patho 4 CV - Vickers

oxygenated blood enters left atrium through the aortic valve -> through mitral/bicuspid valve ->left ventricle -> pumps blood out the aorta -> arteries -> arterioles -> capillaries -> venules -> veins -> vena cava -> deox blood enters right atrium -> thru tricuspid valve -> right ventricle -> thru the pulmonary valve -> pulmonary artery -> lungs to be oxygenated -> pulmonary veins -> oxygenated blood reenters left atrium

take blood away from the heart to tissues

collects blood from body tissues and takes it back to the R side of the heart where it is pumped to the lungs for reoxygenation

SA node -> AV node -> bundle branches -> Purkinje fibers

during diastole the ventricles relax and the mitral and tricuspid valves open to allow blood to enter the ventricles passively from the atria; at the end of diastole the atria contract and propel remaining blood into ventricles & AV valves shut to prevent backflow into atria

during systole the ventricles contract and the pulmonary and aortic valves open to allow blood to flow out of the heart to the tissues and lungs; the AV valves are closed to prevent blood flowing back into the atria

mitral and aortic

tricuspid and pulmonic

pulmonary embolism

will clog in foot and cause ischemia

artery b/c it causes ischemia of a body part

SA node

8 liters per minute

SV X HR

won't have to figure that on the test

pulse, BP, appearance, color, skin moisture,

pale and diaphoretic, v/s, mottled (white/yellow/purple due to ischemia of tissues), grey, capillary refill, MM

amount of blood the heart must pump with each beat due to amnt of blood coming from veins

how much pressure that is required for the heart to pump blood out

decreased CO

increase CO without increases the workload of the heart

drugs that affect preload and afterload

amount of blood the heart pumps in a minute

will increase CO

1. sit pt on side of the bed and let legs hang off so blood volume stays in the legs

2. give them diuretics to decrease BV

3. give them drugs that vasodilate - will decrease volume coming to heart

will keep blood volume in legs and decrease preload

vasodilators - decrease preload

increases it b/c small vessels increase pressure needed to get blood through

causes blood vessels to be constricted that more volume comes to heart and afterload is increased - heart is overworked

they make prob worse

interventions are all to counteract compensatory mechanisms of the body

increase CO, decrease preload & afterload

ability of the heart to change its force of contractions

digoxin, lanoxin

mean arterial pressure

• (2 X diastolic) + systolic
•                 3

must be at least 60

2/3 of the cardiac cycle is spent in diastole

can decrease CO

histamine, serotonin, kinins, prostaglandins, blood vessels, endothelial control of vasodilation and vasoconstriction, NO (nitrous oxide)

increases blood flow to area

vasoconstriction = less blood flow to the area

VASOCONSTRICTION = less blood flow to the area

Prostaglandin E - vasodilator - increases

Prostaglandin F - vasoconstrictor - decreases

nitrous oxide

powerful vasodilator produced by the endothelial lining of arteries - increases blood flow to an area

microcirculation

70 year old has had ischemia a while and collateral circulation has had time to develop

nitroglyceran to keep collateral circulation open and decrease chest pain

vagus

slowed

Have them "vagal down"  bear down like having a bowel movement

excitatory influence on heart rate and contractility

vagal can cause decrease BF to the brain and MI

will give them stool softeners

bearing down in any way

holding breath in anticipation of pain, etc

LDL

1. cholesterol

2. triglycerides

swelling in the legs

elevate legs

in arterial will keep legs down to try to increase BF

hyperlipidemia, PAD, Raynaud disease, aneurysms,

small intestine and liver

atherosclerosis

lowers it by transporting it back to liver to be excreted

moderate alcohol intake and exercise

smoking

genetic basis - not necessarily r/t what they eat or the size of the person

obesity and high calorie diets

DM

statins that work on liver and have it decrease cholesterol production

all adults 20 yrs and older have a fasting lipoprotein profile done q 5 yrs

< 200 mg/dL

HDL > 40mg/dL

turns liver off at night

can damage the lining of the arteries, atherosclerosis will occur at the site of damage and arteries become more sticky due to smoking so the debris sticks to the artery more easily

coronary heart disease

• 1. high LDL
• 2. family Hx of premature CHD in 1st degree relative
• 3. current cigarette smoking
• 4. hypertension
• 5. low HDL
• 6. DM
• 7. hypercholesterolemia
• 8. male gender until women hit menopause

no risk factors - 160mg/dL or less

2 or more risk factors - <130 mg/dL

high risk factors - (with CHD) - < 100 mg /dL

very high risk factors (acute coronary syndromes) - < 70mg/dL

more risk factors = develop at earlier age

they damage the arteries

sugar makes everything sticky and speeds atherosclerosis

teach them they need to bake food and that they can't eat everything they want just because they have the med

find out who is doing the cooking and teach them

• 1. fatty streaks
• 2. fibrous atheromatous
• 3. complicated lesion

present in CH but not sure they lead to atherosclerotic lesions

clinical atherosclerosis

lesion is a gray or pearly white elevated thickening of the vessel

• 1. hemorrhage
• 2. ulceration
• 3. scar tissue deposits

thrombosis caused by slow turbulent blood flow in the region of the plaque and ulceration of the plaque

complicated lesion b/c it can rupture and cause inflammatory process to occur which can lead to 100% occlusion

anticoagulants, clot buster to disintergrate the clot and restore blood flow

• 1. smoking cessation
• 2. hypertension
• 3. hyperlipidemia
• 4. type II DM

• 1. age
• 2. gender
• 3. genetic factors
• 4. race

believed to increase risk for atherosclerosis by inhibiting anticoagulant cascade ass. and causing endothelial damage

CRP - C-reactive protein

atherosclerosis

damage to endothelial vessel layer

• 1. smoking
• 2. immune mechanisms
• 3. mechanical stress - hypertension
• 4. unstable plaques and complicated lesions

depends on vessel involved and how much narrowing there is

ischemia V/S infarction - perfusion decrease v/s tissue death

atherosclerosis of the coronary artery

peripheral artery disease -

atherosclerosis / narrowed arteries reduce blood flow to the legs

most common in 70-80 year old men

• 1. hypertension
• 2. DM II
• 3. hyperlipidemia
• 4. cigarettes
• 5. CHD / atherosclerosis in other areas

vasculitis of the med sized arteries of the hands and feet - become inflamed and swell - eventually block off the arteries and can cause ischemia of distal tissue

AKA Buerger disease

affects men b/t ages 25-40 who are heavy cig smokers

intermittent claudication - pain with walking

muscle is ischemic and requires more blood flow when being used - will do anaerobic respiration and cause lactic acid build up = pain in muscle

at rest the pain goes away

arterial: S/S of decreased blood flow/ischemia  thin/shiny skin, atrophy of leg muscle (chicken legs), cool extremity, popleteal and pedal pulses are weak or absent, hair loss on legs, elevation of leg causes color to blanch in leg, becomes deep red when leg is in dependent postion (dangling), brittle toenails,

dopplar the pulse and document it if found

not elevated

NO- they may have nerve damage due to decreased blood flow and may not be able to feel if it gets too hot

can cause burns that will be hard to heal b/c of decreased BF

• 1. walking (slowly) to the point of claudication usually is encouraged b/c it increases collateral circulation
• 2. avoidance of injury
• 3. no smoking
• 4. Tx hypertension
• 5. decrease lipids
• 6. DM treatment

will cause vasodilation and increase BF and decrease pain

stop smoking

functional disorder caused by intense vasospasm of arteries & arterioles in the fingers and less often in the toes

• 1. walk until it hurts and then rest and tell them why (increased collateral BF)
• 2. need to avoid injury r/t decrease healing
• 3. watch diet and weight if high cholesterol
• 4. keep BG under control if DM

smoking - inflames vessels and cuts of blood flow to extremities = ischemia and amputation

usually in fingers and toes then advances proximally and will have to keep getting amputations

healthy young women

• 1. smoking
• 2. cold
• 3. emotional stress

fingers

• 1. protect from cold
• 2. decrease stressors/ triggers
• 3. avoid injury r/t decreased BF
• 4. no smoking
• 5. Ca channel blockers
• 6. Run hands under warm water

Ca channel blockers b/c treat spastic arteries

viagra

decreases spasms of arteries - given for spastic arteries

Hx of vasospastic attacks

extremely low BP

if fingers are injured (paper cut) they will not heal well r/t decreased BF

when BF is restored it hurts

weakened area of an artery causes small spherical dilation (outpouching) of the vessel at a bifurcation

usually in aorta

abdominal aortic aneurysm

• 1. umbilical pulsation - DO NOT PRESS ON IT
• 2. Xray for other things - asymptomatic usually

man in their 70's b/c they have high blood pressure

causes increased pressure and increased ballooning out of the aneurysms and possible rupture

more in ppl over 50 and more in men

• 1. atherosclerosis
• 2. hypertension

elow the level of the renal artery and involve the bifurcation of the aorta and proximal end of the common iliac arteries

in the middle the blood is moving quickly and around the edges the blood is pooling

• after Tx procedures must watch for clots
• ---monitor I&O for renal clot
• ---monitor perfusion

• 1. < 5cm will just watch it
• 2. > 5cm will go to surgery
• 3. go to surgery if it is getting larger also
• 4. interventional radiography - put in a graft to stabilize the aneurysm (Dacron graph)

may have hypertension and atherosclerosis

will have bad outcome

1. come in q 6 mo for ultrasound

ultrasound, echo, CT, MRI

a life threatening condition where a longitudinal tear in the intimal layer of the vessel or separaion of the vessel wall occurs & involves hemorrhaging into the vessel wall and creating a blood-filled cavity -

• 1. pulsatile mass at umb
• 2. mid mild abd pain
• 3. lumbar discomfort due to enlargement pressing on a nerve - dissecting triple A will cause back pain
• 4. stasis of blood may cause thrombosis

must watch for clots

I&O if above renal artery - have a urometer in the foley bag

• 1. atherosclerosis
• 2. degeneration of vessel media

• 1. atherosclerosis
• 2. hypertension

men 40-60 yrs with Hx of hypertension or in younger ppl with conn. tissue diseases

• 1. excruciating pain that is tearing or ripping feeling
• 2. BP usually moderately elevated
• 3. in late stages BP will drop due to blood loss

• 1. TEE
• 2. history
• 3. phys exam
• 4. CT scans
• 5. MRI

transesophageal echo

numb throat and shine light down esophagus to view the chambers of the heart and watch pumping and valves

must be NPO before and after until gag reflex is good

mean arterial pressure - avg pressure in the arterial system during ventricular contraction and relaxation and is a good indicator of tissue perfusion

90-100 mmHg

• BP control
• monitor for S/S of hypvolemic shock

CO & peripheral vascular resistance

BP = CO X PVR

radius of the arterioles

stimulation sent to cardiovascular center in the lower pons and medulla where info is integrated -> autonomic NS stimulation to maintain homeostasis

PNS - impulses to heart through vagus nerve

pressure sensitive receptors located in the walls of blood vessels and the heart

• 1. ANS stimulation
• 2. barorecptors
• 3. arterial chemoreceptors
• 4. RAAS
• 5. vasopressin/ ADH

sense drop in O2 and cause widespred vasoconstriction -> increases BP

ant pit - vasoconstrictor

kidneys regulate with higher level of Na and water elimination

genetic hypertension that doesn't need Dx test to diagnose it - can Dx with family Hx and phys exam

may do Dx test if adopted and don't know family Hx

primary hypertension

primary/essential - cause unknown - genetic

AA and more severe HTN

not responsive to BP meds

• 1 family Hx of HTN
• 2. race - AA
• 3. age
• 4. T2DM
• 5. hyperlipidemia
• 6. obesity
• 7. metabolic syndrome

early DX and intervention

• 1. gigh Na intake
• 2. excessive calorie intake
• 3. obesity
• 4. phys inactivity
• 5. excessive alcohol consumption
• 6. sleep apnea

high BP, obesity, high BG, & hyperlipidemia

• 1. may be asymptomatic
• 2. symptoms that may be present are r/t long-term effects of HTN on the organ systems of the body

sleep apnea

kidneys, heart, eyes, and blood vessels

creatinine

increases workload on the left ventricle and causes renal insufficiency

need at least 2 or more BP readings to Dx

• 1. weight reduction
• 2. regular phys activity
• 3. reduce dietary NA intake
• 4. moderation of alcohol intake

use a stepwise approach

usually will send for a heart cath

if have renal insufficiency cannot give the dye for heart cath b/c damages kidney

renal insufficiency

make sure to check creatinine on labs and notify MD if it is abnormal - this is a nursing responsibility

HTN caused by another disease process

• 1. renal hypertension
• 2. disorders of adrenocorticosteroid hormones
• 3. phenochromocytoma

yes, but they need meds to protect their kidneys - mucomyst - tastes horrible

secondary HTN accelerated and potentially fatal form

may have white coat syndrome

• 1. young AA men
• 2. women with HTN of pregnancy
• 3. ppl with renal and collagen diseases

• 1. first choice diuretics - hctz
• 2. add another drug
• 3. add another drug of diff category (helps better than just increasing mg)
• 4. will pick diff drugs for diff race b/c act diff
• ----Ca channel blockers work better for AA

• 1. sudden marked elevations in blood pressure
• 2. diastolic values >120mmHg
• 3. HA
• 4. restlessness
• 5.confusion
• 6. stupor
• 7. motor and sensory deficits
• 8. visual disturbances
• 9. convulsions
• 10. coma

check the BP!!!

hypertensive encephalopathy & BP

give meds to lower BP - give them slowly to avoid sudden drop in BP

will bottom out BP & can cause strokes

abnormal drop in BP upon sitting up or standing that also causes increase in heart rate

• 1. tachycardia
• 2. dizziness
• 3. syncope - fainting

any anti-HTN drug can cause it

elderly

• 1. reduced blood volume
• 2. drug-induced HTN
• 3. aging
• 4. bed rest and immobility
• 5. disorders of ANS function
• 6. dehydration or too much dialysis

do orthostatic BP readings

if testing for dehydration or too much dialysis

dilated or tortuous veins of the lower extremities which can lead to venous insufficiency

• 1. impaired flow in deep venous channels
• 2. DVT
• 3. pressure on abd veins caused by obesity
• 4. tumor
• 5. pregnancy
• 6. standing position
• 7. heavy lifting
• 8. incompetent valves

• 1. visualization
• 2. doppler ultrasound flow
• 3. angiograph

• 1. over 50 years old
• 2. family Hx exp in women
• 3. nurses - standing a lot

• 1. unsightly appearnace
• 2. aching in the lower extremities
• 3. edema

compression stockings

• 1. elastic support stockings
• 2. sclerotherapy
• 3. surgical treatment

valve leaflets damaged rendering them incapable of closure - emptying of deep veins cannot occur

• 1. tissue congestion
• 2. edema
• 3. brown pigmentatin of skin
• 4. stasis dermatitis
• 5. stasis or venous ulcers

over the ankle and lower leg due to chronic venous HTN

S/S that occur in chronic venous insufficiency

• 1. stasis of blood - immobility
• 2. vessel wall injury - trauma and surgery
• 3. increased blood coagulabiluty - use of oral contraceptives

• 1. 50% are assymptomatic
• 2. fever
• 3. malaise
• 4 elevated WBC
• 5. elevated sedementation rate
• 6. positive Homan's sign

• 1. early abulation
• 2. support stockings
• 3. sequential pneumatic compression device
• 4. prophylactic anticoagulation
• 5. ankle flexion & extension **

• 1. venography
• 2. ultrasonography
• 3. D-dimer

• 1. edema severe
• 2. will have pulses
• 3.

accumulation of fluid in the pericardial cavity due to injury,

blood flow

why they need to do this and other things so they will comly

means pt is at risk for blood clots but not that they have them

shouldn't get up

no TEDs and Kendalls on swollen leg

other leg - yes

life-threatening,slowing of the heart due to rapid compression of the heart due to the accumulation of lfuid, pus, or blood in the pericardial sac r/t trauma, cardiac surgery, cancer, or uremia

decreased CO and bradycardia

key to Dx ***pulsus paradoxus - drop in BP when pt takes a breath

fluid will keep heart from filling during diastole

cardiac tamponade

pull fluid off pleural effusion

decreased CO

So much fluid in thoracic cavity, when take a breath there is too much pressure in there and BP drops

inflammation of the pericardial sac due to viral infections, after cardiac surgery, connective tissue disorders

echocardiogram  ECG

acute pericarditis

more in men than women

usually take ASA & naproxen/aleve and send home

depends on causative agent

• 1. chest pain
• 2. pericardial friction rub
• 3. EKG changes
• 4. pain relieved by sitting up and leaning forward and slow shallow breaths

• 1. clinical manifestations
• 2. chest X-ray
• 3. ECG
• 4. echo

left anterior descending that feeds blood to left ventricle and the circumflex branches

feeds blood to back of heart, SA and AV nodes

atherosclerosis - obesity, smoking, DM, hypertension, high cholesterol

right coronary artery

12 lead ECG- to show if there are probs and where they may be located:  can show if RCA or left coronary artery is blocked, etc

firing of SA node can be interrupted b/c ischemia to this area can kill SA node and they will have to have a pacemaker

left anterior descending coronary artery

first usually several cm of LAD & L circumflex or the entire length of RCA

plaques that contain a lot of collagen and fibrous conn tissue that makes it less likely to rubture - obstructs blood flow

angina that is precipitated by increase work demands of the heart and can be aleviated with rest

will occur with phys exertion, exposure to cold, and emot distress

• 1. occurs at rest and lasts more than 20 minutes
• 2. it is severe and described as frank pain of new onset
• 3. it occurs with a pattern that is more severe, prolonged, and frequent

ischemic death of myocardial tissue

• C/O:
• 1. severe pain
• 2. crushing pain - sitting on chest
• 3. may radiate to L arm, neck, and jaw
• 4. NV
• 5. not relieved by rest or sublingual nitroglycerin

spasms of the coronary arteries that occur during rest

variant or vasospastic angina

Ca channel blockers

Ca channel blockers

can rupture and cause platelet adhesions & thrombus formation

platelet adhesions- fatty plaque covered in fibrin

• inflammatory response -> block artery completely
• clot busters

within 6 h

if normal pain changes in any way need see/call MD - can mean blockage is worse

women & DM - NV, back pain, jaw/tooth pain

DM pt - have neuropathy

1. EKG changes - T-wave inversion, ST segment depression or elevation & dev of Q-wave

2. serum markers:  myoglobin, creatine kinase MB (CK-MB), troponin I & triponin T

non Q-wave MI

MONA - morphine, oxygen, nitro, aspirin (chewed)

also - analgesic agents, B-adrenergic blockers(block EPI & NE), nitrates

thrombolytics and revascularization need to be initiated within 60-90 min of onset of symptoms

Q-wave MI

rule out MI

12 lead ECG to see if any ST elevation & ROMI panel

STEMI

NSTEMI

if have elevated ST will also have increased triponin = STEMI

If don't have elevated ST but have increased triponin = NSTEMI

enzyme released from heart muscle when it is damaged

the the higher triponin = more damage to heart muscle

STEMI

QRS complex elevated so much it looks like a tomb stone with ST elevation

• 1. sudden death
• 2. heart failure
• 3. cardiogenic shock
• 4. pericarditis
• 5. thromboemboli
• 6. rupture of the heart
• 7. ventricular aneurysms
• 8. may see increased temp due to necrotic tissue
• 9. arhythmias

pt may spike fever r/t inflammatory response to necrotic tissue - still need to contact MD

decreased circulation of blood due to heart failure

myoglobin & CK-MB will be released with ANY muscle damage

triponin is heart muscle specific

deterioration of the heart muscle

progressive cardiac hypertrophy and dilatin and impaired pumping ability of 1 or both ventricles due to alcohol abuse, drug abuse, or genetic - have a gigantic heart

• 1. heart failure/CHF S/S:
• 2. EF 40% or less- ejection fraction (decreased L ventricle function)
• 3. dyspnea on exertion
• 4. paroxysmal nocturnal dyspnea - suddenly feel like can't breathe in middle of night
• 5. orthopnea (orthopnea X5 = need 5 pillow to prop up)
• 6. fatigue
• 7. ascites
• 8. peripheral edema
• 9. S3 or S4
• 10. ventricular arrhythmias
• 11. thrombus

echo, chest Xray, TEE (transesophageal), cardiac cath

• 1. digitalis to increase contractility
• 2. decrease workload of heart - decrease preload and afterload -> increases CO

enlarged heart

uncommon, life-threatening infection of the endocardial surface of the heart and valves - may see vegetations on the valves

how well left ventricle is working

normal is in 50's

lower than 20 = heart transplant

will show on echo/ECG

1. a damaged endocardial surface & portal of entry by which the organism gains access to the circulatory system

2. presence of valvular disease, prosthetic heart valves, or congenital heart defects provides an env conductive to bacterial growth

cardiac cath report

the EF of the pt

• 1. ACE inhibitors
• 2. diuretics
• 3. dangling legs

infective endocarditis when have teeth cleaned b/c blood from teeth will take bacteria to the heart

may give prophylactic ABX before and after dental cleaning to prevent it

pt with valvular probs:  valve replacement, congenital valve probs

surgery, urology procedures

TEE

• 1. fever & S/S of infection
• 2. petechial hemorrhages causes by vegetations breaking off

take ABX before and after dental cleaning

blood cultrues, echo, TEE

antibiotic therapy

blood cultures should be drawn first - make sure that this gets done - may start ABX before returned but must be drawn to get accurate data

acute, immune-mediated, multisystem inflammatory disease following a group A B-hemolytic strep throat infection - causes valvular probs

about 1-4 weeks after strep infection

ABX can prevent the strep from damaging the valves of the heart

group A - Bhemolytic strep

• 1. ask if they have had sore throat
• 2. draw labs- anti-streptolysin O titer

antistreptolysin O titer is positive

• 1. echo
• 2. sed rate
• 3. C-reactive protein
• 4. TEE
• 5. antibiotics
• 6. positive strep titer)

children 5-15

mitral and aortic valves

anti-inflammtory drugs

infective endocarditis b/c they may have sustained valvular damage

probably not- usually already gone

narrowing of the valve orifice and failure of the valve leaflets to open normally

valve is closed when it should be open

2 causes:  may be born with stiff valve or can be RHD

narrowing of the mitral valve that causes left atrium enlargement

can be caused by RHD

as they age may have more valve probs and need valve replacement

if mitral stenosis occurs can cause left atrium to have extra work getting blood through

narrowing of the aortic valve that causes it to be closed during systole when it should be open

RHD or Ca depositis that occur as age (elderly)

person who had RHD and the elderly

enlarged L ventricle due to increased work to get blood through aortic valve

will eventually cause L-sided heart failure -> may have to have surgery to prevent this

permits backward flow to occur when the valve should be closed

open when should be closed

increased workload for the heart r/t having to repump regurgitated blood

RHD or congenital

mitral valve prolapse - form of rugurgitating valve

usually occurs in young women

RHD

enlarged L atrium b/c  blood comes back into atrium during systole and has to be pumped back into ventricle

RHD

L ventricular failure b/c blood goes into aortic valve and blood goes back into the L ventricle to be repumped

women and genetic / in families

• 1. tachycardia
• 2. palpitations especially under stress

ask about diet: 

any caffeine/energy drinks

Ask about stress also:  if under a lot of stress may need a B-blocker until stress is alleviated

caffeine, alcohol, and cigarettes

cardiac output - amnt of blood the heart pumps each minute - normally 8L/min

reflects the loading condition of the heart a the end of diastole

shows venous return to the heart

represents the force that the contracting heart must generate to eject blood from the filling heart - systemic vascular resitance

mechanical performance of the heart

will increase work of heart even more if preload is higher

will increase preload and afterload

give ACE inhibitors

may dangle legs before meds are started

laying flat - they will feel like they are drowning

digoxin

will decrease heart rate

• 1. Frank-Starling mechanism - heart muscle stretches -> remodeling -> heart failure b/c stretching causes permenant damage and muscle won't go back (loses elasticity)
• 2. sympathetic nervous system
• 3. RAAS
• 4. natriuretic peptides

• 1. acute MI
• 2. hypertension
• 3. cardiomyopathy
• 4. renal failure

right and left sided

• 1. AMI - acute MI
• 2. valvular defects - mitral or aortic stenosis/regurg
• 3. hypertension - resistance in the vessels increases workload on heart -> heart failure

acute MI

• 1. S/S
• 2. history and physical
• 3. lab- BNP - brain natriuretic peptid - shows ventricular failure
• 4. EKG
• 5. chest x-ray
• 6. echo

• 1. decreased CO
• 2. pulmonary congestion:  crackles (air moving through water), will see on Xray
• 3. orthopnea
• 4. frothy pink sputum
• 5. paroxysmal nocturnal dyspnea
• 6. fatigue
• 7 dyspnea on exertion

• 1. L sided failure
• 2. pulmonary disease -COPD (not pulm congestion like left sided failure)
• 3. Cor pulmonale - increased R ventricle side due to chronic pulmonary hypertension

enlargement & failure of R ventricle due to pulmonary hypertension

COPD - blue bloater

will show pulmonary congestion

ventricular function - if it starts to go down means they are improving

L sided heart failure

BNP

BNP will go down

because L causes fluid to back up to lungs then backs up to R ventricle -> increases work of R ventricle - R sided failure

R sided

• blood backs up everywhere in body and fluid escapes everywhere
• 1. peripheral edema (3+, 4+, extreme)
• 2. GI congestion - blood backs up in GI tract
• 3. liver congestion & hepatomegaly
• 4. ascites
• 5. splenomegaly
• 6. JV distention

R sided heart failure

relieving symptoms and improving the quality of life with long-term goal of slowing, halting, or reversing cardiac dysfunction

• 1. decrease preload
• 2. decrease afterload
• 3. increase contractility
• 4. possible fluid restriction
• 5. salt restriction
• 6. weigh daily
• 7. drugs - diuretics, digoxin, ACE inhibitors, beta blockers

accumulation of fluid in lungs

• 1. SOB
• 2. cyanosis
• 3. tachycardia
• 4. cool
• 5. frothy, pink sputum
• 6. crackles
• 7. pt will want to sit up, restless, anxious

• 1. digoxin
• 2. diuretics
• 3. vasodilators
• 4. O2
• 5. may need face mask or mechanical ventilation

• 1. nonprogressive stage in which the normal compensatory mechanisms prevent large changes in circulatory function
• 2. progressive state, in which the shock becomes progressively worse
• 3. irreversible stage in which the shock has progressed to such an extent that all forms of therapy  are insufficient to save the person's life

failure of heart to pump

Congestive heart failure

MI

BP drops

no fluid- heart not pumping so won't do any good

• 1. decrease workload of heart
• 2. O2
• 3. vasodilators ?
• 4. vasoconstrictors
• 5. aortic balloon pump

do not give fluids to raise BP

diminished blood volume

• 1. hemorrhage
• 2. severe burns
• 3. vomiting or diarrhea

• 1. thirst
• 2. tachycardia
• 3. cool and clammy skin
• 5. decreased UO
• 6. restlessness
• 7. can lead to apathy
• 8. stupor and coma

1. vasoconstrictors - dopamine, levafed

necrotic tissue in extremites r/t decreased blood flow

• 1. treat cause
• 2. O2
• 3. fluids
• 4. blood
• 5. vasoconstrictors

give them O-

fluid shifts out of vessels:  char. by loss of blood vessel tone, enlargement of the vascular compartment, and displacement of the vascular volume away from the heart and circulation

• 1. neurogenic shock
• 2. anaphylactic shock
• 3. septic shock

• 1. acute resp distress syndrome
• 2. acute renal failure
• 3. GI complications
• 4. DIC
• 5. multiple organ dysfunction syndrome -MODS

distributive and hypovolemic

cardiogenic shock