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Biology 2401 > CARDIO PATHO > Flashcards

CARDIO PATHO Flashcards

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1
Q

Define atherosclerosis.

A

Fibrous fatty lesions (“plaques”) that form in large and medium sized arteries, resulting in reduced flow rate causing ischemia to supplied organ/tissue

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2
Q
  1. What is the effect of atherosclerosis on the blood vessel wall thickness and elasticity, and on the rate of blood flow?
A

Increased wall thickness, decreased elasticity

Reduced vessel radius which causes reduced flow rate

Ischemia to supplied organ/tissue

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3
Q
  1. Which four general blood vessels are principally affected?
A

Aorta, femoral, carotid and coronary

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4
Q
  1. Describe the steps involved in the development of atherosclerosis.
A

Damage (hyperlipidemia, turbulent blood flow) causes increased endothelial permeability to plasma protein and lipids. These enter sub-endothelial layer

Migration of monocytes and other leukocytes into sub-endothelial layers occurs

Monocytes differentiate to macrophages, ingest lipid and transform into lipid filled “foam cells”

Macrophages release ROS and other toxic substances that further damage tissue, as well as growth factors that cause secretion of extracellular matrix (collagen & elastin) and proliferate smooth muscle that grows over the plaque

Deposits often become calcified = atherosclerotic plaques

Plaques protrude into vessel lumens, partially blocking blood flow

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5
Q
  1. What is the significance of low density lipoproteins to this disease?
A

LDLs are oxidized by ROS in plaques and then phagocytized by macrophages

There is a strong association between high levels of plasma LDLs and the development of atherosclerosis

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6
Q
  1. Be familiar with predisposing risk factors for atherosclerosis.
A

Elevated cholesterol

High blood pressure leads to endothelial cell damage

Obesity

Diabetes

Smoking

Sedentary lifestyle

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7
Q
  1. Define coronary artery disease and ischemic heart disease.
A

Coronary artery disease = atherosclerosis of the coronary arteries

Ischemic heart disease = a disease characterized y ischemia (reduced blood supply) of the heart muscle)

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8
Q
  1. Describe the relationship between coronary artery disease (CAD) and ischemic heart disease (IHD).
A

CAD is the most common cause of IHD

Since coronary artery disease is the major cause of ischemic heart disease, the 2 terms are often used interchangeably

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9
Q

Which regions of the heart are affected by blockages in the right coronary, and vessels leading from the left coronary arteries? (You don’t need to separate out the regions from the individual vessels leading from the left coronary artery.)

A

The right coronary artery supplies mostly the right ventricle and posterior regions of heart

The left coronary artery supplies mostly the left ventricle and interventricular septum

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10
Q
  1. Describe the mechanisms that regulate myocardial blood flow.
A

Autonomic control: parasympathetic and sympathetic (complicated)

Local autoregulatory control: vasoactive mediators released from heart muscle cells and blood vessel walls produce vasodilation or constriction of coronary blood vessels to match metabolic / oxygen demands of cardiac muscle

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11
Q
  1. When is myocardial blood flow the highest?
A

Diastole

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12
Q
  1. Why is the subendocardial region of cardiac muscle most sensitive to ischemia?
A

Have most difficulty obtaining adequate blood flow

When the ventricles contract (systole) the heart muscle compresses muscle capillaries, reducing blood glow

Muscle here is usually damaged first if the blood supply is reduced

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13
Q
  1. Why is the collateral circulation of the myocardial blood flow a potential life-saving feature?
A

Many connections called anastomoses exist between smaller coronary arteries

During acute ischemia the anastomoses dilate within seconds, providing an alternative path for blood flow

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14
Q
  1. Describe the two types of plaque that can form and identify which one is associated with what type of ischemic heart disease.
A

Stable plaque = thicker cap, less likely to rupture. Involved in stable angina

Unstable plaque = has more lipid in core, thinner cap. Is more likely to rupture, involved in acute coronary syndrome

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15
Q
  1. Define angina pectoris and differentiate between stable angina and unstable angina, including: a. the differences in underlying pathology of each condition b. the distinctive diagnostic clinical features of each condition regarding: i. the pattern and duration of pain. ii. the effect of exercise and emotional stress on the signs/symptoms. iii. the effect of short acting vasodilators such as glycerol trinitrate (GTN) on the signs and symptoms.
A

Angina pectoris pains radiate from the substernal region of the best to the jaw and down the arms

Stable angina: chest pains caused by transient myocardial ischemia not severe enough to cause necrosis, brought on through physical exertion/emotional stress, myocardial blood flow cannot respond to increased demand for blood due to narrowing of one or more coronary arteries by stable atherosclerotic plaque

Unstable angina: the surface of an unstable plaque experiences small disruptions, leading to the development of small thromboses (clots, made up mostly of platelets), which cause periods of partial occlusion, periods of occlusion not long enough to cause permanent damage or death, very important to recognize unstable angina as it may predict eventual myocardial infarction, requires immediate hospitalization for rest, observation and treatment: oxygen, aspirin (reduce clotting), nitrates (vasodilator), morphine

Differentiating between stable and unstable:

Stable angina:

Plaque intact, partially obstructing coronary artery

Pain predictably brought on by physical exertion/emotional stress

Symptoms last less than 15 minutes

Symptoms relieved by glycerol trinitrate = nitroglycerin) vasodilator

Effects of ischemia on myocardium are temporary / no necrosis

Unstable angina

Chest pain is sudden and unpredictable

Chest pain is not in response to exertion or stress, but is spontaneous

Pain generally more severe, lasts longer than with stable angina

Plaque movement or small thrombi formation results in temporary ischemia

May lead to life threatening myocardial infarction

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16
Q
  1. Define Acute Coronary Syndrome and be able to describe: a. differences in underlying pathology regarding: i. Unstable angina, ii. Non-ST segment elevation Myocardial Infarction (Non-STEMI) iii. ST-segment elevation Myocardial Infarction (STEMI) b. the distinctive diagnostic clinical features for each above condition regarding: i. the pattern and duration of pain. ii. whether the event occurs at rest or only as a result of stress iii. the effect of short acting vasodilators such as glycerol trinitrate (GTN) on the signs and symptoms.
A

ACS represents a spectrum of ischemic heart diseases: ranging from unstable angina to myocardial infarction

Acute coronary syndrome:
Pain may persist longer than 20 minutes, depending upon the type of ACS, Pain may increase in severity, May have previous history of unstable angina as risk factor, Symptoms not relieved by short acting vasodilators (glycerol trinitrate), In most cases of unstable angina there is recovery and the effects are temporary

NSTEMI or STEMI: Immediate result of extensive or complete coronary occlusion, Blood flow is severely impeded or ceases in vessels beyond occlusion except for small amount of collateral flow, Produces acute ischemia in the myocardium supplied by the vessel, and varying degrees of ischemic injury and necrosis

STEMI MI: The clot lodges permanently in the vessel and the entire thickness of the myocardium becomes ischemic, This type MI is associated with ST segment Elevation on ECG “STEMI”, Serious: requires immediate emergency intervention

Non-STEMI MI: The clot does not completely occlude the vessel, resulting in partial ischemia: only sub endocardium affected, Sometimes transient ST elevation, then T wave inversion

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17
Q
  1. Describe the ECG changes related to myocardial infarction and be able to distinguish between STEMI and Non-STEMI ECG traces.
A

STEMI = ST segment elevation of ECG

Non – STEMI = transient ST elevation then T wave inversion

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18
Q
  1. Describe the usual manifestations of ACS, be familiar with the atypical symptoms, and explain the meaning of the term “silent MI”.
A

Abrupt onset, severe and crushing pain (usually substernal, radiating to the left arm, neck or jaw), gastrointestinal complaints, complaints of fatigue and weakness, tachycardia, anxiety, restlessness, feelings of doom, pale cool moist skin

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19
Q
  1. Identify and describe the three main causes of death through myocardial infarction. Know which one is the most common cause of death.
A

Fibrillation of heart: Main cause of death in STEMI is ventricular fibrillation, Cardiac output is 0 due to erratic electrical impulses and abnormal conduction pathways in damaged myocardium

Decreased cardiac output:
(cardiogenic shock), Pumping ability reduced, may be exacerbated by “systolic stretch” = dead muscle forced outward by pressure, Heart failure and peripheral ischemia result

Rupture of heart: Can occur several days after infarct as muscle fibres necrose and degenerate and the heart wall stretches thin, Systolic stretch increases to the point when finally the heart ruptures

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20
Q
  1. List the measures involved in immediate care of ACS.
A

Oxygen therapy, nitroglycerin, bed rest, pain relief, 12 lead ECG & ECG monitoring, beat blockers = slow HR, lengthen diastole, anticoagulant therapy (aspirin, platelet inhibitors), possibly angioplasty / bypass surgery

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21
Q
  1. Describe the key aspects of care (rest and pain management) and their rationale.
A

Rest:

Cellular death determined by: degree of ischemia due to infarct & workload on the heart since it increases O2 demand, When the heart becomes highly active coronary arteries dilate to supply healthy muscle with O2 and nutrients, This reduces the collateral circulation that may be assisting the damaged muscle during recovery

Pain:

Normally cannot “feel” our heart – but ischemic myocardium can produce severe “crushing pain”, Experienced in central chest, down left arm, sometimes chin, Believed to relate to release of lactic acid and mediators of inflammation, Pain relief in itself is important – but also because pain increases stress > increase cardiac output = increase workload on the heart

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22
Q
  1. Describe the clinical manifestations that occur with atherosclerosis of the aorta, cerebral, peripheral and coronary arteries.
A

Aorta: mainly thrombus formation (could lead to hypertension or emboli) and weakening of the vessel wall (lead to aneurism)

Medium-size arteries, the result is mainly ischemia and infarction due to vessel occlusion: Obstruction of cerebral arteries = stroke, Obstruction of peripheral arteries can cause significant pain and disability in extremities, Obstruction of coronary arteries is the major cause of ischemic heart disease and can lead to heart attacks

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23
Q
  1. Define hypertension and possible results.
A

A consistent elevation of systemic arterial blood pressure (a sustained systolic BP of >140mmHg or a diastolic pressure of >90mmHg)

Increased risk for myocardial infarction, kidney disease, stroke

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24
Q
  1. Are most cases of hypertension due to primary or secondary causes?
A

Primary

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25
Q
  1. Be familiar with factors that can lead to primary hypertension.
A

Combination of genetics and the environment

Family history, age, gender, race, high dietary sodium intake, insulin resistance, cigarette smoking, obesity

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26
Q
  1. The increase in blood pressure is due to one or both of what 2 changes in the circulatory system?
A

Increase in circulating blood volume & increased peripheral resistance

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27
Q
  1. Describe 3 factors that can interact to produce these changes.
A

Increased activity of the sympathetic nervous system – increases HR and vasoconstriction

Overactivity of renin-angiotensin-aldosterone system – increases blood volume and pressure (by retaining sodium and water in kidneys), increases vasoconstriction

Chronic inflammation results in the release of chemicals that can alter vessel wall smooth muscle tone

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28
Q
  1. Why is hypertension called the “silent disease”?
A

Early stages have no symptoms/signs, other than elevated blood pressure

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29
Q
  1. Be familiar with examples of damage that can be caused by sustained hypertension.
A

Most clinical manifestations become evident when damage to other organs occur: coronary heart disease, kidney disease, CNS dysfunction (stroke), impaired vision

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30
Q
  1. How is hypertension diagnosed?
A

Determined by several BP measurements at different times (3-5 visits, depending upon the measurement), as well as CBC, urinalysis, blood chemistry, ECG, to exclude secondary hypertension and assess target-organ damage

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31
Q
  1. Describe treatment for primary hypertension.
A

Includes lifestyle modification: exercise, lose weight, stop smoking, as well as diuretics, other antihypertensives

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32
Q
  1. Describe the two classifications of hypertension during pregnancy.
A

Pre-existing: present before pregnancy, or appears before 20 weeks

Gestational: occurs at or after 20 weeks

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33
Q
  1. Why would hypertension develop during pregnancy, and be familiar as to what conditions it might lead.
A

Unknown – thought to be due to a decrease in placental blood flow, leading to release of toxic compounds (cytokines, reactive oxygen products) that cause changes in blood vessel walls throughout body

Risk for development of: preeclampsia, liver failure, kidney failure, heart disease, respiratory distress, DIC, generalized edema

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34
Q
  1. What manifestations would result in the diagnosis of preeclampsia?
A

Hypertension (either gestation or pre-existing)

Proteinuria

Adverse conditions such as persistent or new headache, visual disturbances, persistent abdominal pain, elevated liver enzymes

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35
Q
  1. Describe eclampsia and its possible cause.
A

Occurrence of convulsions and possible coma, possibly brought about through the development of blood clots in cerebral vessels

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36
Q
  1. What is the effect of gestational hypertension on the fetus?
A

Decrease in placental blood flow involved in gestational hypertension also affects the fetus, frequently resulting in infants who are small for gestational age, and the frequent need for early delivery

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37
Q
  1. What is the definitive cure for preeclampsia?
A

Birth of baby and accompanying delivery of placenta

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38
Q
  1. Define orthostatic hypotension.
A

Specific decrease in blood pressure within 3 min of moving to a standing position, causing dizziness, fainting

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39
Q
  1. What is the pathophysiology behind orthostatic hypotension?
A

Normal mechanisms that occur to maintain BP when standing up (increased HR, increased arteriolar and venous constriction) do not function

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40
Q
  1. Give a common cause for orthostatic hypotension, and describe how it is treated.
A

By the use of certain medications, although can be caused by other conditions

Treatment is through alleviating the cause. If not possible, can be managed by learning ways to cope

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41
Q
  1. Describe an aneurism, possible causes and manifestations.
A

Local outpouching of vessel or heart chamber wall, usually in the abdominal aorta, most commonly cause by atherosclerosis and hypertension

Manifestations depend upon where the aneurysm is, and involve the production of pressure on local structures. May also be asymptomatic until they rupture. Rupture causes extreme pain and hypotension

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42
Q
  1. Be familiar with causes of thrombi, and what thrombi can do.
A

Caused by any condition that promotes activation of coagulation (surgery, infection, low BP, inflammation)

Can occlude the artery/vein, or can break off to form a clot

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43
Q
  1. Define embolism.
A

Obstruction of a vessel by an embolus (air bubble, fat, dislodged thrombus). No matter how tiny, it will eventually lodge in a vessel

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44
Q
  1. What is the difference in origin between pulmonary and arterial emboli?
A

Pulmonary arise form venous side or in the right heart

Arterial arise from left heart and associated with thrombi that occur after trauma

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45
Q
  1. Define varicose veins.
A

Veins in which blood has pooled, producing distended, tortuous, and palpable vessels

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46
Q
  1. Describe two reasons for why varicose veins commonly occur in the legs.
A

There are no valves in the inferior vena cava or the common iliac veins, making the veins in legs responsible for supporting the blood in the vessels. If pressure increases in abdomen, this increases the strain on these valves

Standing for long periods of time also puts extra strain on these valves, as the leg muscles are not being used to pump blood back heart

47
Q
  1. Describe how varicose veins develop.
A

If a valve in a vein is damaged, a section of the vein is subjected to the pressure of a larger volume of blood under the influence of gravity

The vein swells and edema develops in the surrounding tissue

This can damage the remaining upstream valves in the vein, making them unable to maintain normal venous pressure

Tends to happen in the external veins, as the deep veins are supported by muscle, bone and connective tissue (external veins have only the subcutaneous fat and connective tissue)

48
Q
  1. Be familiar with risk factors for developing this condition, and how this condition can be treated.
A

Standing long periods, crossing legs at the knee, age, female, family history, obesity, pregnancy, deep venous thrombosis and previous leg injury

Treatment for varicose veins can include wearing compression socks, physical exercise, surgical ligation and stripping of the affected vein

49
Q
  1. Define CVI (don’t just say what the letters stand for)
A

Inadequate venous return over a long period of time

50
Q
  1. To what two complications can CVI lead? What is a symptom of CVI?
A

This can lead to increased venous pressure, which results in edema, which can interfere with delivery/removal of nutrients/waste products. Additionally, the lower flow rate of the blood through capillaries allows leukocytes to migrate into the tissues, which causes inflammation when inflammatory compounds are released into the tissue

Symptoms include darkening of the skin of the feet and ankles

51
Q
  1. If delivery of nutrients to the tissues becomes sufficiently poor, what two problems can result? (Know what a stasis ulcer is).
A

Edema can interfere with the delivery of oxygen and nutrients to tissues to the point that stasis ulcers develop and infection occurs even with minor injury

52
Q
  1. Define DVT and be familiar with risk factors.
A

The development of a thrombus in deep vein

Venous stasis (due to immobility, hip fracture, joint replacement, spinal cord injury are major risk factors) - allows pooling of clotting factors

Impaired cardiac function (acute myocardial infarction, congestive heart failure)

Venous endothelial damage (due to intravenous drug use/groin injection)

Hypercoagulable states (due to inherited disorders, pregnancy)

53
Q
  1. Describe the development of DVT, and be familiar with means to lower risk of occurrence.
A

Clotting factors and platelets accumulate (often near valve) and form thrombus

Inflammation around the thrombus promotes further platelet aggregation and the thrombus grows

Because the vein is deep in the leg, it is usually asymptomatic (may get edema if vessel is obstructed)

Prevention is important (early ambulation after pregnancy or surgery, the use of support stockings, prophylaxis with anticoagulants

54
Q
  1. Define pericarditis and be familiar with some causes.
A

Acute inflammation of the pericardium: fever, pain

Various causes (idiopathic, infection, surgery)

55
Q
  1. Define cardiomyopathy.
A

Diverse group of diseases that primarily affect the myocardium

56
Q
  1. Describe two examples of cardiomyopathy and their effects on heart function.
A

Dilated cardiomyopathy

Increased ventricular volume, which causes impairment of systolic function of one or both ventricles

Hypertrophic cardiomyopathy

Thickening of septum, which decreases left ventricular size and may obstruct outflow of left ventricle

57
Q
  1. What is one of the most common acquired causes for a valvular disfunction?
A

Rheumatic heart failure

58
Q
  1. Which valves in the heart are most commonly affected? Why?
A

Aortic and mitral

Because the pressures across the valves in systole is much higher

59
Q
  1. Describe the two types of disruptions that can occur with a valvular dysfunction.
A

Stenosis: narrowing of valve opening, causing turbulent flow and enlargement of emptying chamber

Incompetent (regurgitant) valve: permits backward flow

60
Q
  1. What is a “heart murmur”?
A

Sounds made by abnormal flow

61
Q
  1. What is a disrhythmia / arrhythmia?
A

A change in the normal rhythm of the heart beat

Range from occasional “missed”, more rapid or slower beats, to serious disturbances that impair the pumping ability of the heart

62
Q
  1. What are the two general causes for disrhythmias?
A

Abnormal rate of impulse generation from the SA node or other pacemaker

Abnormal conduction of impulses through the heart’s conduction system

63
Q
  1. Define sinus rhythm, brachycardia, tachycardia and sinus arrhythmia.
A

Normal heartbeat

Slow heartbeat

Fast heartbeat

Irregular heartbeat (during respiration)

64
Q
  1. Describe atrial fibrillation. Why can this be sometimes asymptomatic? What is the greatest danger?
A

Completely disorganized and irregular atrial rhythm accompanied by completely irregular ventricular rhythm. Causes pooling of blood in atria

Ventricular filling is not totally dependent on atrial contraction, so these arrhythmias may be asymptomatic

Many sites within the atria are generating their own electrical impulses, leading to irregular conduction of impulses to the ventricles that generate the heartbeat

65
Q
  1. Describe atrioventricular node abnormalities (heart block).
A

Occurs when conduction is excessively delayed or stopped at the AV node or bundle of His

Partial heart block (slower conduction – leads to first, second degree) to total heart block (no transmission – leads to third degree, where ventricles contract on their own, but cardiac output is greatly reduced)

Not all atrial beats getting through to the ventricles

66
Q
  1. Describe ventricular fibrillation and asystole.
A

Ventricles quiver but do not contract – ineffective in ejecting blood (no cardiac output, so death within minutes if not corrected)

No electrical activity in the heart / absence of a heartbeat (“flatline”)

Disorganized electrical signals: ventricles quiver instead of contract. Patient unconscious as blood is not pumped to the brain. Immediate defibrillation is indicated. May occur in MI

67
Q
  1. Describe the purpose of cardiopulmonary resuscitation (CPR) and defibrillation, and identify the context in which it is appropriate to use each in regards to the ECG trace.
A

Purpose is to “massage” the heart with sufficient force to circulate sufficient blood throughout the body and throughout the heart muscle to maintain life. Performed when heart has stopped beating (asystole). (it is possible (but unlikely) that, with the heart muscle receiving sufficient oxygen, it may begin to beat spontaneously)

Purpose is to interrupt the irregular electrical signals that are causing the ventricles to vibrate and not produce sufficient cardiac output. Once these signals have been stopped, it is possible for the heart to begin beating in a rhythmic fashion. Performed when the ventricles are fibrillating

68
Q
  1. What is heart failure?
A

When the heart is unable to generate an adequate cardiac output

69
Q
  1. What two factors interact to produce cardiac output? Which of these factors is reduced in heart failure?
A

Stroke volume and heart rate

Decrease in stroke volume

70
Q
  1. Upon what three characteristics does stroke volume depend?
A

Preload, afterload, myocardial contractility

71
Q
  1. What are the two possible consequences of heart failure?
A

Inadequate perfusion of tissues

Increased pulmonary capillary pressures

72
Q
  1. Be familiar with the main causes and risk factors for heart failure.
A

Hypertension, dilated cardiomyopathy, and valvular heart disease

73
Q
  1. Define preload.
A

Volume of blood in the ventricle at the end of diastole

74
Q
  1. What two factors determine preload?
A

Amount of blood entering ventricle during diastole & blood left in ventricle after systole (depends upon the strength of the contraction and the resistance to ventricular emptying)

75
Q
  1. What is the Frank-Starling Law of the Heart?
A

The more stretched the ventricle wall, the greater the force of the contraction (up to maximum value). Therefore, the more blood that is in the ventricles, the stronger the contraction will be (= greater stroke volume)

76
Q
  1. Define afterload and describe the characteristic that would be a good indicator of this.
A

Resistance to ejection of blood from the left ventricle

Peripheral vascular resistance is usually a good index of afterload

77
Q
  1. What is a synonym for inotropy?
A

Contractility

78
Q
  1. Define inotropy.
A

Contractility (force of contraction) of muscle is the ability of the actin and myosin of the heart muscle to interact and shorten against a load. Increases cardiac output, independent of preload and afterload

79
Q
  1. Name two diseases that would affect inotropy, and identify whether contractility would increase or decrease.
A

Ventricular hypertrophy: increases contractility (more muscle present)

Myocardial infarction: decreases contractility (some muscle replaced by scar tissue)

80
Q
  1. Define systolic heart failure.
A

The decrease in ejection fraction means that there is more blood left in the ventricle after contraction, thus increasing preload. The increased preload leads to pulmonary or peripheral edema

81
Q
  1. Identify (and understand the examples for each) three causes for systolic heart failure.
A

Decreased contractility, volume overload, pressure overload

82
Q
  1. Define diastolic heart failure.
A

A decrease in cardiac output caused by decreased filling of the left ventricle during diastole caused by reduced chamber size (left side only)

83
Q
  1. Identify (and understand the example for each) three causes for diastolic heart failure.
A

Decrease expansion of the ventricle (pericardial effusion)

Increase wall thickness and reduce chamber size (hypertrophic cardiomyopathy)

Delay diastolic relaxation (myocardial ischemia) (decreased energy for calcium pumps)

84
Q
  1. What is the result of diastolic heart failure, and how does this happen?
A

Results in pulmonary edema, as blood backs up into pulmonary circulation, thus increasing pulmonary pressure

85
Q
  1. Define left heart failure.
A

Inability to supply sufficient output to systemic circulation

86
Q
  1. What is left heart failure commonly called?
A

Congestive heart failure

87
Q
  1. Describe the consequence of left heart failure, and how this arises.
A

When decreased cardiac output to the systemic circulation occurs, blood accumulates in the left side of the heart, and then in the pulmonary circulation, causing increased pulmonary venous pressure. If this exceeds osmotic pressure in capillaries, fluid enters the lung tissue = pulmonary edema

88
Q
  1. Be familiar with the common causes of left heart failure.
A

Hypertension, acute MI, cardiomyopathy

89
Q
  1. Define right heart failure.
A

Inability of right ventricle to move deoxygenated blood from systemic circulation into the pulmonary circulation

90
Q
  1. Describe the consequences of right heart failure and how these arise.
A

Pressure then rises in systemic venous circulation, leading to peripheral edema and congestion of the viscera

91
Q
  1. Identify the most common cause of right heart failure and describe how this occurs.
A

Left heart failure:

Left heart failure creates increased pulmonary pressure

This backs up into the right ventricle, which is poorly equipped to compensate, so will dilate and fail

92
Q
  1. Define cor pulmonale, and be familiar with the diseases that can be a cause.
A

When right heart failure occurs independently of left heart failure, in response to pulmonary disease (that increases pulmonary pressure)

COPD, cystic fibrosis, ARDS

93
Q
  1. Be familiar with the diseases that can be a direct cause of right heart failure.
A

MI, cardiomyopathies, valvular disease

94
Q
  1. Describe three compensatory mechanisms for heart failure: why they are activated, or their purpose in being activated, and how they bring about harm to the heart.
A

Sympathetic nervous system activation: to increase blood pressure and cardiac output. However, the increase in heart rate and contractility actually put more strain on the already weakened heart

RAAS activation: one of the most important results of decreased cardiac output is decreased renal blood flow (as a result of decreased blood pressure), which leads to activation of the RAAS (which also leads to release of ADH). The vasoconstriction that results increases afterload, and the increase in blood volume increases preload, both of which put more strain on the heart

Hypertrophy: increases in pressure causes myocytes to increase in width, leading to a disproportionate thickening of the walls, which may increase ischemia. Increases in volume (water/salt retention) causes myocytes to increase in length, leading to thinning of the ventricular walls and dilation, possibly resulting in impairment of contraction

95
Q
  1. Explain the phrase “decompensated heart failure”.
A

Clinical syndrome in which a structural or functional change in the heart leads to its inability to eject and/or accommodate blood within physiological pressure levels

96
Q
  1. Be familiar with, and be able to explain, the symptoms for heart failure.
A

Dyspnea = shortness of breath

Orthopnea = sitting up helps relieve dyspnea

Fatigued and tires easily

Decreased urine output

Edema = especially in lower extremities

97
Q
  1. List the treatments for heart failure and explain why they would be used.
A

Concentrates on decreasing preload (salt restriction and diuretics (decrease blood volume)) and afterload (weight management (less fat = less peripheral arterioles and capillaries)

Digitalis (improve stroke volume), beta blockers (decrease heart rate and contractility), O2 therapy

98
Q

100.Define shock.

A

An acute failure of the circulatory system to supply the body with an adequate blood supply, resulting in cellular hypoxia

99
Q

101.Describe the basic cellular effects of shock.

A

If sufficient oxygen is not delivered to the cell, it switches to anaerobic respiration, which produces far less ATP

Without sufficient ATP, the cell’s sodium/potassium pump operates poorly

The intra/extra cellular concentrations of sodium, potassium and calcium are not maintained, interfering with functioning of nervous and muscular systems

100
Q

102.Describe 3 positive feedback loops that result in ever-increasing tissue hypoxia and tissue damage.

A

1: with sodium entering cell, water from interstitial fluid follows. The drop in interstitial fluid then pulls water out of the vascular system, which results in a drop in blood pressure. Decreased volume in the vascular system intensifies the decrease in perfusion of tissues, which decreases aerobic respiration, which decreases ATP production

101
Q

103.What is the consistent sign of shock?

A

Hypotension

102
Q

104.Be familiar with symptoms of shock.

A

Being sick, weak, cold, hot, dizzy, confused, afraid, thirsty, short of breath

103
Q

105.What is the treatment for shock?

A

Must remove underlying cause

Generally, IV fluid to expand blood volume

104
Q

106.Describe the condition of cardiogenic shock and its effect on the heart

A

Enough blood volume, but decreased cardiac output due to decreased contractility, increased preload and increased afterload

Decrease in blood pressure causes responses (increase in epinephrine, RAAS) that increase oxygen/nutrient demand of the heart which puts further strain on the heart, resulting in it becoming incapable of pumping an adequate volume

105
Q

107.Identify the condition that often leads to cardiogenic shock.

A

Usually follows MI

106
Q

108.Describe the condition of hypovolemic shock and its causes (3).

A

Not enough blood volume, caused by loss of whole blood (hemorrhage), plasma (burns) or interstitial fluid (diarrhea or diuresis) in large amounts

107
Q

109.What compensatory mechanisms does the body employ to counteract hypovolemic shock?

A

HR and vasoconstriction increase

Interstitial fluids moves into blood

Liver and spleen add to blood volume

RAAS is activated, as is ADH

108
Q

110.Describe the condition of distributive shock.

A

Result of massive vasodilation such that, although the volume of the blood has not changed, the amount of space containing the blood has increased, resulting in a decrease in BP below the required to drive nutrients across capillary membranes to the cells

109
Q

111.Describe the condition of neurogenic shock. Be familiar with the causes.

A

Result of massive vasodilation resulting from overstimulation of the parasympathetic NS and under stimulation of the sympathetic NS

Trauma to the spinal cord or medulla, anaesthetic agents, severe pain

110
Q

112.Describe the condition of anaphylactic shock, its cause and its treatment.

A

Release of histamine and other compounds by mast cells as a result of a type I hypersensitivity results in vasodilation and vascular permeability to the point of peripheral pooling and tissue edema

Results from widespread hypersensitivity reaction, known as anaphylaxis

Smooth muscle constriction can result in laryngospasm, bronchospasm and diarrhea

Treatment involves intramuscular administration of epinephrine to cause vasoconstriction and reverse airway constriction

111
Q

113.Define the condition of septic shock.

A

Severe infection with a microorganism has 2 possible effects: the microorganism releases toxins that stimulate an overwhelming inflammatory response, and/or there is an overwhelming inflammatory response to the microorganism itself

Common type of vasodilatory shock

112
Q

114.What manifestation differs between vasodilatory (distributive) shock and other categories of shock?

A

Manifestation differs from types of non-vasodilatory shock in that the skin is warm and flushed (non-vasodilatory types of shock constrict blood vessels, thus decreasing blood flow to skin (skin becomes cool and pale) while distributive types of shock produce dilation of blood vessels)

113
Q

115.Describe the condition of obstructive shock, and its most common cause.

A

Results from mechanical obstruction of the flow of blood through the central circulation

Most common cause is pulmonary embolism (other causes include cardiac tamponade, pneumothorax)

Elevated right heart pressure occurs

Significant decrease in cardiac output

Biology 2401 (30 decks)

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