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Patho 2 (Path 311) > Mod 5 CV Disorders > Flashcards

Mod 5 CV Disorders Flashcards

1
Q

What are 3 types of Hypertension?

A

Primary, secondary, or malignant

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2
Q

Etiology of Primary Hypertension?

A

Occurs w/o evidence of other diseases

  • largely idiopathic but has many contributing factors ranging from family history to lifestyle factors
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3
Q

Etiology of Secondary Hypertension?

  • What are the most common causes?
A

Caused by other diseases/complication’s in the body. The main are:

  • Renal disease
  • Excess Adrenocorticosteroids
  • Coarctation of the Aorta
  • Pregnancy
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4
Q

Why are the majority of cases of Secondary Hypertension caused by Renal Disease?

A

Usually atherosclerotic in origin (decreased blood flow to the kidneys)

  • Results in retention of salt and water (due to stimulation of the RAA system) leading to hypertension
  • (sum) The system vasoconstricts bc of low blood flow. Renin releases ACE II —> vasoconstriction. Long term RAA state is bad.
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5
Q

What is Cushing’s syndrome?

A

Body makes too much cortisol (hormone related to stress response)

  • Rare pituitary disorder that is progressive
  • Seen w/excess adrenocorticosteroids
  • Increased cortisol = increased BP
  • Suppresses immune system by reducing production of WBC
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6
Q

What is Excess Adrenocorticosteroids associated with?

A

Seen in primary hyperaldosteronism.

  • leads to secondary hypetension
  • Cushing’s syndrome
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7
Q

Why does excess adrenocorticosteroids cause secondary hypertension?

A

Excess mineralocorticoids, like aldosterone, can lead to increased sodium and water retention, resulting in elevated blood pressure.

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8
Q

Why does Coarctation of the Aorta cause secondary hypertension

A

Causes reduced blood flow to the kidneys —> triggers the RAA system

  • Water retention and hypertension result
  • Viscous cycle?
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9
Q

What stage of hypertension is associated as a hypertensive crisis?

A

Malignant Hypertension (most severe)

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10
Q

What is the origin of Malignant Hypertension?

  • expected course?
A

Occurs when someone w/secondary hypertension develops an accelerated and potentially fatal form of the disease.

  • Can result in Stroke and end organ damage
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11
Q

What is Malignant hypertension defined as (categorically)?

A

Elevations in blood pressure with diastolic pressures > 120mmHg

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12
Q

What is the cascading effect of malignant hypertension?

  • Whats the worst outcomes at its end stage?
A

Can end with Stroke and end organ damage.

  • Causes severe damage to the vascular system
  • Can result in encephalopathy and cerebral edema
  • Convulsions and coma in severe cases
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13
Q

How does Malignant Hypertension manifest?

A
  • Headaches and confusion
  • Motor and sensory deficits
  • Visual disturbances
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14
Q

What is encephalopathy?

A

Dysfunction or disease of the brain that results in altered brain function, which can manifest as a wide range of neurological symptoms.

  • Brain function and structures are affected basically
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15
Q

Pathophysiology of Hypertension in the body?

  • what are the 2 mechanisms of failure?
  • what are the long term consequences?
A
  1. Decreased blood flow to target organs leads to a cascade of varying consequences.
  • Compensation leading to increasing blood volume and blood pressure (vasoconstriction) via kidneys (one example)
  1. Damage to vascular endothelium that causes the lumen to narrow as a result of plaque forming (healing response). Leads to decreased blood flow distally.
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16
Q

What is the expected Pathophysiology of target organ damage in the Heart because of hypertension?

A

Causes hypertrophy of the LV, increasing the risk of ischemia/MI

  • LV has to work harder
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17
Q

What is the anticipated Pathophysiology of Cerebrovascular target organ damage due to hypertension?

  • Cerebrovascular = blood flow in the brain
A

Leads to increased risk of stroke

  • secondary degree bleed or clot
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18
Q

What is the expected Pathophysiology of target organ damage in the Peripheral Vasculature because of hypertension?

A

Leads to the development of atherosclerosis

  • Atherosclerosis is the build up of fat (and other substances) on the arterial walls aka plaque
  • Leads to blood clots and increased resistance
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19
Q

What is the expected Pathophysiology of target organ damage in the Renal system because of hypertension?

A

Stimulation of RAA system

  • worsens hypertension because it stims the retention of water and salt (fluids) causing a increase in blood volume and blood pressure
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20
Q

Clinical manifestations of Hypertension?

A

Increased BP

  • usually asymptomatic (if early)
  • headaches
  • Often the first symptoms are due to complications of hypertension can expect things like chest pain, stroke symptoms, or CHF symptoms
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21
Q

Management of Primary Hypertension?

A

Lifestyle changes

  • Weight loss
  • Reduced sodium intake
  • Regular physical activity
  • Mod in alcohol intake
  • Smoking cessation
  • Healthy diet
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22
Q

What is the clinical definition of Coronary Artery Disease (CAD)

A

Narrowing of 1 or more coronary arteries due to a build up of fatty deposits within the arterial wall.

  • Results in reduced blood flow, causing less O2 and nutrients to be delivered to the heart muscles by the affected arteries
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23
Q

What is a lack of blood flow referred to as?

A

Ischemia

  • When in the heart in the case of coronary artery disease, it is referred to as ischemic heart disease
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24
Q

What are risk factors of Coronary Artery Disease (CAD)

A
  • Increased cholesterol
  • Diabetes
  • Hypertension
  • Smoking
  • Age (Men > 45 y___Women > 55 y)
  • Family history
  • Physical inactivity
  • Obesity
  • Stress
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25
Q

How can you prevent Coronary Artery Disease (CAD)?

A
  • Lifestyle changes (healthy diet, regular exercise, limit smoking and alcohol intake)
  • Control blood pressure
  • Control blood sugar
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26
Q

Pathophysiology of Coronary Artery Disease (CAD)?

A

An atherosclerotic process.

  • Cholesterol and calcium deposited beneath endothelium
  • Fatty streaks develop
  • Scar tissue formation at sites result in plaques
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27
Q

What is the make up of plaque?

  • Is Plaque hard or soft?
  • is it natural?
A

Cholesterol and calcium deposits that settle and harden

  • Firm outer layer w/soft inner core of cholesterol
  • Cholesterol is a natural part of aging, but risk factors accelerate it
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28
Q

What are the 2 main causes of Coronary Artery Disease?

A
  1. Lumen narrows
  2. Plaque Ruptures (etiology of most MIs)
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29
Q

What is the most common cause of origin for MI’s?

A

Plaque Rupture

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30
Q

Why is Lumen Narrowing a problem?

  • why does it lead to Coronary Artery Disease (CAD) ?
A

Results in decreased blood flow to the myocardium

  • Chronic ischemia can lead to myocardial fibrosis and decreased ventricular wall compliance
  • causes a decreased ejection fraction, cause heart can’t pump well
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31
Q

how does Coronary Artery Disease (CAD) present when the lumen narrows?

A

Chest pain because of resulting ischemia

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32
Q

why are Plaque Ruptures a problem?

  • snow ball effect?
A

Plaque rupture exposes the lipid core, which results in platelet adherence (lead to thrombosis/blood clots)

  • Clot development further narrows the lumen and may result in complete occlusion (and MI)
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33
Q

What are clinical manifestations of Coronary Artery Disease (CAD)

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 (chest pain)
  • SOBOE
  • Jaw/back/arm pain (mostly in men), especially left-sided
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34
Q

What lab tests help diagnose/identify Coronary Artery Disease (CAD), but are not definitive?

  • aka non-diagnostic (2)
A
  • High Cholesterol levels
  • High levels of C-reactive protein (CRP)
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35
Q

What are C-Reactive Proteins (CRP)?

A

Marker of inflammation, produced by liver

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36
Q

what exam findings help diagnose Coronary Artery Disease (CAD)?

A
  • Lab tests (CRP & cholesterol levels)
  • ECG
  • Cardiac Stress Test
  • Thallium Stress Test
  • Coronary Angiography
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37
Q

How does a ECG help diagnose Coronary Artery Disease (CAD)?

A

May reveal ischemia, MI, or rhythm disorders

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38
Q

How does a Cardiac Stress Test help diagnose Coronary Artery Disease (CAD)?

A

ECG may show exertional myocardial ischemia

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39
Q

How does a Thallium Stress Test help diagnose Coronary Artery Disease (CAD)?

A

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

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40
Q

What is the gold standard for diagnosing Coronary Artery Disease (CAD)?

A

Coronary Angiography

  • best evaluates the extent and locations of blockages
  • Indicates whether Tx should include angioplasty or CABGs
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41
Q

How is a Coronary Angiography performed?

A
  • Catheter is inserted into a artery (usually femoral) and threaded up the aorta to the openings of the coronary arteries
  • Dye is injected and fluoroscopy captures the image of blood flow
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42
Q

What is non invasive management of Coronary Artery Disease?

A
  • Lifestyle change (healthy diet, exercise, limit smoking/alcohol)
  • Medical Management
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43
Q

What drug classes are used to treat Coronary Artery Disease? (6)

A
  • Daily low-dose aspirin
  • Statins
  • Nitroglycerin
  • β - blockers (lols)
  • Calcium Channel blockers (pines and 1 zem)
  • ACE inhibitors (prils)
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44
Q

What are invasive treatments (management) of Coronary Artery Disease

A
  • Angioplasty = Percutaneous Transluminal Coronary Angioplasty (PTCA)
  • Stenting
  • CABG
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45
Q

How does Angioplasty or Percutaneous Transluminal Coronary Angioplasty (PTCA) manage Coronary Artery disease

A

Results in widening of the artery and plaque being flattened against the wall of the artery

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46
Q

What is the process of Angioplasty or Percutaneous Transluminal Coronary Angioplasty (PTCA)?

A

Often done at the time of angiography

  • A balloon tipped catheter is threaded into coronary artery
  • When balloon is in position, it is inflated. Flattening the walls of the artery
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47
Q

How does Stenting manage Coronary Artery disease?

A

Helps prevent restenosis or at least lengthen the time before it occur so.

  • Prevents renarrowing basically
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48
Q

How is Stenting performed?

A

Often done during angiography.

  • Stents are inserted, often done w/PTCA
  • very similar to PTCA its basically another step
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49
Q

How does Coronary Artery Bypass Graft (CABG) help w/Coronary Artery Disease?

A

Blocked parts of the arteries are bypassed by grafting a vessel above and below the blockage

  • vessel used for grafting is usually the Saphenous vein, internal mammaary artery, or radial artery
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50
Q

When is Coronary Artery Bypass Graft (CABG) performed?

A

Treats Severe Coronary Artery Disease (CAD) that has not responded to meds or PTCA.

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51
Q

What vessels are used for Coronary Artery Bypass Grafting?

A

Vessel used for grafting are usually the Saphenous vein, internal mammaary artery, or radial artery

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52
Q

How are the numbers of Coronary Artery Bypass Grafts (CABG) listed/recorded?

A

CABGx1 = one operation

Refers to how many grafts they’ve done

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53
Q

What are different Coronary Artery Bypass Graft (CABG) methods?

A
  • Traditional approach
  • Off pump or Beating heart
  • MICAB/MICS
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54
Q

What is the traditional method for a Coronary Artery Bypass Graft (CABG)?

  • pros and cons?
A

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

  • Pros = still heart
  • Cons = pump time, cutting through breast bone
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55
Q

What is the Off pump or Beating heart method for a Coronary Artery Bypass Graft (CABG)?

A

Full Sternotomy but heart is not stopped

  • no bypass machine is required
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56
Q

What is the MICABS/MICS method for Coronary Artery Bypass Grafts (CABG)?

A

No sternotomy; Access via intercostal region

  • Typically for from of the heart vessels; 1 or 2
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57
Q

What are the risk factors of Myocardial Infarction (MI)?

A

Most MI’s are caused by a ruptured atherosclerotic plaque, so the risk factors for the development of CAD are also risk factors for an MI!

  • Smoking/drugs/alcohol
  • Hyperlipidemia
  • Diabetes melkite’s
  • Poorly controlled HTN
  • Type A personality
  • Family history/sedentary lifestyle
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58
Q

Etiology of Myocardial Infarctions?

A

AN area of the myocardium is deprived of O2 because of:

  • Decreased supply of O2
  • Increased O2 demand
59
Q

CAD causes that would lead to decreased O2 demand?

  • snowball affect?
A

A decrease in O2 supply for CAD or arterial faults can result from insufficient blood flow or absence. Most commonly, they lead to Myocardial Infarction. The following are reasons why that could happen:

  • Plaque rupture and thrombus formation
  • Vasospasm of coronary artery
  • Hypoxia
  • Profound Hypotension
  • Embolus to coronary arteries
  • Aneurysm of coronary artery
  • Arteritis
60
Q

What are reasons that would cause increased O2 demand from a cardio stand point?

A
  • Inotropic drugs
  • Cocaine
  • Ampetamines
  • Ephedrine
61
Q

where are the most severe sites for infarctions?

A

RCA and LCA because they supply blood for the whole body

62
Q

What are the stages of a myocardial Infarction (MI)

A

Myocardium deprived of O2 -> Ischemia -> Injury and than infarction

63
Q

What is Reperfusion injury?

A

When blood supply is restored to an area of the body that has experienced a period of reduced or interrupted blood flow, typically as a result of ischemia (lack of blood flow).

  • sudden reintroduction of oxygen can cause a burst of oxidative stress, resulting in the production of harmful molecules called reactive oxygen species (ROS). These molecules can damage cells and tissues.
64
Q

What can the area of infarction be described as?

A

Transmural or Subendocardial

65
Q

What is a transmural infarction?

A

when the area affected by a infarction reaches full thickness of myocardium

66
Q

What is a subendocardial infarction?

A

When an area of infarction only affects partial thickness of myocardium

67
Q

what is the time frame of a Myocardial infarction and injury?

A
  • 0-30 mins = reversible injury
  • 1-2 hrs = onset of irreversible injury
  • 4-12 hrs = beginning of necrosis
68
Q

How long does necrosis and development of scar tissue occur?

A

Continued necrosis and development of scar tissue occurs up until 8th week post-infarct

69
Q

When is the risk of myocardial rupture greatest?

A

At 4-7 days post-infarct

  • tougher fibrotic scar tissue starts to form a 7-10 days post-infarct
70
Q

What are the most common clinical manifestations of Myocardial Infarctions (MI)

A

1/3 MI’s are silent

  • Pain/discomfort (tightness/radiating pain)
  • Dyspnea
  • Atypical presentation is common in women, elderly, or long standing diabetics = higher mortality
71
Q

What is our first indicator of a myocardial infarction (MI)?

  • what do we look at next?
A

If you’re having a heart attack, it may take longer to have spikes in blood, which is why we look at myoglobin first

  • High myoglobin
  • High Troponin is next, the wave form is more important to look at than the number itself
72
Q

What are common presentations of a Myocardial Infarction on a ECG?

A
  • ST segment depression or elevation
  • T wave peaking, flattening, or inversion
  • Q wave is deepening or widening, potential loss of R wave resulting in a deep QS wave
73
Q

How many people have diagnostic changes on their initial ECGs with Myocardial Infarctions (MI)

A

50%

74
Q

What are the two classifications of a Myocardial Infarction (MI) based on ECGs?

  • Don’t mix this up with area of affect
A

STEMi and Non-Stemi

75
Q

How many continues leads are necessary to confirm changes in a myocardial infarction (MI)?

A

2 or more leads, and they need to be next to each other

76
Q

What is a STEMI classified Myocardial Infarction?
- How do they Dx?

A

Pts presentation and St elevation on 2 or more contiguous leads provides immediate Dx (w/o need of cardiac enzymes)

  • Means Pt. can be considered for re-perfusion therapy
77
Q

What is Non-Stemi classified Myocardial Infarction?
- How do they Dx?

A

Relies on serum markers (ECG alone doesn’t confirm)

  • the pattern is important
78
Q

What tool helps locate areas of ischemia, infarct, or injury?

A

12 Lead ECG

79
Q

How does a 12 lead ECG give us information on the location of blockage in a artery?

A

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

80
Q

When is ST segment elevation considered pathological?

A

If it occurs in 2 or more anatomically contiguous leads

81
Q

What leads would indicate a lateral injury in the heart?

A

Leads 1, AVL, V5, and V6

82
Q

What leads would indicate a Inferior injury in the heart?

A

Leads II, III, and aVf

83
Q

What leads would indicate a Septal injury in the heart?

A

V1 and V2

84
Q

What leads would indicate a Anterior injury in the heart?

A

V3 and V4

85
Q

Management of Myocardial Infarction?

A
  • Medical support (supportive and pharmaceutical) -> think the mnemonic MONA
  • Repercussion therapy
86
Q

What are medical interventions/support active care to manage Myocardial Infarctions?

A

“MONA”

  • Morphine (Pain relief and vasodilator = reduced afterload)
  • Oxygen (increase O2 content = increase myocardial blood supply)
  • Nitrates (Vasodilating effects)
  • Aspirin (Reduce platelet aggregation)
  • B-blockers (Reduce SNS stim, post MI and reduce afterload)
87
Q

What category of Pts should have reperfusion therapy?

  • how is reperfusion therapy initiated?
A

Patients with STEMI, treat with:

  • Thrombolytics
  • Angioplasty
88
Q

Which patients should not be given Nitrates?

A

Those w/a inferior STEMI

  • Nitrates refer to nitroglycerin
89
Q

What is reperfusion therapy?

  • Methods?
A

The goal is to reduce mortality and limit the infarct size via

  • Thrombolytics (clot buster)
  • Percutaneous Coronary Intervention(PCI)
  • CABG
90
Q

How do Thrombolytics initiate reperfusion therapy?

A
  • Dissolve the blood and platelet clots
  • Best if used within 60-90 mins of onset
  • Risk of bleeding must be considered
91
Q

What is Heart Failure defined as?

A

The inability of the heart to pump enough blood to meet the bodies metabolic needs

  • may affect left or right ventricles (or both)
92
Q

Should Cor pulmonale and right heart failure be referenced as interchangeably?

A

Cor Pulmonale involves PVR not necessarily due to the right heart

  • usually Right Heart Failure (RHF)
  • Right side heart failure is usually secondary to something else
93
Q

How can heart failure be classified under?

A

High output or Low output (which can be systolic/diastolic in origin)

94
Q

What is Left sided Heart Failure caused by and what is the resulting snowball affect?

A

Caused by failure of the left ventricle to move blood from the lungs out of the body

  • Results in blood backing up into the pulmonary system
95
Q

What is Right sided Heart Failure caused by and what is the resulting snowball affect?

A

Caused by failure of right ventricle to pump the returning venous blood out to the lungs.

  • Results in blood backing up into systemic circulation
96
Q

What does it mean when a heart is Supranormal, but still inadequate

A

The heart has high output due to the heart working fast, but w/o the heart being filled in time.

  • aka high need, but unable to meet requirements
97
Q

What is High output Heart Failure?

A

When there is excessive need for cardiac output.

  • uncommon
98
Q

What is Low output Heart Failure?

A

Impaired pumping ability of the heart caused by disorders -> secondary?

  • Can be **systolic/diastolic in origin (and both)
99
Q

What is Low output Systolic Heart Failure?

  • Etiology?
A

Impaired ejection of blood from the heart during systole.

  • Results from conditions that either impair the contractility of the heart or Produce a volume or pressure overload on the heart
  • Results in decrease stroke volume and thus a decreased ejection fraction
100
Q

What disorders could lead to low output systolic heart failure?

A

Anything that decreases stroke volume and ejection fraction:

  • CAD
  • Prior MI
  • A-fib
  • Valve disease/dysfunction
  • alcohol
  • infection
  • cardio myopathy
101
Q

What is low output diastolic heart failure?

A

Impaired relaxation of the heart during diastole

  • results in decreased stroke volume
  • Anything that restricts diastolic filling
  • Increased ventricular thickness (and thus decreases chamber size)
  • Delay diastolic relaxation (fibrosis)
102
Q

What disorders could lead to low output diastolic heart failure?

A

Anything that restrict diastolic fill properly:

  • Ventricular hypertrophy from long term hypertension
  • aortic stenosis
  • diabetes
  • Constrictive pericarditis
103
Q

Add stuff on this

A
104
Q

What are indirect causes of Heart Failure?

A
  • Fluid overload
  • Renal failure
  • Sepsis
105
Q

What are the most common direct causes of heart failure?

A
  • Myocardial ischemia
  • Myocardial infarction
106
Q

What are direct causes of heart failure?

A
  • Myocardial ischemia
  • Myocardial infarction
  • Arrhythmias
  • Heart valve lesions
  • Congenital malformations
  • Pericarditis
  • Cardiomyopathies
107
Q

What factors cause right heart failure (cor pulmonale)?

A
  • COPD
  • Pulmonary Embolism
  • Pulmonary Hypertension
108
Q

What are indirect causes of Heart Failure?

A
  • Fluid overload
  • Renal failure
  • Sepsis
  • factors that cause RHF (cor pulmonale) bc all right sided failure is secondary
109
Q

What symptoms are associated w/left sided heart failure?

A
  • Exertional dyspnea
  • Orthopnea
  • PND
  • Cough
  • Frothy, blood-tinged sputum
  • Cyanosis
  • O/A: Fine/coarse crackles,
    “cardiac” wheezes
  • Increased PAWP
110
Q

What is Paroxysmal nocturnal dyspnea?

A

SOB that awakens Pt 1-2 hrs after falling asleep.

  • Usually relieved by moving into upright position
  • Exertional dyspnea or orthopnea can be expected
111
Q

What is Orthopnea?

A

Discomfort/SOB when laying down

112
Q

What symptoms are associated w/Right sided heart failure?

A
  • Peripheral/dependent edema
  • Fatigue
  • JVD
  • Hepatomegaly
  • Ascites
  • Cyanosis
  • Increased CVP
113
Q

What 2 factors are expected in the event of Heart failure?

A
  1. Inadequate Cardiac Output (CO)
  2. Compensatory mechanisms

Inadequate CO from whatever origin can trigger compensatory mechanisms

114
Q

What compensatory mechanisms get triggered by heart failure?

A

To be specific, inadequate cardiac output triggers the following:

  • Frank starling mechanism (stretch)
  • Increased SNS activity
  • RAA mechanism
  • Myocardial hypertrophy
115
Q

Briefly describe the frank starling mechanism

A

Increased preload = increased stretch = increased force of contraction = increased stroke volume.

  • Frank starling mech is normally responsible for maintaining normal CO
  • Heart can overstretch though
116
Q

How does the frank starling mechanism compensate for heart failure?

A

When end diastolic volumes increase (reflected by increased PAWP and CVP)

  • the mech becomes ineffective when the myocardial fibers overstretch
  • CO can’t increase w/increased physical activity
117
Q

How and why does the SNS mechanism trigger as a result of Heart failure?

A

Increased SNS activity is triggered by a decrease in SV and CO.

  • Leads to systemic vasoconstriction in order to maintain perfusion to vital organs despite lower SV
  • Also increases HR and contractility
118
Q

Why is a increase in SNS activity problematic in heart failure?

A

Increased SVR leads to increased afterload and further myocardial demand

119
Q

Why/how does heart failure trigger the RAA system?

  • What does the trigger cascade look like?
  • end results?
A
  1. Decreased SV and CO results in decreased perfusion in the kidneys.
  2. kidneys respond by releasing renin which activates the RAA system
  3. Aldosterone causes sodium and water retention = increases blood volume
  4. Angiotensin II causes vasoconstriction
  5. Culmination of the above increases end diastolic volumes and increased CO via frank starling mech
120
Q

What is the main problem with compensatory mechanisms?

A

inefficiencies and failure lead to volume problems

  • Snowballs into frank starling mech (overstretch)
  • leads to decompensated heart failure
121
Q

What does increased SVR lead to in decompensated heart failure?

A

Increase in myocardial demand

122
Q

What does increased HR lead to in decompensated heart failure?

A

Increase in myocardial demand, shortens diastole

123
Q

What does stimulation of the RAA system lead to in decompensated heart failure?

A

Increases in filling pressure, further contributes to fluid overload worsening clinical manifestations

124
Q

What does stimulation of the Frank Starling Mechanism lead to in decompensated heart failure?

A

Overstretch in myocardial fibers

125
Q

How does Myocardial Hypertrophy lead to in decompensated heart failure?

A

Increase in myocardial oxygen requirements, may reduce chambers size causing diastolic failure (ventricle gets more muscular and large = less space in chaber)

126
Q

How does heart failure present on a CxR?

A
  • Cardiomegaly
  • Left heart failure = diffuse bilateral infiltrates (butterfly pattern), pleural effusions, kerley B lines
127
Q

What exams can be used to help diagnose heart failure?

A
  • Echocardiography
  • ECG (see MI or abnormal arrhythmias)
128
Q

What are acute treatments for heart failure? (3)

  • acute = active but short term
  • list the primary’s in this card
A
  1. Preload reduction via diuretics (and others)
  2. Afterload reduction via B-blockers
  3. Inotropic support (use w/caution) via milrinone, digoxin, dobutamine, dopamine, NE etc.
  • O2 and NIPPV during this if pulmonary edema is present
129
Q

What drugs can be given to reduce preload?

A
  • Diuretics
  • Nitroglcerin
  • morphine
130
Q

What are acute treatments for pulmonary edema?

A
  1. Oxygen and NIPPV
  2. Diuretics
131
Q

What drugs can be given to reduce afterload?

A
  • B-blockers
  • Nitroglyercin, nitroprusside
  • ACE inhibitors
132
Q

Why does CPAP work well for CHF?

A

CPAP pushes back fluid and surfactant back to where it should be

133
Q

What does a 1:1 ratio on a intra aortic balloon pump mean?

A

It inflates/deflates for every beat of the heart

134
Q

If a patient is on BiPAP for heart failure, what back up rate should you ensure is used?

A

4

  • Ensure they’re getting ventilated
  • Ensure they’re hitting their rates and Vts
135
Q

When using NIPPV for heart failure (acute treatment) when would you use BiPAP vs CPAP?

A
  • BiPAP = SOB and has WOB
  • CPAP = no WOB
136
Q

Aside from a back up rate, what should you monitor and ensure is set appropriately on the patient?

A

Titrate IPAP to appropriate Vt

137
Q

What are general/long term treatments for heart failure?

A
  • Restriction of dietary sodium
  • Diuretics
  • Nitroglycerin or long acting nitrates
  • ACE inhibitors/B-blockers
  • Cardiac rehab
138
Q

What are 2 types of Valvular Disorders?

A

Stenosis and Incompetence

139
Q

What are Valvular Disorders defined as?

A

A disorder that can affect any one of the 4 heart valves

140
Q

What are Incompetence mechanical disruptions in Valvular Disorders?

A

Valve does not close properly; resulting in regurgitant flow

141
Q

What is reflected by poor valvular function?

A
  • Obstruction in the flow of blood (stenotic valve disorder)
  • Allowing backward flow of blood (regurg)
142
Q

Why would stenosis occur?

A

Narrowing can be caused by thickening of stenotic valve leaflets

143
Q

Why would a Transesophageal echocardiography (TEE) be used for patients in prolonged a.fib?

A

Need to make sure there isn’t a big clot before we cause their valve to shut and push further into further if there is one

Patho 2 (Path 311) (15 decks)

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