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Acute Care NP Exam > Cardiovascular Disorders > Flashcards

Cardiovascular Disorders Flashcards

1
Q

How do you measure cardiac output

A

Cardiac output = HR x stroke volume
Stroke volume is how much blood is moved with each beat

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2
Q

Central Venous Pressure - how do we measure it and what can it tell us?

A

Central Venous Pressure can be measured with a central line.
It goes into the Right Atrium
It also can tell us what the preload might be
In sepsis, the CVP gets low because of decreased preload
Normal is between 8-12mmHg

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3
Q

What is wedge pressure and how is measured?

A

Filling pressuring in the left atrium
It is measured with a pulmonary catheter
Helps determine functionality of the Mitral valve

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4
Q

What happens during diastole?

A

The filling of the ventricles with the opening of the tricuspid valve (RV) and the mitral valve (LV)

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5
Q

What happens during systole?

A

The contraction of the ventricles with the opening of the aortic valve (LV) and the pulmonic valve (RV)

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6
Q

Mean arterial pressure

A

Mean arterial pressure (MAP) is the average pressure exerted on the arteries and serves as a surrogate for measuring afterload, which is the pressure against which the LV must eject blood.

MAP = (2XDBP + SBP)/3

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7
Q

What does aortic stenosis sound like?

A

Systolic, “blowing”, rough harsh murmur at 2nd right ICS, usually radiating to the neck

Remember that it radiates to the neck**

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8
Q

What does mitral stenosis sound like?

A

Loud S1 murmur, low pitched, mid-diastolic; apical “crescendo” rumble

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9
Q

How does an ACE-I affect the Renin-Angiotensin-Aldosterone System (RAAS)

A

When BP falls, kidneys release Renin.
Renin cleaves Angiotensinogen into Angiotensin I which then works its way to the lung.
Angiotensin I is then cleaved into Angiotensin II by angiotensin converting enzyme (ACE).
Angiotensin II causes the blood pressure to rise.
When BP rises, the adrenals will retain salt. If BP gets too high, adrenals will release salt in order to release water in order to drop the BP

In an ACE-I, Angiotensin I is never converted into Angiotensin II so it cannot raise the BP.

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10
Q

AV Blocks

A

1st Degree: Prolonged PR interval always followed by QRS
2nd Degree Type 1 - Wenckebach: PR interval lengthens until a QRS is dropped
2nd Degree Type 2 - Mobitz: PR interval is usually normal however some P waves are not conducted and the beat is therefore dropped.
3rd Degree - Complete Heart Block: Para-systole, P waves and QRS are independent, wide QRS

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11
Q

Causes and treatment of hypertensive emergency

A

-Abrupt cessation of antihypertensives
-Cocaine or meth use (don’t use beta blockers with cocaine or meth - causes increase in BP)
-Pre-eclampsia or eclampsia

Treatment - Nicardipine infusion, Hydralazine or labetalol
-Or can restart home meds slowly

HTNsive Emergency defined as SBP>180 and DBP>120 with evidence of end organ damage.
-papilledema, proteinuria, hematuria, renal failure, AMS, EKG changes (ST depressions)

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12
Q

The 5 P’s of Peripheral Vascular Disease

A

Pallor
Poikilothermy (cold)
Parasthesias
Pulses (decreased)
Pain (claudicaton)

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13
Q

Management of an acute ischemic limb

A

Presentation: Cold, pulseless, cyanotic

Consult vascular surgery
Heparinize empirically
CT Angio to find where the occlusion is
Thrombectomy to remove if possible
Amputate if needed

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14
Q

Management of HLD

A

Statins - inhibit HMG CoA reductase - good at decreasing LDL
Fibrates - good for lowering triglycerides and increasing HDL
Niacin - lowers triglycerides, lowers LDL and increases HDL

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15
Q

What is a scoring measuring that can be used to determine risk for ACS?

A

HEART SCORE

History
EKG
Age
Risk Factors
Troponin

0-3 is low risk
4-6 is medium risk and should consider observation
7-10 is high risk and should observe and treat

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16
Q

Three types of Acute Coronary Syndrome

A

STEMI - ST elevations. Usually caused by a plaque rupture in one of the larger coronary arteries causing a clot

NSTEMI - EKG shows no ST elevations (could be ST depressions) but troponin is elevated. Could be caused by narrowing of a larger artery or occlusion of a smaller vessel

Unstable angina - Whereas most CAD causes symptoms during exertion, the symptoms will appear at rest.

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17
Q

When should not give Nitro during a STEMI

A

When ST changes are in the inferior leads (II, III and AVF) because it is R sided and thought to be more preload dependent. Nitro could drop preload.

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18
Q

Priorities for ACS

A

ASA 81mg chewed - makes platelets less sticky

Nitroglycerin 0.4mg SL every 5 minutes as needed for chest pain (except in inferior MI) - this will cause vasodilation and decrease BP to hopefully get blood passed the clot.
- Short half life. Can reverse with fluids

Oxygen if necessary

Morphine 2-4mg IV with caution
- Lowers anxiety and pain but can drop BP and preload

If STEMI - give heparin and revascularize with either PCI or thrombolytics

If NTEMI - give heparin, get ECHO and then consider coronary angiogram

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19
Q

What is the timeframe for PCI after onset of cardiac symptoms

A

within 3 hours
Otherwise you will need thrombolytics

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20
Q

When is CABG indicated?

A

If the CAD is noted to be affecting the:

left main coronary artery
Three major vessels (LAD, LCX, RCA)
Diffuse disease not amenable to PCI

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21
Q

Cardiogenic Shock: Causes, symptoms and treatment

A

Acute pump failure, usually by massive MI because a large enough portion of the heart does not move d/t ischemia

Signs and symptoms include: hypotension, pulmonary edema, tachyarrhythmia, oliguria, acidosis, and cyanosis

Largely fatal

Treatment includes:
Revascularization
Antiarrythmic agents
Vasopressors
VAD
Balloon Pump

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22
Q

Basics of how a Balloon Pump works

A

Utilized in cardiogenic shock and is a place holder for a CABG
Inserted through the femoral vein into the aorta
It will time itself with an EKG and inflate during diastole in order to push blood into coronary arteries and hopefully past occlusion
It deflates just prior to systole, helping to empty and suck out the LV
Creates a larger MAP

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23
Q

Differences in systolic and diastolic Heart Failure

A

Systolic Dysfunction: Failure of the heart’s pumping function - HFrEF
–Ejection fraction drops
–Increase in fluid to the lungs (crackles) because of LV backwards pressure
–results in fluid in the tissue because of RV backwards pressure into the vasculature causing dependent edema.

Diastolic Dysfunction: Failure of the heart’s filling function - HFpEF
–EF is largely normal (50-65%)
–Inadequate stroke volume because of hypertrophy of the ventricular wall

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24
Q

Risk factors for Heart Failure

A

AsCVD
Viral infections of the heart muscle (myocarditis)
Severe ETOH use - ETOH cardiomyopathy
Arrhythmias

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25
New York Heart Association Classes of Heart Failure
New York Heart Association Classes of Heart Failure: Class I: No symptoms with any activity Class II: Limitation only with strenuous exertion. No limitation with mild exertion Class III: Limitation with exertion but no dyspnea at rest Class IV: Dyspnea at rest
26
Treatment of CHF
Medications: --ACE-I/ARB to stabilize remodeling and improve BP (ACE-I first line treatment) --Digoxin for HR control --Diuretics to help with fluid retention Lifestyle modifications: --Physical activity as tolerated --Treat sleep apnea --Weight reduction --Sodium restriction (no more than 1500mg per day) --Fluid restriction (no more then 1.5L per day for NYHA Class III and IV
27
Digoxin - How does it work and what does it treat?
Used to treat A-fib Slows heart rate and increase the force of contraction Very narrow therapeutic window so you need to check a level to avoid toxicity --rapidly deadly, severe bradycardia and hypotension
28
Management of decompensated Heart Failure
Could present with severe hypoxia and/or hypo- or hypertension Could happen over days to weeks and they could develop worsening edema. Could happen very suddenly over minutes and cause flash pulmonary edema --Sudden change in afterload Treatment is ensuring adequate gas exchange (O2 BiPAP, CPAP, intubation) and afterload reduction (nitrates) Lasix takes an hour or so to work and will not help with flash pulmonary edema
29
Hypertrophic Cardiomyopathy: Causes and treatments
Often genetic Cardiac myocytes increase in size and therefore the ventricular wall increases as well Often happens in athletes due to constant exertion Can cause sudden death due to VT Can present as diastolic heart failure Treated with pure beta 2 antagonists - Atenolol
30
Takotsubo Cardiomyopathy
Broken Heart Syndrome Transient condition which causes increased contraction at the LV base, ballooning of the LV apex, disordered response to catecholamine stress Presents like CHF with systolic dysfunction but on EKG shows anterior STEMI but patent coronary arteries on cardiac cath Usually results in a few days - can give metoprolol and consider balloon pump
31
Peripartum cardiomyopathy
Form of dilated cardiomyopathy that occurs during pregnancy for unknown reasons Often confused with normal sxs of pregnancy (SOB, leg swelling) but progress to more overt signs of CHF (crackles on exam) Treatment is to deliver the baby
32
Inflammatory myocarditis
Can be caused by infection --Insect borne infections (Borrelia burgdorferi causes Lyme Disease or Trypanosoma cruzi which causes Chagas' Disease - Central/South America) --Parvovirus B19, Coxsackie --Hypersensitivity after infection with Strep Pyogenes Presents as CHF with systolic dysfunction Treatment is focused on underlying causes - treating the infection
33
Alcoholic Cardiomyopathy
Caused by constant high intensity exposure to large amount of alcohol, causing myocardial cell death leading to dilated cardiomyopathy Presents as CHF with systolic dysfunction Most common in males ages 30-50 (not common for regular CHF to present in this age group) Treatment focuses on cessation of ETOH
34
Mitral Stenosis: Causes, symtoms, treatment
Almost always caused by Rheumatic heart disease, which is a type II hypersensitivity reaction during the later phases of a strep pyogenes infection (strep or scarlet fever left untreated) which causes a thickened mitral valve, thickened chordae tendinae and hypertrophied left ventricle. Sxs are that of CHF Findings include diastolic murmur heard best at the apex with the bell and sometimes an S3 Often asymptomatic but for symptomatic disease, treatment is the same as CHF and AF (risk for arrhythmias) Treated surgically with by valvuloplasty (percutaneous balloon) or mitral valve replacement
35
Aortic stenosis: Causes, symptoms, exam findings and treatments
Caused simply by aging in 50% of cases but also congenital bicuspid aortic valve, or rheumatic heart disease Common symptoms are exertional syncope, angina, CHF Exam findings reveal a loud murmur, usually @ RUSB, occasionally an S4 (Tennessee) and displaced PMI Treatment is with long acting nitrites in order to reduce afterload. Aortic valve replacement is generall the surgical treatment but sometimes can be done with TAVR
36
Aortic Regurgitation
Can be acute (endocarditis) or chronic (aging, Marfan's syndrome, congenital bicuspid valve) Sxs include that of CHF but frequently with a pronounced shock presentation Water hammer pulse - high peak of systole and falls again, intense peaks.
37
Mitral regurgitation: Causes, sound, treatment
As with aortic regurg, can be acute (endocarditis) or chronic (aging, connective tissue) Regurgitant jet - squirt of blood back into the LA. Can hear it when listening to the back. Treatment of chronic MR is focused on afterload reduction (to lower LVEDP) but for acute MR, an IABP can be used for systolic unloading until the patient can be stabilized for emergency mitral valve repair
38
Tricuspid regurgitation
Backflow of blood into the RA during systole Chronic TF can be caused by Cor Pulmonale (isolated RV failure related to pulmonary hypertension but acute can be caused by endocarditis Symptoms are that of backward RV failure: ascites, hepatomegaly, edema and JVD Exam findings including A-fib and a systolic murmur at the LLSB that intensifies with deep inspiration Treatment of the underlying disease is the most important but if necessary, surgical repair is utilized (never replaced)
39
Physical exam findings of endocarditis
Persistent fever New heart murmur Weight loss Night sweats Coughing Vascular phenomena: septic emboli, Janeway lesions (small, not painful macules on the palms and soles), fingernail hemorrhages, renal infarct, splenic infarcts Immunologic phenomena: Glomerulonephritis, Osler's nodes (painful red nodules in the distal phalanges), Roth's spots on retina
40
Treatment of endocarditis
Usually accompanied with CHF so treatment includes afterload reduction and adequate gas exchange Generally a high-dose long term (months) course of IV penicillin G or Vancomycin IV is selected but tailored therapy is needed based on culture results Surgical debridement is often needed but need to control infection first
41
What size thoracic aortic aneurysm should be considered for repair
A thoracic aorta >4.5cm is considered aneurysmal and any aneurysm >6cm should be considered for repair
42
What happens in an aortic dissection?
Dissection usually occurs before rupture. It usually involves the intima tearing away from the media and blood spilling into a newly formed space. Most often presents with chest pain radiating to the back with a "ripping" or "tearing" character. Involves unequal blood pressures in the upper extremities Diagnosed by CT angiography
43
When should an abdominal aortic aneurysm be considered for repair?
An abdominal aorta >3cm is considered to be aneurysmal and those >5.5 should be considered for repair
44
Who is most likely to develop a thoracic aortic aneurysm?
Those under 40 - Marfan's or Ehlers-Danlos Those over 40 - HTN Also family hx of TAA is more likely to develop one
45
What is the most common cause of an abdominal aortic aneurysm?
Most often caused by AsCVD of the lower extremities but HTN plays a role as well Pressure is backing up from the legs into the abdominal aorta
46
What are the symptoms/presentation of an abdominal aortic aneurysm?
Exam findings include an often pulsatile abdominal mass with an associated bruit Decreased pulses in the legs Diagnosed most sensitively by CT angiography
47
Aortic Aneurysm Dissection/Rupture Stepwise Management
1) Assure a patent airway 2) Establish two large bore IVs 3) Lower blood pressure rapidly with medications and keep MAP at 60 -Esmolol, Labetalol - beta blockers also lower the HR - keep it less than 100 -Nicardipine 4) Restore any volume loss with IV crystalloid then colloid (consider activation of the "massive transfusion protocol") 5) Call cardiothoracic and/or vascular surgery
48
Treatment of aneurysms
Tight BP control! Frequent exams by ultrasound to monitor for increase in size or for dissection (every few months) If stable, then nothing really to do, just keep BP under control Could consider surgery but would want to consider the age of the patient and risk for poor outcomes
49
How does pericarditis present?
Pericarditis is an acute inflammation of the pericardium (sac in which the heart sits) Presents as chest pain, which is pleuritic and positional (relieved if sitting up, worse if lying down) and dyspnea On EKG, ST elevation or depression that is global or does not follow a coronary territory, CXR with slightly increased silhouette, labs show slightly increased ESR/CRP
50
Causes of pericarditis
Viral infections - Coxsakie, EBV, Varicella, HIV --Treatment is symptomatic and usually involves NSAIDs --Can be managed at home and will go away Uremic from chronic kidney failure --Treatment involves hemodialysis to remove excess urea Neoplastic - from cancers of the chest
51
Pericardial effusion - Causes and How is it diagnosed
Pericardial effusion is a collection of fluid inside the pericardium Causes are varied but usually transudative (from CHF) and sometimes exudative (from cancers of the chest) Sometimes the result of bleeding - trauma to the chest Diagnosis is made by echocardiogram
52
Beck's Triad for Pericardial Tamponade
Beck's Triad: --Decreased blood pressure --Distant heart sounds --Distended juglar veins
53
Symptoms and Treatment of Pericardial Tamponade
--Beck's Triad --Pulsus Paradoxus - Decrease in the systolic BP by >10mmHg on inspiration --Narrow pulse pressures --Low EKG voltage - needs to conduct through extra fluid Treatment is to increase the preload (IVF) to push back against the pericardium so the heart can fill Emergency pericardiocentesis may be needed
54
Risk factors of Venous Thromboembolism (VTE)
Virchow's Triad --Stasis of blood flow --Endothelial injury --Hypercoagulation Known acquired risk factors: --Older age --Major surgery and/or orthopedic surgery --Cancers --Immobilization --Pregnancy --Central venous catheters --chemotherapy --Smoking --Oral contraceptive use
55
Clinical assessment tool assess the probability of a VTE
Wells Score: Active cancer treatment within the last 6 months Calf swelling >3cm Swollen unilateral superficial veins Unilateral pitting edema Previous documented DVT Swelling of entire leg Localized tenderness along the deep venous system Paralysis, paresis or recent cast immobilization of lower extremity Recently bedridden >3days or major surgery requiring regional or general anesthetic in the past 12 weeks Alternative diagnosis at least as likely: -2 points High probability if greater than 2
56
Stepwise Prevention of VTE in hospitalized patients
Low risk: Minor surgery, stay inpatient for less then 2 days --Early ambulation Moderate Risk: Patients who are neither high nor low risk --Enoxaparin or Unfractionated Heparin (if GFR <40) --Consider sequential compression device High Risk: Elective hip or knee surgery, acute spinal cord injury with paresis, multiple traumas, cancer --As above but can also consider warfarin --Should have sequential compression device
57
Treatment for VTE
1) Parenteral anticoagulation (unfractionated heparin, low-molecular weight heparin, fondaparinux) for 5 days 2) Then switch to oral anticoag If the VTE was provoked (s/p surgery) then continue oral anticoags for 3 months. If the VTE was unprovoked then oral anticoags should be continued for longer IVC filter can be placed if the VTE is very small and could move or for people that cannot tolerate anticoagulation
58
Treatment for symptomatic bradycardia
Atropine Can be given every 3-5 minutes PRN but DNE 3mg atropine total If unsuccessful, will need transcutaneous pacing If transcutaneous pacing is unsuccessful, will need a transvenous pacing wire
59
Supraventricular tachycardia - definition and treatment
Very rapid rate (upwards of 200 bpm) P waves are not often visible, buried in the T wave QRS is narrow First treat with vagal maneuvers (trendelenburg and then have them bear down) If that is unsuccessful, give adenosine 6mg IV rapid push. If that is unsuccessful give additional 12mg IV rapid push If that is unsuccessful consider cardioversion
60
Treatment of Atrial Flutter
Calcium channel blocker or beta blocker Sawtooth appearance because of rapid flutter of atria
61
Treatment of Atrial Fibrillation
Rapid A-fib is usually treated with diltizem 10mg IV every 15 mins --Think about why they are having A-fib (new? Sepsis? hypoMg? Hyperthyroid? ETOH/substances?) Consider DOAC for outpatient (Eliquis, Xarelto, Pradaxa) given less risk for bleeding complication --CHA2DS2VASc score ---CHF, Hypertension, Age >75 (2pts), Diabetes, Stroke (2pts), Vascular disease, Age 65-74, Sex category (female) ASA if young and otherwise healthy
62
What is the gold standard for diagnosis of coronary artery disease?
Coronary angiography
63
Which valves are considered AV and which are considered semilunar?
AV = atrioventricular (Mitral, tricuspid) Semilunar = aortic, pulmonic
64
What do S1 and S2 correspond to?
In S1, the AV valves close and semilunar valves open In S2, the AV valves open and the semilunar valves close
65
What does S3 sound like and what does it suggest?
Ken-tuck-y Caused by increased fluid states (heart failure, pregnancy) In pregnancy, it is a normal finding The number 3 looks like a fat person - too much fluid
66
What does S4 sound like and what does it suggest?
Ten-ne-ssee Stiff ventricular wall (MI, left ventricular hypertrophy, chronic HTN) The number 4 looks stiff - stiff ventricular wall, hypertrophy
67
Grades of murmurs
1/6: Barely audible 2/6: Audible but faint 3/6: Moderately loud: easily heart 4/6: Loud, associated with a thrill 5/6: Very loud, heard with one corner of the stethoscope off the chest 6:6: Loudest
68
What does mitral regurgitation sound like?
Systolic murmur at 5th ICS, mid clavicular line; may radiate to base or left axilla Musical, blowing, or high pitched, may follow S3 Know that it radiates to the base or the axilla***
69
What does aortic regurgitation sound like?
Diastolic "blowing" murmur at 2nd left ICS
70
How do you remember which type of valvular disease is systolic and which are diastolic
Ms. Ard and Mrs. Ass Mitral Stenosis Aortic Regurgitation Diastolic Mitral Regurgitation Aortic Stenosis Systolic
71
Where are murmurs heard? Which intercostal space?
5th ICS - apex - mitral 2nd or 3rd - base - aortic
72
Signs and symptoms of (acute) left sided heart failure
Left failure - LUNGS Dyspnea at rest Coarse rales over all lung fields Wheezing, frothy cough Appears generally healthy except for the acute event S3 gallop Murmur of mitral regurgitation (systolic murmur loudest at the apex)
73
Signs and Symptoms of (chronic) right sided heart failure
Right ventricle hypertrophy - Cor Pulmonale Jugular vein distention (JVD) Hepatomegaly, splenomegaly Dependent edema: Result of increased capillary hydrostatic pressure Paroxysmal nocturnal dyspnea Appears chronically ill Diffuse chest wall heave Displaced point of maximal impulse Abdominal fullness Fatigue on exertion S3 and/or S4
74
What causes AV nicking?
AV nicking is a distorted blood vessel in the eye. It is caused by chronic HTN
75
Management (Pharm) of HTN
Thiazide type diuretics are used for first line treatment Non African American: --Thiazide Diuretics --ACE-I --ARB --Calcium Channel Blockers African Americans: --Thiazides --Calcium channel blockers Diabetics: --ACEI (or ARB if cannot tolerate ACEI) Adults with CKD: ACEI
76
Presentation and management of hypertensive urgency
180/110 May or may not have a severe headache, SOB, epistaxis or severe anxiety Treatment: Oral therapies (such as clonidine) Parenteral therapies are rarely needed
77
Presentation of hypertensive emergency
180/120 Requires immediate (within 1 hour) blood pressure reduction to prevent or limit target organ damage BP may be less than 180/120 with any of the following: -Malignant hypertension -Hypertensive encephalopathy -Intracranial hemorrhage -Unstable angina -Acute MI -Acute heart failure -Dissecting aortic aneurysm -Eclampsia
78
Management of hypertensive emergency
ICU admission Parental administration of antihypertensives -Nicardipine drip -Nitroprusside drip For most complications of hypertensive emergency, SBP should be lowered <140. --For aortic dissection, it should <120 Without compelling complications, SBP should be reduced by no more than 25% within the first hour, then if stable to 160/100 within the next 2- hours and then cautiously to normal during the following 24-48 hours.
79
What is angina and what are the types?
Angina is decreased blood flow through the vessels leading to tissue ischemia ***Not caused by obstruction but rather decreased blood flow Stable - Exertional - most common Prinzmetal's Angina - (variant/vasospastic) - Occurs at various times, including rest ----Caused by influx of calcium - therefore these pts are treated with CCB ----Also notable for ST-elevation Unstable (pre-infarction, rest or crescendo, coronary syndromes) Microvascular - Metabolic syndrome
80
Symptoms of stable angina and physical exam findings
Symptoms: Characteristic chest discomfort lasting several minutes Exertional is usually precipitated by physical activity: subsides with rest Nitroglycerin shortens or prevents attacks Physical exam findings: Usually ST depressions on EKG May see signs of peripheral arterial disease Levine's Sign - Clenched fist sign over the chest Transient S4 not uncommon during angina
81
Lab exam findings for angina and treatment
EKG may be normal with down sloping of the ST segment or T-wave peak or inversion Serum lipids will be elevated Coronary angiography is the definitive diagnostic procedure but not indicated solely for diagnosis Treatment: ASA 81mg PO Daily Can consider starting Nitrates, Beta blockers or CCB
82
Normal findings for Lipid Panel: Total Cholesterol: Very low density lipoprotein (VLDL)/Triglycerides: Low Density Lipoprotein (LDL): High Density lipoprotein (HDL):
Total Cholesterol: Desirable <200 Very low density lipoprotein (VLDL) - Triglycerides: <150 Low Density Lipoprotein (LDL): <100 High Density lipoprotein (HDL): >40
83
Statin therapy - high intensity, moderate intensity and low intensity Who gets which type of statin?
High Intensity Statin Therapy: -Daily dose lowers LDL by >50% --Atorvastatin 40-80mg Daily --Rosuvastatin 20-40mg Daily Moderate Intensity Statin Therapy: -Daily dose lowers LDL by 30-50% --Atorvastatin 10-20mg Daily --Rosuvastatin 5-10mg Daily --Simvastatin 20-40mg Daily --Pravastatin 40-80mg Daily --Lovastatin 40mg Daily --Fluvastatin 80mg Daily --Pitavastatin 2-4mg Daily Low Intensity Statin Therapy: -Daily dose lowers LDL by <30% --Simvastatin 10mg Daily --Pravastatin 10-20mg Daily --Lovastatin 20mg Daily --Fluvastatin 20-40mg Daily --Pitavastatin 1mg Daily
84
Physical exam findings in ACS
Dysrhythmia common S4 very common Wheezing Pulmonary crackles Low grade fever during first 48 hours Tachycardia
85
Location of MI on EKG I, aVL: II, III, aVF: V leads (precordial leads) or V3 and V4:
I, aVL: Lateral II, III, aVF: Inferior V leads (precordial leads) or V3 and V4: Anterior
86
Normal ranges for INR and PT
INR: 0.8-1.2 Coumadin therapeutic: 2-3 If too low, need more coumadin. If too high, need Vit K PT: 11-16 Therapeutic 1.5-2.5 x normal
87
Classic clinical presentation and physical exam findings in Peripheral Vascular Disease
Problem with the arteries Caused by atherosclerosis Peak incidence: 40-70 years old HLD, Smoking, Diabetes Usually first complain of calf pain (claudication) which progresses to pain at rest Physical exam: Shiny/hairless skin Dependent redness Pallor Cyanosis Ulcerations Reduced pulses
88
Laboratory diagnostics in peripheral vascular disease
Doppler ultrasound to evaluate flow Ankle Brachial index*** X-rays may show calcification Arteriography: most definitive
89
Classic clinical presentation and physical exam findings for chronic venous insufficiency
Impaired venous return More common in women Symptoms: -Aching of the lower extremities relieved by elevation -Edema after prolonged standing -Night cramps of the lower extremities Physical exam findings: -Trophic changes in brownish discoloration -Stasis leg ulcers -Edema of lower extremities -Dermatitis may be common -Cool to touch
90
What is May-Thurner syndrome?
Compression of the left common iliac vein by overlying right common iliac artery Causes LLE DVT
91
How do you treat acute wheeping dermatitis caused by chronic venous insufficiency?
Tap water compress Hydrocolloid dressings For less acute dermatitis - hydrocortisone cream
92
Cardiogenic shock - Hemodynamics
Only type of shock with an initially high wedge pressure -Decreased Cardiac Output/Cardiac Index -Increased Central Venous Pressure -Increased Wedge Pressure -Increased Systemic vascular resistance -Decreased SVO2
93
What are the two types of shock with an initially high CVP
Cardiogenic and Obstructive
94
What is the only type of shock that has an initially high Wedge Pressure
Cardiogenic

Acute Care NP Exam (22 decks)

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