🏩- Cardiac Test Flashcards
Preload
Is the amount of blood in the ventricles at the end of diastole
“Stretching of the 💕 muscle”
Frank starlings law
The more blood that fills the ventricle, the more blood will be pumped
^ volume = ^ stretch = ^ contraction
Afterload
Resistance to flow the ventricle must overcome to open the semilunar valves and eject its contents
Myocardial contractility
The force of the mechanical contraction
Renin Angiotensin Aldosterone System
The release of Aldosterone promotes Na and water re absorption in the kidneys, which increases circulating fluid volume
Aldosterone
Is made by the adrenal gland when K+ are increased
Aldosterone causes Na+ to be reabsorbed by the DCT and collecting duct and K+ to be secreted by the DCT and collecting duct.
^aldosterone = ^BP
ADH
Antidiuretic hormone
“Makes you urinate less”
ADH increases water reabsorption in the DCT by stimulating cells to insert aquaporins into the apical epithelial cell memebrane
Brain natriuretic peptide
Released from heart tissue when fluid volumes are high
BNP is made in the heart and shows how well the heart is working
Too much= bad
What are the 2 left coronary artery branches
Left anterior descending branch
Circumflex branch
Right coronary artery
Branches to right marginal branch and posterior interventricular branch
Left anterior descending branch supplies ?
Supplies both ventricles , anterior interventricular septum , anterior wall of the heart
Circumflex branch supplies ?
Left atrium and the posterior wall of the left ventricle
Right marginal branch supplies ?
Lateral aspect of right atrium and ventricle
Posterior interventricular branch supplies ?
Posterior aspect of both ventricles and interventricular septum
Anasarca
Generalized edema - due to prolonged congestion of the liver
Rubor
Dusky pink appearance on the extremity indicates arterial insufficiency
S1
- Closure of mitral and tricuspid valves
- Softer and longer
- lower left sternal border
S2
- closing of aortic and pulmonic valves
- shorter than s1
- higher pitched
- base of heart
Gallops
Late diastolic sound
Baroreceptors
Located in the carotid sinus, aorta
“Pressure receptor” /stretch
^Bp= stretching receptors= decrease heart rate
Prehypertension range
Systolic : 120-139
Diastolic : 80-89
Stage I HTN range
Systolic : 140-159
Diastolic : 90-99
Stage II HTN range
Systolic : greater than 140
Diastolic : greater than 100
Patients with diabetes should have a BP less than what
130/90
Hypotension
BP less than 90/60
Maybe inadequate for providing sufficient nutrition to the body’s cells
Normal range for MAP
70-100 mmHg
Ape to Man ❤️ sounds
Aortic: R 2nd intercostal
Pulmonic: L 2nd intercostal
Erbs point: L 3rd intercostal
Tricuspid: lower L eternal border; 4th intercostal
Mitral: L 5th intercostal; midclavicular line
S3 heart sound associated with
❤️ failure or too much fluid
Primary (essential) hypertension
Most common
Results in damage to vital organs
Has no identifiable medical cause; multifactorial polygenic condition
Causes medial hyperplasia (thickening) or arterioles
Common risk factors for the development of essential hypertension
Obesity
Smoking
Stress
Family history
Secondary hypertension
Is characterized by elevations in blood pressure due to a specific cause
Common causes of secondary hypertension
Renal disease Primary aldosteronism Pheochromocytoma Cushing's syndrome Medications
Pheochromocytoma
Hormone-secreting tumor that can occur in the adrenal glands
{common cause of secondary hypertension}
Malignant hypertension
> 200/150
Rapidly increases, morning headaches, blurred vision, dyspnea, uremia
Untreated leads to renal failure, left ventricular failure, stroke
What is the best indicator of fluid balance
Weight
2.2 lb= 1 kg= 1L of fluid
What are the 5 regulators of blood pressure
RAAS Baroreceptors ADH ANP BNP
Salt substitutes are high in what ?
Potassium
Metoprolol
Cardioselective beta blocker
Interferes with RAAS to lower BP; lower HR through sympathetic response
*Monitor closely for:
Bradycardia, hypotension, orthostatic hypotension, heart block, cough, rebound hypertension
CAN CAUSE HYPOGLYCEMIA
Examples of beta blockers
Nonselective or cardioselective
Propranolol , carvedilol , carteolol or atenolol , bisoprolol , metoprolol
Examples of alpha 2 agonist
Centrally acting
Clonidine, methyldopa, guanfacine
Examples of alpha 1 blockers
Doxazosin , prazosin , terazosin
Prazosin
Alpha 1 blocker
Promotes vasodilation through sympathetic response
Lower vldl and ldl ; raises hdl
OFTEN PRESCRIBED TO TREAT BENIGN PROSTATIC HYPERTROPHY (bph)
*Monitor for:
Hypotension , orthostatic hypotension, rebound hypertension , reflex tachycardia , fluid retention
Clonidine
Side effects include sedation, dry mouth and nasal mucosa, bradycardia (due to increased vagal stimulation of the SA node as well as sympathetic withdrawal) orthostatic hypotension and impotence
Constipation, nausea and gastric upset are also associated
Fluid retention and edema
What are the 5 types of diuretics
- Osmotic (mannitol to decrease ICP)
- Carbonic anhydrase inhibitors (diamox)
- Loop diuretics (furosemide)
- Thiazides (hydrochlorothiazide)
- Potassium- sparing (spironolactone)
Furosemide
Loop diuretic
Very potent- water, Na, K, Ca, Mg
Highly protein bound
*monitor closely for:
Hypokalemia, electrolyte imbalance, hypotension, digitalis toxicity, HYPERglycemia, renal function, dehydration, intake and output and falls
*education:
Importance of K supplement, fluid restriction, daily weight, monitor BS levels
Hydrochlorothiazide
Thiazide diuretic
Ca is retained
DECREASE K INCREASE CA
Don’t give in those with renal dysfunction
*monitor closely for:
Hypotension, hypercalcemia, hypokalemia, electrolyte imbalance, digitalis toxicity, lithium toxicity, HYPERGYLCEMIa, renal function
-check BUN and creatinine levels before use
Spironolactone
Potassium sparing diuretic
Potassium is retained
Least effective at removing excess fluid
SHOULD NOT be given with acei’s or arbs
*monitor closely for:
Hyperkalemia , electrolyte imbalance, renal function, hypotension
Lisinopril
Ace inhibitors
Interferes with RAAS to lower BP
DO NOT take with K+ sparing diuretic
CRITICAL TO LOOK FOR ANGIOEDEMA
What are some side effects of ace inhibitors
Cough Potassium EXCESS Taste changes Orthostatic hypotension Lower gfr (kidney function)
Losartan
Angiotensin II receptor blocker (arb)
More costly than acei’s , used as second choice
*Monitor for:
Hypotension , rebound hypertension , reflex tachycardia , hyperkalemia
Normal range of troponin
Less than 0.03 ng/ml (undetectable)
Normal range of CK-MB
O-3% ng/ml
Normal range of total cholesterol
Less than 200 mg/dl
Normal range of tryglycerides
Less than 150 mg/dl
Normal range of HDL
Greater than 50 mg/dl
Normal range of LDL
Less than 100 mg/dl
*less than 70 for those with heart disease
Less than 130 for individuals who are at low risk for coronary artery disease
What levels are checked to confirm ❤️ attack
Troponin and CK-MB
HDL
Good cholesterol
Legend can be increased with exercise (higher the better)
Removes cholesterol from blood and takes it to the liver
LDL
Bad cholesterol
Picks up cholesterol from the blood and takes it to the cells
Triglycerides
Levels are increased from eating simple sugars or drinking alcohol. Associated with heart and blood vessel disease
**wait 2 months after ❤️ attack, surgery, infection, injury or pregnancy to check levels
Electrocardiograph
ECG
assess the electrical conduction system of the heart
Graphic recording of electrical activity in heart
12 leads- 12 angles
Can identify dysrhythmias, new or old heart muscle damage, electrolyte abnormalities and/or cardiac hypertrophy
Echocardiogram
Used ultrasound to provide information on the size and pumping function of the heart, blood volume status and valve function and integrity
Provides pictures of the hearts valves and chambers
Trans esophageal echocardiogram
TEE
Places ultrasound transducer in the throat to provide information posterior from the ❤️
Nuclear stress test
If patient can’t walk on treadmill isotopes are injected to visualize areas of poor perfusion in the heart
Ejection fraction
A measurement of the amount of blood pumped out of the left ventricle with each heartbeat
70-90 ml ejected per ventricle per stroke
50ml of blood remains in each ventricle at the end of systole
Normal range of ejection fraction
55-70 percent
Hemodynamic monitoring
Invasive system provides quantitative information about vascular capacity, blood volume, pump effectiveness, tissue perfusion
Aka swangans carheter
Supraventricular arrhythmias
Arrhythmias that begin in the atria
“Supra” means above
Name 9 causes of arrhythmias
- Coronary artery disease
- High BP
- Changes in the heart muscle (cardiomyopathy)
- valve disorders
- electrolyte imbalances in the blood, Na or K
- Injury from a ❤️ attack
- the healing process after heart surgery
- caffeine, smoking, stress
P wave
Atrial depolarization and contraction
QRS wave
Ventricle contraction / depolarization
T wave
Ventricle repolarization and filling
How long is each small box on an ekg
0.04 seconds
How long is each large box on an ekg
0.2 seconds
5 big blocks is how long ? 30 big blocks is how long ? On an ekg
5- 1 second
30- 6 seconds
How long is a normal PR interval
0.12-0.2 seconds
3-5 small boxes
How long is a normal QRS complex
0.04-0.1 seconds
1-2 1/2 small boxes
What does the PR interval measure
The measure of time it takes an electrical impulse to depolarize the atria and travel to the ventricles
Time from SA mode to bundle
What are the SIX steps to read an ekg
1 determine the ❤️ rate (count # of spikes in 6 sec block and X by 10)
2 determine the heart rhythm (regular or irregular)
3 analyze the P waves (present or uniform)
4 measure the PR interval (length)
5 measure the QRS duration (length)
6 interpret the rhythm (what is it)
Atrial fibrillation
Many impulses begin and spread through the atria
Results in disorganized , rapid and irregular rhythms
NO P WAVES ON EKG
Irregularly irregular
Premature ventricular contraction
Are wide and atypical (or bizarre looking) QRS complexes that fire earlier than expected from within the ventricles
Ventricular tachycardia
Defined as 3 or more PVC’s in a row.
First thing to do is check for a pulse
What to do if in VT WITH a pulse
Medication .. give lidocaine
Pulseless VT
Describes a patient who is in cardiac arrest
Do cpr and SHOCK them
Ventricular fibrillation
Life threatening dysrhythmia that needs to be treated immediately
Occurs when ventricle has multiple chaotic impulses rapidly firing
NO P or ORS WAVES PRESENT - rhythm on ekg is shaky or quivering
Use: chest compressions, SHOCK, medication
Ventricular asystole
No measurable electrical activity originating from the heart
FLAT LINE
DONT SHOCK
Ventricular asystole
No measurable electrical activity originating from the heart
FLAT LINE
DONT SHOCK
Ventricular fibrillation
Life threatening dysrhythmia that needs to be treated immediately
Occurs when ventricle has multiple chaotic impulses rapidly firing
NO P or ORS WAVES PRESENT - rhythm on ekg is shaky or quivering
Use: chest compressions, SHOCK, medication
Pulseless VT
Describes a patient who is in cardiac arrest
Do cpr and SHOCK them
What to do if in VT WITH a pulse
Medication .. give lidocaine
Ventricular tachycardia
Defined as 3 or more PVC’s in a row.
First thing to do is check for a pulse
Premature ventricular contraction
Are wide and atypical (or bizarre looking) QRS complexes that fire earlier than expected from within the ventricles
Atrial fibrillation
Many impulses begin and spread through the atria
Results in disorganized , rapid and irregular rhythms
NO P WAVES ON EKG
Irregularly irregular
What are the SIX steps to read an ekg
1 determine the ❤️ rate (count # of spikes in 6 sec block and X by 10)
2 determine the heart rhythm (regular or irregular)
3 analyze the P waves (present or uniform)
4 measure the PR interval (length)
5 measure the QRS duration (length)
6 interpret the rhythm (what is it)
What does the PR interval measure
The measure of time it takes an electrical impulse to depolarize the atria and travel to the ventricles
Time from SA mode to bundle
How long is a normal QRS complex
0.04-0.1 seconds
1-2 1/2 small boxes
How long is a normal PR interval
0.12-0.2 seconds
3-5 small boxes
5 big blocks is how long ? 30 big blocks is how long ? On an ekg
5- 1 second
30- 6 seconds
How long is each large box on an ekg
0.2 seconds
How long is each small box on an ekg
0.04 seconds
T wave
Ventricle repolarization and filling
QRS wave
Ventricle contraction / depolarization
P wave
Atrial depolarization and contraction
Name 9 causes of arrhythmias
- Coronary artery disease
- High BP
- Changes in the heart muscle (cardiomyopathy)
- valve disorders
- electrolyte imbalances in the blood, Na or K
- Injury from a ❤️ attack
- the healing process after heart surgery
- caffeine, smoking, stress
Supraventricular arrhythmias
Arrhythmias that begin in the atria
“Supra” means above
Hemodynamic monitoring
Invasive system provides quantitative information about vascular capacity, blood volume, pump effectiveness, tissue perfusion
Aka swangans carheter
Normal range of ejection fraction
55-70 percent
Ejection fraction
A measurement of the amount of blood pumped out of the left ventricle with each heartbeat
70-90 ml ejected per ventricle per stroke
50ml of blood remains in each ventricle at the end of systole
Nuclear stress test
If patient can’t walk on treadmill isotopes are injected to visualize areas of poor perfusion in the heart
Trans esophageal echocardiogram
TEE
Places ultrasound transducer in the throat to provide information posterior from the ❤️
Echocardiogram
Used ultrasound to provide information on the size and pumping function of the heart, blood volume status and valve function and integrity
Provides pictures of the hearts valves and chambers
Electrocardiograph
ECG
assess the electrical conduction system of the heart
Graphic recording of electrical activity in heart
12 leads- 12 angles
Can identify dysrhythmias, new or old heart muscle damage, electrolyte abnormalities and/or cardiac hypertrophy
Triglycerides
Levels are increased from eating simple sugars or drinking alcohol. Associated with heart and blood vessel disease
**wait 2 months after ❤️ attack, surgery, infection, injury or pregnancy to check levels
LDL
Bad cholesterol
Picks up cholesterol from the blood and takes it to the cells
HDL
Good cholesterol
Legend can be increased with exercise (higher the better)
Removes cholesterol from blood and takes it to the liver - where it is used to make bile and then excreted in feces
What levels are checked to confirm ❤️ attack
Troponin and CK-MB
Normal range of LDL
Less than 100 mg/dl
*less than 70 for those with heart disease
Less than 130 for individuals who are at low risk for coronary artery disease
Normal range of HDL
Greater than 50 mg/dl
Normal range of tryglycerides
Less than 150 mg/dl
Normal range of total cholesterol
Less than 200 mg/dl
Normal range of CK-MB
O-3% ng/ml
Normal range of troponin
Less than 0.03 ng/ml (undetectable)
Losartan
Angiotensin II receptor blocker (arb)
More costly than acei’s , used as second choice
*Monitor for:
Hypotension , rebound hypertension , reflex tachycardia , hyperkalemia
What are some side effects of ace inhibitors
Cough Potassium EXCESS Taste changes Orthostatic hypotension Lower gfr (kidney function)
Lisinopril
Ace inhibitors
Interferes with RAAS to lower BP
DO NOT take with K+ sparing diuretic
CRITICAL TO LOOK FOR ANGIOEDEMA
Spironolactone
Potassium sparing diuretic
Potassium is retained
Least effective at removing excess fluid
SHOULD NOT be given with acei’s or arbs
*monitor closely for:
Hyperkalemia , electrolyte imbalance, renal function, hypotension
Hydrochlorothiazide
Thiazide diuretic
Ca is retained
DECREASE K INCREASE CA
Don’t give in those with renal dysfunction
*monitor closely for:
Hypotension, hypercalcemia, hypokalemia, electrolyte imbalance, digitalis toxicity, lithium toxicity, HYPERGYLCEMIa, renal function
-check BUN and creatinine levels before use
Furosemide
Loop diuretic
Very potent- water, Na, K, Ca, Mg
Highly protein bound
*monitor closely for:
Hypokalemia, electrolyte imbalance, hypotension, digitalis toxicity, HYPERglycemia, renal function, dehydration, intake and output and falls
*education:
Importance of K supplement, fluid restriction, daily weight, monitor BS levels
What are the 5 types of diuretics
- Osmotic (mannitol to decrease ICP)
- Carbonic anhydrase inhibitors (diamox)
- Loop diuretics (furosemide)
- Thiazides (hydrochlorothiazide)
- Potassium- sparing (spironolactone)
Clonidine
Side effects include sedation, dry mouth and nasal mucosa, bradycardia (due to increased vagal stimulation of the SA node as well as sympathetic withdrawal) orthostatic hypotension and impotence
Constipation, nausea and gastric upset are also associated
Fluid retention and edema
Prazosin
Alpha 1 blocker
Promotes vasodilation through sympathetic response
Lower vldl and ldl ; raises hdl
OFTEN PRESCRIBED TO TREAT BENIGN PROSTATIC HYPERTROPHY (bph)
*Monitor for:
Hypotension , orthostatic hypotension, rebound hypertension , reflex tachycardia , fluid retention
Examples of alpha 1 blockers
Doxazosin , prazosin , terazosin
Examples of alpha 2 agonist
Centrally acting
Clonidine, methyldopa, guanfacine
Examples of beta blockers
Nonselective or cardioselective
Propranolol , carvedilol , carteolol or atenolol , bisoprolol , metoprolol
Metoprolol
Cardioselective beta blocker
Interferes with RAAS to lower BP; lower HR through sympathetic response
*Monitor closely for:
Bradycardia, hypotension, orthostatic hypotension, heart block, cough, rebound hypertension
CAN CAUSE HYPOGLYCEMIA
Salt substitutes are high in what ?
Potassium
What are the 5 regulators of blood pressure
RAAS Baroreceptors ADH ANP BNP
What is the best indicator of fluid balance
Weight
2.2 lb= 1 kg= 1L of fluid
Malignant hypertension
> 200/150
Rapidly increases, morning headaches, blurred vision, dyspnea, uremia
Untreated leads to renal failure, left ventricular failure, stroke
Pheochromocytoma
Hormone-secreting tumor that can occur in the adrenal glands
{common cause of secondary hypertension}
Common causes of secondary hypertension
Renal disease Primary aldosteronism Pheochromocytoma Cushing's syndrome Medications
Secondary hypertension
Is characterized by elevations in blood pressure due to a specific cause
Common risk factors for the development of essential hypertension
Obesity
Smoking
Stress
Family history
Primary (essential) hypertension
Most common
Results in damage to vital organs
Has no identifiable medical cause; multifactorial polygenic condition
Causes medial hyperplasia (thickening) or arterioles
S3 heart sound associated with
❤️ failure or too much fluid
Ape to Man ❤️ sounds
Aortic: R 2nd intercostal
Pulmonic: L 2nd intercostal
Erbs point: L 3rd intercostal
Tricuspid: lower L eternal border; 4th intercostal
Mitral: L 5th intercostal; midclavicular line
Causes of ventricular asystole
Common primary cause in the presence of CAD , AMI
Electrolyte disturbances, drug effect, acidosis, hypoxia
How to treat ventricular asystole
DONT SHOCK
transcutaneous (external) pacing - initiate early
Epinephrine - increases diastolic BP and blood flow to the brain
Atropine - suppresses excessive vagal (parasympathetic) tone
Coronary artery disease
Arteries that are clogged and hardened by cholesterol and fatty buildup restrict blood flow to the heart muscle
What are the symptoms of a heart attack in women
- pain or discomfort in the chest, left arm or back
- unusually rapid heartbeat
- shortness of breath
- nausea or fatigue
Cardiovascular disease and menopause
Early menopause (before age 50) or surgical menopause , the risk of cardiovascular disease is also higher , especially when combined with other risk factors
After menopause, cardiovascular disease becomes more of a risk for women because of the reduced level of estrogen in the body
Reduced levels of estrogen related to cardiovascular disease can cause what
- changes in the walls of blood vessels that may cause plaque and blood clots to form
- increase in LDL decrease in HDL
Arteriosclerosis
Thickening or hardening of arterial wall often associated with aging
Atherosclerosis
Type of arteriosclerosis involving formation of plaque within arterial wall
How are lipids transported through the blood
Packaged as lipoproteins
Normal range of platelets
150,000 - 400,000
Normal range of fibrinogen levels
200-400
Normal prothrombin time
12-13 seconds
Normal partial thromboplastin time PTT
25-35 seconds
Normal international normalized ratio INR
0.8 - 1.2
Normal range of BNP
Less than 100
Nursing interventions for cholesterol
- evaluate total serum cholesterol levels and lifestyle changes
- nutrition therapy (low fat: no fried,fast, whole milk, red meats)
- drug therapy
- smoking cessation
- exercise
List the 5 classes of antihyperlipidemics
1 bile-acid sequestrants
Cholestyramine (questran)
2 fibrates
Gemfibrozil (lopid)
3 nicotinic acid
Niacin (niaspan)
4 cholesterol absorption inhibitor
Ezetimibe (zetia)
5 HMG-CoA reductase inhibitor
Atorvastin (Lipitor)
HMG- CoA reductase inhibitors (statins)
Used in reducing blood lipid levels
*patient education:
TAKE AT BEDTIME, report any muscle weakness or aching immediately, diet and medication compliance
*monitor closely for:
Liver enzyme levels, creatinine kinase levels, rhabdomyolosis
What are some side/adverse effects of HMG-CoA reductase inhibitors (statins)
- may cause gastrointestinal upset
- may cause liver damage
- rhabdomyolosis
- may rise the risk of diabetes in women
Fenofibrate
Lopid
Decreases triglycerides more than increasing HDL , take before meals , gi side effects
Type: fibrate , antihyperlipidemic
Ezetimibe
Zetia
Blocks cholesterol absorption, take with meals , very well tolerated usually in combination therapy
Type: cholesterol absorption inhibitor, antihyperlipidemic
Cholestyramine
Questran
Bind bike acids in the small intestine, preventing their return to the liver , bound cholesterol is excreted in the stool
Take before meals, may cause constipation
Interact with most drugs including anticoagulants, digoxin, hormones, antibiotics
Type: bile-acid sequestrants, antihyperlipidemics
Niacin
Niaspan
Mechanism of action unknown, take with food
Many side effects including significant vasodilation, flushing and gi distress
Type: nicotinic acid, antihyperlipidemic
Claudication manifestations
(Pain on walking)
- foot, calf, thigh or buttock pain
- pain worse with exertion
- pain relived with several minutes rest
- pain relieved in dependent position
Objective assessment of the vascular system
- decreased skin temperature
- shiny skin
- hairless
- dystrophic toenails
- distal extremity color change with position
- skin pallor with elevation
- skin rubor when leg dependent
- bilateral leg diminished pulses
- slow wound healing
- impotence
Dystrophic toenails
Thick, yellow , brittle
Vascular ultrasound
Noninvasive ultrasound method (also called duplex study) used to examine the blood circulation in the arms and legs
What does noninvasive mean
The procedure doesn’t require the use of needles, dye, radiation or anesthesia
Arteriogram and pre/post care
Visualizing vasculature to assess for structures, bleeding, and other abnormalities
NPO
Dye
Assess for shellfish/iodine allergy
Peripheral arterial disease
Alters natural flow of blood through arteries and veins of peripheral circulation
Deprives lower extremities of O2 and nutrients
Legs more frequently than arms
Peripheral vascular disease
Aka arteriosclerosis obliterans
Manifests as insufficient tissue perfusion caused by existing atherosclerosis
Advanced pvd/pad may manifest as
Mottling in a “fishnet pattern” , pulselessness, numbness or cyanosis
Paralysis and cold extremity
Gangrene
*poorly healing injuries or ulcers in the extremities help provide evidence of preexisting pvd
SIX P’s of acute arterial occlusion/insufficiency
PAIN of loss of sensory nerves 2nd to ischemia
PULSELESSNESS
POIKILOTHERMIA (coldness)
PALLOR caused by empty superficial veins and no cap refill
PARESTHESIA and loss of position sense
PARALYSIS
What are the 2 most common locations of peripheral arterial diseases
Aortoiliac bifurcation
Femoral bifurcation
Manifestation of pain in PAD vs PVD
PAD- intermittent claudication, rest pain may be present, worsens with elevation
PVD- achy, heaviness, exercise and elevation decrease pain
Manifestation of skin color/temp in PAD vs PVD
PAD- absence of hair, thin, shiny skin, thick toenails, pale with dependent rubor and cool
PVD- brown discoloration, dependent cyanosis, may be warmer
Manifestation of sensation in PAD vs PVD
PAD- decreased
PVD- pruritis may be present
Manifestation of pulses in PAD vs PVD
PAD- decreased to absent
PVD- present , may be difficult to palpate related to edema
Manifestation of edema in PAD vs PVD
PAD- may be present, but usually absent
PVD- present, worse at the end of the day
Manifestation of muscle mass in PAD vs PVD
PAD- reduced in chronic disease
PVD- unaffected
Manifestation of ulcers in PAD vs PVD
PAD- small painful ulcers in pressure points
PVD- broad shallow slightly painful ulcers of the ankle and lower leg
Management of PAD
- Smoking cessation
- Skin care
- Exercise
- Diet change
- Promote arterial flow (reverse trendelenburg, fleece boots, elevated heels)
- medications (trental, cilostazol, asa, clopidogrel, L-arginine)
Doppler ultrasound
Evaluation of audible arterial signals measurement of limb pressures
Ankle-brachial index
Used to diagnose PAD. Compares blood pressure in your ankle to blood pressure in your arm
Normal range of ABI
1.0 or greater
(With a range of 0.90 to 1.30)
Less than 0.9 in either leg is diagnostic of PAD
Four stages of chronic PAD
Stage I- asymptomatic
Stage II- claudication
Stage III- rest pain
Stage IV- necrosis/gangrene
Inflow vascular disease Manifests as
Discomfort in lower back, buttocks, thighs
Outflow vascular disease manifests as
Burning or cramping in valves, ankles, feet, toes
How to asses for PAD in dark skinned patients
Skin and nail beds for dull, lifeless color
Soles of feet and toenails
Percutaneous trandluminal angioplasty
Minimally invasive method of improving arterial blood flow.
A cannula is inserted into or above an occluded or stenosed artery , the occluded artery is then dilated with a ballon catheter
Atherectomy
Used to improve blood flow to the ischemic limbs of people with PAD.
for very hard, calcified stenotic lesions that aren’t amenable to balloon angioplasty
Goal is removal of the plaque by breaking it into micro fragments
Varicose veins
Distended, protruding veins that appear darkened and tortuous
Collaborative care: Elastic stockings Elevation of extremities Sclerotherapy Surgical removal of veins Radio frequency energy to heat veins
Phlebitis
Management/complications
Inflammation of superficial veins
Management- warm, moist, soaks; elastic stockings
Complications- tissue necrosis, infection, pulmonary embolism , pain
Virchows triad
Venous thrombosis occurs via 3 mechanisms:
Decreased flow rate of the blood, damage to the blood vessel wall and an increased tendency of the blood to clot
Signs of pulmonary embolism
Shortness of breath
Chest pain
Petechiae
Decreases O2 sat
Assessment of VTE
- calf or groin tenderness or pain
- sudden onset of unilateral swelling of leg
- localized edema
- venous flow studies
- d dimer (indicative of clots)
Normal range of d dimer
Less than .5
A global market of coagulation activation and measuring fibrin degradation products produced from fibrinolysis (clot breakdown)
Nonsurgical management of VTE
Rest, preventative measures
Drug therapy: Unfractionated heparin Low-molecular weight heparin Warfarin Thrombolytics
Anticoagulants
Prevent clot formation in veins through inhibition of fibrin
Antiplatelets (antithrombotics)
Prevent clot formation in arteries through inhibition of platelet activity
Thrombolytics
Dissolve boosts that have already formed
Heparin
Anticoagulant
Monitored via PTT
do NOT give with antiplatelet therapy, IM injections
*monitor closely for:
Thrombocytopenia HIT, bleeding, hypotension
What is the antidote for heparin overdose
Protamine sulfate
Enoxaparin
Low-molecular weight heparin
Given SQ
Patients may give their own injections
*monitor closely for:
Bleeding hypotension
Antidote is protamine sulfate
Coumadin
Anticoagulant
Given PO
*monitor closely for
Bleeding, hypotension, tarry stools, drug interaction
Antidote: vitamin K
Normal INR levels
Normal: less than 1.4
Therapeutic Coumadin range: 2.0-3.0
Higher risk therapeutic Coumadin range: 2.5-4.0
Antiplatelets
Oral ex: aspirin, clopidogrel, prasugrel, dipyridamole with ASA
IV ex: reopro, aggrastat, integrelin
Oral dosing used for prophylaxis, IV dosing used for ACS
oral dosing must be stopped 7 days before surgery
Do NOT give with NSAIDS
Thrombolytics
Promote rapid destruction of thrombus
Must be given within narrow time frame/Given IV
Ex: streptokinase , urokinase, tPA
*monitor for
Baseline blood counts, bleeding, tachycardia , increased pulse/decreases pressure
“Usually end in -ase”
Abdominal aortic aneurysm
Outpouching or dilation of the arterial wall of the latter portion of the descending segment of the aorta
- seen in men most often 40-70
- asymptomatic usually
- back pain and abdominal pain will follow with growth of mass
What are signs of an abdominal aortic aneurysm
Swelling Bleeding out Diminished pulses Flush/warm upper Pale lower BACK PAIN/PRESSURE
What is something to do when an abdominal aortic aneurysm is suspected
Check BP in right vs left arm
Saccular aneurysm
Projects from only one side of the vessel
Fusiform aneurysm
An entire arterial segment becomes dilated
Tricuspid valve location vs Bicuspid (mitral) valve location
Triscuspid - R side
Bicuspid - L side
