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Surgery > Cardiovascular from PANCE Pearls > Flashcards

Cardiovascular from PANCE Pearls Flashcards

1
Q

What is Angina

A

Substernal chest pain often brough on by exertion

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2
Q

What causes Angina

A

CAD
Coronary Artery Spasms
Pulmonary HTN
Hypertrophic Cardiomyopathy

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3
Q

What are risk factors for Angina

A

DM
Hyperlipidemia
HTN
Smoking

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4
Q

Sx of Angina

A

Substernal chest pain
May radiate to arm, lower jaw, back, shoulder
Short duration

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5
Q

Dx of Angina
Best non-invasive
Gold Standard

A

EKG: ST Depression with exertion, T wave inversion
Stress is best non-invasive screening
Coronary Angiograph is Gold Standard and Definitive dx

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6
Q

What is a Cath

A

Coronary Angiography

Outlines coronary artery anatomy, determines location and extent of CAD

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7
Q

What are indictions for PTCA (Percutaneous Transluminal Coronary Angioplasty) or PCI (Percutaneous Coronary Intervention

A

Used for 1 or 2 vessel disease not involving main left coronary artery + Normal or near normal left ventricular function

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8
Q

What are indications for CABG (Coronary Artery Bypass Graft)

A

Left main coronary artery disease
Sx 3 vessel disease
Left Ventricular EF

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9
Q

How does Nitroglycerin work

A

Increased myocardial blood supply, so increases oxygen and collateral blood flow
Decreases Demand which will reduce cardiac work and decrease preload

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10
Q

How do beta-blockers work

A

Increases myocardial blood supply
Decreases Demand
1st line drug for chronic management

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11
Q

How do Calcium Channel Blockers work

A

Increased myocardial blood supply
Decreases Demand
Used in patients not able to use beta-blockers

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12
Q

How does Aspirin work

A

Prevents platelet activation/aggregation

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13
Q

What is Acute Coronary Syndrome

A

Symptoms of acute MI due to acute plaque rupture and coronary artery thrombosis
Includes unstable angina, NSTEMI, and STEMI

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14
Q

What causes Acute Coronary Syndrome

A

Atherosclerosis caused by plaque rupture

Coronary artery vasospasms, usually due to cocaine, Prinzmetal’s variant angina

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15
Q

Sx of Acute Coronary Syndrome

A

Anginal Pain
Sympathetic stimulation: Anxiety, Diaphoresis, Tachycardia, N/V, Palpitations, Dizziness
Silent MI: atypical sx such a abdominal pain, dyspnea without chest pain

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16
Q

Dx of Acute Coronary Syndrome

A

EKG
Unstable Angina and NSTEMI: T wave inversion/ST Depression
STEMI: ST elevations

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17
Q

What does the location of Q waves or ST elevation tell you about where the MI occured

A

V1-V4: Anterior. Involves Left Anterior Descending
I, aVL, V5, V6: Lateral. Involves Cirucumfelx
I, aVL, V4, V5, V6: Anterolateral. Involves LAD or CFX
II, III, aVF: Inferior. Involves Right Coronary Artery
ST DEPRESSION in V1-V2: Posterior. Involves RCA, CFX

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18
Q

What are 2 main cardiac markers and what does the timing of their apperace mean

A

CK/CK-B: Peaks 12-24 hours, Baseline at 3-4 days

Troponin: Peaks 12-24 hours, Baseline 7-10 days

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19
Q

What is Prinzmetal’s Angina

A

Coronary Spasm that leads to transient ST elevations

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20
Q

Sx of Prinzmetal’s Angina

A

Ches pain at rest, usually in the mornings with hyperventilation, emotional stress or cold exposure. Not usually due to exertion

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21
Q

Dx of Prinzmetal’s Angina

A

EKG: Transient ST elevations (usually resolve wth CCB and NTG)
Angiography: No fixed stenosis seen

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22
Q

Tx of Prinzemtal’s Angina

A

CCB, NTG as needed

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23
Q

What is Heart Failure

A

Inability of the heart to pump sufficient blood to meet the metabolic deamns of the body at normal filling pressures

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24
Q

What causes Heart Failure

A

CAD

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25
Q

What causes Left sided HF

A

CAD and HTN

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26
Q

What causes Right sided HF

A

Left sided HF

Pulmonary disease

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27
Q

What is the pathophysiology behind CHF

A

An insult leads to increased afterload, increased preload, decreased contractility
Injured heart tries to make short term compensation tha promotes cardiovascular deterioration
Sympathetic nervous system is activated, myocyte hypertrophy/remodeling, RAAS activation, fluid overload, ventricular remodeling

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28
Q

Sx of Left Sided HF

A

Increased venous pressure from fluid backing up into lungs
Dyspnea, Orthopnea, Paroxysmal Nocturnal Dyspnea
Pulmonary Cognestion: Rales, Rhonchi, pink frothy sputum
HTN, Cheyne Stoke’s
Dusky pale skin, Diaphoresis

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29
Q

Sx of Right sided HF

A

Increased systemic venous pressure, see signs of systemic fluid retention
Peripheral Edema
Jugular Venous Distention
Anorexia, N/V, Hepatosplenomegaly, RUQ tenderness, Hepatojugular Reflex

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30
Q

Dx of CHF

A

Echo: Can test Ejection Fraction
CXR: Cephalization of flow, Kerley B lines, butterfly pattern, Cardiomegaly, Pleural Effusions
Increased BNP (Ventricles release BNP during volume overload)

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31
Q

Tx of CHF

A

Ace-Inhibitors: 1st line. Decreased mortality
Beta-Blockers: Decreased mortality
Diuretics: Treats sx
Digoxin: Treats sx

32
Q

What are the meds that decreased mortality in CHF

A

Ace-I, ARB, Beta-Blocker, Nitrates, Some Diuretics (Hydralazine, Spironolactone)

33
Q

What it the outpatient tx for CHF

A

Ace-I + Diuretic, eventually add Beta-Blocker

Implantable Cardioverter Defibrillator if EF

34
Q

Hospital management of CHF

A

LMNOP

Lasix, Morphine, Nitrates, Oxygen, Position

35
Q

What is Hypertensive Urgency

A

BP of 220/120 without end organ damage

36
Q

Tx of Hypertensive Urgency

A

Reduced BP by 25% in first 24-48 hours using oral agents

37
Q

What is Hypertensive Emergency

A

BP of 220/120 with acute end-organ damage

Encephalopathy, hemorrhage, Acute Coronary Syndrome, HF, Aortic Dissection, AKI, Proteinuria

38
Q

Tx of Hypertensive Emergency

A

Reduce BP by 10% in the first hour then another 15% the next 2-3 hours using IV agents

39
Q

What is Peripheral Arterial Disease

A

Atherosclerosis of the lower extremities

40
Q

Sx of Peripheral Artery Disease

A

Intermittent Claudication: Pain/Discomfort with exercise/walking and relieved with rest
Resting leg pain (advanced disease)
Acute Arterial Embolism: Parasthesias, Pain, Pallor, Pulselessness, Paralysis, Poikilothermia, Livedo Reticularis (mottling with arteriolar occlusion)
Gangrene, Ulcers

41
Q

What will you see on physical exam with Peripheral Artery Disease

A

Decreased or absent pulses, Bruits
Atrophic skin chanes (thin, shiny skin, hair loss, thickened nails)
Pale on elevation, dusky red with dependency
LATERAL malleolar Ulcers

42
Q

Dx of Peripheral Artery Disease
Screening
Gold Standard

A

Ankle-Brachial Index is most useful screening
Angiography: Gold standard
Duplex Ultrasound

43
Q

Tx of Peripheral Artery Disease

A

Platelet Inhibitors: Cilostazol, ASA, Plavix
Revascularization: PTA, Bypass grafts, Endarterectomy
Supportive: Foot care, Exercise
Amputation if severe/grangrene

44
Q

What is an Abdominal Aortic Aneurysm

A

Focal dilation of aortic diameter at least 1-1.5 times diamter measured at level of renal arteries
>3.0cm is considered aneurysmal
Usually occurs Infrarenally

45
Q

What are risk factors for Anuerysms

A 
Atherosclerosis
Age >60yrs
Smoking
Caucasian Males
Hyperlipidemia, DM, Marfan's
46
Q

Sx of Aneurysm

A

Most are asymptomatic an are incidental findings
Acute Leakage is rapidly fatal
Severe back or abdominal pain, syncope, Hypotension, Pulsatile abdominal mass, Flank Ecchymosis
Ripping chest pain = Thoracic Dissection

47
Q

Dx of Aneurysm
Initial test
Gold Standard

A

Ultrasound is first test
CT is test of choice for thoracic
Angiogram is gold standard
MRI/MRA

48
Q

Tx of Aneurysm

A

3-4cm: Monitor via ultrasound every year
4-4.5cm: Monitor via ultrasound every 6 months
>4.5cm: Vascular Surgeon Referral
>5.5cm: Immediate surgical repair

49
Q

What is an Aortic Dissection

A

A tear in the innermost layer of aorta (Intima)

50
Q

What leads to an Aortic Dissection

A

Intimal wall tear leads to propagation of tear

51
Q

Risk factors for Aortic Dissection

A

HTN, Age, Vasculitis, Trauma, Collagen Disorders

52
Q

Sx of Aortic Dissection

A

Sudden onset of severe, tearing chest/back pain
Variation in pulses between left and right arm
HTN
New Aortic Regurgitation

53
Q

Dx of Aortic Dissection

Gold Standard

A

CXR: Wide mediastinum
CT scan with contrast
MRI Aniography is Gold Standard
Trans Esophageal Echocardiography

54
Q

Tx of Aortic Dissection

A

If in ascending: Surgery

If descending: Medical management with Labetalol

55
Q

What is Giant Cell Arteritis

A

A vasculitis

56
Q

What should you associate with Giant Cell Arteritis

A

Polymyalgia Rheumatica

57
Q

Sx of Giant Cell Arteritis

A

New onset, unilateral tempral headache
Jaw Claudication with Mastication
Acute Vision changes (if not treated will lead to blindness!)
Fatigue, weight loss, anorexia, fevers, night sweats

58
Q

Dx of Giant Cell Arteritis

A

Increased ESR, Increased CRP

Temporal Artery Biopsy: See Mononuclear Lymphocyte Infiltration, Ultinucleated Giant Cells

59
Q

Tx of Giant Cell Arteritis

A

High Dose Corticosteroids: 40-60mg/day x6 weeks

Methotrexate and Azathioprine

60
Q

What is Superficial Thrombophlebitis

A

Inflammation of superficial vein and or thrombus

Associated with IV cath, Trauma, pregnancy, varicose veins

61
Q

Sx of Superficial Thrombophlebitis

A

Local Phlebitis: Tenderness, pain, induration, edema, erythema along coure of superficial vein

62
Q

Dx of Superficial Thrombophlebitis

A

Venous Duplex Ultrasound: Noncompressible vein with clot and vein wall thickening

63
Q

Tx of Superficial Thrombophlebitis

A

Supportive: Elevation, Warm Compress, NSAIDS, compression Stockings
If Aseptic: NSAIDS, Heparin, Warfarin
Septic: IV Abx (Penicillin + Aminoglycosides)
Phelebectomy if extensive

64
Q

What is a Deep Venous Thrombosis

A

Most important consequence of PE

65
Q

What are risk factors for DVT

A

Vrichow’s Triad: Venous Stasis, Endothelial Damage, Hypercoagulability

66
Q

Sx of DVT

A

Unilateral swelling/edema of lower extremity
Calf Pain/Tenderness
Homan’s Sign: Calf Pain with dorsiflexion while knee is flexed
Phlebitis: Local warmth, erythema, palpable cord

67
Q

Dx of DVT

A

Venous Duplex Ultrasound: 1st line
D-Dimer: Negative r/o DVT, Positive need more workup
Venography: Gold Standard

68
Q

Tx of DVT

A

Anticoagulation: UF Heparin, LMW Heparin, Warfarin

IVC Filter

69
Q

What are Varicose Veins

A

Dilated, Tortuous Superficial Veins secondary to defective valve structure and function of superficial veisn

70
Q

Sx of Varicose Veins

A

Often asymptomatic but cause cosmetic damage
Dull ache or pressure sensation worse with prolonged standing and relieved with elevation
VENOUS STASIS ULCERS: Severe varicosities resulting in skin ulceration

71
Q

Tx of Varicose Veins

A

Conservative: Elevation, Compression Stockings, Avoid Prolonged Standing
Sclerotherapy, Radiofrequency or laser ablation

72
Q

What is Chronic Venous Insufficiency

A

Vascular incompetency of either deep and or superficial veins

73
Q

Sx of Chronic Venous Insufficiency

A

Leg pain: Burning, Aching, Throbbing
Pain worse with prolonged standing/sitting
Improves with leg elevation or walking
Leg edema, Stasis Dermatitis
Brownish Hyperpigmentation
Venous stasis ulcers are usually MEDIAL MALLEOLUS

74
Q

Dx of Chronic Venous Insufficiency

A

Ankle/Brachial Index
Trandelenburg Test: Slow filling at ankle suggests perforator competency
Ultrasound

75
Q

Tx of Chronic Venous Insufficiency

A

Elevation, Compression Stockings
Ulcer Treatment: Wet to dry dressings, skin grafting, hyperbaric oxygen if severe, control edema
Venous valve transplant

Surgery (12 decks)

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