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Patho > Cardiovascular Emergencies > Flashcards

Cardiovascular Emergencies Flashcards

1
Q

What is ischemia?

A

decreased blood (and oxygen) supply to a body organ or part, usually due to functional constriction or actual obstruction of a blood vessel

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2
Q

What is infarction?

A

necrosis or death of tissues due to local ischemia

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3
Q

What is necrosis?

A

localized tissue death that occurs in grounds of cells or part of a structure or an organ in
response to disease or injury

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4
Q

What is gangrene?

A

death of body tissue due to lack of blood flow or bacterial infection

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5
Q

What is perfusion?

A

the process or act of pouring over or through, especially the passage of a fluid through a
specific organ or area of the body

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6
Q

What is a thrombus?

A

stationary mass of clotted blood or other formed elements that remains attached to its place of origin along the wall of a blood vessel

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7
Q

What is an embolus?

A

a mass of clotted blood or other formed elements (such as bubbles of air, calcium fragments or fat) that circulates in the blood stream until it becomes lodged in a vessel, obstructing circulation

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8
Q

What is preload?

A

volume of blood returning to the right atrium of the heart

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9
Q

What is afterload?

A

pressure/force the left ventricle must obtain to open the aortic semilunar valve and pump
blood into systemic circulation

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10
Q

What do arteries do?

A

-carry oxygenated blood from the heart to all tissues in the body
-also responsible for regulating blood pressure and capillary flow

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11
Q

What do veins do?

A

provide a return pathway to the heart and play an important role in providing the preload required to maintain cardiac contraction

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12
Q

What is dislipidemia?

A

-A condition of imbalance of the lipid components of the blood
-Cholesterol and triglycerides combine with water-soluble transport proteins in order to travel through the bloodstream - this transport molecule is called a lipoprotein
-Characterized by increased triglycerides, increased total blood cholesterol, increased LDL cholesterol and decreased HDL cholesterol

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13
Q

What is a low density lipoprotein (LDL)?

A

the primary transport molecule for cholesterol liver to target tissues, aka - “bad cholesterol”

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14
Q

What is high density lipoprotein (HDL)?

A

-the primary transport molecule for cholesterol from tissues back to the liver, aka - “good cholesterol”

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15
Q

What is cholesterol?

A

a lipid molecule with many functions including membrane and hormone synthesis

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16
Q

What are some risk factors for LDL cholesterol?

A

-Smoking
-Excessive alcohol consumption
-Sedentary lifestyle
-Poor dietary intake
-Type 2 diabetes
-Genetic predisposition
-Many of these risk factors will also decrease HDL levels, worsening the imbalance

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17
Q

What is arteriosclerosis?

A

an abnormal hardening and thickening of the arteries

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18
Q

What is atherosclerosis?

A

a form of arteriosclerosis characterized by the formation of fibrofatty lesions in the Intima lining of large and medium-sized arteries

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19
Q

What causes atherosclerosis?

A

-Atherosclerosis is, at its core, an inflammatory condition
-Several triggers exist that create lesions and plaque build-up in the intimal layer of the artery
-Atherosclerotic plaque consists of smooth muscle cells (SMCs), macrophages/leukocytes, collagen and elastin fibres, platelets, and a large lipid
core

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20
Q

How does the buildup of atherosclerotic plaque occur?

A
  1. A trigger causes initial endothelial injury
  2. Migration and adhesion of inflammatory cells to the injury site
  3. The foam cells begin to accumulate, which increases the progression of the lesion. Foam cells die and deposit their contents (necrotic debris and lipids) into the vascular wall (contained by the SMC and ECM)
  4. Atherosclerotic plaque is contained in the bulging vascular wall (reduction of blood
    flow) and is prone to rupture (hemorrhage) or thrombotic vessel occlusion
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21
Q

What are the clinical manifestations of atherosclerosis?

A

-Typically do not become evident for over 20 years of plaque build up
-Depend on the vessels involved and the extent of vessel obstruction
-Atherosclerotic plaque exerts its effect through narrowing of the vessel producing ischemia, sudden vessel obstruction (thrombosis, embolism), aneurysm formation (weakened vessel wall) with possible rupture
-Larger vessels tend to produce aneurysms as a high-risk complication and smaller vessels tend to be more prone to vessel occlusion

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22
Q

What is peripheral artery disease/peripheral vascular disease?

A

-A disorder of the circulation in the extremities
-Can produce ischemia, pain, impaired function and, occasionally, infarction and tissue necrosis
-Caused by atherosclerosis/arteriosclerosis in peripheral arteries

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23
Q

What are the clinical manifestations of peripheral vascular disease?

A

-Symptoms don’t start until there is a 50% narrowing of the vessel
-Pain with walking (commonly in the calf), vague complaints of muscle aches and/or numbness
-Atrophy of leg muscles and thinning of the skin and subcutaneous tissue
-Weak or absent peripheral pulses (popliteal/ pedal) with signs poor perfusion (pale/mottled while elevated or deep red while dependent, delayed cap refill, cool to touch)
-Can progress to necrosis, ulceration, gangrene and amputation

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24
Q

What is Raynaud disease/phenomenon?

A

-A functional disorder caused by intense vasospasm of the arteries and arterioles in the
fingers and (occasionally) toes
-Exposure to cold or strong emotions causes vasoconstriction in the fingers (blood shunting) producing temporary, and self-limiting, ischemia
-Cause can be unknown or a direct byproduct of a previous vessel injury (frost bite, prolonged use of heavy/vibrating machinery, etc.)

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25
Q

What are the clinical manifestations of Raynaud disease?

A

-Distal pallor/cyanosis, cold sensation/altered sensory perception
-Following the spasm - intense redness, throbbing, paresthesia

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26
Q

What is an aneurysm?

A

-An abnormal localized dilation of a blood vessel that can occur in both arteries and veins
-Aneurysms can be classified according to their cause, location and anatomical features

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27
Q

What is a true aneurysm?

A

bounded by a complete vessel wall and the blood remains within the vascular compartment

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28
Q

What is a false aneurysm?

A

a localized dissection or tear in the inner wall of the artery with formation of an extravascular hematoma (causing vessel enlargement)

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29
Q

What is a berry aneurysm?

A

a true aneurysm that consists of a small, spherical dilation of the vessel at a bifurcation (usually found in the circle of Willis)

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30
Q

What is a fusiform aneurysm?

A

a true aneurysm that involves the entire circumference of the vessel with gradual
and progressive vessel dilation - these vary in diameter and length

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31
Q

What is a saccular aneurysm?

A

a true aneurysm that extends over part of the circumference of the vessel (appears “sac-like”)

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32
Q

What is a dissecting aneurysm?

A

a false aneurysm resulting from a tear in the intimal layer of the vessel that allows blood to enter the vessel wall, dissecting its layers to create a blood-filledcavity

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33
Q

What causes an aneurysm?

A

-Atherosclerosis (and its risk factors) is a common cause as is degeneration of the tunica media
-Weakness that leads to aneurysm formation may be due to congenital defects, trauma, infections or atherosclerosis
-As the tension/pressure in the vessel increases, so does the size of the aneurysm -eventually may rupture
-Even an unruptured aneurysm may cause damage by exerting pressure on adjacent structures and interrupting blood flow

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34
Q

What are the clinical manifestations of an anuerysm?

A

-Often asymptomatic until vessel rupture
-Other symptoms (pre-rupture) are dependent upon the vessel location
-May produce pain, discomfort - severe/significant if ruptured
-Pulsatile masses may be present in some

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35
Q

What is a ruptured aneurysm?

A

-A ruptured aneurysm is a significant life threat and must be treated immediately in an operating room
-Location of aneurysm will dictate the specific symptoms, but pain is typically unbearable and rapid blood loss will quickly progress to hypovolemic shock, an altered LOC, and death
-Observe for signs of shock (increased HR/RR, declining BP, pallor, etc.) and prepare for resuscitation

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36
Q

What is a dissecting aortic aneurysm?

A

-An aortic dissection is an acute life threatening condition that involves hemorrhage into
the vessel wall with longitudinal tearing that forms a blood- filled channel
-Can occur anywhere along the length of the aorta but it is most common in the ascending aorta and descending (thoracic) aorta (just distal to the subclavian artery)

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37
Q

What are the clinical manifestations of a dissecting aortic aneurysm?

A

-Abrupt and excruciating pain described as tearing or ripping
-Ascending Aorta - anterior chest
-Descending - mid upper back (between scapula)
-Hypovolemic shock
-Difference in bilateral blood pressures

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38
Q

What are varicose veins?

A

-Dilated veins of the lower extremities (usually superficial)
-Often lead to secondary problems of venous insufficiency
-Prone to rupture with minimal direct trauma - easily managed with direct pressure and often does not require any further medical intervention

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39
Q

What is deep vein thrombosis (DVT)?

A

-The presence of thrombus, and the accompanying inflammatory response, in the wall of a deep vein - most commonly in the lower extremities
-Pulmonary embolism (PE) is a significant complication of DVT

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40
Q

What is Virchow’s Triad?

A

-Stasis of blood (prolonged flights, bed rest, SCI)
-Increased blood coagulability (clotting deficiencies, oral contraceptive use, hormone therapy, cigarettes)
-Vessel wall injury (trauma, post-surgery, IVs, infection)

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41
Q

What are the clinical manifestations of DVT?

A

-Often asymptomatic (usually because the vein isn’t completely occluded)
-S&S can be related to the inflammatory process - pain, swelling, deep muscle tenderness, fever, general malaise
-Other findings are dependent on location of the thrombus
-Most commonly occurs below the knee (calf pain/tenderness, swelling, redness, warm to touch)

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42
Q

What is hypertension?

A

-A sustained elevation of arterial blood pressure (typically ≥140mmHg)
-The primary risk factor for cardiovascular disease

43
Q

What is primary HTN?

A

presence of hypertension without evidence of a specific causative clinical condition

44
Q

What is secondary HTN?

A

elevation in blood pressure because of another disease or condition

45
Q

What are the risk factors for primary HTN?

A

-Advancing age, gender (higher incidence of HTN in males, higher incidence of adverse complications in females)
-Family history/genetic predisposition
-High sodium diet, dyslipidemia
-Tobacco use, alcohol consumption
-Sedentary lifestyle, obesity, insulin resistance

46
Q

What are the clinical manifestations of hypertension?

A

-Increased perfusion pressure can damage target organs and increased intravascular pressure can damage endothelial cells (causing inflammation and atherosclerosis)
-Perfusion Pressure - the pressure required to push blood through the vessels in a specific area
-A major risk factor for atherosclerosis (elevated vascular pressure promotes endothelial damage)
-Predisposes people to coronary artery disease (CAD), heart failure, MIs, strokes and peripheral artery disease (PAD)
-Increases the workload on the left ventricle by increasing afterload
-High glomerular pressures decrease filtration and can lead to kidney disease
-Predisposes people to cognitive impairment, dementia and retinopathy

47
Q

What are the clinical manifestations of a hypertensive emergency?

A

-A rare, but potentially fatal, complication of hypertension
-Characterized by a sudden and sustained spike in blood pressure (>180/120mmHg)
-This acutely worsens target organ damage and must be dealt with promptly
-Complications can include Ischemia stroke, cardiac ischemia and retinal hemorrhage

48
Q

What is orthostatic hypertension?

A

-Abnormal drop in blood pressure (of at least 20mmHg) on assumption of the standing position
-Changes in blood pressure may or may not be accompanied by clinical symptoms or may be asymptomatic
-Dizziness, syncope (fainting)

49
Q

What is endocarditis?

A

-Inflammation of the inner lining of the heart (endocardium) most caused by an infectious
agent
-Endocardium is continuous the heart valves and the inner lining of the aorta as it exits the left ventricle

50
Q

What causes endocarditis?

A

-A very common cause of endocarditis is illicit IV drug use
-Usually, the heart valves are initially affected with destructive lesions composed of infectious organisms and cellular debris enclosed in a mesh of fibrin strands of clotted blood
-The lesions can spread from the valves and, in some cases, spread through the different layers of the heart

51
Q

What are the clinical manifestations of endocarditis?

A

-Initial symptoms include fever, chills and other signs of systemic infection (elevated HR, RR, general malaise, SOB, muscle aches/weakness, etc.)
-Complications can include the formation of emboli - this includes a coronary artery embolism (MI, cardiac ischemia)
-Myocarditis or pericarditis can develop should the lesions spread through the different heart layers
-Congestive heart failure can be a result of valve destruction

52
Q

What is myocarditis?

A

-Inflammation of the myocardium (muscular layer of the heart)
-A form of primary cardiomyopathy

53
Q

What causes myocarditis?

A

-Usually caused by a viral infection but may also be bacterial or fungal in origin
-Occasionally can be caused by hypersensitivity to certain drugs or an autoimmune process
-May be self-limiting and only requiring supportive care, or may become life threatening and require aggressive medical intervention

54
Q

What are the clinical manifestations of myocarditis?

A

-Manifestations vary dependent on causative agent and severity of infection
-Signs of infection (fever, chills, malaise, etc.)
-Formation of emboli is possible
-Inflammatory mediators cause increased coagulability while an irritated myocardium produced a decrease in contractility
-Signs of heart failure/cardiogenic shock

55
Q

What is pericarditis?

A

-Inflammation of the pericardium
-The pericardium is a double layered membrane composed of a fibrous layer and 2 serous layers (visceral and parietal)
-Between the 2 serous layers of the pericardium is the pericardial space/cavity containing serous fluid (pericardial fluid) that lubricates and protects the heart during movement/contraction
-Pericarditis promotes an increase in capillary permeability allowing plasma proteins to enter the pericardial fluid
-This can promote adhesion and scarring between the 2 serous layers

56
Q

What are the clinical manifestations of pericarditis?

A

-Chest pain, pericardial friction rub (auscultated), and ECG changes
-Chest pain described as an abrupt in onset, sharp and located in the precordial area (just superficial to the heart) - may radiate to the neck, back, abdomen or side
-Pain is typically worse with deep breathing, coughing, swallowing and positional changes
-Pain is often relieved by sitting upright and a bit forward - allows for easier venous return and reduced pressure on the pericardium
-Classic ECG changes associated with pericarditis include widespread ST segment elevation and PR segment depression

57
Q

What is pericardial effusion?

A

an accumulation of fluid in the pericardial cavity - usually as a result of an inflammatory or infectious process

58
Q

What is pericardial tamponade?

A

fluid in the pericardial space accumulates to the point of compression on the heart that reduces cardiac output

59
Q

What are the clinical manifestations of pericardial effusion/tamponade?

A

-Beck’s Triad - JVD, muffled heart sounds, hypotension
-Pulsus paradoxus - weakened or absent arterial pulse during inspiration
-Normally, the decreased intrathoracic pressure during inspiration accelerates venous return (increased right sided filling)
-As the right atria fills, it bulges into the LV causing a slight decrease in LV filling, SV, and SBP - this process is amplified when there is excessive pressure on the heart from a tamponade
-ECG changes - nonspecific T-wave changes and low QRS voltage

60
Q

What are cardiomyopathies?

A

-A group of diseases of the myocardium associated with mechanical and/or electrical dysfunction
-Usually exhibits inappropriate ventricular hypertrophy or dilation
-Cardiomyopathies may be confined to the heart or part of a generalized systemic disorder that may lead to cardiovascular death or heart failure

61
Q

What is primary cardiomyopathy?

A

heart disorders confined to the myocardium

62
Q

What is secondary cardiomyopathy?

A

myocardial changes that occur with a variety of
systemic disorders

63
Q

What is coronary artery disease (CAD)?

A

-Impaired coronary blood flow, usually caused by atherosclerosis
-Can lead to myocardial ischemia, angina, myocardial infarction (MI), cardiac arrhythmias, heart failure, or sudden heart death
-CAD is divided into Acute Coronary Syndrome (ACS) and Chronic Ischemic Heart Disease

64
Q

What are the risk factors for CAD?

A

cigarette smoking, HTN, dyslipidemia, diabetes, advancing age, obesity, and sedentary lifestyle

65
Q

What are the coronary arteries?

A

-Two main coronary arteries arise from the coronary sinus just above the aortic valve
-The left coronary artery (LCA) divides into the left anterior descending (LAD) and circumflex arteries
-The right coronary artery (RCA) becomes the posterior descending artery and supplies the posterior heart, septum, SA and AV nodes
-The larger coronary arteries lie in the surface of the heart (epicardium) while smaller branches penetrate the myocardium

66
Q

What is anastomoses?

A

-cross-connection between adjacent channels (collateral circulation)
-Anastomotic channels exist between the smaller branches of coronary arteries - as CAD progresses, these channels will increase in size

67
Q

What are coronary veins?

A

Venous system that drains the deoxygenated blood from the myocardium through the coronary sinus into the right atrium

68
Q

What happens if there is an imbalance in myocardial oxygen?

A

An imbalance between supply and demand can lead to myocardial ischemia, MI or sudden cardiac death

69
Q

What is myocardial oxygen supply?

A

-Determined by the capillary inflow and the ability of hemoglobin to transport and deliver O2
-Ischemia can occur, in absence of decreased coronary flow, due to hypoxia, anemia, or CO poisoning

70
Q

What is myocardial oxygen demand?

A

-MVO2 is determined by HR, SV and systolic pressure/myocardial wall stress
-HR - higher the rate, higher the oxygen demand. Elevated rates also cause a decrease in diastolic filling time
-SV - increased force of muscle contractions require an increase in oxygen (exercise, inotropes, sympathetic response)
-LV wall stress - the average tension that individual muscle fibres must generate to shorten (contract) against intraventricular pressure

71
Q

What is chronic ischemic heart disease?

A

-When blood flow through the coronary arteries does not meet the metabolic demands of the heart
-Most often due to atherosclerosis but may also be caused by vasospasm
-Main types of chronic ischemic heart disease include: Stable angina, variant (vasospastic) angina, and silent myocardial ischemia

72
Q

What is silent myocardial ischemia?

A

-When myocardial ischemia occurs without the presence of cardiac chest pain
-It can range from mild, non-infarction ischemia to full myocardial infarction
-Patients may present to emerge with atypical symptoms (fatigue, nausea, malaise, etc) and end up finding elevated serum biomarkers indicating they have had ischemia/infarction

73
Q

What is stable angina?

A

-Imbalance between coronary blood flow and metabolic demands resulting in ischemic chest pain
-Often the initial manifestation of CAD
-An increase in baseline MVO2 (physical exertion, exposure to cold, emotional stress) causes cardiac chest pain
-Symptoms of stable angina typically resolve within minutes of rest (sometimes with the help of nitroglycerin) - should they not resolve within 5-10 minutes the pain is likely more significant (myocardial infarction)

74
Q

What are the clinical manifestations of stable angina?

A

-Ischemic chest pain
-Constricting, squeezing, suffocating, pressure, or heaviness
-Pain is usually consistent and not reproducible (able to worsen) with coughing, inspiration, palpation, or movement
-Located usually precordial (retrosternal/ substernal) or epigastric and may radiate
to the left shoulder, jaw or arm (usually left)

75
Q

What is nitroglycerin?

A

-A nitrate medication that causes vasodilation reducing preload and arterial pressure
-Reduction in MVO2 (myocardial oxygen demand) and, hopefully, eliminates the chest pain
-Mechanism of Action - within the body, nitro converts to nitric oxide (NO) which relaxes the smooth muscle in blood vessels
-Nitro does not eliminate obstruction, it merely reduces MVO2

76
Q

What is vasospastic angina?

A

-Cardiac ischemia caused by coronary vasospasm
-Can be brought on by minimal exercise or spontaneously while at rest
-May be self-limiting or may lead to cardiac dysrhythmias and even death
-Exact cause is unknown but may be associated with hyperactive sympathetic nervous system, altered NO production, cocaine (and other amphetamines)

77
Q

What is acute coronary syndrome (ACS)?

A

-Includes unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI)
-Indicates an acute and severe obstruction in coronary blood flow that requires immediate
medical intervention to prevent death or permanent cardiac damage
-ACS is typically associated with ECG changes and serum biomarkers

78
Q

What ECG changes present with ACS?

A

-T-wave inversion, ST-segment elevation, and development of an abnormal Q wave
-ECG changes may not be present at onset of symptoms and will progress/change as infarction/ischemia continue
-ST-segment and T-wave represent ventricular repolarization - ischemic tissue has a shortened repolarization period and reduction in resting membrane potential

79
Q

What are serum biomarkers?

A

-ACS labs should be drawn promptly upon arrival to the ED but ECG changes indicative of cardiac ischemia, and clinical presentation should prompt the start of treatment
-Presence of serum biomarkers may take hours to show up in blood work
-Elevated cardiac troponin and creatine kinase levels indicate myocardial damage (aka “CK and tropes”)
-As myocardial cells become necrotic, they release their intracellular contents into the blood stream

80
Q

What is troponin?

A

-a regulatory protein found in muscle cells that aids in the contraction of the actin-myosin filaments
-cardiac muscle tissue has specific cardiac troponins that can be differentiated from skeletal muscle cells

81
Q

What is creatine kinase?

A

intracellular enzyme found in muscle cells responsible for converting creatine phosphate into ATP

82
Q

What is unstable angina?

A

-Angina is unstable when the pain occurs while at rest and does not subside promptly without intervention
-The fibrous cap of an atherosclerotic lesion either
ruptures or thins significantly exposing the lipid core which promotes platelet aggregation and inflammatory infiltration
-Can cause thrombus formation with can further obstruct the artery without resolution, UA can result in ischemia significant enough to cause
infarction
-The fibrous cap can become worn down, thinned or ruptured by ongoing hypertension
-Will not present with serum biomarkers in their lab results

83
Q

What is myocardial infarction?

A

Cardiac muscle death

84
Q

What is Non-ST-segment Elevation Myocardial Infarction (NSTEMI)?

A

-Associated with symptoms of cardiac ischemia and the presence of serum
biomarkers and the absence of ST-segment elevation
-May progress to a STEMI if left untreated
-As with unstable angina, an atherosclerotic lesion may develop a thrombus should the fibrous cap rupture or thin enough to promote platelet aggregation
-Should the thrombus grow enough, it may obstruct coronary circulation enough yo cause distal infarction
-Continued pressures on the thrombus may also cause it to become dislodged and eventually stop and obstruct a smaller vessel

85
Q

What are the similarities and differences between UA and NSTEMI?

A

Similarities:
-Ischemic chest pain, may be resolved/improved with nitro, may present with minor ECG changes (t-wave inversion, ST depression)

Difference:
-UA has no elevation in serum biomarkers and NSTEMI presents with elevation in serum biomarkers

86
Q

What is a STEMI?

A

-An acute STEMI is characterized by ischemic death of myocardial tissue
-Area of infarction is determined by the coronary artery that is affected and by its distribution of blood flow
-Occurs with a complete obstruction of a coronary artery due to a thrombus/embolus
-Decrease in contractile function occurs within 60 seconds of onset and irreversible damage within 20-40 minutes
-Medical emergency that can rapidly lead to death
-Common to deteriorate into a lethal cardiac arrhythmia called ventricular fibrillation (VF)
-ASA - inhibits platelet aggregation and will prevent the thrombus from getting worse, but it will not decrease the already formed thrombus
-Nitro can be administered in an attempt to reduce MVO2 but it will not do anything to change/reverse infarction

87
Q

What is a right sided STEMI?

A

-STEMI that affects the right side of the heart can
cause death of the pacemaker cells (SA node)
-May present with bradycardia and hypotension
-Nitro relaxes smooth muscle to reduce MVO2, any administration of nitro could drastically alter the hearts already limited ability to provide adequate CO for systemic tissue perfusion

88
Q

What are the classic manifestations of ACS?

A

-Ischemic chest pain
-Constricting, squeezing, suffocating, pressure, or heaviness
-Pain is usually consistent and not reproducible (able to worsen) with coughing inspiration, palpation, or movement
-Located usually precordial (retrosternal/substernal) or epigastric and may radiate to the left shoulder, jaw or arm (usually left)

89
Q

What are other associated symptoms of ACS?

A

-Shortness of breath
-GI complaints (nausea, vomiting)
-Epigastric discomfort (may be mistaken for indigestion)
-Fatigue, weakness
-Anxiety, tachycardia, feeling of impending doom
-Skin - pale, cool, diaphoretic
-Female patients often have atypical presentations of cardiac ischemia (may be absent of chest pain) whereas males tend to have more classic presentations

90
Q

What is heart failure?

A

-A complex syndrome resulting from any functional or structural disorder of the heart that
results in low cardiac output and/or pulmonary congestion
-Can result from any heart condition that reduces the pumping ability of the heart
-Usually a progressive disease but may be the result of an acute problem (STEMI)
-Can be classified as either right sided or left sided but long-term failure typically involves both

91
Q

What is right sided heart failure?

A

-Right ventricle fails, there is a reduction in the deoxygenated blood moving into the pulmonary circulation and a decrease in left ventricular
cardiac output
-Blood isn’t pumping into the pulmonary circulation, it backs up into the systemic
venous system, causes an increase in right ventricular and right atrial end diastolic
pressure as well as systemic venous pressure
-Common side effect of right sided heart failure is peripheral edema
-Further venous congestion causes systemic organ problems
-Blood backs into the hepatic vein causing hepatomegaly, portal hypertension and all of its side effects
-Severe right failure can cause JVD in patients presenting sitting or standing
-Causes include anything that impedes blood flow through the lungs (left heart failure and pulmonary hypertension are the most common
causes)

92
Q

What is pulmonary hypertension?

A

-HTN within the pulmonary circulation (arterial)
o Commonly occurs in patients with chronic pulmonary disease (COPD), severe pneumonia, pulmonary embolism (PE) or aortic or mitral valve stenosis - also caused by left sided heart failure
-Pulmonary vessels constrict in the presence of hypoxemia and hypercapnia (opposite to the response in systemic circulation)
-Compensatory mechanism to promote gas
exchange

93
Q

What is Cor Pulmonale?

A

right heart failure resulting from disease of the lungs or the pulmonary

94
Q

What is left sided heart failure?

A

-Impairment of the left ventricle decreases systemic cardiac output and causes a backup of blood into the left atrium and pulmonary circulation
-Backup causes a rise in pulmonary venous pressure
-When pressure in the pulmonary capillaries exceeds the capillary osmotic pressure, intravascular fluid shifts into the interstitium of the lungs and ultimately the alveoli
-Fluid is called pulmonary edema, commonly occurs at night when patients are lying supine and
gravitational forces are no longer at play
-Common causes of left ventricular failure are hypertension (progressive), acute MI (acute failure), and valve disorders
-As pulmonary pressure rises, left sided heart failure often progresses to right sided heart failure

95
Q

What are the compensatory mechanisms used by the body to combat heart failure?

A

-Sympathetic response (increased HR, SV, vasoconstriction)
-Frank-Starling - since SV is usually decreased, in order to maintain CO the heart requires an increase in preload – kidneys reabsorb sodium in an effort to increase fluid volume
-RAAS - reduction in renal blood flow triggers this system
-ANP - increased ANP secretion due to water retention and promotes fluid loss
-Myocardial Hypertrophy - enlargement of the ventricles by myocytes and non myocytes can lead to fibrosis and remodeling of the heart tissue, typically leads to worsened cardiac function, replaces normal conduction cells which often leads to cardiac arrhythmias

96
Q

What is acute heart failure?

A

-Heart failure may be a gradual and progressive process or an acute and emergent onset
-Symptoms of both mechanisms may often become severe and require medical
intervention
-Usually, the emergent symptoms are a result of increased pulmonary edema causing shortness of breath
-Rapid development of pulmonary edema due to acute heart failure is called: Acute Cardiogenic Pulmonary Edema (ACPE) and presents a significant life threat due to a lack of gas exchange – sometimes referred as “flash edema”

97
Q

What are the clinical manifestations of heart failure?

A

-Exertional SOB
-Orthopnea (SOB while lying supine)
-Paroxysmal nocturnal dyspnea (sudden SOB during sleep)
-Bilateral crackles on auscultation (coughing pink frothy sputum indicates significant congestion)
-Wheezes (bronchospasm caused by irritation of the bronchi due to pulmonary edema - cardiac asthma)
-Fluid retention and edema (pitting edema in the distal extremities - usually ankles)
-May also present as diffuse weight gain, ascites, hydrothorax (pleural effusion)
-Nocturia - increase in urination at night
-While patient is supine, the excess edema recirculates and makes its way to the kidneys where it gets excreted in urine
-Weakness, fatigue, mental confusion

98
Q

What is shock/circulatory failure?

A

an acute failure of the circulatory system to supply peripheral tissues and organs with an adequate blood supply, resulting in cellular hypoxia

99
Q

What are the causes of shock?

A

-Altered cardiac function (Cardiogenic)
-Decreased fluid/blood volume (Hypovolemic)
-Vasodilation with maldistribution of blood flow (Distributive)
-Obstruction of blood through the circulatory system (Obstructive)

100
Q

What is cardiogenic shock?

A

-Occurs when the heart fails to pump blood sufficiently to meet the body’s demands
0Decreased CO, hypotension, hypoperfusion, tissue hypoxia
-Common causes include: Acute MI, sustained arrhythmias, CHF, end-stage CAD or cardiomyopathy

101
Q

What is a myocardial contusion?

A

-Bruising to the heart that may occur with deceleration forces that cause the heart to collide with the sternum or spinal column
-Characterized by local tissues contusion, hemorrhage, edema and myocardial damage
-Direct or indirect damage (edema) to coronary arteries may cause disruption in myocardial blood flow – ischemia
-Disruption/damage to conductive cells may produce cardiac arrhythmias
-Damage to the left ventricle may cause fluid backup into the lungs (left-sided heart failure)

102
Q

What is myocardial rupture?

A

-When one of the walls of the heart is ruptured or penetrated due to blunt or penetrating trauma
-Almost always fatal
-Can produce pericardial tamponade, arrhythmias, hypovolemic shock, heart failure, etc.

103
Q

What is commotio cordis?

A

-If the patient receives significant blunt force trauma to the chest during ventricular repolarization (specifically the upstroke of the T- wave) it may cause sudden cardiac arrest, presenting with ventricular fibrillation (VF)
-Typically occurs during the relative refractory period or supernormal excitatory period
-These patients typically respond well to prompt defibrillation
-A rare condition, usually occurs as a sports injury

Patho (9 decks)

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