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Pathophysiology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Vericose Veins

A

A vein in which blood has pooled.

Distended, tortuous, and palpable veins.

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2
Q

Risk factors of vericose veins

A
  • prolonged standing
  • Age
  • Family history
  • Obesity
  • Pregnancy (extra fluid volume)
  • History of deep vein thrombosis
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3
Q

Chronic Venous Insufficiency (CVI)

A

Inadequate venous return over a long period due to varicose veins or valvular incompetence.

Ulcers form as a result of lack of blood flow. Tissues aren’t getting nutrients.

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4
Q

Results of CVI

A
  • Venous hypertension
  • Circulatory stasis
  • Tissue hypoxia (in low areas of lower extremeties)

These lead to inflammatory reaction in vessels and tissues

This leads to fibrosclerotic remodeling of the skin

This leads to ulcers

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5
Q

Manifestations of CVI

A
  • Edema of lower extremeties
  • Hyperpigmentation of the skin of the feet and ankles
  • Venous stasis ulcers
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6
Q

Stasis ulcers

A

Metabolic demands of cells not being met.

Jagged and uneven. Brown pigment

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7
Q

Deep Vein Thrombosis

A

Obstruction of venous flow leading to increased venous pressure. This happens from an accumulation of platelets and clotting factors, forming a thrombus.

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8
Q

Triad of Virchow

A
  1. Venous stasis: immobilty/age
  2. Venous endothelial damage: trauma or meds
  3. Hypercoagulable states: cancer/oral contraceptive usage
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9
Q

Thrombus

A

Clot attached to vessel walls

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10
Q

Embolus

A

Thrombus that breaks off and travels blood stream

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11
Q

Manifestations of Deep Vein Thrombosis

A
  • Pain
  • Redness
  • Heat
  • Swelling distal to the spot of embolism
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12
Q

Superior Vena Cava Syndrome

A

Progessive occlusion of the superior vena cava that leads to the venous distension of upper extremities and head.

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13
Q

Number one cause of Superior Vena Cava Syndrome

A

Bronchogenic cancer. SVCS is an oncology emergency.

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14
Q

Manifestations of Superior Vena Cava Syndrome

A
  • Blood pools in upper extremities and head
  • Edema around heart
  • Distended veins in the head and neck
  • Headaches (cerebral edema)
  • Visual disturbances (cerebral edema)
  • Purple/red coloration in head and neck
  • capillary refill prolonged
  • Tight skin
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15
Q

Hypertension

A

Consistent elevation of systemic arterial blood pressure. All stages of hypertension are associated with increased risk for target organ disease events (MI, kidney disease, stroke) Sustained 140/90+

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16
Q

Types of hypertension

A
  • Primary hypertension
  • Secondary hypertension
  • Complicated hypertension
  • Malignant hypertension
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17
Q

Isolated systolic hypertension

A

Sustained systolic blood pressure reading that is greater than 140 mmHg and a diastolic measurement that is less than 90 mmHg

Associated with cardiovascular disease (heart failure) and cerebrovascular events (strokes)

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18
Q

Elevations in systolic pressures are caused by

A
  • Increases in cardiac output (more out/pumped harder)
  • Total peripheral vascular resistance after the heart

Can be one, the other, or both

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19
Q

Risk factors for primary hypertension

A
  • Family history
  • Advancing age
  • Gender (Men-younger, women-older)
  • Ethnicity
  • Excessive salt intake
  • Glucose intolerance
  • Smoking
  • Obesity
  • Heavy drinking
  • Hypokalemic, Hypocalcemic, Hypomagnesia (chronically)
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20
Q

Progression of hypertension

A

Genetics and environment can cause:

  • Insulin resistance
  • Dysfunction of the RAAS system or faulty levels of naturitic peptides
  • Inflammations

Which lead to:

  • increased peripheral resistance or
  • increased blood volume

Which leaves you with
-sustained hypertension
Can be combo of events

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21
Q

Secondary hypertension

A

Caused by systemic disease process that raises peripheral vascular resistance or cardiac output.

Renal artery stenosis, renal parenchymal disease, pheochromocytoma, drugs (birth control, steroids)

Treat the underlying disease

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22
Q

Complicated hypertension

A

Chronic severe hypertension that leads to tissue and vessel damage and eventually leads to organ damage.

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23
Q

Organs damaged by complicated hypertension

A
  • Heart
  • Kidneys
  • Brain
  • Eyes
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24
Q

Cardiovascular complications of sustained hypertension

A
  • Left ventricular hypertrophy
  • Smooth muscle hypertrophy and hyperplasia
  • Fibrosis of the tunica intima and tunica media
  • Angina pectoris
  • Heart failure
  • Coronary artery disease
  • Myocardial infarction
  • Sudden death
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25
Q

Result of cells being under constant pressure to work and do more

A

hypertrophy

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26
Q

Mycardial hypertrophy leads to

A
  • Heart failure
  • M.I.
  • Death

Muscle becomes less effective. Bigger cells need more oxygen, adds to the cycle

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27
Q

Affects on the kidneys by complicated hypertension

A
  • Nephrosclerosis (hardening of the kidneys)
  • Renal arterial sclerosis (plaque within renal arteries)
  • Renal insufficiency
  • Renal failure
  • Protienuria from chronic hypertension
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28
Q

Affects on the brain by complicated hypertension

A
  • Cerebral thrombosis
  • Ischemia
  • Strokes
  • Cerebral edema
  • Aneurisms
  • Hemorrhage
  • Vascular dementia
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29
Q

Affects on the eye by complicated hypertension

A
  • Retinal vascular sclerosis
  • Increased pressures
  • Hemorrhage
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30
Q

Malignant hypertension

A

Form of complicated hypertension. Progresses rapidly–diastolic pressure is usually more than 140 mmHg.

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31
Q

High arterial pressure of malignant hypertension leads to

A
  • Disregulation of bloodflow to cerebral capillary beds in the brain
  • Cerebral edema*
  • Cerebral disfunction*
  • life threatening
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32
Q

Orthostatic Hypotension

A

Decrease in both systolic and diastolic blood pressure upon standing. Occurs with rapid position change.
Decrease of 20 mmHg (systolic) and 10 mmHg (diastolic)

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33
Q

Types of orthostatic hypotension

A
  • Acute orthostatic hypotension

- Chronic orthostatic hypotension

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34
Q

Risk for acute orthostatic hypotension

A
  • Alkalosis
  • Acidosis
  • Meds
  • Fluid shift
  • Prolonged immobility
  • Exhaustion
  • Starvation
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35
Q

Risk for Chronic orthostatic hypotension

A
  • Idiopathic

- Could be secondary to an endocrine disorder

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36
Q

Aneurysm

A

Localized dilation or out-pouching of a vessel wall or cardiac chamber.
Can be true or false.

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37
Q

True aneurysm

A

Involve all three layers of the arterial wall and are best described as a weakening of the vessel wall.
Weakened portion of the arterial wall, so under pressure, it pops out.

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38
Q

Types of true aneurysm

A
  • Fusiform*
  • Saccular
  • most common
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39
Q

False aneurysm

A

Pulsating, encapsulated hematoma attached to the vessel wall. Blood leaks out of small rupture, but gets trapped in layer of vessel wall.

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40
Q

Most susceptible to aneurysm

A

Aorta (abdominal or thoracic)

—Abdominal aorta aneurysm most common

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41
Q

Manifestations of aneurysm

A

Depend on location/size/type

  • Pain
  • Hypotension if ruptured
  • Mostly asymptomatic
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42
Q

Fusiform aneurysm

A

a localized dilation of an artery in which the entire circumference of the vessel is distended. The result is an elongated, tubular, or spindlelike swelling.

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43
Q

Saccular aneurysm

A

a localized dilation of a small area of an artery, forming a saclike swelling or protrusion.

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44
Q

Dissecting aneurysm

A

The splitting or dissection of an arterial wall by blood entering through a tear of the inner lining or by interstitial hemorrhage.

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45
Q

Causes of Vericose Veins

A
  • Trauma to sephenous veins (running up thigh) that damages one or more valves (low pressure system)
  • Gradual distension. Veins not meant to be flexible. Gravity pooling blood in the veins stretches the vein and it can’t recoil.
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46
Q

Thrombus

A

Blood vessel that remains attached to the vessel wall

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47
Q

Risk factors for thrombi

A
  • Internal irritation (inflammation)
  • Traumatic injury (burns)
  • Infection
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48
Q

Threats to circulation from thrombi

A
  • Occlusion

- thromboembolus

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49
Q

Embolism

A

Detached thrombus that becomes mobile

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50
Q

Types of embolism

A
  • Clots
  • Air bubbles
  • Fat
  • Amniotic fluid
  • Aggregate of cancer cells
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51
Q

Pulmonary emboli

A

Typically originate in the venous system.

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52
Q

DVT emboli

A

Originate in lower extremeties

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53
Q

Arterial emboli

A

Originate in left side of the heart

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54
Q

Manifestations of emboli

A
  • Ischemia distal to the site of obstruction.
  • Organ disfunction
  • Pain
  • Infarction may occur with total occlusion of artery or vein
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55
Q

Peripheral vascular disease

A

Atherosclerotic disease of the arteries that profuses the limbs

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56
Q

Types of peripheral vascular diseases

A
  • Buerger disease

- Raynaud disease/phenomenon

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57
Q

Buerger disease

A

Inflammatory disease of the peripheral arteries. Characterized by formation of thrombi filled with inflammatory and immune cells with vasospasm.

Over time, thrombi organize and become fibrotic.
Fibrotic thrombi lead to occlusion.
>Occlusion and obliteration of arteries inhibits oxygen to profuse to the extremities.

Obliterates small and medium arteries.

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58
Q

Causes/risk factors of Buerger Disease

A

· Smoking
· Young age
· Males
· Peripheral ischemia

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59
Q

Manifestations of Buerger disease

A

·Pain
·Cyanosis via ischemia (bluish/purple coloration of the skin)
·Rubor (redness) of the skin due to dilated capillaries
·Hair loss of affected extremity (due to nutrient loss and physiological prioritizing)
·Thin, shiny skin
·Hardened, malformed nail beds

Advanced disease progress:
·Potential for gangrene and amputation
·Stroke
·Mesenteric disease
·joint pain
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60
Q

Raynaud’s disease/phenomenon

A

Attacks of vasospasm in the small arteries and arterioles of the fingers and toes.

Blood vessels in affected individuals demonstrate imbalance in vasodialaters and vasoconstricters.

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61
Q

Cause of Raynaud’s disease

A

Idiopathic. No known cause

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62
Q

Cause of Raynaud’s phenomenon

A

secondary effect from another disease (collagen vascular disease, vasculitis, hypertension, hypothyroidism) or environmental conditions (smoking, cold)

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63
Q

Causes/Risk factors of Raynaud’s d/p

A 
·Changes in temperature
·Cold temperature
·Emotional stress
·Young age
·Females
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64
Q

Manifestations of Raynaud’s d/p

A 
During attack:
·Pain
·Cyanosis via ischemia (bluish/purple coloration of the skin)
·Numbness due to ischemia
·Pallor
·Cold sensations in affected areas
·Bilateral attacks

As blood flow returns:
·Rubor
·Throbbing pain
·paresthesias (prickling)

Prolonged attacks:
·Thickened skin
·Brittle nails
·Ischemia leads to ulcerations and gangrene

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65
Q

Atherosclerosis

A

· Characterized by thickening and hardening of the vessel wall via buildup of lipid laden macrophages in the vessel wall
· THE risk factor for every vascular risk factor (PAD, MI, CAD, etc)
· Progressive disease, typically occlusions are throughout the body

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66
Q

Simple description of formation of atherosclerosis

A

Caused by accumulation of lipid-laden macrophages within the arterial wall, which leads to the formation of a lesion called a plaque

Epithelial injury>Accumulation of lipid-laden macrophages>fatty streak>fibrous plaque>complicated plaque

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67
Q

First step of atherosclerosis formation

A

Atherosclerosis begins with injury to the endothelial cells that line artery walls. Injured cells become inflamed and cannot make normal amounts of anti-thrombic and vasodialating cytokines.

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68
Q

What occurs as a result of endothelial injury in development of atherosclerosis

A

Macrophages bind to inflamed endothelial cells. (Other types of immune/inflammatory cells bind also.) These macrophages release inflammatory cytokines and enzymes that further injure vessel walls. Oxidation of LDL occurs due to the inflammatory process and recruit monocytes that results in more macrophages. Oxidized LDL feeds macrophages transforming them into lipid-laden macrophages.

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69
Q

Result of lipid-laden macrophage accumulation in development of atherosclerosis

A

Lipid-laden macrophages accumulate in large amounts to form a lesion on the walls of arteries called a fatty-streak. Fatty streaks produce radicals and additional inflammatory mediations and recruit T-Cells. All these result in progressive damage to the vessel wall.

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70
Q

Development of plaques in progression of atherosclerosis

A

Macrophages also release growth factors that stimulate smooth muscle cell proliferation. In the damaged area, smooth muscle cells proliferate, produce collagen, and migrate over the fatty streak, forming a fibrous plaque.

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71
Q

Types of plaque formation in atherosclerosis

A
  • Fibrous plaque

- Complicated plaque

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72
Q

Fibrous plaque

A

Formed after smooth muscle cells in damaged area proliferate and produce collagen. Cover the fatty streak and occlude vessels.

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73
Q

Fatty streak

A

First grossly visible lesion in the development of atherosclerosis. Formed from accumulation of lipid-laden macrophages. Damage vessel walls.

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74
Q

Lipid-laden macrophages

A

Macrophages that have engulfed oxidized LDL. Create foam cells that become fatty streaks

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75
Q

Complicated plaque

A

Fibrous plaques that have ruptured. Thrombi form due to platelet adhesion and the clotting cascade. Thrombi may suddenly occlude affected vessel.

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76
Q

Infarction

A

a localized area of tissue that is dying or dead, having been deprived of its blood supply because of an obstruction by embolism or thrombosis.

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77
Q

Three layers of vessel walls

A
  • Tunica intima (thin layer of endothelium)
  • Tunica Media (smooth muscle that constricts/dilates in arteries)
  • Tunica Adventitia (connective tissue)
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78
Q

Risk factors for atherosclerosis (or any vascular disease: CAD, PAD, MI)

A 
· Smoking
· Hypertension
· Family history
· Diabetes mellitus
· Autoimmune disorders
· Obesity
· Sedentary lifestyle
· Increased Low Density Lipoprotiens/Decreased High Density Lipoproteins
· Age
· Males or females post-menopause
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79
Q

Manifestations of atherosclerosis

A

Result from inadequate perfusion of tissues because of obstruction
· Pain
· Disability
· Transient ischemic events (associated with stress or exersize)
· Tissue infarction (in presence of complicated plaque)

80
Q

Peripheral arterial disease

PAD

A

Atherosclerotic disease of arteries that perfuse the limbs, particularly lower extremities.

81
Q

Risk factors of Peripheral Arterial Disease

A

Same as atherosclerosis. Can’t have PAD without atherosclerosis

82
Q

Manifestations of Peripheral Arterial Disease

A

At first, may be asymptomatic.

Hallmark sign: intermittent claudication. (Pain with ambulation that’s relieved with rest.)

Complete obstruction of blood flow may occur, causing:

  • Pain
  • Loss of pulse
  • Skin color changes
83
Q

Someone has pain while walking. The pain gets better when they sit and rest. What disease could they have?

A

Peripheral arterial disease

84
Q

Coronary Artery Disease

A

atherosclerotic occlusion (or ANY lesion that causes a narrowing) of the coronary arteries (The arteries that supply the heart with its Oxygen to continue to pump)
(it is mostly due to atherosclerosis. So for my studying purposes, CAD is an atherosclerotic PARTIAL occlusion of the Coronary Arteries)
-Christine Morton

85
Q

Effects of Coronary Artery Disease

A

Atherosclerotic plaque #1 cause:

  • Ischemia (temporary)
  • Persistent ischemia can lead to infarction (death of tissues)
  • Imbalance between myocardial demand and blood supply to coronary arteries.
  • Lack of oxygen to heart
86
Q

Risk factors of Coronary Artery Disease

A

Same as atherosclerosis.

87
Q

Ischemic attack

A

Tissues without oxygen for up to 20 minutes. Reversible

Cause breaks in electrical conduction of impulses: dysrhythmia/failure to contract/heart failure.

88
Q

Causes of myocardial ischemia

A

Atherosclerosis (Coronary artery disease)

  • Hypovolemia/hypotension (not enough blood supply)
  • Dysrhythmia
  • Increased demand of the heart
89
Q

Events that occur due to myocardial ischemia

A
  • Stable angina pectoris
  • Prinzmetal angina
  • Silent ischemia
90
Q

Stable angina pectoris

A

Recurrent/predictable chest pain that. Rest repairs blood flow, alleviates pain.

91
Q

Pathophysiology of stable angina pectoris

A
  • Gradual narrowing of the coronary vessels due to plaque.
  • Artery is hardened because of plaque

Body can not respond to increase of myocardial demand.

92
Q

Manifestations of stable angina pectoris

A
  • Substernal chest discomfort (pain or pressure)
  • Profuse sweating
  • Pain radiates
  • Dyspnia (short of breath due to pain)
  • Pallor (pale due to pain)
93
Q

Prinzmetal angina

A

Abnormal vasospasm of coronary vessels. Results in unpredictable chest pain (often at rest or at night) and has a cyclical pattern of occurrence.

Relatively benign.

94
Q

Silent ischemia

A

Seldom detectable symptoms. Could be linked with diabetes millitus or chronic stress.

95
Q

Manifestations of silent ischemia

A

Few detectable symptoms. The ones that do appear are vague.

  • fatigue
  • malaise
  • Can form into unstable angina
96
Q

EKG signs of ischemia

A
  • ST segment depression
  • T wave inversion
  • ST segment elevation (most serious)
97
Q

Acute coronary syndromes

A
  • Transient ischemia
    • Unstable angina
  • Sustained ischemia
    • M.I. (STEMI/nonSTEMI)
98
Q

Result of stable plaque

A

Stable angina

99
Q

Paths of acute coronary syndromes

A

Transient ischemia>Unstable angina>Sustained ischemia>Myocardial infarction (non-STEMI or STEMI)>Myocardial inflammation and necrosis

100
Q

Transient ischemia

A
  • Unpredictable.

- Precursor to a stroke.

101
Q

Unstable angina EKG reading

A

ST segment depression

T wave inversion

102
Q

Myocardial infarction categories

A
  • STEMI

- non-STEMI

103
Q

non-STEMI

A

non-ST elevated myocardial infarction. Only damage to the myocardium (middle layer of heart tissue.)

104
Q

STEMI

A

ST elevation myocardial infarction. More serious because there’s an indication of damage to all three layers of the heart tissue.

Requires immediate intervention.

  • Cell death (infarction)
  • Can lead to heart failure due to formation of scar tissue
105
Q

Three layers of heart tissue

A
  • Epicardium (outer)
  • Myocardium
  • Endocardium (inner)
106
Q

Changes in the heart due to myocardial infarction

A
  • Myocardium becomes cyanotic with ischemia after 10 seconds
  • Oxygen demand increases leading to anaerobic metabolism causing acidic environment
  • Cell death occurs in 20 minutes
  • Myocardial stunting in area of infarction (stops contracting) that lasts hours to days
  • Hibernating myocardium. Area stops in an attempt to lower demand.
  • Myocardial remodeling occurs once tissue blood flow is restored. Hypertrophy/loss of contraction of the heart distal to the infarction. Trying to compensate.
  • Wound repair: 10-14 days after infarction
107
Q

Biomarker from myocardial infarction (one example)

A

Triponin

108
Q

Manifestations of MI

A

First signs:

  • Sudden, severe chest pain (crushing, radiating, etc)
  • Sweating
  • Dyspnia
  • Nausea/vomiting

Men:

  • Chest pain
  • Arm pain
  • Shortness of breath

Women:

  • Nausea/vomiting
  • Jaw pain
  • Fatigue
  • Back pain
109
Q

Complications of MI

A
  • Death (depending on area of infarction)

- Electrical instability

110
Q

Left ventricular failure is

A
  • also called congestive heart failure
  • can be further categorized into systolic and diastolic failure
  • most causes of heart failure result from dysfunction of the left ventricle
111
Q

Three types of pericardial disorders:

A
  • acute pericarditis
  • pericardial effusion
  • constrictive pericarditis
112
Q

Causes of acute pericarditis

A

unknown or viral

113
Q

Manifestations of acute pericarditis

A
  • sudden on set of chest pain with fever
  • difficulty swallowing
  • restlessness
  • irritability
  • tachycardia
  • friction rub with stethoscope
  • pulsus paradoxus
114
Q

Pulsus paradoxus is a

A

decrease in systolic blood pressure of >10 mmHg with inspiration

it is suggestive of cardiac tamponade, which is life- threatening

115
Q

Pericardial effusion

A

accumulation of fluid in pericardial cavity

116
Q

Causes of pericardial effusion

A

could be infection or underlying issue

117
Q

Pulsus paradoxus can also be defined as

A

when arterial blood pressure during expiration exceeds arterial pressure during inspiration by more than 10 mm Hg

118
Q

Manifestations of pericardial effusion

A
  • muffled heart waves
  • weak and thready pulse
  • dull chest pain
  • dyspnea
119
Q

Cardiac tamponade

A

fluid compresses heart so much that it can’t beat, which leads to circulatory stoppage

this is connected with pericardial effusion

120
Q

Constrictive pericarditis

A

heart is not as flexible; fibrous scarring with occasional calcification causes layers of pericardium to adhere, obliterating the pericardial cavity and subsequently lowering cardiac output

develops gradually

121
Q

Causes of constrictive pericarditis

A

commonly idiopathic

122
Q

Manifestations of constrictive pericarditis

A
  • exercise intolerance
  • dyspnea on exertion
  • fatigue
  • anorexia

Clinical assessments show:

  • edema
  • jugular vein distention
  • hepatic congestion
  • T wave inversion
123
Q

Disorders of the myocardium: cardiomyopathies

A

-occur on left side of heart
-are a result of remodeling after effect of neurohumoral response to ischemic heart disease or hypertension
diabetes can also be a cause
-often idiopathic, but may be secondary to other disease

124
Q

Types of cardiomyopathies

A
  • Dilated
  • Hypertrophic
  • Restrictive
125
Q

Dilated cardiomyopathy

A
  • causes impaired systolic function
  • the extra blood in the heart leads to dilation and we end up with systolic heart failure
  • left ventricle because rounder
126
Q

Manifestations of dilated cardiomyopathy

A
  • dyspnea
  • fatigue
  • jugular vein distention
  • edema
  • weakened LV
127
Q

Hypertrophic cardiomyopathy

A

is a hypertrophy of septum walls which cause restriction and leads to thickened wall and smaller cavity

can have LA dilation

128
Q

Manifestations of hypertrophic cardiomyopathy

A
  • dysrhythmias
  • angina, syncopy (fainting)
  • dsypnea on exertion
  • palpitations
129
Q

Restrictive cardiomyopathy

A

Restrictive filling and increased diastolic pressure of either or both ventricles

LV cavity is normal size, but LA is dilated because of reduced diastolic compliance

It’s called restrictive because it’s restricting diastole so the decreased diastolic function doesn’t let LV relax

Cause is often idopathic

130
Q

Manifestations of restrictive cardiomyopathy

A

similar to constrictive pericarditis because we have hardening and stiffening of myocardium

Manifestations of constrictive peri are

  • exercise intolerance
  • dyspnea on exertion
  • fatigue
  • anorexia
131
Q

Rheumatic fever

A

systemic, inflammatory disease which can ultimately lead to rheumatic heart disease if left untreated

causes scarring and deformity of cardiac structures when untreated

132
Q

Cause of rheumatic fever

A

a delayed immune response due to group A hemolytic streptococcus

133
Q

Characteristics of acute rheumatic fever

A

is a febrile illness

shows inflammation of joints, skin, nervous system and heart

134
Q

Manifestation of acute rheumatic fever

A
  • fever
  • enlarged lymph nodes
  • joint pain
  • nausea
  • vomiting
135
Q

Aschoff bodies

A

a form of granulomatous inflammatory lesions within the heart, seen in acute rheumatic fever

136
Q

Most common cause of valvular injury

A

Rheumatic fever

137
Q

Valvular dysfunctions

A

are disorders of the endocardium

138
Q

Valvular stenosis

A

is when valve is restricted leading to myocardial hypertrophy

139
Q

Types of valvular stenosis

A

Aortic

Mitral

140
Q

Aortic stenosis

A

most common type of valvular abnormality. Orifice of the aortic valve narrows causing resistance to clood flow from the left ventricle into the aorta. Develops gradually

141
Q

Three common causes of aortic stenosis

A
  • congenital bicuspid valve problems
  • degeneration with aging
  • inflammation damage caused by rheumatic heart disease
142
Q

Manifestations of aortic stenosis

A
  • angina
  • syncopy
  • dyspnea
  • decreased stroke volume
  • Narrowed pulse pressure
  • Slowed heart rate
  • Delayed pulse
143
Q

Mitral stenosis

A

impairs blood flow from LA to LV

valve leaflets harden and become fibrous and fuse, LA pressure increases if LA is backed up

144
Q

Causes of mitral stenosis

A

occurs in patients with history of Rheumatic heart disease and autoimmunity to strep

145
Q

Manifestations of mitral stenosis

A
  • pulmonary congestion

- pulmonary edema

146
Q

Types of valvular regurgitation

A

Aortic
Mitral
Tricuspid

147
Q

Aortic regurgitation

A

inability of aortic valve leaflets to close properly during diastole

ejected blood flows back into LV, causing hypertrophy, dilation of LV

continued hypertrophy causes heart failure

148
Q

Manifestations of aortic regurgitation

A
  • widened pulse pressure resulting from increased stroke volume and diastolic backflow
  • dysrhythmias
149
Q

Pulse pressure

A

is the difference btwn systolic and diastolic blood pressures, normally 30 to 50 mmHg

150
Q

Causes of aortic regurgitation

A
  • congenital (bicuspid valvue)

- acquired (often idopathic)

151
Q

Mitral regurgitation

A

permits backflow of blood from LV to LA during ventricular systole

152
Q

Causes of mitral regurgitation

A

many possibilities, including:

  • mitral valve prolapse
  • rheumatic heart disease
  • infective endocarditis
  • MI
153
Q

Manifestations of mitral regurgitation

A
  • pulmonary hypertension

- heart failure

154
Q

Tricuspid regurgitation

A

usually associated with dilation and failure of RV

leads to volume overload in RA and RV

155
Q

Causes of tricuspid regurgitation

A

secondary to pulmonary hypertension

less commonly caused by rheumatic heart disease and infective endocarditis

156
Q

Manifestations of tricuspid regurgitation

A
  • peripheral edema

- jugular vein distention

157
Q

Infective endocarditis

A

infection and inflammation of the endocardium - especially the cardiac valves

158
Q

Pathophysiology and development of infective endocarditis

A
  1. Endocardial damage from trauma, congenital heart disease or valvular heart disease
  2. leads to inflammation and thrombus formation
  3. then blood-borne microorganism (bacteremia) have much better chance at adherence and increase in clotting factor
  4. which leads to fibrin and thrombus formation, proliferation of microorganisms
  5. then microorganisms aggregate into infective endocardial vegetations
159
Q

Manifestations of infective endocarditis

A
  • fever
  • malaise
  • weight loss
  • changed cardiac murmur
  • petechial lesions on skin
  • conjuctive and oral mucosa
  • Janeway lesions
  • Osler nodes
160
Q

Dysrhythmias

A

disturbance of hearth rhythm

ranges from occasional “missed” or rapid beats to severe disturbance that affects the pumping ability of the heart

161
Q

Cause of dysrhythmias

A
  • abnormal rate of impulse generation or abnormal impulse conduction
  • MI causes scar tissue in purkinje fibers
162
Q

Types of dysrhythmias

A

Sinus Bradycardia
Atrial Tachycardia
Ventricular Standstill (Asystole)

163
Q

Sinus Bradycardia

A

effect is increased preload and decreased mean arterial pressure (MAP)

slow heartbeat

164
Q

Mean Arterial Pressure (MAP)

A

we want it above 60

normal heart beat range is between 60 and 100

165
Q

Causes of sinus bradycardia

A
  • hyperkalemia
  • vagal nerve stimulation
  • age
166
Q

Atrial Tachycardia

A

effect is decreased filling time, decreased MAP and increased myocardial oxygenation demand

rapid heartbeat

167
Q

Causes of atrial tachycardia

A
  • electrolyte disturbances (mostly potassium)
  • hypoxia
  • elevated preload
  • age
168
Q

Ventricular standstill (asystole)

A

effect is no heartbeat and no cardiac output

169
Q

Causes of ventricular standstill

A
  • profound ischemia
  • MI
  • hyperkalemia
  • acidosis
170
Q

Zone of ischemia

A
  • Wider than zone of infarction.

- Reversible, can heal

171
Q

Zone of hypoxic injury

A
  • Damage to cell, but no cell death.

- Might or might not totally heal.

172
Q

Zone of infarction

A
  • Localized.
  • Unable to heal.
  • Area of scar tissue after infarction.
173
Q

Conventional or major risk factors for atherosclerotic disease that are non-modifiable

A
  • Advanced age
  • Male gender or women after menopause
  • -Family history
174
Q

Modifiable risk factors for Atherosclerotic disease

A
  • Dislipidemia (abnormal concentrations of lipoproteins)
  • Hypertension
  • Cigarette smoking
  • Diabetes/insulin resistance
  • Obesity
  • Sedentary lifestyle
  • Atherogenic diet
175
Q

Heart failure

A

The heart is unable to generate an adequate cardiac output, causing inadequate perfusion of tissues

176
Q

Types of heart failure:

A
  • Left systolic
  • Left diastolic
  • Right side heart failure
177
Q

Causes of left systolic heart failure

A

Contractility reduced by:

-M.I. (most common)

178
Q

Cardiac output

A

Depends on the heart rate and stroke volume. Amount ejected from the heart.

179
Q

Stroke volume

A

Influenced by three major determinants:

  • Contractility
  • Preload
  • Afterload
180
Q

Left Systolic Heart Failure

A

An inability of the heart to generate and adequate cardiac output to perfuse vital tissues. Contractility is reduced by diseases that disrupt myocyte activity, namely MI due to scar tissue formation.
-Walls of the heart become distended with increased volume, which further disrupts contractility.

181
Q

Ejection fraction

A

The fraction of blood that is ejected from ventricles with each heartbeat. Given in a percentage. Marker: 40%

182
Q

Manifestations of Left Side Heart Failure

A
  • pulmonary congestion
    • Dyspnea
    • Orthopnia (shortness of breath when lying flat)
    • Cough with pink frothy sputum
    • Pulmonary edema causes crackle sounds in the lung
  • Cyanosis
  • Fatigue
  • Decreased cardiac output
  • Inadequate perfusion of tissues in the system
  • Variable BP
  • Abnormal heart sounds
183
Q

Diastolic Heart Failure

A

Heart failure with preserved ejection fraction. Normal stroke volume and cardiac output.

Decreased compliance of the LV ending with too much volume in LV after relaxation as a result of thickening of ventricular walls.

184
Q

Causes of diastolic heart failure

A
  • Myocardial hypertrophy
  • Ischemia
  • Valve dysfunction
  • Pericardial disease
185
Q

Right Side Heart Failure

A

Inability of the RV to provide adequate blood flow into the lungs. As pressure in the pulmonary circulation rises, the resistance to right ventricular emptying increases. The right ventricle is poorly prepared to compensate for this increased afteload and will dilate and fail.

186
Q

Manifestations of right side heart failure

A
  • Dilation of RV
  • Peripheral maifestations
    • peripheral edema
    • Fluid buildup in the abdomen
    • Jugular vein distension
    • Enlarged liver or spleen
187
Q

Shock

A

Cardiovascular system fails to perfuse the tissues adequately, thus impairing cellular metabolism.

188
Q

Types of shock

A
  • Cardiogenic
  • Hypovolemic
  • Septic
189
Q

Final common pathway in all types of shock

A

Impaired cellular metabolism—Cells switch from aerobic to anaerobic metabolism. Energy stores drop, and cellular mechanisms relative to membrane permeability, action potentials, and lysozome release fail.

190
Q

Results of anaerobic metabolism

A
  • Activation of the inflammatory response
  • Decreased circulatory volume
  • Acidosis
191
Q

Predictive route of MODS

A

Lungs>liver/kidney>GI>Heart

192
Q

Transient ischemia

A

Temporary ischemia, less than 20 minutes, that leads to unstable angina

193
Q

Unstable angina

A

Reversible; shows that atherosclerotic plaque has become complicated and you are at risk for an MI

194
Q

Sustained ischemia

A

Lasts more than 20 minutes. Leads to myocardial infarction (STEMI/nonSTEMI)

195
Q

Aortic stenosis leads to

A
  • Hypertrophic cardiomyopathy
  • Dysrhythmias
  • MI
  • Heart failure
196
Q

Mitral stenosis leads to

A
  • Pulmonary hypertension
  • RV failure
  • Pulmonary edema

Pathophysiology (6 decks)

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