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CMC > Cardiovascular Conditions > Flashcards

Cardiovascular Conditions Flashcards

1
Q

What is coronary artery disease?

A

cardiovascular condition, involves narrowing or blockage of coronary arteries due to atherosclerosis.
-impedes blood flow to myocardium, leading to ischemia (with pain: angina pectoris)
-potentially resulting in ACS or MI

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2
Q

What is acute coronary syndrome?

A

term used to describe a range of conditions associated with sudden, reduced blood flow to the heart.
-3 entities: STEMI, NSTEMI, and unstable angina

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3
Q

What causes ACS?
What is the pathophys?

A

the rupture of an atherosclerotic plaque in a CA, leading to partial or complete blockage of blood flow

-disruption of plaque triggers platelet aggregation and thrombus formation. results in ischemia and potential necrosis of myocardial tissue. extent of damage depends on duration and severity of ischemic event.

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4
Q

CAD can lead to _________ , or progress to ______.

A

angina pectoris

ACS

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5
Q

s/s ACS

A

CP or discomfort that may radiate to shoulders arms, neck, jaw, back.
-described as pressure or squeezing
-dyspnea, diaphoresis, nausa, syncope

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6
Q

Dx of ACS

A

ECG
cardiac biomarkers

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7
Q

Why ECG for dx ACS?

A

differentiates between stemi and nstemi/ unstable angina

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8
Q

What does NSTEMI ECG usually show?

A

ST segment depression or T wave inversion

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9
Q

Cardiac biomarkers for dx ACS

A

Troponins.
-elevated indicate myocardial necrosis and help differentiate between NSTEMI and unstable anginga

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10
Q

ACS management

A

pharm:
1. antiplatelet agents (aspirin and P2Y12 inhibitors)
2. anticoagulants
3. beta blockers
4. ACE inhibitors
5. statins

reperfusion therapy:
-PCI
-thromobolysis

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11
Q

What do ST segement elevations signify?

A

COMPLETE blockage of one or more CAs
(indicates acute transmural ischemia)

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12
Q

Pathophys of STEMI

A

results from rupture of atherosclerotic plaque followed by thrombosis, leading to occlusion of the CA.

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13
Q

risk fac

Risk Factors of STEMI (preluding one)

A
  1. HTN
  2. HLD
  3. smoking
  4. DM
  5. family hx CAD
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14
Q

clinical manifestations of STEMI

A

CP (pressure or squeezing) radiating to left arm, neck, or jaw
diaphorsis
dyspnea
nausea
sometimes syncope

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15
Q

post STEMI reperfusion management

A
  1. antiplatelet therapy with aspirin and P2Y12 ihibitors (clopidogrel)
  2. AC with heparin or LMWH
  3. BB to reduce myocardial oxygen demand
  4. ACE inhibitors prevent ventricular remodeling
  5. statins for lipid management
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16
Q

NSTEMI is characterized by

A

partial blockage of a CA, result is reduced blood flow to heart muscle

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17
Q

How is a NSTEMI identified?

A

by cardiac biomarkers, such as troponins, indicating myocardial injury

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18
Q

Pathophy of NSTEMI

A

CA plaque ruptures or erodes, leading to thrombus formation. Not completely obstructied, so some perfusion of myocardium is allowed, BUT insufficient to meet metabolic demands, esp during exertion or stress.

mismatch between o2 supply and demand causes ischemia and myocardial necrosis

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19
Q

clinical manifestations of NSTEMI

A

similar to other forms of ACS, including CP or discomfort that may radiate to arm, neck, jaw, back. (often pressure like)
dyspnea, diaphoresis, nausea, fatigue

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20
Q

Dx of NSTEMI

A
  1. ECG: may show nonspecifc changes (ST depression or T wave inversion)
  2. cardiac biomarkers ** (Troponin I or T)
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21
Q

Management/ Tx of NSTEMI

A

Pharm:
1. antiplatelet agents (aspirin and P2Y12 inhibitors)
2. AC (heparin)
3. BB
4. statins
5. nitrates**

procedure (not all cases)
- PCI

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21
Q

What diagnostic tool helps differentiate between NSTEMI and unstable angina?

A

cardiac biomarkers (Troponin I or T) as they are sensitive indicators of myocardial cell injury

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22
Q

Unstable angina is characterized by_______
and indicates________

A

unexpected CP or discomfort typically at rest or with minimal exertion.

indicates sudden reduction in blood flow to heart muscle, often due to plaque rupture and subsequent thrombus formation in CA

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23
Q

How do stable and unstable angina differ?

A

stable: predictable pattern and relieved by rest or nitro
unstable: unexpected. occurring at rest or with minimal exertion

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24
Q

pathophy of unstable angina

A

disruption of atherosclerotic plaque, leading to platelet aggregation and partial occlusion of CA

(so there is an imbalance between O2 supply and demand)

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25
Q

What is the difference between unstable angina and MI?

A

the partial occlusion of unstable angina does not result in myocardial necrosis

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26
Q

s/s unstable angina

A

-new onset CP (may radiate)
-worsening anginal symptoms (dyspnea, diaphoresis, nausea, syncope)
-angina at rest lasting more than 20 min

*immediate medical eval as may escalate to MI

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27
Q

Dx of unstable angina

A
  1. ECG (may show ST depression or T wave inversion)
  2. cardiac biomarkers (Troponin) remain normal or only slightly elevated since no myocardial necrosis
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28
Q

Management unstable angina

A
  1. anti-ischemic therapy with nitrates and BB
  2. antiplatelet therapy (aspirin, possibly P2Y12 inhibitors like clopidogrel)
  3. AC (heparin)

depending on risks: coronary angiography, PCI, CABG

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29
Q

What is cardiac tamponade?

A

accumulation of fluid in pericardial space, which exerts increased pressure on the heart
impairs ability to fill properly during diastole, leading to *decreased cardiac output and hemodynamic instability *

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30
Q

What are some causes of tamponade?

A

trauma, malignancy, infection, uremia, post MI syndrome

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31
Q

pathophy of cardiac tamponade

A

rapid or excessive accumulation of pericardial fluid overwhelming compensatory mechanisms of heart.

-as intrapericardial pressure rises, it surpasses intracardiac pressures, leading to impaired ventricular filling.

-result is reduced stroke volume and CO (manifests as hypotension and shock)

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32
Q

What is Beck’s Triad? What does it indicate?

A

hypotension, JVD, muffled heart sounds

tamponade

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33
Q

Dx of tamponade

A

assessment, but confirmed with imaging (echo)

Echo shows pericardial effusion and signs of chamber collapse (RA and ventricualr collapse during diastole)

ECG changes: low voltage QRS complexes and electrical alterans due to swinging movement of heart within fluid-filled pericardium

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34
Q

M

Management of tamponade

A

hemodynamics stabilization with IV fluids to augment preload and maintain CO.
-pericardial fluid drainage through pericardiocentesis (using echo guidance) or sx intervention (pericardial window)

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35
Q

What are cardiomyopathies?

A

a group of diseases that affect the heart muscle, leading to impaired cardiac function

resulting in HF, arrhythmias, sudden cardiac death

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36
Q

4 main types of cardiomyopathy

A
  1. dilated
  2. hypertrophic
  3. restrictive
  4. arrythmogenic RV cardiomyopathy (ARVC)
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37
Q

described dilated CM.

causes?

s/s?

A

enlargement and impaired contraction of LV, leading to systolic dysfunction.

-idiopathic or secondary to ischemic heart disease, alcohol abuse, or viral infections

-s/s of HF (dyspnea, fatigue, peripheral edmea)

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38
Q

described hypertrophic CM (HCM).

causes?

s/s?

A

abnormal thickening of myocardium, particular affecting interventricular septum. It can obstruct blood flow out of the LV.

-often inherited in an autosomal dominant pattern.

-CP, syncope, palpitations. *risk for sudden cardiac death due to arrhythmias

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39
Q

described restrictive CM.

causes?

s/s?

A

stiffening of ventricular walls, leading to impaired disatolic filling *without * significant systolic dysfunction

-can be caused by infiltrative diseases such as amyloidosis or hemochromatosis

-s/s:exercise intolerance and right sided HF symptoms (ascites, hepatomegaly)

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40
Q

Dx of cardiomyopathies

A

clinical evaluation
imaging (echo, MRI)
somtimes genetic testing

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40
Q

described arrhythmogenic RV CM.

causes?

s/s?

A

replacement of myocardial tissue with fibrofatty tissue in RV, leading to arrhythmias

-genetic disorder

-palpitations or syncope. risk for sudden cardiac death.

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41
Q

management of CM

A

depending on the type and severity

may include meds like BB or ACE inhibitors
lifestyle mod
ICDs
sx: septal myectomy for HCM

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42
Q

contributors to dysrhythmias

A

electrolyte imbalances, ischemic heart disease, MI, congenital heart defects

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43
Q

generalized tx of arrhythmias

A

antiarrhythmic drugs, AC for thrombus prevention, cardioversion, catheter ablation, pacemaker or defibrillator

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44
Q

classic HF symptoms

A

dyspnea, fatigue, fluid retention (leading to pulmonary congestion or peripheral edema)

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45
Q

two main types of HF

A

Heart Failure with Reduced Ejection Fraction (HFrEF) and Heart Failure with Preserved Ejection Fraction (HFpEF)

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46
Q

HFrEF: systolic or diastolic dysfunction?

A

systolic. heart muscle weakens and cannot contract effectively

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47
Q

HFpEF: systolic or diastolic dysfunction?

A

diastolic. heart loses ability to relax and fill properly during diastole.

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48
Q

Pathophys of heart failure overview

A

involves neurohormonal activation, including the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. These initially compensate for decreased CO, but eventually exacerbate myocardial damage and worsen HF.

compensatory mechanisms lead to vasoconstriction, sodium and water retention, and increased cardiac workload.

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49
Q

Dx of HF

A
  1. history and physical exam
  2. dx tests like echo to asses EF and identify structural abnormalities
  3. Biomarkers (B-type Natriuretic Peptide BNP or N-terminal pro-BNP) crucial for diagnozing and monitoring severity of HF
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50
Q

management of HF overview

A

-lifestyle mod (sodium restrict, fluid management, exercise, no smoking)
-pharm
-device therapy or surgery

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51
Q

Pharm management of HF

A

-ACE inhibitors
-BB
-diuretics
-aldosterone antagonists
-and sometimes ARNIs (angiotensin receptor-neprilysin inhibitors)

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52
Q

advanced HF therapies (devices and surgeries)

A

-CRT cardiac resynchronization therapy
-implantable cardioverter-defibrillators (ICDs)
-mechanical circulatory support (LVADs)
-transplant

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53
Q

Hypertensive urgency criteria
and s/s

A

SBP > 180mmHg or DBP >120 mmHg without evidence of acute target organ damage.
-severe headache, SOB, epistaxis

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54
Q

TX HTN urgency

A

GRADUALLY reduce blood pressure over 24 to 48 hours using oral antiHTN meds

(rapid= possible cerebral hypoperfusion)

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55
Q

hypertensive emergency criteria and s/s

A

similar BP parameters but accompanied by acute, life threatening target organ damage. ex: hypertensive encephalopathy, acute MI, acute LV failure with pulm edema, aortic dissection, acute renal failure

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56
Q

management of hypertensive emergency

A

prompt reduction of MAP by 20-25% within first hour, using IV antiHTN agents
-sodium nitroprusside, labetalol, or nicardipine

subsequent BP reduction should be gradual over next 24 to 48 hours to minimze risk of ischemic complications

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57
Q

What can cause hypertensive emergencies?

A

nonadherence to meds
autonomic dysregulation
secondary causes like pheochromocytoma or renovascular hypertension

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58
Q

examples of inflammmatory and infectious heart conditions

A

myocarditis, pericardities, endocarditis, rheumatic heart disease

59
Q

What is Myocarditis?
Causes?

A

inflammation of the heart muscle (myocardium), often caused by viral infections such as Coxsackievirus.
-also bacterial inx, autoimmune dz, exposure to toxins

60
Q

s/s myocarditis

A

range from mild CP to fatigue to severe HF and arrhythmias

61
Q

Dx myocarditis

A

markers for inflammation
ECGs
echo
cardiac MRI

62
Q

Tx myocarditis

A

symptom management
address cause
may need mechanical support

63
Q

What is pericarditis?
causes?

A

inflammation of pericardium (fibrous sac around heart)

-idiopathic
-infections
-post MI infarction (Dressler’s syndrome)
-systemic inflammation like lupus

64
Q

s/s pericarditis

A

sharp BP, worse with inspiration or lying flat
pericardial friction rub
ECG changes (diffuse ST elevation)

65
Q

Tx pericarditis

A

NSAIDs
colchicine
corticosteroids (in refractory cases)

66
Q

What is endocarditis?
causes?

A

infection of inner lining of heart chambers and valves

-bacteria entering bloodstream and adhering to damaged endocardial tissue or prosthetic valves

67
Q

s/s endocarditis

A

fever
new or changed heart murmurs
petechiae
embolic phenomena

68
Q

dx endocarditis

A

BCx
echo

69
Q

Tx endocarditis

A

prolong abx therapy
surgery if need valve repair or replacement

70
Q

What is rheumatic heart disease?

A

sequela of rheumatic fever, an inflammatory disease following group A streptococcal pharyngitis.

71
Q

What is the primary valve impacted by rheumatic heart disease?

A

mitral valve
leads to chronic valvular damage

72
Q

Tx for rheumatic heart disease

A

prevention through early abx tx of streptococcal infections

73
Q

What is pericardial effusion?

A

accumulation of excess fluid in pericardial cavity, the space between the heart and pericardium (double walled sac surround heart)

74
Q

How much fluid is normally in the percardial sac?

A

15-50ml

75
Q

etiology of pericardial effusion

A

so many.

  1. inflammatory conditions (pericarditis)
  2. infectious dx (bact, fung, viral)
  3. malignances (primary or metastatic)
  4. autoimmune disorders (lupus, RA)
  5. trauma
  6. Dressler’s syndrome (post MI)
  7. hypothyroidism
  8. renal failure
  9. certain meds
  10. radiation therapy
76
Q

pathophys of pericardial effusion

A

imbalance in fluid production and reabsorption, or due to pathological processes, excess fluid accumulates

77
Q

s/s of pericardial effusion

A

asymptomatic
CP, SOB, orthopnea, cough, fatigue

(due to compression of nearby structures and impaired cardiac function–> can lead to tamponade)

78
Q

dx of pericardial effusion

A

echo
CXR
CT scan
MRI
ECC: low voltage QRS complexes or electrical alterans can suggest significant effusion

79
Q

tx pericardial effusion

A

small: observation
large: pericardiocentesis and drainage via pericardial window or pericardiectomy in recurrent cases

80
Q

What is pulmonary edema?

A

accumulation of excess fluid in the alveoli and interstitial spaces of the lungs, leading to impaired gas exchange and respiratory distress.

often associated with left sided HF–> increased pressure in pulm circulation

81
Q

pathophys of pulmonary edema

A

imbalance between hydrostatic and oncotic pressures in pulmonary capillaries. When LV function is compromised, like in MI or CM, there is backflow of blood into pulmonary veins and capillaries. This increased hydrostatic pressure forces fluid out of the capillaries into the alveolar spaces, overwhelming the lymphatic drainage system and leading to edema.

82
Q

s/s pulmonary edema

A

dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough (may = frothy pink sputum)

crackles or rales
tachypnea
tachycardia
signs of hypoxia (cyanosis)

83
Q

Dx pulmonary edema

A

CXR- bilateral infiltrates
echo
ABG: hypoxemia and resp alkalosis (hyperventilation)

84
Q

Management pulmonary edema

A

underlying cause and symptom relief
oxygen
diuretics (reduce fluid overload via renal excretion of sodium and water)
vasodilators like nitroglycerin to decrease preload and afterload (increase CO)
mech vent or NIPPV

85
Q

What is syncope?

A

sudden, temporary loss of consciousness typically caused by decrease in blood flow to the brain. It is a symptom. Can indicate cardiac and non-cardiac conditions.

86
Q

How does syncope happen?

A

there is a transient drop in cerebral perfusion, which can result form

-decreased CO
-vasodilation
-hypovolemia

cardiac related usually stems from arrhythmias, structural heart diseases, or ischemic heart conditions
(ex. sick sinus syndrome (bradyarrhythmia) or VT, aortic stenosis, HCM)

87
Q

Noncardiac causes of syncope

A

vasovagal reactions
orthostatic hypotension
situational triggers (coughing, swallowing)

88
Q

most prevalent type of syncope

A

vasovagal syncope. due to exaggerated autonomic response that causes vasodilation and bradycardia

89
Q

What is orthostatic hypotension a result of?

A

inadequate autonomic response to postural changes, leading to blood pooling in lower extremities,

90
Q

syncope management

A

underlying cause
cardiac: may need med or device
vasovagal: lifestyle mod (more salt), hydration, avoid triggers
orthostatic: gradual position changes and compression garments

91
Q

describe mitral stenosis

A

blood flow is not able to pass through valve from left atrium to left ventricle properly, leading to increased pressure in the left atrium and pulmonary circulation

92
Q

s/s mitral stenosis

A

SOB, fatigue, palpitations

93
Q

What causes mitral stenosis?

A

often rheumatic fever leading to thickening and fusion of the valve leaflets

94
Q

Describe mitral regurgitation and

A

blood flow flows backward into left atrium during systole, leading to volume overload in left atrium and ventricle, potentially resulted in left sided heart failure

95
Q

what causes mitral regurgitation?

A

mitral valve prolapse
ischemic heart disease
infective endocarditis

96
Q

describe aortic stenosis

A

calcification and narrowing of the aortic valve restricts blood flow from LV into aorta

97
Q

s/s aortic stenosis

A

exertional dyspnea, angina, syncope due to reduced CO

98
Q

describe aortic regurgitation

A

occurs when aortic valve fails to close properly during diastole, causing blood to leak back into left ventricle. results in volume overload and eventual left ventricle dilation and hypertrophy

99
Q

name some causes of tricuspid and pulmonary valve disorders

A

-congenital defects (usually pulmonary)
-secondary to other cardiac conditions like pulmonary hypertension
-RV enlargement or failure (tricuspid)

100
Q

Dx and Tx of valvular disorders

A

echo (structure and function)
depending on severity. pharm (diuretics, vasodilators). surgery (repair/replacement)

101
Q

common vascular conditions

A

atherosclerosis, PAD, aneurysms, venous insufficiency, DVT, PE

102
Q

describe atherosclerosis

A

buildup of plaque within arterial walls, leading to narrowed or blocked arteries. Can result in CAD, CVA, PAD. PAD specifically affects arteries in legs and feet, causing pain, cramping, and potential tissue loss due to inadequate blood flow

103
Q

describe aneurysms

A

abnormal dilation or ballooning of a blood vessel wall, most commonly seen in aorta.
can rupture–> hemorrhage

104
Q

describe venous insufficiency

A

occurs when veins are unable to efficiently return blood to heart, often due to damaged valves within the veins. can lead to varicose veins, swelling, skin changes, and ulcers.

Chronic venous insufficiency may require compression or surgery to improve venous return.

105
Q

dx and tx of vascular conditions

A

-doppler US or angiography
-lifestyle mod
-pharm: antiplatelet or AC
-endovascular interventions
-surgical procedures

106
Q

describe acute arterial occlusion

A

sudden blockage of an artery, usually in lower extremities, resulting in rapid decrease in blood flow to the affected area. medical emergency due to potential for tissue necrosis if not treated. blockage can occur due to an embolus, which is often a blood clot that travels from another part of the body, or a thrombus, which forms at the site of occlusion

107
Q

s/s of acute arterial occlusion

A

6 Ps
-pain (severe and sudden)
-pallor
-pulselessness
-paresthesia (result of nerve ischemia)
-paralysis (result of severe ischemia affecting motor function)
-poikilothermia

108
Q

Dx of acute arterial occlusion

A

clinical exam and imaging
doppler US.
gold standard: angiography to visualize arterial blockage and plan tx

109
Q

Tx of acute arterial occlusion

including long term management

A

initially: AC with heparin to avoid clot propagation
thromolytic therapy to dissolve if within timeframe
Sx: embolectomy or thrombectomy
sometimes- bypass if direct removal not feasible.

long term: Antiplatelet therapy and lifestyle modification

110
Q

risk factors for arterial occlusion

A

HTN, HLD, DM

111
Q

the pathophysiology of acute venous thrombosis involves what traid?

A

Virchow’s triad
-venous stasis (prolong immobility, long flight, bedrest)
-endothelial injury (trauma, surg procedure)
-hypercoagulability (genetic factors- factor V Leiden mutation or malignancy, pregnancy)

112
Q

s/s DVT

Dx DVT

A

swelling, pain, warmth, redness in affected limb

some asymptomatic

Doppler US

113
Q

Tx DVT

A

focus is on preventing clot propagation and embolization while minimizing bleeding risks
AC cornerstone of treatment with LMWH, UFH, or DOACs

if sig risk for limb ischemia or massive PE: thrombolytic therapy or surg.

114
Q

DVT prevention

A

compression stockings, pharm prophylaxis for hospitalized patients. education on lifestyle mod (exercise, hydration)

115
Q

describe aortic aneurysm

A

dilation of the aorta, occurring anywhere along its length. Arises due to weaking of arterial wall, leading to localized enlargement.

116
Q

how are aneurysms classified?

A

by location:
TAA- chest
AAA- abdomen

117
Q

risk factors for aneurysms

A

age
HTN
smoking
genetics: Marfans
atherosclerosis

118
Q

s/s of aneurysms

A

asymptomatic until pressing on structures or rupture

119
Q

describe aortic dissection

A

tear in intimal layer of aorta’s wall, allowing blood to flow between the layers of the vessel walls. This creates a false lumen and can compromise blood flow to vital organs.

120
Q

How are dissections classified?

A

2 main systems: Stanford and DeBakery
Stanford: Type A (involves ascending aorta) and Type B (not involving ascending aorta)

DeBakery: also includes location and extent

121
Q

pathophysiology of aortic dissection and aneurysm

A

degeneration of elastic fibers in arterial wall and increased proteolytic activity that weakens structural integrity.

aneurysm: leads to dilation

dissection: rupture under hemodynamic stress

122
Q

s/s of aneurysms and dissections

A

aneurysm: back or abdominal pain when big enough
dissection: sudden onset severe chest or back pain (tearing/ripping)

123
Q

dx of aneurysms and dissections

A

US for AAA
CT angio for dissections

124
Q

Management of aneurysms and dissections

A

larger aneurysm: open repair or endovascular stent grafting

dissection:
A: emergent surgical repair
B: BP control

125
Q

hyperlipidemia is

A

a medical condition with elevated levels of lipids in the blood, including cholesterol and triglycerides.

126
Q

HLD is a significant risk factor for

A

cardiovascular diseases, such as CAD, stroke, PAD

127
Q

How is HLD classified?

A

primary: often genetic

secondary: from lifestyle factors or other medical conditions

128
Q

how is cholesterol transported in the blood?

A

by lipoproteins, primarily low-density lipoprotein (LDL) and high density lipoprotein (HDL).

129
Q

LDL vs HDL

A

low density cholesterol: often referred to as bad cholesterol as high levels can lead to plaque buildup in arteries, increasing risk of atherosclerosis,

high density cholesterol: considered good as it helps remove LDL cholesterol from bloodstream

130
Q

What do high triglycerides contribute to?

A

hardening or thickening of the arterial walls, increasing risk of CV events

131
Q

contributors to HLD

A

-poor diet
-obesity
-sedentary
-smoking
-excessive alcohol consumption
-certain conditions like diabetes and hypothyroidism -

132
Q

dx of HLD

A

-fasting lipid panel test: assesses total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides

133
Q

HLD management: list possible medications

A

statins:

ezetimibe:

fibrates and omega 3 fatty acids:

PCSK9 inhibitors:

134
Q

HLD management: lifestyle modification

A

heart healthy diet low in sat fat and cholesterol, physical activity, healthy weight, no smoking

135
Q

how do statins work?

A

lower LDL by inhibiting the enzyme HMG-CoA reductase, involved in cholesterol synthesis

136
Q

how does ezetimibe work?

A

reduces intestinal absorption of cholesterol

137
Q

how do fibrates and omega 3 fatty acids work?

A

lower triglycerides

138
Q

who are PCSK9 inhibitors for?

A

those with familial hypercholesterolemia or those not responding to statins alone.

139
Q

complications that can occur post vascular intervention (angiography, angioplasty, stent placement)

A

hematoma
pseudoaneurysm
arteriovenous fistula
RP bleed
arterial occlusion

140
Q

describe hematoma
s/s
tx

A

accumulation of blood at site of vascular access, often due to inadequate hemostasis post procedure.
localized swelling, bruising pain
small: resolve spontaneously; large: may compress structures/ need intervention

141
Q

what is a pseudoaneurysm?

A

occurs when blood leaks out of an artery but is contained by the surrounding tissue, forming pulsatile mass. Also results often from inadequate closure of arterial puncture site.

142
Q

clinical presentation and tx of pseudoaneurysm

A

palpable mass with bruit on auscultation

US guided compression or thrombin injection

143
Q

what is an arteriovenous fistula?

presentation

tx

A

occurs when there is abnormal connection between an artery and a vein, usually due to inadvertent puncture during procedure. can lead to altered hemodynamics and may have bruit/thrill over site.

sx intervention if large or symptomatic

144
Q

What is retroperitoneal hemorrhage?

A

serious complication where there is bleeding in RP space.

can occur due to high puncture sites in femoral artery, leading to vessel injury.

145
Q

s/s RP bleed

tx

A

back pain
hypotension
tachycardia

prompt fluid resuscitation and possible sx

146
Q

what is an arterial occlusion?

s/s

tx

A

blockage of an artery used for access, often due to thrombosis or dissection

limb ischemia: 6 Ps

AC or surgical revascularization

CMC (4 decks)

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