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CVD Diseases Flashcards

1
Q

Management for Primary Hypertension

Pharmacological

A

Which drugs are used are dependant upon the severity of hypertension and any undyling disorders

  • ß-blockers: Class II Antiarrhythmic
  • ACE Inhibitors
  • Duiretics
  • Calcium Channel Blockers
  • Nitroglycerin/Nitroprusside
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2
Q

ß-blockers: Class II Antiarrhythmic

A
  • Reduce HR and force of contraction (not a desirable side effect), by blocking B1 receptors on the heart.
  • Used in angina and to treat hypertension.
  • Sympatholytic Drug
    • Opposes the downstream effects of postganglionic nerve firing in effector organs innervating the sympathetic nervous system (fight or flight)
    • Ex. Metoprolol
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3
Q

Diuretics

A

Help your kidney to get rid of extra water and salt from you body through your pee

Because there is less overall fluid in your blood vessels the pressure will be lower

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4
Q

Diuretics

Examples

A

Hydrochlorothiazide

Furosemide

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5
Q

Calcium Channel Blockers

A

Block the entry of calcium into the muscle cells of the heart and arteries

Calcium is critical to help pass electrical signals in the heart as well as constrict the arteries

By blocking calcium it will in turn dilate the arteries and decrease the force of contraction in the heart

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6
Q

Calcium Channel Blockers

Examples

A

Verapamil

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7
Q

Nitroglycerin/Nitroprusside

A

Potent vasodilators

Used in acute management

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8
Q

Causes of Secondary Hypertension

A

Renal Disease

Excess Adrenosorticosteroids

Co Arctation of the Aorta

Pregnancy

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9
Q

Secondary Hypertension

Renal Disease

A
  • Responsible for majority of 2° HTN
  • Usually atherosclerotic (hardening and narrowing of arteries) in origin
    • Decreased blood flow to the kidneys
  • Results in the retention of salt and water (due to the stimulation of RAA system)
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10
Q

Secondary Hypertension

Excess Adrenosorticosteroids

A

Seen in primary hyperaldosteronism and Cushing’s syndrome

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11
Q

Secondary Hypertension

Co Arctation of the Aorta

A

Coarctation of the aorta —Is a narrowing of the aorta, meaning your heart must pump harder to force blood through the aorta.

Coarctation of the aorta is generally present at birth (congenital). The condition can range from mild to severe, and might not be detected until adulthood, depending on how much the aorta is narrowed.

It will reduced blood flow to the kidney’s triggering the RAA system which results in water retention and HTN results

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12
Q

RAA System

A
  • When blood volume or sodium levels in the body are low, or blood potassium is high, cells in the kidney release the enzyme, renin.
  • Renin converts angiotensinogen, which is produced in the liver, to the hormone angiotensin I.
  • An enzyme known as ACE or angiotensin-converting enzyme found in the lungs metabolizes angiotensin I into angiotensin II.
  • Angiotensin II causes blood vessels to constrict and blood pressure to increase. Angiotensin II stimulates the release of the hormone aldosterone in the adrenal glands, which causes the renal tubules to retain sodium and water and excrete potassium.
  • If the renin-angiotensin system becomes overactive, consistently high blood pressure results.
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13
Q

Secondary Hypertension

Pregnancy

A
  • Pregnancy induced hypertension (PIH)
    • Elevated blood pressure throughout pregnancy
  • Precampsia
    • Serious disorder characterized by the onset of acute hypertension after 24thweek
    • Accompanied by proteinuria and edema
  • Eclampsia
    • Life threatening form of toxemia cause severe convulsions, coma, kidney failure, and possibly death
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14
Q

Treatment of Secondary Hypertension

A

Treat the underlying cause

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15
Q

Malignant Hypertension

A

AKA Hypertensive Crisis

Occurs when someone with second degree hypertension develops an accelerated and potentially fatal form of the disease

Characterized by a sudden marked elevation in blood pressure with systolic pressure (>180 mmHg) and diastolic pressure (>120 mmHg)

Causes severe damage to the vascular system

Can result in encephalopathy, cerebral edema, coma, convulsion, and stroke and organ damage

Manifests as headache, confusion, motor and sensory deficit and visual disturbances

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16
Q

Hypertension Pathphysiology

Plaque does not rupture

A
  1. Damage to vascular endothelium
  2. Healing plaque formation
  3. Lumen narrowing
  4. Decreased blood flow distally
  5. Decreased blood flow to kidney
  6. Stimulation of RAA system
  7. Increased blood volume
  8. Increased blood pressure
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17
Q

Hypertension Pathphysiology

Plaque Ruptures

A

Thrombus

Lack of blood flow to organ

Ischemia/Infarction to area distal to blockage

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18
Q

Target Organ Damage

Hypertension

A
  • Heart
    • Hypertrophy of LV, risk of ischemia/MI
  • Cerebrovascular
    • Increased risk of stroke (2°bleed or clot)
  • Peripheral Vascular
    • Development of atherosclerosis and arteriosclerosis
  • Renal
    • Stimulation of renin-angiotensin system (which worsens HTN)
  • Retinal
    • Damage to vasculature and resulting vision problems, increased intraocular pressure can cause retinal separation
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19
Q

Hypertension

Clinical Manifestation

A

Increased BP!

Usually an asymptomatic disease (especially initial few decades)

Occasionally can result in headaches

Often the first symptoms are due to complications of the HTN

E.g., Chest pain, stroke symptoms, CHF symptoms

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20
Q

Coronary Artery Disease

A

A narrowing of one or more coronary arteries due to a build-up of fatty deposits within the arterial wall

This will result in a reduced blood flow and subsequently less oxygen and nutrients delivered to the heart muscles that are reliant upon the affected arteries

Lack of blood flow will lead to ischemia of the heart

CAD is also known as ischemic heart disease

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21
Q

Atherosclerosis

A

Atherosclerosis- Plaque build up in the arteries

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22
Q

Ischemia vs Infarction

A

Ischemia-When blood flow to the heart muscle is obstructed

Infraction is caused by ischemia and is an area of tissue/organ necrosis

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23
Q

Coronary Artery Disease

Risk Factors

A
  • Increased cholesterol
  • Diabetes
  • Hypertension
  • Smoking
  • Age
    • Men > 45 y
    • Women > 55 y
  • Family history
  • Physical inactivity
  • Obesity
  • Stress
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24
Q

Coronary Artery Disease

Prevention

A
  • Lifestyle changes!
    • “Heart-healthy” diet, regular exercise, quit smoking, limit alcohol intake
  • Control blood pressure
  • Control blood sugars
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25
Q

Atherosclerotic Process

A
  • Cholesterol and calcium is deposited beneath the endothelium in the lining of the artery to develop fatty streaks
    • Scar tissue formation at these sites will result in plaques
  • Plaques have a firm outer layer with a soft inner core of cholesterol
  • This deposition of cholesterol and calcium is a natural part of the aging process, however, having risk factors accelerates it.
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26
Q

What is the Pathopyshiology of CAD

A
  1. Atherosclerotic Process
  2. Luman Narrowing
  3. Plaque Rupture
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27
Q

CAD Pathyphysiology

Lumen Narrowing

A

Results in decreased blood flow to the myocardium, resulting in ischemia which can cause chest pain

Chronic ischemia can lead to myocardial fibrosis and can decrease ventricular wall compliance

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28
Q

CAD Pathophysiology

Plaque Rupture

A

When there is a plaque rupture it will expose the lipid core resulting in platelet adherence (clot development)

The clot development will further narrow the lumen and can result in a complete occlusion and myocardial infarction

This is the etiology of most myocardial infarctions

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29
Q

CAD Clinical Manifestations

A
  • These are “non-specific” and can appear gradually as the coronary arteries slowly narrow.
  • Heartburn
  • Palpitations
  • Dizziness or fainting
  • Nausea or vomiting
  • Diaphoresis
  • Exertional Angina
  • SOBOE
  • Jaw/back/arm pain
    • Especially left-sided
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30
Q

CAD Lab Findings

A
  • Non-Diagnostic
  • High cholesterol levels
  • High levels of CRP
    • C-Reactive Protein which is a protein produced in the liver in response to inflammation
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31
Q

CAD

ECG

A

May reveal ischemia, MI or rhythm disorders

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32
Q

CAD

Cardiac Stress Test

A

ECG may show exertional myocardial ischemia

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33
Q

CAD

Thallum Stress Test

A

Combines nuclear imaging of the blood flow to the myocardium at rest and under exertion

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34
Q

CAD

Coronary Angiography

A

Gold Standard-The best way to diagnose CAD and evaluate the extent and locations of the blockages. This is the only test that indicates whether treatment should include angioplasty or CABGs

Uses a catheter inserted into an artery (usually femoral) and threaded up the aorta to the openings of the coronary arteries

Dye is injected at this point and fluoroscopy captures the image of the blood flow

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35
Q

CAD

Treatment

A
  • Non-Invasive
    • Lifestyle Changes
    • Medical Management
  • Invasive
    • Angioplasty
    • Stenting
    • CABG
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36
Q

The drop in heart disease is due to

A

The phenomenal drop in the heart disease death rate over the past 30 years has been due more to reducing risk factors than to advances in treatment.

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37
Q

CAD

Medical Management

A
  • Daily Low Dose Aspirin
    • ​Will help to prevent clotting
  • Statins
  • Calcium Channel Blockers
  • Nitoglycerin
  • B-Blockers
  • ACE Inhibitors
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38
Q

Drug: Statins

A

Chemical which makes cholesterol

Ex. Atorvastatin (Lipitor)

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39
Q

Angioplasty

A

Angioplasty=Percutaneous Transluminal Coronary Angioplasty (PTCA)

If necessary if it often done at the same time as an angiography

A balloon tippe catheter is threaded into the affected coronary artery. When the balloon is positioned at the blockage it will be inflated. This will result in a widening of the artery as the plaque will be flattened against the arterial wall.

Arteries treated with angioplasty alone can still undergo restenosis (1/3 of cases within 6 months)

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40
Q

Drug: B-Blockers

A

Beta blockers, also known as beta-adrenergic blocking agents, are medications that reduce your blood pressure.

Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline.

When you take beta blockers, your heart beats more slowly and with less force, thereby reducing blood pressure. Beta blockers also help blood vessels open up to improve blood flow.

Beta blockers aren’t usually prescribed for blood pressure until other medications, such as diuretics, haven’t worked effectively.

Beta blockers generally aren’t used in people with asthma because of concerns that the medication may trigger severe asthma attacks.

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41
Q

B-Blockers Examples

A

Will end in -olol

Acebutolol (Sectral)

Metoprolol (Lopressor, Toprol-XL)

Nadolol (Corgard)

Propranolol (Inderal LA, InnoPran XL)

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42
Q

ACE Inhibitor

A

Angiotensin converting enzyme inhibitors (ACE inhibitors) are medications that slow (inhibit) the activity of the enzyme ACE, which decreases the production of angiotensin II. As a result, blood vessels enlarge or dilate, and blood pressure is reduced.

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43
Q

ACE Inhibitor

Examples

A

Ends in -pril

benazepril (Lotensin)

lisinopril (Prinivil, Zestril, Qbrelis)

perindopril (Aceon)

ramipril (Altace)

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44
Q

Retenosis

A

the recurrence of abnormal narrowing of an artery or valve after corrective surgery.

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45
Q

Stenting

A
  • If necessary can be done at the same time as an angiography
    • Stents are used more often than not.
  • The goal is to help prevent restenosis, or at least lengthen the time before restenosis occurs
  • Use of drug-impregnated stents reduces risk of restenosis.
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46
Q

Angioplasty vs. Stent

A

In an angioplasty the balloon will be expanded several times in order to force the plaque against the wall and then will be completely removed from the body

In a stent the mesh will remain in the body

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47
Q

CABG

A

Used to treat severe CAD or CAD that has not responded to medical therapy or PTCA

The blocked arteries will be bypassed through grafting a vessel above and below the blockage

The vessels that are used most often for grafting are most commonly the saphenous vein, internal mammary artery or radial artery

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48
Q

What are the different CABG Methods

A

Traditional Approach

Off Pump or Beating Heart

MICABS/MICS

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49
Q

CABG Methods

Traditional Approach

A

Full sternotomy, heart is stopped and heart-lung bypass is used

Pros: still heart;

Cons: “pump time”

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50
Q

Median Sternotomy

A

Median sternotomy is a type of surgical procedure in which a vertical inline incision is made along the sternum, after which the sternum itself is divided, or “cracked”.

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51
Q

CABG Methods

“Off-Pump” / Beating Heart

A

Full sternotomy but heart is not stopped (no bypass machine is required)

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52
Q

CABG Methods

MICABS/MICS

A

MI-Minimally Invasive

No sternotomy; access through the intercostal region

Typically for front of the heart vessels; 1 or 2 vessels

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53
Q

CABG Surgeries

A

These surgeries are generally very successful with low rates of complications.

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54
Q

Myocardial Infarction

A

Blood flow to the heart decreases or stops, damaging the heart muscle, which can help in

Decreased ejection fraction

Shortness of breath

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55
Q

Myocardial Infarction

Risk Factors

A
  • Most MI’s are caused through a ruptured atherosclerotic plaque
    • The risk factors for the development of CAD are also risk factors for an MI
  • Age
  • Smoking/illicit drugs
  • Hyperlipidemia
  • Diabetes mellitus
  • Poorly controlled HTN
  • Type A personality
  • Family history
  • Sedentary lifestyle
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56
Q

Myocardial Infarction

Decreased Supply of O2

A

A decreased supply of oxygen can result from a lack of sufficient blood flow or an absence of blood flow

Plaque rupture and thrombus formation

Vasospasm of coronary artery

Hypoxia

Profound Hypotension

Embolus to coronary arteries

Aneurysm of coronary artery

Arteritis

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57
Q

Aneurysm

A

An aneurysm is a localized, abnormal, weak spot on a blood vessel wall that causes an outward bulging, likened to a bubble or balloon.

Aneurysms are a result of a weakened blood vessel wall, and may be a result of a hereditary condition or an acquired disease.

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58
Q

Increased O2 Demand

A
  • Inotropic Drugs
    • Increased contractility
    • Because the heart is working harder there is an increased demand of oxygen
  • Cocaine and Amphetamines
    • Beta and alpha receptors
    • Sympathetic receptors for an increased sympathetic response
  • Ephedrine
    • Stimulant
    • Often used as a medication for hypotension and spinal anesthesia
  • Exercise
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59
Q

Myocardial Infarction

Pathophysiology

A
  • Regardless of etiology, whether it be a lack of blood supply, decreased blood supply, or increased O2 demand, there will be an area of myocardium that is deprived of oxygen
    • This lead to the development of ischemia, then an area of injury, and then finally an infarction
    • Ischemia will be on the outer border
  • During an area of injury there is the ability for the muscle to repair itself, but it will not be 100% repaired as there is a lot of extra fibrinogen, fat deposits, etc
  • Reperfusion injury is also an important component of the pathophysiology.
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60
Q

Area of Infarction

A

The area of infarction can be described as transmural or subendocardial based on the thickness of the injury

Transmural-Full thickness of myocardium

Subendocardial-Partial thickness of myocardium

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61
Q

Myocardial Infarction

Time Frames

A
  • 0-30 Minutes
    • Reversible injury
  • 1-2 Hours
    • Onset of irreversible injury
  • 4-12 Hours
    • Beginning of necrosis
  • There will continue to be necrosis and development of scar tissues occurs up until 8th week post infarct
  • The risk for myocardial rupture is greatest at days 4-7 post infarct
    • As the tougher fibrotic scar tissue starts to form 7-10 days post infarct
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62
Q

Myocardial Infarction

Atypical Presentation

A

Common among women, elderly and longstanding diabetics

Results in higher mortality

Can be mistaken with a GI problem such as reflux or heart burn

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63
Q

Myocardial Infarction

Clinical Manifestations

A
  • Pain/Discomfort
  • Dyspnea
  • Nausea +/- vomiting
  • Anxiety– impending doom
  • Lightheadedness
  • Syncope
  • Cough
  • Pale
  • Diaphoresis
  • Dysrhythmias
  • Hypertension
    • 2° to anxiety or pain
  • Hypotension
    • Indicates ventricular dysfunction and failure
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64
Q

Myocardial Infarction

Clinical Manifestations-Pain and Discomfort

A

Tightness, pressure or squeezing

Usually substernal and radiating down left arm

Can involve the jaw, right arm, epigastrum (right above stomach) and back

Often perceived as GI!

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65
Q

Myocardial Infarction

Types of blood markers

A

Myoglobin

CK-MB

Total CK

Troponin I

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66
Q

Myocardial Infarction

Blood Markers-Myoglobin

A

Very sensitive and early marker of myocardial necrosis, but is not specific for MI

Levels will begin to rise within 1 hour with peaks within 4-8 hoursWill return to normal by 36 hours

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67
Q

Myocardial Infarction

Blood Markers CK-MB

A

Levels will begin to rise within 4 hours and peak at 24 hours

Levels will subside by 3 days

Not specific to MI

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68
Q

Myocardial Infarction

Blood Markers Total CK

A

Enzyme of cardiac damage

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69
Q

Myocardial Infarction

Blood Markers Troponin I

A

Troponin I is detectable at 3-6 hours with peaks at ~26 hours and remains elevated for up to 14 days

This is a highly sensitive test

The pattern and numbers are important

This is a main test (#1 test choice for marker) and a marker of damaged tissue right after an MI where it will have an exponential increase (gotta check over several hours) and then decline over days

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70
Q

Myocardial Infarction

ECG

A

Only ~50% of patient will have diagnostic changes on their initial ECG

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71
Q

Myocardial Infarction

ECG-ST Segments

A

Depression (ischemia)

Elevation (infarction)

ST segment elevation is only considered pathologic if it occurs in two or more anatomically contiguous leads!

72
Q

Myocardial Infarction

ECG-T Wave

A

Peaking, flatten, or inversion

T waves associated with potassium levels

If the T wave is irregular it tends to not be due to an MI but rather it is often caused by hyperkalemia

73
Q

Myocardial Infarction

ECG-Q Wave

A

Deepening and widening of Q Wave

Loss of R wave resulting in a deep QS wave

74
Q

Myocardial Infarction

12 Leads and Coronary Arteries

A

The 12 lead ECG helps to locate areas of ischemia, infarct or injury

When a specific coronary artery is blocked it can result in predictable changes of specific leads

75
Q

Myocardial Infarction

12 Leads and Coronary Arteries-Lateral Injury

A

Leads I, aVL, V5, V6

76
Q

Myocardial Infarction

12 Leads and Coronary Arteries-Inferior Injury

A

Leads II, III, aVF

77
Q

Myocardial Infarction

12 Leads and Coronary Arteries-Septal Injury

A

V1, V2

78
Q

Myocardial Infarction

12 Leads and Coronary Arteries-Anterior Injury

A

V3, V4

79
Q

Classifications of MI

STEMI

A
  • The patient’s presentation and ST elevation on 2 or more contiguous leads provides an immediate diagnosis
    • Without the need of cardiac enzymes
  • This means that the patient can be considered for re perfusion therapy
  • Those with STEMI should have reperfusion therapy: thrombolytics or angioplasty
80
Q

Classifications of MI

Non- STEMI

A

The ECG alone will not confirm the MI and we have to rely on the serum markers (the pattern is important)

81
Q

Myocardial Infarction

Medical Management

A

*ACLS will use the acronym MONA for initial pharmacological therapy

  • Morphine
    • Analgesic for pain relief and vasodilator effects which results in reduced afterload and systemic pressure
  • Oxygen
    • Will increase oxygen content and therefore increasing oxygen supply
  • Nitrates
    • Vasodilator effect to decrease systemic vascular resistance and afterload
  • Aspirin
    • Reduces platelet aggregation by preventing them from sticking together
  • Beta Blockers
    • Reduce SNS stimulation (reduce HR) post MI and reduce afterload
    • Decrease oxygen demand and hypertension
82
Q

Myocardial Infarction

Reperfusion therapy

A
  • Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a MI
  • The goal is to reduce mortality and limit the infarct size
  • Methods
    • Thrombolytics
      • Dissolve blood and platelet clots
      • Best is used within 60-90 minutes of onset
      • Should be given by EMT
      • Risk of bleeding must be considered, because you will have a time period when there is no clotting factors avalible
    • Percutaneous Coronary Interventions (PCI)
    • CABG
83
Q

Heart Failure Definition

A

Inability for the heart to meet the metabolic demands of the body

84
Q

Types of Heart Failure

A

Right sided-Cor Pulmonale

left sided

Both sides affected

85
Q

Classifications of heart failure

A
  • High output
  • Low output
    • Can be systolic or diastolic in origin
86
Q

Left vs Right Sided Heart Failure

A

Although the initial event that leads to heart failure may be right-sided or left-sided in origin, long-term heart failure usually involves both sides!

Because the circulatory system is a closed system when one side starts getting backed up it will eventually affect the other side

87
Q

Cor Pulmonale

A
  • Cor pulmonale is the enlargement and failure of the right ventricle in response to an increased vascular resistance from the lungs
  • Chronic pulmonary heart disease will usually result in right ventricular hypertrophy
    • Hypertrophy is an adaptive response to a long term increase in pressure as muscle cells will grow thicker in order to increase the contractile force and move the blood against a greater resistance
88
Q

Left Sided Heart Failure

A
  • There is a failure in the left ventricle to move blood to the body causing poor systemic perfusion
    • Decreased systemic perfusion will lead to vasoconstriction (increased SVR)
    • There will be a normal or increased BP that is needed to maintain cerebral and coronary perfusion
  • Blood will also back up into the pulmonary system causing pulmonary congestion and can lead to right ventricular failure as the right side of the heart will pump against the increased PVR which will lead to a decreased RV output
    • When the RH fails there is a decreased pulmonary congestion giving a false look of improvement
89
Q

Left Sided Heart Failure

Hemodynamics

A

Increased

PAWP

HR

Decreased

CO

Pulse pressure

90
Q

Right Sided Heart Failure

A

Due to failure of the right ventricle to pump blood out to the lungs

Results in blood backing up into the systemic circulation

Backwards Failure

Decreased RV output leading to venous congestion

Forward Failure

Decrease RV output -> Decreased pulmonary perfusion ->Decreased LV filling ->Decreased LV output -> systemic perfusion

91
Q

Right Sided Heart Failure

Hemodynamic Profile

A

Increased

CVP

92
Q

High Output Heart Failure

A

Uncommonform of heart failure that can occur when there is an excessive need for cardiac output due to an increase in peripheral demand

The heart is “supranormal” and yet still inadequate

Can occur when there is an increased blood volume (excess water and/or salt), excess fluid, chronic and severe anemia, etc.

93
Q

Low Output Heart Failure

A

Caused by a disorder that will impair the pumping ability of the heart

May be systolic or diastolic in origin

Many patient will have elements of both

94
Q

Low-Output Systolic (Systolic Failure)

A

Heart failure with reduced ejection fraction (HFrEF)

Impaired ejection of blood from the heart during diastole

95
Q

Low-Output Systolic (Systolic Failure) Causes

A
  • Results from conditions that either
    • Impair contractility of the heart
    • Produce a volume or pressure overload on the heart
  • Ex. CAD, previous MI, A-Fib, Valve disease/dysfunction, alchol, infection, cardio myopathy, etc
96
Q

Low-Output Systolic (Systolic Failure) Results

A

Results in a decreased stroke volume and in turn a decreased ejection fraction

97
Q

Low-Output Diastolic (Diastolic Failure)

A

Heart failure with a preserved ejection fraction (HFpEF)

Ejection fraction will remain the same at 50% or become lower

Impaired relaxation of the heart during diastole

Will result in a decreased stroke volume

There will be an increase in muscle mass without dilating

98
Q

Low-Output Diastolic (Diastolic Failure) Causes

A

Restrict diastolic filling

Increase ventricular thickness

Thus decrease chamber size

Delay diastolic relaxation (fibrosis)

Ex. Ventricular hypertrophy from long term HTN or aortic stenodid, diabtese, constrictive pericarditis

99
Q

Direct Causes of Heart Failure

A
  • Most Common
    • Myocardial ischemia
    • Myocardial infarction
  • Arrhythmias
    • The heart is not pumping in proper sequence (ex. A-fib) so blood does not pump well and will stay in the atrium
    • Clots can also form if the heart is pulling for some time
  • Heart valve lesions
    • Opening and closing problems
  • Congenital malformations
  • Pericarditis
    • Inflammation of sac around the heart
  • Cardiomyopathies
100
Q

Indirect Causes of Heart Failure

A
  • Fluid overload
  • Renal failure
  • Sepsis
    • Biggest issue
    • Causes membrane variable of well weaken, so fluid will enter more easily
    • Vasodilation of blood vessel
  • Causing RHF (Cor Pulmonale)
  • **Nitric Oxide
    • COPD
    • PE
    • Pulmonary HTN
101
Q

Left Sided Heart Failure

Clinical Manifestations

A
  • Exertional Dyspnea
  • Orthopnea
    • The heart is not pumping when the patient lying down and fluid will back up into the lugs
  • Peripheral Edema
    • Late stage
  • Paroxysmal Nocturnal Dyspnea (PND)
    • The heart is not pumping properly when sleeping or when the body is relaxing and fluid will back up into the lungs so when the patient wakes up they will have SOB and wheezes
  • Cough
  • Frothy, blood tinged sections
    • Fluid backs up from the vasculature bringing up RBC
    • Frothy because of surfactant (creates bubbles)
  • Cyanosis
  • Increase PAWP
    • Backed up pressure from the left ventricle due to fluid overload
    • Distinguishes heart failure and non-cardiac infections
    • ~4-12 mmHg
102
Q

Left Sided Heart Failure

On Auscultation

A

Fine/Coarse crackles due to the fluid

“Cardiac” wheezes

103
Q

Left Sided Heart Failure

Clinical Manifestation

A
  • Peripheral/dependent edema
    • Dependant Edema=Gravity related swelling in the lower body
  • Fatigue
  • JVD
  • Hepatomegaly
    • Due to a backup of blood in the liver
  • Ascites
    • Abnormal accumulation of fluid in abdominal (peritoneal) cavity
    • When the right side of the heart loses its pumping power, blood will back up into the veins
  • Cyanosis
  • Increased CVP
104
Q

Heart Failure

Inadequate Cardiac Output

A

This is the end result of different etiology’s

This is what will trigger different compensatory mechanisms

105
Q

Heart Failure Compensatory Mechanisms

A

Frank-Starling Mechanism

Increased SNS activity

Renin-Angiotensin Mechanism

Myocardial Hypertrophy

106
Q

Frank-Starling Mechanism

A
  • In a normal heart this will be the mechanism that is responsible for the heart pumping the blood it receives and matching the output of the two ventricles
    • Increased preload will increase stretch which increases force of contraction and ultimately increase stroke volume
  • During heart failure this mechanism is responsible for maintain normal CO in the face of end diastolic volumes
    • This is reflected by an increase in PAWP and CVP
  • This mechanism become ineffective when the myocardial fibers become overstretched
    • Thus CO can not increase with an increase in physical activity
107
Q

Compensation Mechanism for HF

Increased SNS Activity

A
  • SNS will be stimulated through a decrease in SV and CO
  • Leads to (all of the below is an attempt to maintain perfusion to vital organs)
    • Systemic vasoconstriction
      • This may lead to increased afterload and further increase in myocardial demand
    • Stimulation of the heart
      • Increased HR
      • Increased contractility
  • Norepinephrine
    • Increases SVR
108
Q

Renin-Angiotensin Mechanism

A
  • Decreased SV and CO will result in a decrease perfusion to the kidneys
  • The kidneys will respond through releasing renin which will activate the renin angiotensin aldosterone system
  • End result
    • Aldosterone will cause sodium and water retention resulting in an increase in blood volume
    • Angiotensin II causes vasoconstriction
  • Because this mechanism results in an increase in blood volume there will also be an increase in end-diastolic volume
    • Indirectly this is activating the frank starling mechanism and increase CO
109
Q

Myocardial Hypertrophy

A
  • A long term compensatory mechanism in response to increase work demand
    • The heart is working harder building muscle which will decrease the size of the ventricle
      • Less preload and less fluid that can be ejected
  • This results in an increased in the number of contractile fibers in the myocardium
  • While this mechanism allows for the ventricle to do more work it also results in an increase in myocardial demands and increase myocardial oxygen requirements
110
Q

Decompensated Heart Failure

Increased SVR

A

Further increase myocardial demand

111
Q

Decompensated Heart Failure

Increased HR

A

Increase myocardial demand

Shorten diastole

112
Q

Decompensated Heart Failure

RAA System

A

Further increase filling pressure

Further contributes to fluid overload worsening clinical manifestations

113
Q

Decompensated Heart Failure

Frank Starling Mechanism

A

Ineffective due to over stretched myocardial fibers

114
Q

Decompensated Heart Failure

Myocardial Hypertrophy

A

Increase myocardial oxygen requirements

May reduce chamber size cause a diastolic failure

115
Q

Exam Findign for Heart Failure

CXR

A
  • Cardiomegaly
  • Left sided heart failure
    • Diffuse bilateral infiltrated (butterfly pattern)
    • Pleural effusion
116
Q

Kerley B lines

A

Seen in the CXR with left sided heart failure

These are 1-2 cm thin lines in the peripheral of the lungs

They are peripheral to and external to the pleural surface

They represent thickened subpleural interlobar septal and are unlikely seen at the lung bases

Suggesting pulmonary edema

117
Q

Exam Findings

Echocardiography

A

Useful to diagnose cause of heart failure

118
Q

Heart Filaure Exam Findings

ECG

A

May diagnose cause (MI, arrthymia)

119
Q

Pharmacological Treatment for Preload Reduction

A
  • Diuretics
    • Used to target hypervolemia
    • Inhibit sodium and water reabsorption
    • Will reduce intravascular volume, decrease CVP, decrease right and left heart filling pressures
  • Nitroglycerin
    • Causes systemic venodilation decreasing preload
  • Morphine
120
Q

Pharmacological Treatment for Afterload Reduction

A
  • β-Blockers
    • Inhibit sympathetic nervous system and block alpha 1 adrenergic vasoconstrictor activity
    • Slow down HR and dilate blood vessels
  • Nitroglycerin, Nitroprusside
  • ACE inhibitors
121
Q

Pharmacological Treatment for Inotropic Support

A
  • Use with caution
  • Ex. Milrinone, Inamrinone, digoxin, Dobutamine, Dopamine, and Norepinephrine
  • Increase contractility and can increase oxygen as a result
  • Inotropic agents will help to restore organ perfusion and reduce congestion
122
Q

What to treat for acute pulmonary edema

A

Oxygen & NIPPV!!

123
Q

Treatment for Severe Heart Failure

A

Intra-aortic Balloon Pump

Left Ventricular Assist Device

Heart Transplant

124
Q

Heart Failure and NIPPV

A
  • CPAP is the 1st line of therapy
    • BiPAP if hypercapnia or continued dyspnea
  • The increase FiO2 and Pmean will improve oxygenation
  • The increase intrathoracic pressure and increase PVR due to PPV will cause blood to back up on the right side
    • This will cause distension of the RV and a shift of the septum towards the left side
    • The effectively reduced preload on the left side of the heart and improved output (Frank-Starling Curve)
    • The increased intrathoracic pressure will also reduce transmural pressure resulting in a decreased afterload
  • Will help to open alveoli and get oxygen
    • This pressure will push fluid in the alveoli back to the vasculature
125
Q

General/Long Term Treatment for Heart Failure

A

Restriction of dietary sodium

Diuretics

Nitroglycerin or long-acting nitrates

ACE Inhibitors/β-blockers

Cardiac rehabilitation

126
Q

What is the best predictor of mortality in heart failrue

A

Ejection fraction is the best predictor of mortality!

The lower the EF the worse the prognosis!

127
Q

Valvular Disorders

mechanical disruptions

A
  • Stenosis: This is a narrowing of a valve so that it does not open properly
    • Obstruct blood flow
  • Incompetence: This is a distortion of the valve so that it unable to close completely; results in regurgitant flow.
128
Q

Valvular Disorders

Etiology

A
  • Congenital defects
  • Trauma
  • Ischemic damage
  • Degenerative changes
    • DM and hypercholesteremia are risk factors
  • Inflammation/Infection
    • Rheumatic heart disease
    • Auto-immune diseases (Rheumatoid Arthritis)
    • Endocarditis 2°bacterial infection (IVDU)
  • Neoplasm
  • Connective tissue diseases Eg. Marfan Syndrome
129
Q

Valvular Disorders

Pathophysiology

A
  1. Damage or inflammation of the heart valve leaflets
  2. Healing results in increased collagen content and scaring
    1. Valve leaflets heal together
      1. Valve cannot open properly (Valve stenosis)
    2. Valve leaflets become retracted
      1. Valve cannot close properly (regurgitant valve)
130
Q

Stenotic Valve

A

Distension of the chamber that pumps the blood thru the diseased valve (and thus an increase in pressure)

Impaired filling of the chamber that receives the blood (and thus decrease pressure)

131
Q

Regurgitant/Incompetent Valves

A

There is backward flow thru the valve

This causes distension of the chamber prior to the diseased valve (and thus increase pressure here!)

This places increase work demands on this chamber

132
Q

Valvular Disorders

Clinical Manifestations

A
  • Mild valvular disorders may not produce any signs or symptoms other than a heart murmur.
  • History of heart murmur (or newly developed)
  • Exertional dyspnea**
  • Orthopnea and paroxysmal nocturnal dyspnea
  • Effort-induced fatigue
  • Angina 2°ischemia
  • Palpitations
  • Syncope
  • Signs of heart failure (S & S depend on whether L or R heart failure)
133
Q

Valvular Disorders

Diagnostic Tests

Auscultation of Heart Sounds

A

Valve dysfunction results in turbulent flows replacing the normal laminar flows and result in “murmurs” being heard

Depending on the valve affected there may be extra heart sounds heard

134
Q

Valvular Disorders

Diagnostic Tests

Echocardiogram

A

Allows for viewing of the internal structures of the heart and blood flow patterns

The transesophageal echo is particularly effective in identifying valve disorders

135
Q

Valvular Disorders

Management

A
  • Medical management of associated heart failure
  • Surgical intervention
    • Replace or repair valve– put in pig valve
    • Only done in severe cases
    • Ideal prosthetic valve is not yet invented
  • Percutaneous balloon valvuloplasty
    • For treatment of stenotic valves
136
Q

Cardiomyopathies

A

A group of disorders that affect the heart muscle and diminishes cardiac performance

It can develop as a primary or secondary disorder

137
Q

Cardiomyopathies

Main Types

A

Dilated

Restrictive

Hypertrophic

Arrthymogenic right ventricular dysplasia

138
Q

Cardiomyopathies

Primary Causes

A
  • Idiopathic
  • Genetic
  • Infectious
    • Viral, bacterial, protozoal
  • Toxic
  • Drugs, poisons, ETOH
139
Q

Cardiomyopathies

Secondary Causes

A
  • Other CV disorders
    • Ischemia **
    • Hypertension
    • Valvular disorders
  • Metabolic disorders:
    • DM, hyperthyroidism…
  • Collagen Vascular Disease
    • SLE, RA
140
Q

Dilated Cardiomyopathy

A
  • Most Common
  • This type causes the heart to become enlarged and the myocardium to become weak, thin and floppy
  • Most often idiopathic in origin
  • The affected ventricle is unable to pump the blood it receives, thus,
    • If LV is affected ggLeft heart failure and its manifestations
    • If the RV is affected ggRight heart failure and its manifestations
  • Results in a systolic dysfunction
141
Q

Hypertrophic Cardiomyopathy

A
  • Hallmark is inappropriate, disorganized proliferation of myocardial cells and is caused by a genetic disorder
  • Affects the left ventricle, frequently in the interventricular septal area
  • Results in an obstruction of outward flow
  • Results in both a systolic and diastolic dysfunction
    • Because the left ventricle is smaller
  • The leading cause of sudden cardiac death in pre-adolescent and adolescent children.
    • We don’t know about this until afterwards
142
Q

Restrictive Cardiomyopathy

A
  • This type causes the walls of the ventricles to become stiff but not necessarily thickened
  • It impairs the filling of blood as the ventricle doesn’t relax normally
    • If LV is affected
      • Left heart failure and its manifestations
    • If the RV is affected
      • Right heart failure and its manifestations
  • Results in a diastolic dysfunction
  • This is the least common cardiomyopathy and is often due to infiltration by foreign materials
143
Q

Arrhythmogenic Right Ventricular Dysplasia

A
  • Rare
  • Genetic
    • Two patterns: Autosomal Dominant and Autosomal Recessive
  • Can affect left or right wall
  • Loss of myocardium of the right ventricular free wall (free wall is the ventricle wall that is not the septum
    • Right Ventricular muscle is replaced by fat and fibrous tissue (scar tissue)
      • Scar tissue will affect the conduction of the hert
    • Right ventricle has poor dilating and contracting ability
  • Highly associated with ventricular arrhythmias
144
Q

Cardiomyopathies

Clinical Manifestations

A
  • Ventricular arrhythmias
    • Palpitations
  • Dizziness, lightheadedness, syncope
    • SOBOE
  • Heart Failure
    • Abnormal ECG
  • Sudden Cardiac Arrest
145
Q

Cardiomyopathies

Diagnosis

A

MRI

CT scan

146
Q

Cardiomyopathies Treatment

A

Antiarrhthmic drugs

Catheter Ablation- Will damage the pace maker cells in order to prevent the off firing of the heart

Implantable cardioverter defibrillator

147
Q

Cardiomyopathies

Antiarrhythmic Drugs

A
  • Class I (Na Channel Blocker)
    • Lidocaine, Phenytoin
  • Class II (B-Blocker)
    • Sotalol
    • Slows down HR and helps to decrease SVR
  • Class III (K Channel Blockers)
    • Amiodarone
      • The big problem is that this drug is toxic and will affect the lung (pulmonary fibrosis)
148
Q

Pericarditis

A
  • An inflammation of the pericardium (sac that surrounds the heart)
    • Can be acute or chronic
  • The inflammation can lead to the accumulation of fluid in the pericardial sac
    • Characterized by chest pain, pericardial friction rub and serial ECG changes.
149
Q

Pericarditis Etiology

A
  • Idiopathic
  • Infectious
    • Viral, bacterial, fungal, TB
  • Prior MI
    • 7-10% of MI patients develop this complication
  • Kidney failure
  • Cancer
  • Rheumatoid Arthritis/Scleroderma/SLE
  • Chest trauma
  • Rheumatic Fever
  • Inherited disorder
  • About 1/1000 hospitalized patients are diagnosed with this disorder. Many more are likely to have an mild form that goes undiagnosed.
150
Q

Pericarditis

Pathophysiology

A
  1. Etiological Agent
  2. Infiltrations of WBCs
  3. Pericardial Vasculitis
    1. Pericardial Effusion
      1. Formation of cardiac tamponade
        1. Exudative: Serous, fibrinous, hemorrhagic, purulent, or chylous
      2. Fribrinous, retractions, and adhesion formation
        1. Constrictive pericarditis
      3. Formulation of granulomas
        1. Seen with TB, RA, sarcosiodosis, fungal infections
151
Q

Pericarditis

Clinical Manifestation

A
  • Chest pain
    • Cardinal Symptom
  • Pericardial rub
  • Dyspnea (2° to pain)
  • Dry cough
  • +/- Fever
  • Chills
  • Weakness
  • Signs of tamponade if large effusion present
    • Becks Triad: Distended neck veins, distant heart sounds, hypotension
152
Q

Three Main Signs of Percarditis

A

Chest pain

Dyspnea secondary to pain

Dry cough

Fourth possible sign: Kussmauls sign

153
Q

Constrictive Pericarditis

A

Scarring of the pericardium after one or more episodes of pericarditis

The pericardium becomes thickened and stiff making it hard for the percadium to expand

Results in impaired filling of the heart, thus, diastolic dysfunction

154
Q

Constrictive Pericarditis

Clinical Manifestations

A

Because this results in blood backing up into the extremities and lungs you will see S & S similar to heart failure

Kussmaul’s sign is often seen! (Swelling JVD during insp).

155
Q

Constrictive Pericarditis

CXR

A
156
Q

Pericarditis Diagnostics

A
  • Lab Studies
    • Infectious Etiology
      • Increase WBC and blood cultrues
    • Cardiac Enzyme
      • Increased if myocardial infarction
  • CXR
    • May show pericardial effusion
    • Expanded look at the heart
    • White out
  • ECG
    • 4 classic stages for pericarditis
  • Echocardiography
    • Diagnosed type of effusion
  • CT Scan
    • Diagnosed type of effusion
  • Analysis of Pericardial Fluid
157
Q

Classic Stages of Pericarditis

Stage 1

A

Elevation in all leads

PR segment is depressed

Depression between the end of the P wave and the beginning of the QRS complex

158
Q

Classic Stages of Pericarditis

Stage 2

A

Pseudonormalisation with t wave flattening (transition)

The PR segment will return to normal

159
Q

Classic Stages of Pericarditis

Stage 3

A

Inverted T waves

160
Q

Classic Stages of Pericarditis

Stage 4

A

Normalization

If it gets normal because the electrical conduction is adapting

161
Q

Pericarditis Management

A
  • Treatment depends on etiology
    • E.g. Antibiotics for bacterial pericarditis
    • E.g. Kidney failure causing uremic pericarditis is treated with dialysis
      • Due to the overload of volume
    • Viral will just have to take its course
  • General
    • Analgesics for pain management
    • Steroids for inflammation
162
Q

Pericarditis Management if Effusion if present

A
  • Percardiocentesis
    • Fluid is aspirated from the pericardium
  • Pericardial window
    • A small part of the sac around the heart is removal in order to remove drained excess fluid
  • Pericardiodesis
  • Percardiectomy
163
Q

Pericardiectomy

A

Excision of part of the pericardium

Done for constrictive pericarditis or for chronic recurring pericarditis

Usually only done in severe cases!

30% of patients will have a recurrent episode of pericarditis within 2 years

164
Q

Cardiac Tamponade

A
  • A life-threatening condition in which elevated intra-pericardial pressures impair the filling of the heart during diastole
    • The increased pressure results from an accumulation of fluid in the pericardial sac
    • Results in decreased SV and CO
  • The severity of the condition depends on the amount of fluid present and the rate at which it accumulated
165
Q

Cardiac Tamponade

Etiology

A
  • Trauma
    • Ex. GSW, MVC
  • Cardiac Surgery
  • Cardiac Rupture secondary to MI
  • Pericarditis
    • All the etiology’s
  • Neoplasm
166
Q

Cardiac Tamponade

Pathophysiology

A

The pericardial space normally contains 20-50 mL of fluid

Rapid accumulation of as little as 150 mL of extra fluid can markedly reduce CO

However 1-2L of fluid accumulating slowly may not have any significant effect on CO due to the adaptive stretching of the pericardium

The effusion can be serous, serosanguineous, hemorrhagic, or chylous

167
Q

Acute Pericardial Effusion

A

Increased Pericardial Pressure ► Decreased Diastolic Filling of the Heart ► Decreased SV and CO ►Signs and Symptons of Shock or Heart Failure

168
Q

Chronic Pericardial Effusion

A

Streching of the Pericardium ► Signs and Symptons of Pericardial Effusion

the streaching of the pericardium can lead to additional accumulation of pericardial effusion lead to the acute pathology of pleural effusion

169
Q

Cardiac Tamponade

Clinical Manifestations

A
  • Beck Triad
  • Tachycardias
  • Decreased pulse pressure
  • Pulsus paradoxus
  • May be present with PEA
  • This is life threatening! Patient will present in acute shock!
170
Q

Beck Triad

A

Hypotension

Increased Jugular Venous Pressure

Diminished heart sounds

171
Q

Cardiac Tamponade

Treatment

A
  • Pericardiocentesis
    • ACUTE
      • Subxiphoid percutaneous drainage with an 18 gauge needle
    • Less Acute
      • Will use fluoroscopy/echo to aid
  • Treatment of underlying causes
  • For recurrent tamponade secondary effusions
    • Pericardial window
    • Pericardiodesis
      • Agents introduced into pericardial sac to sclerose the tissue
  • Pericardiectomy
  • If untreated it is rapidly and universally fatal!
172
Q

Disseminating Intravascular Coagulation

A

A paradox in the hemostatic sequence and is characterized by widespread coagulation and bleeding

A stimulus causes hyperstimulation of the clotting pathways

This results in formation of diffuse clots in the microvasculature and depletion of the clotting factors, which can now result in generalized bleeding

173
Q

Disseminating Intravascular Coagulation

Etiology

A

DIC is not a primary disease it occurs as a complicationof a wide variety of conditions

  • Infections-Bacterial, Viral, Rickettsial, Parasitic
  • Shock, Septic, Hypovolemic
  • Trauma-Burns, Severe Head Injury, Snake Bites, Heatstroke
  • Surgical Procedures
  • Other Disease States-Malignancy, Liver Disease, Pancreatitis, SLE
  • Obstetric Conditions-Abruptio placenta, Retained dead fetus, Amniotic fluid embolism
  • Hematologic Conditions- Incompatible Transfusion, Massive Transfusion
174
Q

Disseminating Intravascular Coagulation

A
  1. Stimulus
  2. Hyperactivation of Clotting Pathways
    1. Consumption of Clotting Factors
      1. Bleeding
    2. Diffuse clotting and micro emboli
      1. Organ and tissue ischemia
        1. Organ Failure
      2. Widespread Fibrinolysis
175
Q
A

CBRC (20 decks)

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