PATH - Cardio Flashcards
alterations of Cardio
1
Q
A vein in which blood has pooled
Distended, tortuous, and palpable veins
Caused by trauma or gradual venous distention
A
Varicose Veins
2
Q
3 Diseases of the veins?
A
Varicose Veins
Chronic Venous Insufficiency
Deep Venous Thrombosis
3
Q
stasis
A
not moving
4
Q
Deep Venous Thrombosis?
Factors/Causes?
A
Obstruction of venous flow leading to increased venous pressure
Virchow’s triad – describes causes of DVT:
● Venous stasis
● Venous endothelial damage
● Hypercoagulable states
5
Q
Chronic Venous Insufficiency
A
Inadequate venous return over a long period due to varicose veins or valvular incompetence
• Causes pathologic ischemic changes in the vasculature, skin, and supporting tissues.
• Venous stasis ulcers
6
Q
Venous stasis ulcers
A
ulcerations of skin that occur due to pressure or trauma.
o Develop as a result of the borderline metabolic state of the cells in the affected extremities
7
Q
Progressive occlusion of the superior vena cava.
A
Superior Vena Cava Syndrome
• Leads to venous distention of upper extremities and head.
• Usually caused by bronchogenic cancer and some other cancers.
o As tumors grow they compress the SVC, decreasing its diameter.
8
Q
Generally considered an oncologic emergency rather than a vascular emergency.
A
Superior Vena Cava Syndrome
9
Q
Hypertension
A
is the consistent elevation of systemic arterial blood pressure resulting from increases in total peripheral resistance, circulating blood volume, or both.
10
Q
Normal blood pressure is defined as
A
systolic pressure less than 120 mm Hg and diastolic pressure less than 80 mm Hg.
11
Q
Hypertension - types
A
Primary Hypertension (essential or idiopathic) Secondary Hypertension Isolated Systolic Hypertension (ISH) Complicated Hypertension Malignant Hypertension
12
Q
Affects 92% to 95% of individuals with hypertension
A
Primary Hypertension (essential or idiopathic)
• Hypertension without a known cause
• Appears to be due to a combination of genetic and environmental factors.
13
Q
Primary Hypertension • Risk factors include:
A
o Family history
o Advanced age
o Smoking
o Obesity
o Heavy alcohol consumption (>3 drinks per day)
o Gender (men > women before age 55, women > men after 55)
o Black race
o High dietary sodium intake
o Low dietary intake of potassium, magnesium, and calcium
o Glucose intolerance/diabetes mellitus
14
Q
Underlying mechanisms of primary hypertension
A
Overactivity of the sympathetic nervous system (SNS)
Causes increased heart rate and peripheral vasoconstriction.
Overactivity of the renin-angiotensin-aldosterone (RAA) system
High aldosterone levels cause increased retention of sodium and water.
Angiotensin II causes vasoconstriction and vascular remodeling which increases peripheral resistance.
Abnormal secretion of natriuretic hormones
These modulate renal sodium excretion and retention.
Abnormal levels cause sodium and water retention by the kidneys.
Complex interactions involving insulin resistance, inflammation, and endothelial function.
Contribute to vascular remodeling, increased sodium retention, and effects of SNS and RAA.
15
Q
Caused by a systemic disease process or medication that raises peripheral vascular resistance or cardiac output, such as:
o Renal disease
o Adrenocortical tumors
o Adrenomedullary tumors (pheochromocytoma)
o Drugs (oral contraceptives, corticosteroids, antihistamines).
A
Secondary Hypertension
• If the cause is identified and removed before permanent structural changes occur, blood pressure returns to normal.
16
Q
Defined as a sustained systolic BP that is ≥140mm Hg and diastolic BP that is below 90mm Hg.
• Common in older individuals who have stiffer (noncompliant) blood vessels.
A
Isolated Systolic Hypertension (ISH)
ISH is a risk factor for heart attack, congestive heart failure, and stroke.
17
Q
Isolated Systolic Hypertension (ISH) - Mechanism:
A
o As the cardiac output is ejected into the aorta and its branches, they do not stretch to accept this increased blood volume and pressure rises.
o As this volume is distributed to the tissues during diastole, pressure falls back to normal.
18
Q
Complicated Hypertension
A
Severe or sustained hypertension that begins to affect many other organs in the body.
• Chronic hypertensive damage occurs in the walls of systemic blood vessels.
• Vascular remodeling occurs
• Clinical manifestations result from damage of organs and tissues
19
Q
o Smooth muscle cells undergo hypertrophy and hyperplasia.
o Fibrosis occurs in the tunica intima and tunica media.
A
Vascular remodeling
20
Q
Complicated Hypertension - Clinical manifestations result from damage of organs and tissues (end organ damage):
A
o Heart disease
o Renal disease
o Cerebrovascular accidents
o Damage to retina of eye
21
Q
Malignant Hypertension
A
- Rapidly progressive hypertension in which diastolic pressure is usually above 140mm Hg.
- Organ damage resulting from malignant hypertension is life threatening
22
Q
Malignant Hypertension - Sequelae include:
A
o Encephalopathy - from profound cerebral edema that disrupts cerebral function and causes loss of consciousness. o Cardiac failure o Uremia o Retinopathy o Cerebrovascular accident
23
Q
Treatment for Hypertension
A
- Behavioral changes – weight loss through diet and exercise and salt restriction.
- Antihypertensive drugs
24
Q
Antihypertensive drugs
A
a. Diuretics – enhance urinary fluid loss to reduce blood volume.
b. Beta-blockers – block sympathetic input to heart, reducing contraction strength, cardiac output, and thus lowering blood pressure.
c. ACE-inhibitors – block angiotensin converting enzyme in lungs, so less angiotensin II is formed. This reduces vasoconstriction and aldosterone release.
d. Angiotensin-receptor blockers - cause vasodilation, reduced secretion of angiotensin II, and reduced production and secretion of aldosterone.
e. Calcium channel blockers – restrict entry of calcium into arteriolar smooth muscle, thus producing vasodilation, and into cardiac muscle, causing lower cardiac output.
• Multiple types of drugs may be combined to increase effectiveness.
25
enhance urinary fluid loss to reduce blood volume.
Diuretics
26
block sympathetic input to heart, reducing contraction strength, cardiac output, and thus lowering blood pressure.
Beta-blockers
27
ACE-inhibitors
block angiotensin converting enzyme in lungs, so less angiotensin II is formed. This reduces vasoconstriction and aldosterone release.
28
Angiotensin-receptor blockers
cause vasodilation, reduced secretion of angiotensin II, and reduced production and secretion of aldosterone.
29
restrict entry of calcium into arteriolar smooth muscle, thus producing vasodilation, and into cardiac muscle, causing lower cardiac output.
Calcium channel blockers
30
Multiple types of drugs may be combined to increase effectiveness. T/F
True
31
Antagonists
act against (oppose)
32
Agonists
increase activity of something
33
A significant drop in systolic and diastolic blood pressure upon moving from a lying or sitting position to a standing position.
Orthostatic (Postural) Hypotension
Systolic blood pressure decrease of 20 mm Hg (or greater) or diastolic blood pressure decrease of 10 mm Hg (or greater) within the first 3 minutes of standing.
34
Orthostatic (Postural) Hypotension - Cause
a failure of sympathetic nervous system vasomotor compensatory mechanisms that cause increased heart rate, vasoconstriction, and venous valve closing upon standing.
o Essential to maintaining adequate cerebral perfusion during upright positioning.
35
Orthostatic (Postural) Hypotension - Clinical Manifestations
dizziness, syncope (fainting), or sudden loss of vision or blurred vision.
36
Orthostatic (Postural) Hypotension - Types
* Acute orthostatic hypotension – caused by temporary body alterations like drugs and medications, dehydration, venous pooling, and prolonged inactivity.
* Chronic orthostatic hypotension – caused by underlying diseases like endocrine or metabolic disorders. Or it may be a primary condition caused by degeneration of the CNS with age.
37
Acute orthostatic hypotension
caused by temporary body alterations like drugs and medications, dehydration, venous pooling, and prolonged inactivity
38
Chronic orthostatic hypotension
caused by underlying diseases like endocrine or metabolic disorders. Or it may be a primary condition caused by degeneration of the CNS with age.
39
a local dilation or outpouching of a vessel wall or cardiac chamber.
Aneurysm
40
Aneurysms Primarily develop in the:
o Cerebral arteries (most commonly in the circle of Willis)
| o Thoracic or abdominal aorta
41
Over time __________ grow in size, putting pressure on neighboring structures.
• The wall becomes thinner and weaker, and eventually may rupture, causing stroke or life-threatening hemorrhage.
aneurysms
42
Dissecting aneurysm (aortic dissection)
o Occurs when the tunica media is weakened and the intima is torn, allowing arterial pressure to force blood into the media, dissecting its layers apart.
o The dissection compresses vessels as they leave the aorta, causing acute ischemia and infarction of vital organs such as the brain and kidney.
o Aortic dissection most commonly involves the thoracic aorta.
o Symptoms - abrupt onset of severe chest pain along with syncope and symptoms of organ ischemia.
43
Aortic dissection has a very low mortality rate and is not a surgical emergency.
False - high
44
a clot that remains attached to a vascular wall.
| o Can also form on damaged heart valves and in cardiac chambers (atrial fibrillation, ventricular aneurysms).
thrombus
o Activation of the clotting cascade leads to platelet aggregation and formation of a clot (thrombus) within a vessel, on a cardiac valve, or along the wall of a cardiac chamber.
45
Thrombus - Causes
o Causes are the same as for venous thrombi: intimal injury, stasis of flow, and hypercoagulable states (although these more commonly cause venous thrombosis).
46
Types of Arterial Thrombus Formations
* Thrombus
| * Thromboembolus
47
detached portion of a thrombus that travels through the bloodstream
Thromboembolus
48
If the thrombus or embolus blocks a part of the peripheral circulation, this will cause limb ischemia and tissue infarction (tissue death). T/F
True
o If the thrombus or embolus blocks one of the central arteries, stroke and other types of vital organ infarctions may occur.
o Thromboemboli from the heart valves or chambers frequently travel to the brain, causing stroke.
49
Raynaud Phenomenon and Raynaud Disease
Peripheral Vascular Disease
| • Episodic vasospasm in arteries and arterioles of the fingers, and less commonly the toes.
50
a primary vasospastic disorder related to an imbalance of endothelium-derived vasodilators and vasoconstrictors.
Raynaud disease
51
occurs secondary to other systemic diseases or conditions such as:
o Scleroderma, smoking, pulmonary hypertension, myxedema, and environmental factors
Raynaud phenomenon
52
Vasospasm causes pain and Temperature changes in the skin, especially involving the fingers and toes. T/F
True
• Vasospasm causes pain and color changes in the skin, especially involving the fingers and toes.
• Can occur on exposure to even a small drop in room temperature, or occasionally with vibration or repetitive motion.
53
Most common form of arteriosclerosis.
Atherosclerosis
54
Arteriosclerosis
* Chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls.
* Smooth muscle cells and collagen fibers migrate to the tunica intima, gradually narrowing the arterial lumen.
* Part of the normal aging process, but it is a disease state when it occurs to the point of symptom development.
55
Atherosclerosis is Characterized by
by soft deposits of fat and fibrin in the arterial wall that harden over time (plaques).
56
Hypertension, diabetes, smoking, high LDL levels, aging, autoimmune injury, and possibly bacterial infection by Chlamydia pneumonia can Cause?
Condition name?
• Plaque development
- begins when there is endothelial injury and inflammation
Atherosclerosis
57
Atherosclerosis Progression:
o Endothelial injury causes inflammation.
o Macrophages adhere and release cytokines that further injure the wall.
o Low-density lipoprotein (LDL) in the blood is oxidized and engulfed by macrophages (forming foam cells)
o A fatty streak forms as foam cells accumulate in wall of vessel.
o Fibrous plaque - macrophages release growth factors (mitogens) that promote proliferation of smooth muscle cells in the tunica media. These cells migrate over the fatty streak, produce collagen, and form a fibrous cap over the plaque.
o Plaques undergo calcification, grow, and protrude into the lumen of the vessel, obstructing flow.
o Complicated plaque – a plaque that has ruptured. This initiates thrombus formation and instability and vasoconstriction leading to obstruction of the lumen and inadequate oxygen delivery to tissues.
58
Atherosclerosis is the Secondary risk factor for myocardial infarction, stroke, and peripheral artery disease. T/F
False
| • Atherosclerosis is the PRIMARY risk factor for myocardial infarction, stroke, and peripheral artery disease.
59
any vascular disorder that narrows or occludes the coronary arteries is called
Coronary Artery Disease (CAD)
60
Coronary Artery Disease (CAD) most common cause.
Atherosclerosis is the most common cause.
o Plaques narrow the coronary arteries.
o May rupture and cause sudden thrombus formation and myocardial ischemia and even infarction.
61
Risk factors for CAD are Catagorized as
Conventional or major risk factors
| Nontraditional or novel risk factors
62
Conventional or major risk factors for CAD
* Advanced age
* Gender (men > women before age 55, women > men after age 55)
* High cholesterol/LDL levels*
* Hypertension *
* Smoking *
* Diabetes mellitus and insulin resistance
* Obesity
* Sedentary lifestyle
* Metabolic syndrome
* Atherogenic diet (high in saturated and trans fats)
63
Nontraditional or novel risk factors for CAD
```
Markers of inflammation
o C-reactive protein (CRP)
o Fibrinogen
o Protein C
o Plasminogen activator inhibitor
o Interleukins
o Others
```
Hyperhomocysteinemia
Infection
64
Markers of inflammation
```
o C-reactive protein (CRP)
o Fibrinogen
o Protein C
o Plasminogen activator inhibitor
o Interleukins
o Others
```
65
Myocardial ischemia types
- Ischemic heart disease
- Angina pectoris
- Silent ischemia
- Acute coronary syndromes
66
o Local, temporary insufficiency of the coronary blood supply and oxygen.
o Usually occurs when demand for oxygen rises (increased heart rate)
Ischemic heart disease – caused by CAD and the resultant decrease in blood supply.
67
Angina pectoris -
| Types -
- chest pain caused by myocardial ischemia.
o Stable angina - occurs with exercise and relieved with rest.
o Prinzmetal angina – due to vasospasm of coronary vessels without underlying atherosclerosis
68
Myocardial ischemia occurs unpredictably, often at rest or during sleep.
May result from hyperactivity of the sympathetic nervous system and changes in endogenous vasodilators and vasoconstrictors.
Which type of Angina?
Prinzmetal angina – due to vasospasm of coronary vessels without underlying atherosclerosis
69
Usually transient, lasting approximately 3 to 5 minutes
Substernal chest discomfort, which may radiate to the neck, lower jaw, left arm, and left shoulder, or occasionally, to the back or down the right arm.
Other symptoms include dizziness, shortness of breath, pallor and sweating.
Which Type of Angina?
Stable angina - occurs with exercise and relieved with rest.
70
ischemia without symptoms of chest discomfort.
o Can occur with dysfunction of the autonomic nerves that bring efferent messages from the heart to the brain.
o Common in diabetics, since they often suffer autonomic dysfunction.
Silent ischemia
71
caused by sudden coronary obstruction due to thrombus formation.
Acute coronary syndromes
72
Unstable angina
– severe chest pain that occurs due to rupture of a plaque in a coronary artery.
73
Acute coronary syndromes causes anginal pain that occurs at predictable times (for example, at rest) or with less frequency and severity. T/F
False
| Causes anginal pain that occurs at UNpredictable times (for example, at rest) or with GREATER frequency and severity.
74
Unstable angina is a signal of?
| Symptom of?
myocardial infarction
Acute coronary syndromes
75
If the ruptured thrombus is labile and occludes the vessel for no more than 10 to 20 minutes, myocardial ischemia will be severe but will not result in infarction of the heart. T/F
True
| Anaerobic metabolism is able to support cell function for about 20 minutes.
76
Is a Myocardial infarction classified as an acute coronary syndrome?
Yes
77
Caused by prolonged, unrelieved ischemia that interrupts blood supply to the myocardium.
o Usually due to a ruptured thrombus in a coronary artery.
Myocardial infarction
78
After about ____ minutes of myocardial ischemia, irreversible hypoxic injury causes cellular death and tissue necrosis due to lack of oxygen.
20 Minutes
79
Myocardial infarction Classifications:
o Non-STEMI
| o STEMI
80
Non-STEMI
only affects the myocardium just under the endocardium (subendocardial).
81
STEMI
– damage penetrates all the way from the endocardium to the pericardium (transmural MI). [STEMI = ST-elevated myocardial infarction.] Identifies patients at greatest risk for severe complications and most likely to benefit from rapid intervention
82
Pathophysiology of MI
| Myocardial infarction
o Cellular necrosis results in the release of intracellular enzymes such as troponin I and troponin T, creatinine phosphokinase (CPK-MB), and lactate dehydrogenase (LDH).
o Cellular necrosis is accompanied by release of inflammatory mediators and infiltration of the myocardium with inflammatory cells such as polymorphonucleocytes and macrophages.
83
Structural and functional changes are defined as?
Neurohumoral changes cause structural and functional alterations that contribute to further dysfunction of heart muscle surrounding the infarction.
84
Myocardial infarctions Structural and functional changes are?
Myocardial stunning
Hibernating myocardium
Myocardial remodeling
85
Myocardial stunning
- toxic oxygen radicals and other inflammatory mediators cause temporary loss of contractile function that persists for hours or days after perfusion has been restored.
86
Hibernating myocardium
- Tissue that survives persistent ischemia through metabolic adaptation to prolong myocyte survival until perfusion can be restored.
87
Myocardial remodeling
- Myocyte hypertrophy and loss of contractile function of heart muscle distant from the site of infarction. This process is mediated by angiotensin II, catecholamines, aldosterone, adenosine, and inflammatory cytokines. It can be inhibited by the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and beta blockers after an MI.
88
An increase in plasma enzyme levels is used to diagnose the occurrence of myocardial infarction and indicate its severity. T/F
True
o Elevations of the isoenzymes creatine kinase (CK-MB), troponins, and lactic dehydrogenase (LDH-1) are most predictive of a myocardial infarction.
89
Myocardial infarction Treatments include:
o Revascularization (thrombolytics or PCI)
o Antithrombotics, ACE inhibitors, and beta-blockers.
o Pain relief and fluid management.
90
Dysrhythmias and cardiac failure are the most common complications of acute myocardial infarction. T/F
True
91
Eclampsia is what type of hypertension?
malignant hypertension (Gravidic toxemia)
92
Eclampsia → HELLP means?
● H → hemolysis, breakdown of RBC
● EL → elevated liver enzymes
● LP → low platelet count, causes bleeding
93
Pancoast tumor/syndrome = if malignancy
- Superior vena cava syndrome produced by a malignancy (by primary or metastatic cancer)
94
● Difficult to diagnose when high blood pressure and protein in urine are not present
● Happens with pregnancy → s/s liver pain, swollen legs, reduction of mental ability
● Target organs = brain, heart, liver + bleeding
Eclampsia
95
Usually happens to thin and tall people, triggers tachycardia
Orthostatic (postural) hypotension
96
True aneurysm types
● Fusiform aneurysm (spindle shape)
● Circumferential aneurysm (round)
● Saccular aneurysm (sac on one side of bloodvessel)
97
False aneurysm
● Blood leak but is caught by surrounding perivascular soft tissue
● Clots attached to outside of wall
98
● Most dangerous → collection of blood increases pressure
| ● Breaks through the endothelium and basement membrane between muscular and adventitia
Dissecting aneurysm
99
Types of Aneurysms?
1 True aneurysm
● Fusiform aneurysm (spindle shape)
● Circumferential aneurysm (round)
● Saccular aneurysm (sac on one side of bloodvessel)
2 False aneurysm
3 Dissecting aneurysm
100
Bolus of matter that is circulating in the bloodstream
Embolism
101
Peripheral artery disease
○ Atherosclerosis → is plaque build up
| ○ Arteriosclerosis → is hardening of arteries/vessels due to chronic hypertension
102
Buerger disease
Thromboangiitis obliterans
103
Thromboangiitis obliterans
● Inflammation, narrowing and blockage W/O
| ● Occurs mainly in aging men who smokeplaque
104
Obliteration
closure
105
● Inflammatory disease of peripheral arteries resulting in the formation of nonatherosclerotic lesions
○ digital, tibial, plantar, ulnar, and palmar arteries
● Obliterates the small and medium sized arteries
● Causes pain, tenderness, and hair loss in affected area → follicles don't receive blood
● Symptoms are caused by slow, sluggish blood flow and can lead to gangrenous lesions
Thromboangiitis obliterans (Buerger disease)
106
Raynaud disease is a primary vasospastic disorder of autoimmune origin T/F
True
107
Raynaud phenomenon is Primary to other systemic diseases or conditions
Raynaud phenomenon is secondary to other systemic diseases or conditions
-Collagen vascular disease, smoking, pulmonary hypertension, myxedema, and environmental factors (cold and prolonged exposure to vibrating machinery)
108
claudication
claudication means giving in/surrendering
109
Ex. walk → stop since pain → walk → stop since pain
Intermittent claudication
110
Subendocardial infarction
beneath the endocardium
111
Transmural infarction
across the wall thickness of the heart
112
scarring is formed for?
Repair
113
systolic cardiac failure due to weaker heart walls
Dilated cardiomyopathy
114
Disorders of the Heart Wall can be categorized into?
Disorders of the Pericardium
Disorders of the Myocardium
Disorders of the Endocardium
115
Three Disorders of the Pericardium?
Acute pericarditis
Pericardial effusion
Constrictive pericarditis
116
compression of the heart by fluid in the pericardial sac, which interferes with filling of the heart.
Cardiac tamponade
117
Cardiac tamponade Clinical signs:
- increased venous pressure
- congestion resulting in distention of the jugular veins
- edema
- hepatomegaly
- distant or muffled heart sounds
- poorly palpable apical pulse
- dyspnea on exertion
- dull chest pain.
118
Clinical presentation: Sudden onset of severe anterior chest pain that worsens with respiratory movement or lying down; low-grade fever; sinus tachycardia; friction rub.
Acute pericarditis
119
Acute pericarditis?
| Cause?
* Acute inflammation of the pericardium whereby membranes become inflamed and roughened, often producing exudates.
* May result from infection, drug therapy, or tumors.
120
Clinical presentation: Often asymptomatic unless cardiac compression results
Pericardial effusion
121
Pericardial effusion
Accumulation of fluid in the pericardial sac (cavity), usually secondary to acute pericarditis.
• Clinical presentation: Often asymptomatic unless cardiac compression results.
• Cardiac tamponade – compression of the heart by fluid in the pericardial sac, which interferes with filling of the heart.
o Cardiac function may be severely impaired if the accumulation of fluid occurs rapidly and involves a large volume.
o Clinical signs: increased venous pressure and congestion resulting in distention of the jugular veins, edema, and hepatomegaly; distant or muffled heart sounds, poorly palpable apical pulse, dyspnea on exertion, and dull chest pain.
122
* Cause: Often idiopathic but may result from infection (tuberculosis, gram positive bacteria), radiation exposure, rheumatoid arthritis, or post-surgical scarring.
* Clinical presentation: Asymptomatic in early stages; exercise intolerance, fatigue, dyspnea on exertion develop and worsen over time; symptoms of venous congestion; eventually compresses heart, preventing ventricular filling.
Constrictive pericarditis
123
Constrictive pericarditis
• Fibrous scarring and calcification of the pericardium causes the visceral and parietal pericardial layers to adhere, obliterating the pericardial cavity, resulting in encasement of the heart in a rigid shell over time.
124
Disorders of the Myocardium also called?
Cardiomyopathies
- a diverse group of primary myocardial disorders.
- Classified according to their effects on the heart wall.
125
Disorders of the Myocardium - 3?
Dilated cardiomyopathy (congestive cardiomyopathy)
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
126
the ventricular walls dilate and become thin, resulting in a decreased strength on contraction.
Dilated cardiomyopathy (congestive cardiomyopathy)
127
the ventricular myocardium thickens (hypertrophies).
Hypertrophic cardiomyopathy
128
Asymmetrical septal hypertrophy
– genetic disorder causing enlargement of the interventricular septum.
129
Hypertensive (valvular hypertrophic) cardiomyopathy
- develops secondary to hypertension or valvular stenosis. The ventricles enlarge in an attempt to compensate for the increased workload being placed on the heart.
130
Two Types of Hypertrophic cardiomyopathy?
```
o Asymmetrical septal hypertrophy – genetic disorder causing enlargement of the interventricular septum.
o Hypertensive (valvular hypertrophic) cardiomyopathy - develops secondary to hypertension or valvular stenosis. The ventricles enlarge in an attempt to compensate for the increased workload being placed on the heart.
```
131
- increased rigidity (decreased compliance) of the myocardium from severe scarring (e.g., from radiation therapy) or from infiltration of abnormal substances into the myocardium (e.g., iron in hemochromatosis, or amyloid in amyloidosis).
Restrictive cardiomyopathy
132
Valvular dysfunction
Acute Rheumatic Fever and Rheumatic Heart Disease
Infective Endocarditis
All Forms of ?
Disorders of the Endocardium
133
caused by conditions that damage the heart valves.
| • May be congenital or acquired.
Valvular dysfunction
• Acquired valvular disease can be caused by inflammatory diseases, trauma, tissue degeneration, or infections.
• Most of the acquired valvular disorders involve the aortic and mitral valves.
134
Valvular dysfunction, 2 basic Types?
Valvular stenosis – narrowing of the valve opening. Valvular regurgitation – incomplete closure of a valve
135
Valvular stenosis – 2 types?
Aortic stenosis – narrowing of aortic semilunar valve between left ventricle and aorta.
Mitral stenosis – narrowing of mitral valve between left atrium and left ventricle.
136
Causes: congenital (children), rheumatic heart disease (RHD) (children and adults), or due to degeneration and calcification of the valve with aging (elderly).
• Incomplete emptying of left ventricle results in its hypertrophy and eventual failure.
Name all four categories it's in?
Aortic stenosis
1) Disorders of the Endocardium
2) Valvular dysfunction
3) Valvular stenosis
4) Aortic stenosis
137
Mitral stenosis cause:
| narrowing of mitral valve between left atrium and left ventricle.
* Causes: congenital (children); RHD or bacterial endocarditis.
* Results in hypertrophy and dilation of left atrium due to incomplete emptying; blood backs up into pulmonary system; systemic outflow is decreased; atrial fibrillations and pulmonary edema occur.
138
incomplete closure of a valve.
Valvular regurgitation
139
Valvular regurgitation - 3 Types?
Aortic regurgitation
Mitral regurgitation
Tricuspid regurgitation
140
Tricuspid regurgitation
tricuspid valve fails to close properly: blood leaks back into right atrium.
• Right atrium dilates; right ventricle dilates and hypertrophies; eventually right ventricle fails.
141
Causes of Tricuspid regurgitation
due to failure and dilation of right ventricle, RHD or infective endocarditis.
• Right atrium dilates; right ventricle dilates and hypertrophies; eventually right ventricle fails.
142
one or both of the cusps of the mitral valve billow upward (prolapse) into the left atrium during systole.
Mitral valve prolapse syndrome (MVPS)
| • Most common valve disorder in the United States, especially in young women.
143
* Mitral valve leaflets do not position themselves properly during systole.
* MVPS may be completely asymptomatic or can result in unpredictable symptoms.
* Afflicted valves are at greater risk for developing infective endocarditis.
Mitral valve prolapse syndrome (MVPS)
144
a diffuse, inflammatory disease caused by a delayed immune response to pharyngeal infection by the group A beta-hemolytic streptococci.
Rheumatic fever (RF)
145
Antibiotic therapy given within first 9 days of strep infection usually prevents_____?
Rheumatic fever (RF)
146
Acute Rheumatic fever Caused by?
-fever and inflammation of the joints, skin, nervous system, and heart
o Caused by cross reaction of antibodies against strep with self-antigens on heart, muscle, and brain and joints, resulting in an autoimmune response that inflames and potentially scars these tissues.
• If left untreated, rheumatic fever may lead to rheumatic heart disease.
147
12% of individuals with rheumatic fever develop rheumatic heart disease (RHD). T/F
False
| • 10% of individuals with rheumatic fever develop rheumatic heart disease (RHD).
148
________refers to cardiac complications of rheumatic fever, primarily endocarditis and damage to the heart valves, although myocarditis may also occur.
Rheumatic Heart Disease (RHD)
149
Damage occurs because antibodies bind to the lining of the heart, surface of valves, and connective tissue within the myocardium and trigger an autoimmune response. T/F
True
150
infection and inflammation of the endocardium and often cardiac valves.
Infective Endocarditis
151
Causes: bacteria (most common); sometimes viruses, fungi, rickettsiae, and parasites.
Infective Endocarditis
152
Infective Endocarditis Pathophysiology:
o The endocardium is “prepared,” usually by endothelial damage, for microorganism colonization.
o Blood-borne microorganisms adhere to the damaged endocardial surface.
o These proliferate and promote the propagation of infective endocardial vegetations.
o Vegetations are clumps of microorganisms surrounded by fibrin, which prevents inflammatory cells from reaching them.
153
* In the mildest cases, valvular function may be slightly impaired by vegetations that collect on the valve leaflets.
* If left unchecked, severe valve abnormalities, chronic bacteremia, and systemic emboli may occur as vegetations break off the valve surface and travel through the bloodstream.
* Antibiotic therapy can limit the extension of this disease.
Infective Endocarditis
154
Manifestations of Heart Disease
- Dysrhythmias
| - Heart Failure
155
* Disturbance of the heart rhythm.
* Range from occasional “missed” or rapid beats to severe disturbances that affect the pumping ability of the heart.
* Diagnosed and evaluated by doing an electrocardiogram.
* Different dysrhythmias are characteristic of specific problems in the myocardium and conduction system.
* Can be caused by an abnormal rate of impulse generation or abnormal impulse conduction
Dysrhythmias
156
Heart Failure
• General term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues with oxygen and nutrients.
157
Cardiac output (CO) =
Cardiac output (CO) = stroke volume x heart rate.
158
Stroke volume is determined by:
o Contractility – the strength of cardiac contraction.
Reduced by disease processes that affect muscle cells, including ischemia.
o Preload (or left ventricular end-diastolic volume, LVEDV) – the amount of blood in the ventricle just before it contracts.
Reduced by poor venous return; increased when fluid volume goes up.
o Afterload- pressure the heart must work against to push blood out of the heart.
Primarily determined by peripheral vascular resistance (blood pressure).
159
• Also called congestive heart failure (CHF)
• The most common pattern of heart failure is for one ventricle, usually the left, to fail first.
o The left ventricle has a heavier workload, as well as a greater requirement for oxygen.
• Causes:
o Myocardial ischemia or infarction, cardiomyopathies, valve disorders, hypertension, etc.
Left heart failure
• Decreased cardiac output causes ischemia in all organs, as well as exertional fatigue.
• Pulmonary congestion and edema occur as the weakened left ventricle pumps out less and less blood, producing dyspnea and cough.
160
Left heart failure Pathophysiology:
o Left ventricle is faced with a high workload due to hypertension or valve disorders, or is weakened due to disease. In response:
o Heart muscle undergoes myocardial hypertrophy and ventricular remodeling.
o Results in decreased contractility which causes lower stroke volume and higher LVEDV.
o The heart dilates to accommodate the higher volume so left ventricular preload increases.
o Higher preload stretches the wall and causes further dilation and decreased contractility.
o As the myocardium weakens, cardiac output falls, reducing systemic BP. In response:
Sympathetic nervous system (SNS) releases epinephrine causing vasoconstriction and increased heart rate which raises blood pressure (and afterload).
Decreased kidney perfusion causes activation of renin-angiotensin-aldosterone (RAA) system, which also causes vasoconstriction and increases fluid volume. Together these raise vascular resistance and blood pressure.
161
Right heart failure Causes:
o Chronic pulmonary hypertension caused by left heart failure.
o Chronic lung disease that increases the afterload of the right ventricle.
o Less frequently, cardiomyopathies or MIs of the right ventricle or disorders of the tricuspid or pulmonary semiluner valves.
• Blood backs up into the systemic veins leading into the right atrium, causing venous congestion
162
Clinical manifestations:
| o Jugular venous distension, hepatomegaly, and peripheral edema.
Right heart failure
163
Inability of the heart to supply the body with oxygen and nutrients, despite adequate blood volume and normal or elevated myocardial contractility.
High-output failure
164
The Causes of High-output failure?
extreme exertion, anemia, septicemia, hyperthyroidism, and thiamine deficiency
165
Treatments for heart failure
* Prevention
| * Pharmacologic therapy (just like in acute heart failure)
166
Pharmacologic therapies (just like in acute heart failure) is aimed at?
o Reducing preload with diuretics (including furosemide [Lasix] and spironolactone)
o Reducing afterload with vasodilators (ACE inhibitors, beta blockers)
o Increasing contractility in selected patients (digoxin, pacemaker placement, myoplasty surgery)
• Address underlying cause of heart failure - lipid-lowering agents and percutaneous coronary intervention (PCI) (dilation of narrowed coronary arteries with a catheter).
167
Preventive Treatments for heart failure
dietary changes to limit sodium intake and reduce risk factors for coronary artery disease and hypertension, exercise, and weight loss.
168
Shock
* In shock the cardiovascular system fails to perfuse the tissues adequately.
* This results in widespread impairment of cellular metabolism, involving positive feedback loops, that places the individual on a downward physiologic spiral leading to multiple organ dysfunction syndrome (MODS).
169
Impairment of Cellular Metabolism
Shock
170
Impairment of Cellular Metabolism includes
Impaired oxygen use
| Impaired glucose use
171
Impaired oxygen use
• Underperfusion of vital tissues impairs cellular metabolism due to a lack of oxygen.
When this occurs, cells shift to anaerobic metabolism, which results in:
o A reduction in adenosine triphosphate (ATP) production
o An inability of the cells to maintain their normal membrane electrolyte pumps causing sodium, chloride, and calcium to accumulate in cells, resulting in cellular lysis.
172
Ischemia activates the inflammatory response, causing release of cytokines, lysosomal enzymes, and activators of the clotting cascade. T/F
True
173
Anaerobic metabolism produces lactic acid, which elevates the blood and tissue pH.
False - Lowers
174
What interferes with cellular metabolism and electrolyte balance.
Acidosis
175
If the shock state persists, does multiple organ dysfunction develops.?
Yes
176
Impaired glucose use
* Occurs because less glucose is delivered to the tissues, many disease states cause increased demand for glucose, and glucose uptake is impaired by many toxins and cytokines.
* Once glycogen stores are used up, gluconeogenesis is activated to continue glucose production, but at the expense of protein depletion.
177
Systemic compensation for the shock state includes
includes the release of cortisol, thyroid hormone, and catecholamines (like epinephrine), which increase glucose production from glycogen.
178
As proteins are broken down they release alanine, which can contribute to lactic acid production as well as the release of ammonia and urea, compounds that are toxic to cellular metabolism. T/F
True
179
Muscle dysfunction from protein degradation doesn't contributes to multiple organ dysfunction. T/F
False
180
Types of Shock
```
Cardiogenic shock
Hypovolemic shock
Neurogenic shock
Anaphylactic shock
Septic shock
```
181
Cardiogenic shock - defined
• Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.
182
Cardiogenic shock - causes
o Can occur whenever the heart is unable to generate an adequate cardiac output.
o Severe left heart failure, severe MI (>40% of myocardium damaged), severe dysrhythmias, cardiac tamponade, tension pneumothorax, etc.
183
Cardiogenic shock - Clinical Manifestations
o Pulmonary edema, which causes dyspnea and inspiratory crackles.
o Hypotension and severe underperfusion of vital organs, which causes poor capillary refill, cyanosis, cold clammy extremities, and oliguria.
184
Cardiogenic shock - Treatment:
o Use of pressors such as dobutamine (which increase contractility), careful fluid management, and treatment of the underlying cardiac abnormality if possible.
185
Hypovolemic shock - Causes:
o Dehydration, hemorrhage, burns, severe diarrhea, overuse of diuretics or dialysis, or extreme hyperglycemia or hypercalcemia.
186
Hypovolemic shock is?
o Any condition that can result in the loss of greater than 15% of the intravascular volume
187
Hypovolemic shock - Compensatory mechanisms:
o Increased heart rate (tachycardia)
o Activation of the renin-angiotensin-aldosterone system and release of antidiuretic hormone
o Increased peripheral vascular resistance (vasoconstriction)
o Movement of fluid from interstitial compartment to bloodstream
• If these are inadequate to maintain tissue perfusion, then shock ensues.
188
Hypovolemic shock - Clinical manifestations
o Same as cardiogenic shock but without pulmonary edema
189
Hypovolemic shock - Treatment:
o Reversing the underlying loss of fluid or blood
| o Intravenous fluid administration.
190
Distributive shock
caused by an inability to maintain an adequate peripheral vascular resistance due to vasodilation of the systemic arteries.
Includes neurogenic, anaphylactic and septic shock.
191
Neurogenic shock - Causes:
o Loss of sympathetic stimulation due to injury to the brain or spinal cord, or certain drugs.
o Overstimulation of the parasympathetic nerves due to pain, stress, drugs, or toxins.
192
Neurogenic shock - Pathophysiology:
o Arterioles lose their stimulus to maintain a constant amount of vasoconstriction (loss of vascular tone) and, therefore, peripheral vascular resistance falls.
o This causes the blood volume to be redistributed to nonvital organs, with a loss of blood pressure and underperfusion of tissues.
193
Neurogenic shock - Clinical manifestations:
o Very low peripheral vascular resistance and bradycardia, with neurogenic insult.
194
Neurogenic shock - Treatment:
o Treatment of the underlying insult.
| o Careful patient positioning, the administration of pressors, and appropriate fluid management.
195
Severe allergic reactions.
Anaphylactic shock
196
• Pathophysiology:
o Exposure to high doses of allergen cause an immediate severe immune reaction with production of high levels of IgE. This results in:
o Rapid, widespread degranulation of mast cells, with release of multiple vasoactive and inflammatory mediators, including histamine.
o Profound peripheral vasodilation and increased capillary permeability cause a decrease in blood pressure and tissue perfusion.
• Clinical manifestations:
Anaphylactic shock
197
Anaphylactic shock - Clinical manifestations:
o History of allergies, urticaria (hives), edema, bronchoconstriction causing dyspnea, decreased peripheral vascular resistance, hypotension, and increased bowel sounds.
198
Anaphylactic shock - Treatment:
o Removal of the allergen.
o Administration of epinephrine, corticosteroids, bronchodilators, and fluids.
o Mechanical ventilation may also be required.
199
Septic shock - Causes:
o Gram-positive or gram-negative bacterial infection (or occasionally, fungi or viruses) that overwhelms the body’s defense mechanisms.
• Serious complication of severe trauma, immunodeficiency syndromes, or for the very young or elderly.
200
Multiple organ dysfunction syndrome (MODS)
- organ dysfunction involving many of the vital organs can become overwhelming and cause death
201
Septic shock - PathoPhysiology
o Bacteria must enter the bloodstream.
o Gram-negative organisms release endotoxin (lipopolysaccharide), whereas gram-positive organisms release exotoxin and cell wall components.
o These substances activate macrophages which release inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukins, and nitric oxide.
o These substances, especially nitric oxide, cause widespread vasodilation and hypotension.
o The complement and coagulation systems are also activated.
o This results in what is called the systemic inflammatory response syndrome (SIRS):
Signs: fever, tachypnea, tachycardia, and leukocytosis.
o Numerous cell and tissue complications result, including decreased peripheral resistance, decreased cardiac output, and increased capillary permeability, all of which cause hypotension and decreased tissue perfusion.
o Lactic acidosis, widespread coagulation, and activation of other inflammatory cells occur.
o Hypotension can cause disruption of the intestinal lining, allowing enteric bacteria to enter the bloodstream, and thus aggravating the bacteremia.
o Multiple organ dysfunction syndrome (MODS
202
Septic shock - Clinical manifestations
o Initially: fever, tachypnea, tachycardia, generalized edema and warm, sweaty skin.
o As the SIRS and organ dysfunction progress, the individual may exhibit the clinical manifestations associated with multiple organ dysfunction.
o Laboratory findings include leukocytosis, lactic acidosis, hypoxemia, uremia (elevated blood urea nitrogen and creatinine), and hepatic insufficiency (with elevated liver enzymes).
203
Septic shock - Treatment
o Prompt administration of antibiotics, oxygen, pressors, and careful fluid management.
o Activated protein C is an anti-inflammatory and anticoagulant drug which has been shown to improve outcomes in severe sepsis.
204
Progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury.
Multiple Organ Dysfunction Syndrome (MODS)
205
Multiple Organ Dysfunction Syndrome (MODS) - Causes:
o Septic shock (most common), trauma, burns, and other causes of severe shock with underperfusion of vital tissues.
206
Multiple Organ Dysfunction Syndrome (MODS) - Pathophysiology
o Injury, infection or disease cause endothelial damage, activation of the sympathetic nervous system, release of stress hormones (cortisol, epinephrine, and norepinephrine), and release of inflammatory mediators.
o Inflammatory mediators activate the complement, coagulation and kinin cascades.
o These cause a massive, systemic immune/inflammatory response → SIRS.
o Inflammatory and clotting processes cause maldistribution of blood flow and hypermetabolism.
o Oxygen delivery to the tissues decreases because:
Blood is shunted past selected regional capillary beds, due to inflammatory mediators.
Interstitial edema, due to increased capillary permeability, interferes with oxygen diffusion to tissue cells.
Microvascular thrombi cause capillary obstruction.
o Hypermetabolism occurs to meet the body's increased demands for energy, but over time this depletes oxygen and fuel supplies.
o Decreased oxygen delivery plus hypermetabolism combine to create an imbalance in oxygen supply and demand, in which the reserve supply of oxygen is exhausted and the amount that can be delivered by the circulation is less than the cells need.
o Tissue hypoxia with cellular acidosis and impaired cellular function ensue and result in the multiple organ failure.
207
Multiple Organ Dysfunction Syndrome (MODS) - Common Manifestations:
o Acute respiratory distress syndrome (ARDS) – dyspnea, pulmonary crackles, and cyanosis.
Note: the lungs are often the first system to fail.
o Disseminated intravascular coagulation (DIC) – organ infarction and bleeding
o Acute tubular necrosis (ATN) – decreased urine output, azotemia, and edema
o Liver failure – jaundice, abdominal distension and tenderness, and hepatic encephalopathy
o Heart failure – dyspnea, cough, cyanosis and peripheral edema
o Ischemic bowel – translocation of bacteria into the bloodstream
o Central nervous system (CNS) dysfunction – confusion and coma
208
Multiple Organ Dysfunction Syndrome (MODS) - Treatment:
o Reversal of the primary insult if possible.
o Support for organ failure including mechanical ventilation, activated protein C, dialysis, fluid and electrolyte management, enteral (preferably) or parenteral nutrition, and antibiotics.
209
SIRS - systemic inflammatory response syndrome (SIRS): signs -
: fever, tachypnea, tachycardia, and leukocytosis.
210
Hypotension can cause disruption of the intestinal lining, allowing enteric bacteria to enter the bloodstream, and thus aggravating the bacteremia. T/F
True
211
Bacteria doesn't have to enter the bloodstream for it to be septic shock. T/F
False - Must Enter
212
Worst outcome of Infective Endocarditis is ?
sepsis
213
Infective Endocarditis agents
● Bacteria, viruses, fungi, rickettsiae (transmitted by fleas and rats, similar to lyme disease), and parasites
214
Infective Endocarditis - Pathogenesis
● Prepared endocardium
● Blood-borne microorganism adherence
● Proliferation of the microorganism
215
Cardiac Complications of AIDS
```
~Myocarditis
~Endocarditis
~Pericarditis
~Cardiomyopathy (disease)
~Pericardial effusion
~Pulmonary hypertension
~Antiviral drug-related cardiotoxicity
```
216
Examples of Dysrhythmias
Tachycardia, flutter, fibrillation, bradycardia, premature ventricular contraction (PVC), premature atrial contraction (PAC), asystole
217
inability of the heart to generate adequate cardiac output to perfuse tissues → ventricular remodelling
Systolic heart failure
218
pulmonary congestion, restriction of stroke volume and cardiac output
Diastolic heart failure
219
(1.5L - 5L of blood loss) =
Shock
220
Shock
Cardiovascular system fails to perfuse the tissues adequately
● Impaired oxygen use
● Impaired glucose use
221
```
● Cardiogenic
● Hypovolemic
● Neurogenic
● Anaphylactic
● Septic
All types of
```
Shock
222
strangling of the heart due to fluid between the pericardial membranes
tamponade
223
tamponade happens beacuse of?
Pericardial effusion
224
MVPS
Mitral valve prolapse syndrome (MVPS) → leaflets are pushed back into atria, since chordae tendinae are broken
225
Asculations will sound like a “galloping horse”
Rheumatic fever
