked at AV node Diff med can start this; MI; caffeine Digoxin can result in this as well - popular med Lab work is done to see if you're in the right range, toxicity can result in further abnormal rhythm Is the person symptomatic? Can't tell w taking a pulse Symptoms involved usually Will see on EKG

Junctional Dysrhythmias

(first degree, second degree, third degree full heart block)

Junctional Dysrhythmias

________ - quite slow; PR interval is long (lengthened) Every impulse is conducted to the ventricles, but duration of AV conduction is prolonged Bradycardic - usually asymptomatic otherwise

First degree block

________: AV node prolonged Atria and ventricles contract independently of each other Loss of electrical activity happening - increased Gradual lengthening of interval, gradually lose QRS May need pacemaker to make sure heart is working evenly; not missing beats Most often seen: HF, shock, damaged heart

Second-degree

Form of AV dissociation in which no impulses from the atria are conducted to ventricles Atria are stimulated and contract independently of ventricles Ventricular rhythm is an escape rhythm Seen w severe heart disease; MI; some systemic disease; lovely meds like digoxin can do this too CO is poor CO w ischemia Person may be fainting (Syncope) Ectopic pacemaker may be above / below the bifurcation of the bundle of His Permanent pacemaker Especially being symptomatic

Third Degree (Complete heart block)

Next to no CO Digitalis toxicity Valve problems Electrolyte imbalances What is causing it? Fix it Person can have this and have a pulse; or be considered unstable w no pulse Pulse not normal; not pumping the heart Decreased cerebral blood flow V-tach - life threatening - need CPR done; defibrillation and epinephrine is drug of choice

Ventricular tachycardia

They need CPR, defibrillation All types of MI; CAD; cardiomyopathy Hyperkalemia (high potassium) - cardiac arrest Potassium out of wack needs to be fixed RIGHT AWAY If untreated leads to death

Ventricular Fibrillation

Cardiac Arrhythmias _________: Absence of contractions of heart Flat line in EKG Not breathing, pulseless Not good Advanced cardiac life support

Asystole

_______: Most effective method of terminating VF and pulseless VT Passage of DC electrical shock through the heart to depolarize the cells of the myocardium to allow the SA node to resume the role of pacemaker

Defibrillation

_______ - changes associated w acute coronary syndrome Ischemia Injury Infraction

ECG/EKG

________ ** need to know Brief lapse in consciousness accompanied by a loss of postural tone (fainting) Cardiovascular causes Neurocardiogenic syncope or “vasovagal” syncope (e.g., carotid sinus sensitivity) Primary cardiac dysrhythmias (e.g., tachycardias, bradycardias) Non-cardiovascular causes Hypoglycemia Hysteria Unwitnessed seizure Vertebrobasilar transient ischemic attack

Syncope

Layers of the _______ Serous pericardium (visceral layer; epicardium) Endocardium Myocardium Serous pericardium (parietal layer) Pericardial space Fibrous pericardium

heart

An Infection of the heart valves or the endocardial surface of the heart. Risk factors include previous endocarditis, prosthetic valves, acquired valvular disease other cardiac lesions, and non cardiac condition. Symptoms are nonspecific and can involve multiple organ systems.

Infective Endocardium

Inflammation of the pericardial sac Infectious, non-infectious, and autoimmune Symptoms of progressive, frequent, severe chest pain Hallmark finding in acute pericarditis is the pericardial friction rub. Complications include, pericardial effusion and cardiac tamponade Treatment is geared identifying and treating the underlying cause.

Acute Pericarditis

Inflammation of the myocardium - focal or diffuse Clinical manifestations vary from mild to sudden cardiac death

Myocarditis

Chronic condition Inflammatory disease Affects several connective tissues of the body especially heart, brain, joints or skin Can involve all layers of the heart

Rheumatic fever

Cardiac lesions and valvular deformities Extracardiac lesion Acute rheumatic heart disease can occur as a complication from strep A pharyngitis Chest pain, excessive fatigue, heart palpation, sob, edema

Rheumatic heart disease

_______ Heart Disease The heart has Two atrioventricular valves Mitral Tricuspid Two semilunar valves Aortic Pulmonic

Valvular

Stenosis The valve is restricted Forward blood flow is impeded A pressure gradient is created across the open valve Pressure gradient differences reflect the degree of stenosis

Valvular Heart Disease

Regurgitation Incomplete closure of valve leaflets Results in backward flow of blood

Valvular Heart Disease

The majority of adult cases result from rheumatic heart disease Causes scarring of valve leaflets and chordae tendineae Contractions develop w adhesions between commissures of the leaflets Primary symptom if exertional dyspnea due to decreased lung compliance

Mitral Valve Stenosis

Valve function depends on Intact mitral leaflets Integrity of mitral annulus Chordae tendineae Papillary muscles

Mitral Valve Regurgitation

Valve patency depends on Left atrium Left ventricle An abnormality of any of these structures can result in regurgitation

Mitral Valve Regurgitation

Abnormality of mitral valve leaflets and the papillary muscle of chordae Allows the leaflets to prolapse back into the left atrium during systole Unknown cause

Mitral Valve Prolapse (MVP)

Usually discovered in childhood, adolescence, or young adulthood Those seen later in life usually have aortic stenosis from rheumatic fever/calcification of a normal valve Isolated aortic valve stenosis is almost always of nonrheumatic origin Results in obstruction of flow from left ventricle to aorta during systole Angina Syncope Exertional Dyspnea

Aortic Valve Stenosis

May result from disease of aortic valve leaflets, aortic root, or both Caused by: Infective endocarditis Trauma Aortic dissection

Aortic Valve Regurgitation

Myocardial contractility eventually declines Pulmonary hypertension and right ventricular failure develop Clinical manifestations of sudden cardiovascular collapse - constitutes a medical emergency

Aortic Valve Regurgitation

Very uncommon Tricuspid occurs almost exclusively in patients W rheumatic mitral stenosis IV drug users Have had multiple myocardial biopsies, radiation treatment, anorectic medications Treated w dopamine agonists Pulmonic is almost always congenital Both result in increased blood volume in right atrium and ventricle, respectively

Tricuspid and Pulmonic Valve Stenosis

Diagnostic Studies for _______: Pt history/physical exam Echocardiography and doppler imaging Chest radiograph ECG/EKG Cardiac catheterization

Valvular Heart Disease

Interprofessional Care Prevention of recurrent rheumatic fever and infection endocarditis is essential Treatment depends on the valve involved and severity of disease Medication therapy to treat / control HF Digitalis (positive inotropes) Vasodilators Diuretics B blockers Other medication therapies Anticoagulants Antidysrhythmic Low sodium diet Percutaneous aortic valve replacement Percutaneous transluminal balloon valvuloplasty (PTBV) to split open fused commissures

Valvular Heart Disease

Nursing Assessment Subjective Objective Fever Hepatomegaly Diaphoresis Crackles, wheezes, hoarseness Ascites Abnormal heart sounds Tachycardia Dysrhythmias Hypotension Reduced stamina Excess fluid volume Decreased cardiac output

Valvular Heart Disease

A group of diseases that directly affect the structural or functional ability of the myocardium Dilated, Hypertrophic, Restrictive A diagnosis of cardiomyopathy is made on the basis of the patient’s clinical manifestations and non-invasive and invasive diagnostic procedures. There are two types: primary and secondary. Symptoms may include decreased exercise capacity, fatigue, dyspnea at rest, paroxysmal nocturnal dyspnea and orthopnea, dry cough, palpitations

Cardiomyopathy

__________ - Dilated Ventricles are weaker & get larger Heart muscle is larger and thicker Ventricles stiffen, heart wall do not thicken

Cardiomyopathy

Include disorder of the arteries, veins, and lymphatic vessels

Vascular Disorders

____________ - your limbs :) - everything outside the heart and brain Aneurysmal Atherosclerotic Narrowing & degeneration Risk factors: diet, tobacco, diabetes (damages endothelial tissue in blood vessels - increased glucose levels, Nonatherosclerotic

Peripheral artery disease (PAD)

Progressive narrowing & degeneration of arteries in neck, abdomen & extremities Strong associated w systemic atherosclerosis Higher as age increases (85 30-50% have PAD) Sections of arteries Anyone w diabetes this can happen earlier Usually a marker for systemic problems

Peripheral artery disease (PAD)

What causes them and WHY Risk factors - why? Think bigger picture High cholesterol, increased fats and lipids, obesity, sedentary lifestyle, high BP (hypertension), genetic risk (family history) Marker in blood - C reactive protein** Chronic problem, it will be monitored Homocysteine levels are sometimes elevated as well w atherosclerosis AND blood clots Lipid monitoring ***

Atherosclerosis

In diabetes, tend to be below the knee - loss of sensation, amputation More common in aortoiliac, femoral, popliteal, tibial & peroneal arteries Intermittent claudication (calf pain/leg pain after movement - occurs w movement & goes away in 10 mins after rest) - key for peripheral vascular pain ** Rest pain, chronic Related to ischemia - ischemic pain Reproducible - pain will show up for same thing that caused it over and over Rest pain In forefoot & toes * aggravated by limb elevation Insufficient blood flow More frequent at night

PAD of lower Extremities

when you elevated legs it remains that grey colour

Elevation pallor

Other clinical manifestation Reactive hyperemia - foot gets redder when just sitting there Paresthesia Thin, shiny, and taut skin Loss of hair on lower legs Diminished/absent pedal, popliteal or femoral Elevation pallor Reactive hyperemia Rest pain Occurs in the forefoot or toes and is aggravated by limb elevation Occurs from insufficient blood flow Occurs more often at night

Elevation pallor

_______ complications (at risk for the following) Atrophy of muscles Increased damage from minor trauma Slowed wound healing Increases risk of infection Nonhealing arterial ulcers Gangrene Amputation

PAD

_________ - gangrene, ulcers They will have an amputation within 7 months if they have this critical limb ischemia Ischemia is bad because - no circulation, blood flow change, tissue death (gangrene), risk will increase in diabetes Bypass is most common treatment Proper fitting shoes, nails Bottom of feet need to be looked at, change in sensation

Critical limb Ischemia

What can nurse do? Decrease the risk: Education is huge to decrease risk Tobacco Antiplatelet side effects Non pharmacological - walking/exercise is huge

Critical limb Ischemia

Diagnosis - doppler ultrasound Angiogram, venograms sometimes

Critical limb Ischemia

Acute, sudden Huge interruption in blood supply Thrombus may develop within an artery & cause complete occlusion of blood flow to the tissues "downstream" An embolus may dislodge from within an artery, travel "downstream" and completely occlude artery Think about the 6 P's **** Pain Pallor Pulselessness Paresthesia Paralysis Poikilothermia - the inability to maintain a constant core temperature independent of ambient temperature Anticoagulation therapy, remove clot Revascularization / amputation

Acute Arterial Ischemia

Aka burgers disease No tests for this Non anthrosclerotic inflammatory disorder Might have rest pain, intermittent claudification A nonatherosclerotic, segmental, recurrent inflammatory vaso-occlusive disorder of the small and medium-sized arteries and veins of the upper and lower extremities Sometimes ulcerations, feet hands and arms (smaller areas) Decreasing risk - analgesics * Lots of pain

Thomboangiitis Obliterans

Spastic disorder of cutaneous arteries Fingers & toes Colour change Only a few minutes sometimes for an hour or so Triggered by stress, change in temp is a big one, emotional stress Caffeine & tobacco Diagnosed if persists for > 2yrs Anything that limits vasoconstriction - caffeine, tobacco, and cold Drug of choice - calcium channel blocker (decrease that response)

Raynaud's

Loss of elasticity of media layer of arterial wall causing thinning and bulging of aortic wall ¾ occur in abdominal aorta Also in aortic arch, thoracic aorta Any artery can have aneurysm Congenital or acquired Can be caused by infection, inflammation, trauma (mechanical - outside factor) Men > women for risk; >65 Abdominal aneurysm - big cause of death in elderly Tobacco - major risk factor CAD, PAD, high cholesterol Often asymptomatic - found in regular x ray often High mortality rate Surgery when around 5-5.5 cm Unless person is symptomatic (pain); surrounding area is compressed because of the aneurysm is increasing in size Abdominal - level of renal - that is why we listen for bruits (asymptomatic) Biggest cause in aorta - atherosclerosis Biggest risk, tobacco Can even get intermittent claudication

Aneurysm

A - uniform/intact, has fusiform area (bulging area), bulge is outside the wall Thoracic aneurysm Aorta in that area Chest pain - into back & scapula Mimics gallbladder & liver problems

Aneurysm

__________ (AAA most common) Present w TIAs Hoarseness, dysphagia depending on what is compressed Jugular distension Decreased venous return - edema (in phase & arms)

Ascending Aorta aneurysm

__________ is when you have disruption in the layers Result of trauma Graft didn't hold Leaking arterial line

False aneurysm

Complications Biggest - bleeding - rupture (serious complication related to untreated) Rupture into retroperitoneal space Bleeding may be tamponaded by surrounding structures, thus preventing exsanguination and death. Severe pain May or may not have back or flank ecchymosis (Grey Turner’s sign).

Aneurysm

Rupture into thoracic or abdominal cavity Massive hemorrhage Most patients do not survive long enough to get to the hospital.

aneurysm

90% of people die if rupture - As many as 50% to 90% of people with an aneurysm rupture in their brain get a vasospasm.

aneurysm

Peripheral aspect - ______ is biggest one *

aorta (aneurysm)

Circulation impacted Low BP Tachycardic Pale/ashen/very sick Altered LOC Tenderness

Hypovolemic shock

___________ - like aneurysm but a tear Tear in intimal layer of arterial wall allows bleeding into the media layer and a pool or bulge of blood results Leads to compression & occlusion of surrounding vessels an/or rupture Men at higher risk Any type of aortic disease, heart disorder, connective tissue, heart problems, bowel problems Anytime heart pumps, pressure restricted in that area, increase pressure in that area Can impact blood flow in other areas of the body

Aortic Dissection

Complication (big one) Cardiac tamponade - blood leaking in pericardial sac Compress heart Life threatening Symptoms: Distension in jugular Hypotension ? Heart sounds change (muffled) Narrow pulse pressure Bleeding biggest boy **** Hypovolemic shock Decreased BP (hypotension), tachycardia (trying to exert more blood by going faster), pallor/pale, fearful Imperative that BP is not too high, increase the tear; maintain BP at lower level; lot of intense monitoring

Aortic Dissection

___________ - what do they look like? Where are they usually? Symptoms are what we have been talking about. Often have punched out look (thickened area around it) - mostly over bony prominences Typically toes, heels, prominences of foot "Punched out" well demarcated edges Pale, non granulating, often necrotic base Skin dust, erythema, cool to touch Hairless, thin, brittle skin w shiny texture Toe nails thickened, opaque, maybe lost Gangrene may occur Loss or decreased pulse (dorsalis pedis or tibial arteries) If person has this you are monitoring: Infection Poor healing Any other changes in CWCM Treating w whatever is ordered Doppler ultrasound - to see blood flow in that area - espec. If not healing Ankle brachial indexes 1 to 1.4 is normal number you would see

Arterial Leg Ulcers

Treatment Increase blood flow - surgery Smoking cessation Control diabetes, hypertension, hyperlipidemia Head of bed raised at night may help rest pain Excellent foot & leg care Waling is beneficial Treatment of infections w system antibiotics Analgesics Do not debride ulcers

Arterial Leg Ulcers

Phlebitis Inflammation of a vein Can happen cause of IV or med Redness, tenderness, warm Pt will complain Superficial vein (usually no clot) Deep - as a result of a clot Block Can move May have symptoms Change in circulation, discomfort, redness Do something before it travels If having difficulty breathing suddenly - pulmonary emboli

Venous Disorders

a condition that occurs when a blood clot forms in a vein

Venous thromboembolism

Twisted, distorted, cord looking appearance Can be uncomfortable Achy Caused by wall/valve damage Spider veins appearance is more mild

Varicose

Venous Thrombus / Venous disorders _________: Venous stasis Damage to endothelium Hypercoagulability of blood (elevated clot, thicker and gooey)

Virchow's triad **

At risk of clots because blood is just chillin' ________ can sit there, start to block or move Any problem w the valve will cause stagnation Mostly in people who are obese, heart failure, anything that causes a person to be sedentary (lengthy hospital stay), hip fractures, IV therapy (chemo - very irritating) Estrogen based BC - increases risk of clots

Thrombus

Venous Thrombosis _________ - may palpate a hard area, euthymia, red, warm to touch, temperature (increased WBC) Promote venous returns NSAIDs Venous thrombo-embolism - in deeper veins Systemic Lungs - chance of death (cardiac arrest)

Superficial

Diagnosis of VTE DVT Prevention Mobilization post op Moving limbs Compression stockings Intermittent compression devices Prevention and prophylaxis Drug therapy: Anticoagulant therapy - inhibiting 1 component of the clotting Vitamin K is an antagonists *** can interfere w medications Indirect thrombin inhibitors Direct thrombin inhibitors Factor Xa inhibitors Anticoagulation therapy for VTE prophylaxis Anticoagulation therapy for VTE treatment Thrombolytic therapy for VTE treatment

Venous thromboembolism (VTE)

Commonly called blood thinners - but they don't thin Used to treat DVT or PE Prevent the clot from becoming larger while the body slowly reabsorbs it Reduce the risk of further clots developing

Anticoagulants

Monitor lab results (e.g., PTT) Observe S & S of bleeding, bruising Do not give IM’s, minimize IV - well we never do that stuff unnecessarily anyway (prone to bruising, may bleed more after) Do not take Vit K, avoid certain herbs Limit alcohol use Report blood in urine/stool Report prolonged bleeding Do not take ASA or NSAIDs Report severe headache, stomach ache

Anticoagulant Treatment

Filter inserted inside IVC (large vein that brings blood back to heart) Traps amolus before it reaches the lungs

VTE - inferior vena cava filter

What does _____ mean International normalized ratio test tells you how long it takes for your blood to clot. A test called the prothrombin time (PT) actually measures how quickly your blood clots.

INR

Valve damage Backflow of venous blood Persistent edema Bronze-brown pigmentation (breakdown of blood, iron leaches out and browns the skin - hemocyteric) Thick, hard, fibrous skin Ulceration

Chronic Venous Insufficiency

___________ - itchy, looks like eczema (happens w this) Sores will ooze and crust Treatment is compression stockings, if swelling (elevation), itching w antihistamines & moisturizers; watching for wounds that aren't healing; infection spreading up the legs (cellulitis - redness going in direction that is increasing - mark area w pen on person & document)

Stasis dermatitis

From chronic venous insufficiency Often accompanied by stasis dermatitis & peritus Partial thickness Painful Extensive drainage Can lead to infection, cellulitis Uncomfortable, drain lots, prone to infection

Venous Ulcers

________- - Collaborative care Compression only if no arterial disease Moist dressings Diet high in protein, Vit C, A, and zinc Control of diabetes Reduce obesity Observe for infection Happens w older people, antihistamines (drowsy) increase falls Improve healing - nutrition is very important, supplements (liquid may increase pt adherence) Obesity is a big risk factor too Compression socks need to be measured to person leg - hard to get on, if too tight can cause skin breakdown Need to be replaced and washed (every 4-6 months) Bacteria

Leg Ulcer

Long-term management of venous leg ulcers should focus on teaching the client about self-care measures because the ulcers often recur. Instruct the client and caregiver to avoid trauma to the limbs and teach them proper skin care. Demonstrate the correct application of graduated compression stockings and stress the importance of regular replacement (every 4–6 months).

Chronic Venous Insufficiency & Venous Leg Ulcers

______ - Nursing Care Careful foot & skin care Avoid sitting, standing for long periods Elevate leg frequently if no arterial disease Daily walking program Compression stockings as ordered only if not arterial

Leg Ulcers

Dilated, twisted veins Esophageal varices Hemorrhoids Saphenous veins in legs Primary or secondary (valve damage from DVT)

Varicose Veins

Decreased tissue perfusion and impaired cellular metabolism Imbalance in supply/demand for O2 and nutrients

Shock

Types of _______- *** Cardiogenic (low volume) Hypovolemic (low volume) Neurogenic (distribution) - she said earlier that this one is different Anaphylactic (distribution) Septic (distribution) Obstructive (not on there)

shock

Low Blood Flow __________: Systolic / diastolic dysfunction Compromised CO Precipitating causes Myocardial infarction Cardiomyopathy Blunt cardiac injury Severe systemic or pulmonary hypertension Cardiac tamponade Myocardial depression from metabolic problems Early manifestations are similar to that of a client w decompensated heart failure Looking at cardiac enzymes in lab work Troponin level EKG Chest x ray Echocardiogram Person will be in ICU

Cardiogenic Shock

Three things that RESULT from _______ * Decreased cellular oxygen supply Decreased tissue perfusion Impaired cellular metabolism

shock

Low Blood Flow ____________ - not just bleeding can be loss of other body fluids Absolute hypovolemia: loss of intravascular fluid volume Hemorrhage GI loss (e.g., vomiting diarrhea) Fistula drainage Diabetes insipidus Hyperglycemia Diuresis

Hypovolemic Shock

_________: Results when fluid volume moves out of the vascular space into extravascular space (e.g., interstitial or intracavity space) Termed third spacing

Relative hypovolemia

Clinical Manifestations Anxiety Tachypnea Increased in CO, heart rate Decrease in stroke volume, PAOP, urinary output If loss is >30%, blood volume is replaced 15-30% will be symptomatic - will see more of a response (BP, tachycardic) Respiratory status will change too

Relative hypovolemia

Distributive Shock ___________: Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and can last up to 6 weeks. Can occur in response to spinal anaesthesia (spinal anesthetic) Results in massive vasodilation, leading to pooling of blood in vessels Lost the ability to compensate here because we lost ability to communicate and therefore change* DECREASED HEART RATE - different

Neurogenic shock

Clinical manifestations Hypotension Bradycardia Temperature dysregulation (resulting in heat loss) Dry skin Poikilothermia (taking on the temperature of the environment) - greater risk for hypothermia ***

Neurogenic shock

Distributive Shock ___________ - sudden onset Acute, life-threatening hypersensitivity reaction Massive vasodilation Release of mediators Increased capillary permeability Clinical manifestations Anxiety, confusion, dizziness Sense of impending doom Chest pain Incontinence Swelling of the lips and tongue, angioedema Wheezing, stridor Flushing, pruritus, urticaria Respiratory distress and circulatory failure

Anaphylactic Shock

Distributive Shock _________ - inflammatory response related to infection (30% do not know what caused it) Mortality rate of 15-20% ? W severe sepsis

Septic Shock

__________ = Presence of sepsis with hypotension despite fluid resuscitation Presence of tissue perfusion abnormalities Clinical manifestations Increased coagulation and inflammation Decreased fibrinolysis Formation of microthrombi Obstruction of microvasculature Clinical presentation of sepsis is complex, and no single symptom or group of symptoms is specific to the diagnosis. Hyperdynamic state: increased CO and decreased SVR Tachypnea/hyperventilation Temperature dysregulation Decreased urine output Altered neurological status GI dysfunction Respiratory failure is common. Usually quick

Septic Shock

Develops when a physical obstruction to blood flow occurs, resulting in decreased CO Abdominal compartment syndrome Decreased CO, increased afterload, and variable left ventricular filling pressures Jugular venous distention and pulses paradoxus Rapid assessment and treatment are important to prevent cardiac arrest.

Obstructive Shock

Coronavirus Disease 2019 - people can become _______ w COVID as well Clinically, many patients infected by SARS-CoV-2 present with mild symptoms. About 5% show severe lung injury and/or multiple organ dysfunction syndrome. Many patients meet sepsis criteria; sepsis is the second leading cause of death among patients with COVID-19.

septic

_________ - she doesn't need us to know the stages; we know at beginning no symptoms (we compensate)

Stages of Shock

Initial stage Compensatory stage Progressive stage Refractory stage

Stages of shock

Usually not clinically apparent Metabolism changes from aerobic to anerobic Lactic acid accumulates and must be removed by blood & broken down by liver Process requires unavailable O2

Initial Shock

Clinically apparent Body activates neural, hormonal & biochemical compensatory mechanisms Classic clinical sign is hypotension Vasoconstriction while blood to vital organs maintained Increased venous return to heart, CO, BP Impaired GI motility Cool clammy skin from blood (except with septic) Blood is shunting from lungs and increasing physiological dead space Increased myocardial oxygen demands.

Compensatory Stage

Begins when compensatory mechanisms fail Multiple organ dysfunction syndrome Cardiac problems Liver starts to fail Everything starts to shut down

Progressive Stage

Increasing fluid leaking out Worsening CO More organs worsening - person won't recover

Refractory Stage