Download ah ii exam i study guide part i

AH II EXAM I STUDY GUIDE

Cardiac:PART I
Blood Pressure= “silent killer”
o BP=CO X SVR
 BP= blood pressure, forced exerted by the blood against the walls of the
blood vessels.
 CO= cardiac output, the total blood flow through the systemic or
pulmonary circulation in on minute.
 SVR= systemic vascular resistance (SVR) force opposite the movement of
blood.
o Levels of HTN
 Normal=120/80
 Prehypertension= 120-139/80-89
 Hypertension (HTN) Stage I-140-159/90-99
 Hypertension Stage II=160+/100+
 Hypertension Crisis=180+/110+
 Hypertension Urgency
 Asymptomatic, severe HTN.
 NO EVIDENCE OF TARGET END ORGAN DAMAGE
 BP >180/120mmHg
 Assess for potential evidence of target organ damage
 MEDS: ORAL AGENTS
o BB—labetalol
o ACE inhibitor—captopril
o Alpha 2 agonist—clonidine
 Hypertensive Emergency
 Acute, life threatening
 EVIDENCE OF TARGET END ORGAN DAMAGE
 BP >180/120mmHg
 MEDS:
o IV vasodilators
o Sodium nitroprusside
o Nicardipine
o Fenoldopam mesulate
o Enalapril
o Nitroglycerin
o Primary HTN (95%)
 Excess salt
 Abnormal Arteries
 Increased blood volume
 Genetic disorders
 Stress
o Secondary HTN
 Health Conditions
 Medications
 Recreational Drugs
 Pregnancy
 Hormonal Therapy
o Risk Factors for HTN:
 Changeable
 Obesity
 High sodium
 Alcohol
 Lack of physical activity
 Stress
 Smoking
 Unmodifiable
 Age
 Race
 Family hx
 Gender
 Gestation HTN (during pregnancy)
o How does one get HTN:
 Due to a change in CO or peripheral resistance resulting in increased
pressure damaging lining of the vessels causing the left ventricle to
enlarge
o What does HTN look like:
 Edema due to too much salt causing fluid overload.
 Headaches
 Shortness of breath due to constriction of blood vessels or lack of
exercise.
 Papilledema—in back of the eye the disc will look fuzzy and hazy if edema
is present. Normally the disc will look like a big yellow circle.
 Angina
 Altered speech
 Nocturia
 Balance issues/ dizziness
o Important Labs
 Sodium (Na+)
 Potassium (K+)
 Creatinine
 BUN
 Urine analysis (UA)
 Fasting glucose
 HDL
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Total cholesterol
Lipids
ECG
24hr urine creatinine clearance
GFR (glomerular filtration rate)
Protein
Echocardiogram—shows blockage and structure of the heart
Electrocardiogram (EKG)—shows conduction waves and electricity of the
heart
o Complications
 CVA/Stroke/TIA
 STROKE RECOGNITION:
o F—face uneven?
o A—arm hanging down?
o S—slurred speech?
o T—time, call 911 NOW!
 Transient Ischemic Attack—mini stroke, go get medical attention
if you think you are having one.
 MI
 Pain
o Sudden onset
o Substernal
o Crushing
o Tightness
o Severe
o Unrelieved by nitroglycerin
o Can radiate to back, neck, jaw, shoulder or arm
 Dyspnea
 Syncope (decreased BP)
 N/V
 Diaphoresis
 Weakness
 Denial
 Increased Heart Rate
 TX:
o O2, IV, Meds, decrease Na+, cholesterol and caffeine.
 Heart Failure
 LEFT
o LUNGS
 Cough
 Crackles
 Wheezing
 Blood-tinged sputum
 Tachypnea
Restlessness
Orthopnea
Confusion
Tachycardia
Exertional dyspnea
Fatigue
Cyanosis
Elevated pulmonary capillary wedge pressure
Paroxysmal nocturnal dyspnea
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o
o
o
o
o
o
o
o
o
 RIGHT
o REST OF BODY
 Secondary to chronic pulmonary problems
 Distended jugular veins
 Anorexia
 GI distress complaints
 Dependent edema
 Weight gain
 Fatigue
 Increased peripheral venous pressure
 Ascites
 Enlarged liver and spleen
Left vent. Hypertrophy
 Thickening of myocardium of the left ventricle
Renal damage
 Headaches (HA)
 Decreased ability to concentrate urine
 Polyuria to oliguria
 Increased BUN and Creatinine
 Edema
 Glomerular filtration rate (GFR) progressively decreases from 90
to 30mL/min.
 Mild Anemia
 Increased BP
 Weakness
 Fatigue
Meds for BP:
 ACE Inhibitors—effects blood vessels and everything in blood
vessels.
 ARBs (Angiotensin II receptor blockers)-- effects blood vessels
and everything in blood vessels.
 Beta Blockers (BB)—effects Heart rate
 Ca+2 Channel Blockers—effects heart rate
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Diuretics—effects everything in the blood vessels.
o Thiazides
o Loop
o K+ Sparring
 Centrally acting alpha 2 agonists
 Alpha 1 antagonists
 Vasodilators
Peripheral Vascular Disease
o Arterial Vessels
 Vasoclusive—PA occlusion, emboli (pulmonary embolus)/thrombi
(Formed blood clot), aneurysms (out-pouch of vessel).
 Vasopastic---Raynaud’s phenomenon
o Venous Vessels
 Venous Thrombosis
 Varicose Veins
o Lymphatics
 Lymphedema/Elephantiasis
 Lymphadenitis/Lymphangitis
o Risk Factors:
 Modifiable (changeable)
 Nicotine
 Diet
 HTN
 Diabetes
 Obesity
 Stress
 Sedentary lifestyle
 C-reactive protein—sensitive marker for CV inflammation
 Hyperhomocysteinemia
 Unmodifiable (not changeable)
 Age
 Gender
 Genetics
Vascular Disorders
o Atherosclerosis (larger arteries)/Arteriosclerosis (smaller arteries)—
 lining of the arterial wall thicken with lipids, calcium, carbs, fibrous
tissues, and plaques causing a blockage. Can result in stenosis,
obstruction, aneurysm, ulceration and/or rupture. Reduces flow to
myocardium.
 Manifestations:
 Depends on vessels affected.
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Intermittent Claudication—aching, cramping pain causing fatigue
in legs, relieved by rest. Hang legs down to feel better. Due to lack
of oxygen to arms/legs (periphery).
 CVA
 SOB
RISK FACTORS:
 Smoking
 HTN
 Sedentary lifestyle
 Gender
 Genetics
 Hyperhomocysteinemia
 Older females.
 C-reactive protein
COMPLICATIONS:
 MI
 CVA
 Renal failure
 Syncope
 Occlusion
 Aneurysms
MEDS
 PTA—causes dilation of the vessel and flattening of plaque
o RISKS:
 Dissection
 Hemorrhage
 Hematoma
 Embolus
 Acute arterial occlusion
 Stent Placement
o Distal occlusion
o Intimal damage/dissection
o Dislodgment
 Statins
o HMG-Co-A reductase inhibitors
o Atorvastatin
o Fluvastatin
o Pravastatin
o Simvastatin
 Bile Acid Sequestrants
o Cholestyramine
o Coleselvelam
o Colestipol

Nicotinic Acid Derivatives (Niacin)
o Niacor
o Niaspan
 Fibric acid inhibitors
o Gemfibrizol
o Fenofibrate
 Cholesterol absorption inhibitors
o Ezetimibe
 PLAN OF CARE
 Maintain tissues perfusion
o Increase arterial supply to arteries
o Decrease venous congestion
o Promote vasodilation
o Prevent vascular compression
 Relieve pain
 Maintain skin integrity
 Teach patient about home care and care of site.
o Peripheral Arterial Occlusive Disease—
 partial or full blockage of an artery, usually below the aorta and renal
arteries. Due to atherosclerosis.
 MANIFESTATIONS:
 Intermittent claudication
 Weak
 Unequal peripheral pulses
 Poor cap. Refill
 Poor hair growth
 Atrophy of muscles and skin
 Nail and skin changes
 RISK FACTORS:
 Smoking
 HTN
 Sedentary lifestyle
 Gender
 Genetics
 Hyperhomocysteinemia
 Older females.
 C-reactive protein
 COMPLICATIONS:
 Hemorrhage
 Compartment syndrome
 Infection
 MI
 CVA
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Renal failure
TX
 Surgery—for severe disease
 Endarterectomy
 Bypass Graft
POST-SURGERY
 Supine for 6hrs
 VS and Doppler peripheral pulse q 15min.
o Temp q 4hrs, any signs of postimplantation syndrome
should be reported.
 Access site (femoral or iliac artery)
 Assess site for bleeding, pulse, swelling, pain, hematoma, or skin
changes.
DX:
 Altered peripheral tissue perfusion
 Chronic pain
 Risk for impaired skin integrity
 Knowledge deficient
HOW TO IMPROVE CIRICULATION
 Exercise
 Lower legs increases perfusion
 Stop smoking
 Reduce stress
 Low-fat, protein and zinc.
 Temperature (hot & cold)
PLAN OF CARE
 Maintain tissues perfusion
o Increase arterial supply to arteries
o Decrease venous congestion
o Promote vasodilation
o Prevent vascular compression
o May need surgery
 Monitor for bleeding, fluid imbalance, thrombosis formation,
severe edema/compartment syndrome.
 Relieve pain
 Maintain skin integrity
 Teach patient home care and care of site.
MEDS
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Pentoxifylline--increases erythrocyte flexibility, lowers blood fibrinogen
concentrations, and inhibits neutrophil aggregation and activation
Cilostazol--phosphodiesterase III inhibitor, vasodilates and prevents
platelets from aggregating.
Antiplatelet Agents--ASA or clopidogrel, prevent formation of
thromboemboli, decrease risk of cardiovascular events.

Statins--stabilize plaques, decrease vascular inflammation, decrease
endothelial dysfunction and thrombus formation. Some have effect of
claudication
o Aneurysms (thoracic, abdominal)—
 a weakened point on an arterial wall due to HTN or atherosclerosis.
 Manifestations:
 Pulsating mass in chest or abdomen
 Thoracic dyspnea
 Cough
 Hoarseness
 Loss of voice
 Dysphagia
 RISK FACTORS:
 Congenital
 Trauma
 Disease
 HTN
 Atherosclerosis
 Tobacco
 COMPLICATIONS:
 Rupture
 Arterial occlusion
 Hemorrhage
 Infection
 Ischemic bowel
 Renal failure
 Impotence
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SURGERY
o Depends on location and risk factors
o Thoracic aortic aneurysms
 Endovascular graft procedure--drain spinal fluid to a perfusion
gradient that enhances perfusion
 RISK=neurological perfusion can be interrupted.
 RISK= paraplegia
PRE-OP
o Maintain tissue perfusion/circulation
o Monitor for rupture and other complication
POST-OP
o Maintain tissue perfusion/circulation
o Monitor for arterial occlusion, hemorrhage, infection, ischemic bowel,
renal failure, and impotence.
PLAN OF CARE
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MEDS:
Relieve pain
Maintain skin integrity
Teach patient home care and care of site.
o
Anti-hypertensives
o Dissecting Aorta—
 tear of the intima or media of a diseased aorta due to atherosclerosis and
HTN.
 MANIFESTATIONS:
 Sudden severe ripping pain in anterior chest or back extending to
shoulders, epigastrum or abdomen.
 Cardiovascular symptoms
 Neurological symptoms
 GI Symptoms
 Sweating
 Tachycardia
 RISK FACTORS:
 Congenital
 HTN
 Blunt chest trauma
 Atherosclerosis
 Cocaine use
 Tobacco
 Men and women 50-70y/o
 COMPLICATIONS:
 Rupture
 Arterial occlusion
 Hemorrhage
 Infection
 Ischemic bowel
 Renal failure
 Impotence
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SURGERY
o Depends on location and risk factors
o Thoracic aortic aneurysms
 Endovascular graft procedure--drain spinal fluid to a perfusion
gradient that enhances perfusion
 RISK=neurological perfusion can be interrupted.
 RISK= paraplegia
PLAN OF CARE

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Relieve pain
Maintain skin integrity
Teach patient home care and care of site.
o Arterial Embolus/Thrombus—
 Due to drug abuse or iatrogenic injury causing a blockage of an artery.
Seen w/Atrial fibrillation and trauma injuries.
 MANIFESTATIONS:
 Depends on vessel involved and size.
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 Pain
 Pallor
 Pulselessness
 Paresthesia (numbness/tingling)
 Poikilothermia (cool unable to bear weight)
 Paralysis
RISK FACTORS:
 Congenital
 HTN
 Blunt chest trauma
 Atherosclerosis
 Cocaine use
 Tobacco
 Men and women 50-70y/o
COMPLICATIONS:
 MI
 CVA
 Renal failure
 Hemorrhage
 Compartment sundrome
 Metabolic abnormalities
 Reocclusion
 Arterial dissection
 Distal artery embolism
INTERVENTIONS:
 Emergency embolectomy--through the groin, balloon filter out clot
fragments
 Endovascular--percutaneous mechanical thrombectomy: similar to
angiogram meaning you blast the clot w/water and suction
fragments. Complications of procedures include: arterial
dissection or distal artery embolization.
MEDS:
 Heparin IV—prevents thrombus from enlarging. Reducing further
emboli from forming and necrosis. *(REMEMBER: protamine
sulfate is antidote for Heparin)*
 TPA (tissue plasminogen activator, alteplase) & scuPA or
urokinase plasminogen activator (prourokinase).
o Don’t cause systemic effect on fibrinogen or plasminogen
preventing systemic fibrinolysis. Med is given under x-ray
via catheter straight into emboli.
o DO NOT USE W/ PTS WHO HAVE ACTIVE INTERNAL
BLEEDING, CEREBROVASC. HEMMORHAGE,
UNCONTROLLED HTN, PREGNANT OR WHO’VE HAD
MAJOR SURGERY RECENTLY.
PLAN OF CARE:
 Pre-op
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o Maintain tissue perfusion
o Monitor for rupture and other complications
Post-op
o Maintain tissue perfusion
o Monitor for arterial occlusion, hemorrhage, infection,
ischemic bowel, renal failure, and impotence
Relief of pain
Attain skin integrity
Knowledge deficit/pt self care. Home care.
NO HEART OR COLD
Nothing that could cause trauma (tape, electrodes).
o Raynaud’s Phenomenon—
 intermittent arterial vasoconstriction causing pain, pallor, coldness in
usually fingers and toes. Is primary or idiopathic, there’s no secondary
cause. Due to cold or stress.
 Manifestations:
 White, blue, red color changes in periphery bilateral and
symmetrical.
 Hyperhidrosis
 Pain
 Cold
 RISK FACTORS:
 Women 16-40y/o
 Obstructive lesions
 Autoimmune disease
 COMPLICATIONS:
 Infection
 Gangrene (if underlying vasoclusive disease)
 Syncope (r/t meds)
 PREVETNION
 Avoid trigger (cold/stress)
 MEDICATIONS
 Ca+2 channel blockers—symptom relief
o Nifedipine
o Amlodipine
 PLAN OF CARE:
 Maintain tissues perfusion
 Relief of pain
 Maintain skin integrity
 Knowledge deficit
o Labs for vascular disorders:
 C-reactive Protein
 Homocysteine Levels

Increased risk cerebral vascular, peripheral/coronary artery
disease and VTE
 Factor V Leiden—genetic predisposition to emobli formation. Used for
post-partum or labor patients.
 Lipid panel
 Fasting glucose
 HgbA1c
 BUN/Cr
 24hr urine
 UA
o Diagnostics for vascular disorders:
 Doppler flow study
 Assess flow, architectural abnormalities.
 USED FOR:
o Arterial occlusions
o Embolism
 Exercise testing
 Determines how long a patient can tolerate walking and measure
BP in the ankle (systolic w/walking)
 USED FOR:
o Arterial occlusions
 Duplex ultrasounds
 Determines how long a patient can tolerate walking and measure
BP in the ankle (systolic w/walking)
 USED FOR:
o Arterial occlusions
o Aneurysms
 CT angiography and scanning
 Visualizes cross sections of tissue, volume change in tissues, 3D
w/contrast (CAUTION PTS W/ ALLERGY TO IODINE OR SHELLFISH,
ADMINISTER ACETLYCYSTEINE IF RISK).
 USED FOR:
o Dissecting aorta
o Aneurysms
 Angiography and arteriography
 Inject radio opaque dye into arterial system to visualize vessels
o Reactions to dye:
 SOB dyspnea
 N/V
 Sweating
 Tachycardia
 Numbness of extremities
o Risks vessels damage
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o Acute arterial occlusion
o Bleeding
o Contrast nephropathy
USED FOR:
o Dissecting aorta
o Embolism
o Occlusive disease
o Aneurysms
MRA
 Uses IV contrast dye
 CONTRAINDICATIONS:
o Metal implants
o Old tattoos
 USED FOR:
o Dissecting aorta
 Ankle-Brachial index (ABI)
 A test calculating the ratio of the systolic BP of the ankle w/ the
systolic of the brachial (arm). This helps quantify the degree of
stenosis.
 USED FOR:
o Arterial occlusions
 Transesophageal echocardiogram
 DIagnotitc tool for cardiovascular disease (CVD), heart failure (HF),
valvular disease.
 RISK
o Aspiration
o Resp. depression
o Esophageal perforation
o Vasovagal stimulation
Peripheral Venous Issues
o Venous Thrombembolism/DVT
 Endothelial damage, venous stasis, altered coagulation
 MANIFESTATIONS:
 Affected limb has the following SYMPTOMS:
o Firm
o Edema
o Warm
o Erythematous
o Pain w/ movement, palpation & weight-bearing
 RISKS:
 Hypercoagulation
 Cancer
 Cardiovasc. Disease
 Recent surgery
 Trauma
 Obesity
 Older adults
 Women on hormone therapy containing estrogen.
 COMPLICATIONS:
 Chronic venous occlusion
 Pulmonary embolism
 Ulcers
 Gangrene
 Possible amputation
 MEDS:
 Unfractionated Heparin IV—prevents thrombus from getting
bigger. Decreases risk of more emboli and reduces necrosis.
(PROMTAMINE SULFATE=ANTIDOTE FOR HEPARIN)
 Low molecular weight Heparin—prevent thrombus formation
 Oral anticoagulants (warfarin)-- prevent thrombus formation
(VITAMIN K=ANTIDOTE FOR WARFARIN)
 Factor Xa Inhibitors— prevent thrombus formation
 Thrombolytic therapy—TPA or tissue plasminogen activator
(alteplase)
 Scu-PA
 Urokinase plasminogen activator (prourokinase)
o Chronic venous insufficiency/post-thrombotic syndrome
 Chronic distention of the veins preventing values form fully closing
causing back flow or reflux of blood in the veins.
 MANIFESTATIONS:
 Post thrombotic syndrome resulting from long term venous stasis
causing dilation of superficial veins.
 Edema
 Altered pigment
 Pain
 Stasis dermatitis
 Debilitation
 COMPLICATIONS:
 Venous ulceration
 Infection/cellulitis
 Amputation
 Neuropathy
 MEDICATIONS:
 NONE
 TX:
 Surgery
 Usually preventable.
o Varicose Veins
 Primary
 w/o deep vein involvement
 Reflux of blood and venous stasis
 Secondary
 Due to obstruction of deep veins
 Reflux of blood and venous stasis
 MANIFESTATIONS:
 Dull aches
 Fatigue of leg muscles
 Muscle cramps
 Heaviness in legs
 Nocturnal leg cramps
 Deep vein variscosity
 CHRONIC VENOUS STASIS S/S:
 Pain
 Pigment changes
 Edema
 COMPLICATIONS:
 DVT
 Chronic venous insufficiency/post-thrombotic syndrome
 Venous ulcers
 PREVENTION:
 Avoid activities that cause venous stasis (socks too tight, leave
mark on skin, crossing legs, sitting/standing too long)
 Elevate legs higher than heart
 Walker every hour
 Wear compression stockings
 Weight reduction plans for overweight pts.
 TX:
 Can have surgery (laser, ablations, injections) to remove veins.
o Leg Ulcers
 Alterations in vessels in all blood vessels (arteries, capillaries, veins)
results in inadequate oxygenation and nutrient exchange to the tissues
causing alteration in skin integrity and development of inflamed necrotic
area causing an ulcer.
 MANIFESTATIONS:
 Arterial
o intermittent claudication
o Foot pain
o Ulcers on tips of toes due to ischemia or pressure.

Venous
o Aches
o Heavy pain
o Swelling in lower extremities
o Ulcers on medial or lateral malleolus.
o Discoloration often present due to extravasation of blood
secondary to venous HTN.
o FIND UNDERLYING ISSUE (shoes, injury, inserts of shoes)
 COMPLICATIONS:
 Infection/cellulitis
 Amputation
 neuropathy
 MEDS:
 Anti-infectives (oral antibiotics)
 Compression therapy
 Debridement of wounds—removal of dead tissue
 Dressings
 Antiseptic agents
o Provodine-iodine
o Aetic acid
o Chlorhexidine
o Silver wound products
 Systemic antibiotics
o Based on results of culture/sensitivity.
 TX:
 Compression therapy
 Debridement
 Topical therapies
 Wound tx
 Stimulated healing
 Hyperbaric oxygenation
o Virchow’s Triad
 Triangle that leads to a blood clot.
Stasis of blood flow
Endothelial
Hypercoagulability.
Injury
 Labs of Peripheral venous issues:
o WBC
PT/INR
PTT
Cap refill
Hemoglobin
Doppler study
Infection, poor perfusion & other cultures---LEG ULCERS.
Plan of care for pts w/ peripheral venous issues:
o Altered peripheral tissue perfusion
o Chronic pain
o Risk for impaired skin integrity
o Knowledge deficit
o Alterations in mobility
o Risk for infection/injury
o Imbalanced nutrition
Prevention of peripheral venous issues:
o Compression stockings
o Compression devices
o SQ heparin or low-molecular weight (LMW) heparin, warfarin.
o Elevate lower extremities.
o Deep breathing and active exercises
o Early ambulation
o Avoid sitting/standing for long periods of time.
o Walk q 10min q 1-2hrs.
Lymphatic disorders:
o Lymphangitis
 Acute inflammation/infection of the lymphatic channels secondary to
a focus of infection in an extremity
 Lymph node removal/biopsy/dissection is necessary if a lymph node
becomes obstructed or abscessed.
 MANIFESTATIONS:
 Red streaks extending up from an infection on an extremity
 RISKS:
 Infection
 Inflammation
o Lymphadenitis
 Inflammation or infection of the lymph nodes
 Strep throat
 MANIFESTATIONS:
 Tissues swelling unilaterally r/t obstruction of lymph channels.
 RISKS:
 Infection
 inflammation
o Lymphedema
 Tissues swelling r/t obstruction of lymphatic flow
o
o
o
o
o
o
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PRIMARY
 Congenital malformations
 SECONDARY
 Acquired obstruction.
 MANIFESTATIONS:
 Swelling
 Erythematous
 Tender
 Warm
 Groin, axilla, cervical lymph nodes affected
 r/t infection
 RISKS:
 Congenital malformation
 Lymph node dissection/biopsy
TX FOR LYMPHATIC ISSUES:
 ROM exercises
 External compression devices
 Compression stockings
 Lymphatic drainage therapy
 Meds
 Surgery—excision of SQ tissue, fascia w/ skin grafting to cover the
defect, only if mobility or circulation are severely compromised.
 IF IN LEG: bedrest, and elevate leg.
 Reduce & control edema, prevent infection.
COMPLICATIONS FOR LYMPHATIC ISSUES:
 Post surgery:
 Flap necrosis
 Hematoma
 Abscess under the flap
 Cellulitis
 Spread of redness, will see distinct border
 Alteration in skin integrity allows bacteria to release
toxins and produce under the skin causing infection
 Causes swelling/redness, fever, chills and sweating
 ELEVATE, use warm/moist packs to site q2-4hrs
 Educate pt on prevention of recurrence and about
skin/foot care.
MEDS FOR LYMPHATIC ISSUES:
 Furosemide—prevents fluid overload
 Antibiotics—infection tx
PLAN OF CARE:
 Altered peripheral tissue perfusion
 Chronic pain
 Risk for impaired skin integrity

o
o
o
o
Knowledge deficiency
Alterations in mobility
Risk for injury/ infection
Imbalanced nutrition
Body image disturbance
Coronary Vascular Disorders:
o Preload= vol. of blood in the ventricles at the end of diastole (Relaxation)
 Preload increases in pts w/:
 Hypervolemia
 Cardiac valves regurgitate
 Heart Failure
o Afterload=resistance left ventricle must overcome to circulate blood
 Afterload increases in pts w/:
 HTN
 Vasoconstriction
 Increase afterload=increase cardiac workload
o Cardiac output (L/min)= Heart rate X stroke volume
o Ejection fraction= % of blood ejected. (amount of blood pumped out of
ventricle / total amount of blood in ventricle). (50-55%= low, 5570%=normal, 70+%=high function)
o Pulse Pressure= systolic BP minus diastolic BP (EX: 122/75= 122-75=47)
o Tachycardia=>100BPM
o Bradycardia= <60BPM
o Depolarization—contraction
o Repolarization--relaxation
o P wave—atrial depolarization
o QRS-–ventricular depolarization, atrial repolarization
o T wave—ventricular repolarization
o Chronotrope– HR through SA node
o Inotrope—force of contraction
o Dromotrope—conduction velocity (speed of conduction through heart at AV
node)
o S3—early diastole. Caused by vibration of the ventricular walls. Heard usually
in children and young adults. In elderly if S3 is heard means heart failure.
o S4—late diastole. Resistant ventricular filling, high atrial pressure. Vibration
of valves, supporting structures and ventricular walls. Usually weak left
ventricle caused by atria contracting in effort to overcome failing left
ventricle
o Murmurs—turbulent blood flow cause by valve closing. Graded 1-6
o Mean arterial Pressure (MAP):
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MAP= 1/3 X systolic BP + 2/3 X diastolic BP.
EX:
o BP=120/80
 1/3 X 120=40
 2/3 X 80=53
 40 + 53= 93.
o OR
MAP= systolic BP + (2 X diastolic BP)
3
EX: BP=120/80
120 + (2 x 80)= 280/3=93.
Normal MAP is 70-100, less than 60 is inadequate, it means no
perfusion to major organs.
Coronary Artery Disease:

Risk factors lead to the following disease:
o Atherosclerosis
o Angina Pectoris
 Oxygen supply to the heart muscle does not meet
demand of the heart secondary to atherosclerosis and
assoc. blockage.
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Syndrome characterized by episode of paroxysmal
pain/pressure in the anterior chest due to insufficient
coronary blood flow
Described as tightness, choking or heavy sensation
FACTORS:
 Heavy meals
 Exercise/physical exertion
 Cold
 Stress
TYPES:
 Stable
 Unstable
 New in onset, occurs at rest, worsening
pattern, more frequent, unpredictable,
medical emergency. Fatigue is most
common symptom.
 12 lead EKG
 look for changes in QRS, ST, &T.
 Refractory
 Variant—chronic stable
 Silent Ischemia—chronic stable
MANIFESTATIONS:
 Chronic stable Chest pain that occurs
intermittently over a long period w/ same
pattern of onset, duration and intensity. Lasts 515mins.
 ST segment depression and T wave inversion
 Control w/ drugs
TYPES:
 Silent ischemia
 Ischemia that occurs w/o subjective
symptoms.
 Assoc. w/ diabetic neuropathy
 Confirm w/ ECG changes.
 Prinzmetals’ (variant) ischemia
 Occurs at rest in response to spasm
 In pts w/ a hx of migraine HA’s and
Raynaud’s phenomenon
 Chest pain marked transient ST-segment
elevation (STEMI)
SYMPTOMS: caused by myocardial ischemia*
 Epigastric distress
 Pain radiating to jaw or left arm
 SOB
Sweating
 ATYPICAL SYMPTOMS:
 SOB
 Fatigue
 N/V
 Pain in b/w shoulder blades.
Myocardial Infarction: occurs b/c of sustained ischemia.
 Cardiac cells can withstand ischemic conditions for
~20minutes before necrosis occurs.
 Takes ~4-6hrs for entire heart to become necrotic if
ischemia continues.
 ~12hrs if thrombus doesn’t block full artery for heart to
become necrotic.
 RISK FACTORS:
 Smoking
 Sedentary lifestyle
 HTN
 Drinking
 Diabetes
 Gender
 Genetics

Meds
 Age
 HEALING PROCESS
 24hrs= leukocytes infiltrate area of cell death
 4 days=proteolytic enzymes of neutrophils and
macrophages remove dead tissue.
 6 weeks= scar tissue replaces dead tissues, less
compliant but healed
 Necrotic zone is ID’d by ECG changes (elevated
ST segment, pathologic Q wave)
 MANIFESTATIONS:
 Pain is severe and not relieved by rest, position
change, or nitroglycerin.
 Heaviness, pressure, tight, burning, constriction,
crushing substernal, retrosternal or epigastric
 WOMEN & ELDERLY HAVE ATYPICAL SYMPTOMS
 DIABETIC PTS MAY BE ASYMPTOMATIC DUE TO
CARDIAC NEUROPATHY
 Catecholamine release/ SNS stimulation
 Release of glycogen
 Diaphoretic
 Vasoconstriction of peripheral b.v.
 Ashen, clammy/cool skin
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o
Cardiovascular
 Increase HR, BP then decrease BP due to
decrease in CO.
 Crackles
 Dyspnea
 Jugular vein distention (JVD)
 S3/S4, new murmur sounds.
 N/V
 Vasovagal reflex
 Vomiting due to severe pain
 Fever
 100.4+ in first 24hrs, can last up to 1wk.
 Systemic inflammatory process caused
by myocardial cell death
COMPLICATIONS:
 Dysrhythmias
 Caused
by ischemia, electrolyte
imbalance, SNS stimulation
 Heart Failure (HF)
 When heart cannot contract as well
 Can be subtle or severe
 Cardiogenic Shock
 when oxygen and nutrients supplied to
the tissues are inadequate because of
severe left ventricular failure.
 b/c of left ventricle failure
 need aggressive management
 high mortality rate
 Papillary muscle dysfunction
 Ventricular aneurysms

Cardiac arrest
 Unstable angina
 Bradycardia, heart block
 Tachyarrhythmias
 Left ventricular failure/aneurysm
 Right ventricular failure
 Pericarditis
 DVT & PE
 Systemic embolus
 Cardiac tamponade
 Mitral Regurg
 Ventricular septal defect
 Late malignant ventricular arrhythmias
 Dressler’s syndrome
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o
TX:
M- morphine
O- oxygen
N- nitrates
A- Aspirin
S- Statins
A—ASA
B—beta blockers
Thrombolytics—urokinase /streptokinase
 Stops infarction process by dissolving thrombus.
 Assess for return of ST segment to baseline.
 IV Heparin to prevent re-occlusion
 Analgesics
 Reperfusion therapy
Coronary Surgical Revascularization:
o When PCI failed, failed med. Management.
o Coronary artery bypass graft (CABG):
 Requires
sternotomy
(opening
chest)
and
cardiopulmonary bypass
 Use arteries/veins for grafts
 Minimally invasive
 COMPLICATIONS:
 Bleeding
 Anemia
 Fluid/electrolyte imbalance
 Hypothermia
 Infection
 PRIORITIES-POST-OP:
 Restore CO
 Maintain body temp
 Prevent infection
 Pain control
 Fluid/electrolyte maintenance
 Gas exchange maintenance
 Promote cerebral circulation
 PT IN POST-OP HAS:
 ICU 12-36hrs
 Pulmonary artery catherter
 Intraarterial line
 Pleural/mediastinal chest tube
 Continuous ECG
 ET Tube w/ mechanical ventilation
 Epicardial pacing wires
 Urine cath.
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NG tube
 MONA LISA Mnemonic for acute management of MI
o M- morphine
o O- oxygen
o N- nitrates
o A- Aspirin
o L – loop diuretic
o I – IV access – for bloods, for IV GTN etc
o S – streptokinase (thrombolysis) / PCI - if STEMI
o A – Antiplatelets (e.g. clopidogrel)
Differentiating types of MI
 Transmural MI – this is an infract that causes necrosis of tissue through
the full thickness of the myocardium
 Nontransmural – this is an MI that does not cause necrosis through the
full thickness of the myocardium
 the pain experienced during an MI is related to myocardial ischemia
– if the pain goes away its probably too late to save the heart muscle.
 o Streptokinase is the usual drug used.
 o
BUT – DONT GIVE THROMBOLYSIS TO THOSE WITHOUT ST
ELEVATION!
 ECG Showings – most commonly, a STEMI
 Early – within hours
o o Peaked T wave (very tall T wave)
o o Raised ST segment
Within 24h
o o Inverted T waves – this may or may not persist
o o ST segment returns to normal. Raised ST segments may
persist if a left ventricular aneurysm develops
 Use thrombolysis if:
 The patient has no contra-indications
 they have a STEMI (not NSTEMI)
 angioplasty (PCI) is not available
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Diagnostic studies of cardiovascular system:
o Creatine Kinase (CK)
 Three isoenzymes
 Found in skeletal and myocardial muscle

Raised after any sort of muscle trauma
o CK-MB cardiac specific
 Rise in 4-8hrs, peak 12-24hrs, returns to baseline w/in
3-4 days.
o Myoglobin—seen w/ damaged muscle. Toxic to kidneys.
 Rise in 1-3hrs, peak 4-12hrs, normal w/in 24hrs
 Rabdomyolysis—dying muscle cells.
Troponin T and I-serial
 Rises w/in 3-4hrs, peak 4-24hrs, 1-3weeks detection
 Troponin T is biomarker for heart muscle but not MI
o C-Reactive Protein—marker for inflammation. Risk factor= CAD
o Homocysteine—elevated levels risk for CAD, PVD and stroke
o Cardiac Natriuretic Peptide Markers
 Atrial
 Brain—increase signify HF
 Circulating
- Glucose – not only does this help you treat any diabetes present, but
evidence suggests that patients with a high glucose on admission have
a worse prognosis- thus you should treat these patients more
aggressively.
Lipids – checking for raised cholesterol – although this isn’t
actually necessary as all MI patients are given a potent statin (e.g.
atorvastatin) regardless of the cholesterol level.
o Cholesterol--<200
o LDL--<160, Diabetics and CAD pts <70
o HDL-- >40 is goal
o Triglycerides-- <150
ECG—12lead, holter monitor
Stress Testing—exercise or meds, myocardial ischemia detection
Echocardiography
o TEE
Radionuclide imaging—detects decrease myocardial perfusion
@rest/after exercise
Cardiac catheterization—rt side enter through vein, left side enter
through artery
o Assess catheter for bleeding.
o Assess for arrhythmias
o Cath in groin- 6hr bed rest
o Cath in radius 1hr bed rest
o Report chest pain or sudden discomfort from site
o Assess for contrast against reaction
o COMPLICATIONS:
 MI
 HF
 Death
PREVENTION OF CAD:
o Control cholesterol
o Diet
o Exercise
o Meds
o Manage HTN
o
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Control diabetes
Stop smoking/tobacco
REMEMBER:
o ST Depression= ischemia (reversible)
o ST elevation=infarction (irreversible)
o Unstable MI=troponin levels abnormal
o Unstable angina—troponin levels not affected.
Acute coronary syndrome (ACS)
 Emergent/acute onset of myocardial ischemia resulting
in myocardial tissue death (infarction) if not stopped.
 SPECTRUM:
 Unstable Angina
 NSTEMI= non-ST segment elevation MI, damage
to myocardium
 STEMI—ST segment elevation MI, the most
serious type of ACS. Caused myocardial
infarction and ischemia.
 TX OF STEMI:
 §PCI / Thrombolysis. PCI if available, increase O2
supply. If not, thrombolyse if no PCI's
Beta-blocker – unless contraindicated (e.g. asthma) –
e.g. lisinopril 5mg IV
 ACE-i – start ASAP – usually within 24hours, particularly
if there are signs of LV dysfunction - e.g. lisinopril
 TX OF NSTEMI/UNSTABLE ISCHEMIA:
 § Beta-blocker – unless contraindicated (e.g. asthma)
- e.g. atenolol 5mg IV
 § LMWH – e.g. enoxaparin – for 2-8 days
 § Nitrates – usually given IV
 § Clopidogrel – may be considered in addition to
aspirin, for up to 12 months – especially in patients with
raised troponin. These patients are considered high risk
o
o
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TX of ACS:
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12 lead EKG
Semi-fowlers
MONA
o M- morphine
o O- oxygen
o N- nitrates
o A- Aspirin
Meds for CAD, Angina, ACS & MI:
 Nitroglycerin
 Beta adrenergic blocking agents—chronotropic=decrease rate and
vasodilation
 Ca+2 channel blockers—decreased stroke vol. rate and afterload
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Antiplatelet/Anticoag. Meds
o Aspirin
o Clopidogrel/Ticiopidine
o Heparin
o Glycoprotein IIB/IIA agents
Hyperlipidemia meds
o Statins—inhibit cholesterol synthesis
o Niacin—lower LDL and triglyceride by inhibiting synthesis.
o Fibric acid derivatives—increase HDL
o Bile acid sequestrants—decrease cholesterol and bile
o Ezetimibe
Oxygen
Short-acting nitrates—decrease O2 demand
o Dilate peripheral/coronary veins
o Dilates arteries
o Sub-lingual med or by spray
Long-Acting nitrates
o Reduce angina incidences
o SIDE EFFECTS:
 HA
 Orthostatic hypotension
o Administrations
 Oral—isosorbide dinitrate/mononitrate
 Nitro ointment
 Transdermal patch—controlled release nitro.
Metabolic Syndrome

NEED THREE OR MORE OF THE FOLLOWING:
o Insulin resistance
o Abdominal obesity
o Dyslipidemia
o HTN
o Pro-inflammatory state (C-reactive protein/CRP)
o Prothrombic state- High fibrinogen levels
ECG CALCULATIONS: https://www.youtube.com/watch?v=cfQWo6zqX4E
5 Step Process:
1. Rate= 300/ # of big boxes from one R wave to the next R wave OR, # of R waves in a
6 second strip X 10= BPM
2. Rhythm= regularity of heart beat. Equal distance b/w R waves is the same.
a. Regular—constant/equal distance b/w R waves
b. Irregular—unequal number of big boxes between different R waves. Changes
with each R wave.
3. P-Wave= is there a p-wave for every QRS, and every QRS has a p-wave? No=AV
block, or Pre-atrial complex (PAC).
4. QRS= is there a QRS?
a. Measure length. Normal=0.06-0.11= 1-3 small squares
b. Q wave-over-exaggeration= MI
c. Wide Q wave= PVC, hyperkalemia
d. Narrow Q wave= superventricular tachycardia (>140BPM)
5. P-R Interval
a. P-R interval= 0.12-0.20 = 3-5 small squares
b. Represents atria contraction.
c. Long= 1st degree block
d. Short=junctional rhythm
Normal time per square:
Each square represents 0.04 seconds
Each big square (5 columns of little squares) = 0.20 seconds