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KCSU17 Patho/Pharm Submodule 2 > Cardio Objectives > Flashcards

Cardio Objectives Flashcards

1
Q

four types of shock

A

hypovolemic shock cardiogenic shock distributive shock obstructive shock

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2
Q

hypovolemic shock

A

caused by blood loss, burns, blood loss, diarrhea

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3
Q

cardiogenic shock

A

caused by reduced output, pump failure (MI)

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4
Q

distributive shock

A

caused by anaphylaxis, septic shock, neurogenic shock, all of these cause excessive vasodilation need volume

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5
Q

obstructive shock

A

caused by pulmonary embolism cardiac tamponade tension pneumothorax (collapsed lung)

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6
Q

shock

A

circulatory insufficiency that creates imbalance between tissue O2 supply and demand causing reduction in effective tissue perfusion and suboptimal substage

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7
Q

which hormone is produced at higher levels during shock

A

epinephrine reinforces adrenergic tone early stages, then it is reduced after BP is restored

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8
Q

first compensatory mechanism in shock

A

increase cardiac output in response to insufficient oxygen supply

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9
Q

if increased CO is inadequate… (shock)

A

amount of O2 extracted from Hg by tissues is increased, decreased SVO2

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10
Q

6 main steps in shock response

A
  1. stimulation of carotid baroreceptor stretch relax activates sympathetic NS leading to arterial vasoconstriction = redistribution of blood flow from skin, skeletal muscle, kidney, and splanchnic viscera 2. increase heart rate and contractility causing increase CO 3. venous constriction augments venous return 4. release of vasoactive hormones to increase arteriole and venous tone 5. release of ADH enhances water retention 6. activation of RAAS enhances Na, H20 retention
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11
Q

3 stages of shock

A

pre shock shock end organ dysfunction

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12
Q

edema

A

accumulation of fluid in interstitial tissues ex: pleural effusion and ascites results from disturbance of ECF circulation bt capillaries and interstitial space

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13
Q

factors that regulate edema

A
  1. capillary hydrostatic pressure 2. capillary permeability 3. osmotic pressure 4. lymphatic channels
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14
Q

capillary hydrostatic pressure

A

force pushing fluid from capillaries into extracellular space

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15
Q

capillary permeability

A

determines ease of fluid flow through capillary endothelium

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16
Q

osmotic pressure

A

water attracting proper exerted by proteins in blood that attract fluid from interstitial space back to the capillaries

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17
Q

lymphatic channels

A

collect fluid forced out of capillaries by hydrostatic pressure and return fluid to circulation

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18
Q

pathogenesis of edema

A
  1. increased capillary permeability (swelling and acute inflammation) 2. decreased intravascular oncotic pressure (due to low plasma proteins, via kidney dx, malnutrition, liver dx) 3. increased hydrostatic pressure (heart failure)
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19
Q

arterial thromboembolic dx main cause

A

injury to vessel wall via arteriosclerosis ulceration and rupture of cholesterol plaque

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20
Q

cardioembolic sources of a clot

A

within atrial appendages (potential space) surface of heart valves (valve vegetation/endocarditis) wall motion defect (mural thrombus caused by MI or Afib)

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21
Q

thrombus

A

intravascular clot occurring at site of tissue injury can occur at any vessel (arterial or venous)

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22
Q

emboli

A

detached clot or cholesterol plaque carried into pulmonary or systemic circulation plugs smaller vessel, blocking blood flow and causing necrosis

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23
Q

Virchow’s triad

A
  1. slowing or stasis of blood flow 2. blood vessel wall damage 3. increased coagulability of blood
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24
Q

what might form emboli besides blood

A

malignancy, fat, air, amniotic fluid, foreign particles, sepsis

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25
Q

malignancy thrombosis

A

caused by 3 main things 1.rapid release of thromboplastic materials during treatment 2. platelets and coagulation factors consumed faster than replenished 3. large tumor releasing thromboplastic materials

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26
Q

fat embolism

A

caused by severe bone fracture disrupts fatty bone marrow and adipose tissue emulsified fat globules get sucked into being and carried to lungs

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27
Q

air embolism

A

large amounts of air get sucked into circulation could be from lung injury or or accidentally injected into circulation (IV)

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28
Q

amnionic fluid embolism

A

fluid entered circulation through tear in fetal membrane which then blocks the maternal pulmonary capillaries the material in fluid also activates coagulation mechanisms causing coagulation syndrome

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29
Q

foreign particulate matter embolism

A

particulate matter may injected by substance users that crush and dissolve tablets for oral use

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30
Q

septic emboli

A

infectious endocarditis lesions or with local infections causing thrombosis due to inflammation that are secondarily infected and embolize

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31
Q

predisposing factors to DVT

A

prolonged immobilization (which causes Virchows triad) impaired milking action of leg musculature that normally promotes venous return and stasis of blood veins preventing of normal emptying

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32
Q

if a DVT breaks from the vessel wall…

A

it can travel through the blood stream and lodge into the lungs, causing a pulmonary embolism

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33
Q

large pulmonary emboli

A

complete blockage of main pulmonary artery or major branches obstructing blood flow to lungs

34
Q

consequence of large PE?

A

right side of heart is distended pulmonary a. is congested with blood, increasing pulmonary pressure poor supply to LV, unable to pump adequate blood to brain and other vital organs systemic pressure falls and may go into shock

35
Q

how do you diagnose a PE?

A

contrast CT of chest can do VQ scan

36
Q

treatment of PE

A

anticoagulation drugs unfractionated heparin, LMWH, warfarin

37
Q

heart is no longer able to pump adequate amounts of blood

A

heart failure

38
Q

diastolic heart failure

A

filling problem impaired diastolic relaxation most often caused by ventricular hypertrophy or from poorly controlled HTN or stenotic valve dx usually first

39
Q

systolic heart failure

A

contracting problem impaired squeezing function of heart caused by ischemic heart disease regurgitation of heart disease

40
Q

frank starling mechanism

A

elasticity decrease with failure

41
Q

compensated heart failure

A

heart muscles will stretch and increase force of contraction to pump blood some stretch left patients can be asymptomatic

42
Q

decompensated heart failure

A

diminishing return on hearts ability to stretch and forcefully pumping blood from heart no stretch at all symptomatic

43
Q

aortic aneurysm

A

dilation or out poaching of portion of arterial wall caused by atherosclerosis, HTN, or congenital weakness

44
Q

aortic dissection

A

blood is forced into middle layer of artery false lumen tears as it blood volume two types: Ascending and Descending

45
Q

coarctation of aorta

A

congenital band of fibrous tissue after take off of major branches to upper extremities

46
Q

where is a coarctation typically found ?

A

at the isthmus (close proximity to left subclavian artery)

47
Q

PDA

A

patent ductus arteriosus narrowing severe enough that it is dependent on this neonatal artery once this closes, infants develop heart failure and shock

in coarctation, blood is able to move around/compensate but this closes = low blood supply

48
Q

physical exam of coarctation

A

femoral pulse is weak or absent systolic HTN in upper extremities more common in males than females

49
Q

treatment of coarctation

A

continuous IV infusion of prostaglandin E1 (alprostadil) to vasodilator and maintain ductus arterioles dopamine/dobutamine to improve contractility of those with heart failure surgical pair

50
Q

types of cardiomyopathy

A

dilated cardiomyopathy hypertrophic cardiomyopathy

51
Q

dilated cardiomyopathy

A

enlargement of heart and dilation of chambers impaired action leads to chronic heart failure

52
Q

hypertrophic cardiomyopathy

A

marked hypertrophy of heart muscle , muscle fibers in disarray this then reduces the size of the ventricles (then non compliant in diastole) LV flows into the aorta, thick septum impinges mitral valve, blocking outflow from ventricles heart is unable to fill like it should

53
Q

most common cause of valvular heart disease

A

degeneration

54
Q

infective endocarditis

A

more common in persons with altered anatomy and hemodynamics inciting events include: poor dental health, incisive procedure, prosthetic heart valves, IV drug abuse

55
Q

rheumatic heart disease

A

less common, patients with untreated strep infection causing inflammation damage to the mitral valve

56
Q

mitral valve prolapse

A

one of the leaflets enlarge, stretch, and prolapse into LA during ventricular systole these leaflets may not fit together causing blood to leak back into LA causing mitral regurgitation

57
Q

regulation of normal blood pressure is dependent upon which systems

A

cardiovascular, necrologic, renal and endocrine systems

58
Q

excessive vasoconstriction of the small arterioles

A

HTN this causes: increased diastolic BP, forces heart to create increased force of systolic pressure to get over after load excessive RAAS activation (=vasoconstriction)

59
Q

cardiac effects of HTN

A

increased peripheral resistance –> higher workload of heart –> cardiac wall hypertrophy increased O2 demand and stiff, non complaint ventricle that doesn’t relax –> first heart failure and with time, systolic heart failure

60
Q

vascular effects of HTN

A

increased pressure on walls of arteries –> premature wearing out of vessels, accelerating atherosclerosis causes injury to arterials –> arterial walls weakened and may rupture –> resulting hemorrhage

61
Q

renal effects of HTN

A

constricted renal arterioles –> decrease blood supply to kidneys –> activates RAAS increasing BP –> increased glomerular after pressure result input and degenerative changes in glomeruli tubules –> CKD

62
Q

primary hypertension

A

unknown cause 90% of HTN

63
Q

secondary hypertension

A

from unknown dx, potentially treated and potentially curable etiologies or secondary HTN: polycystic kidney disease, renal after stenosis, coarctation of aorta endocrine causes (hyperthyroid, pituitary or adrenal tumors)

64
Q

atherogenic

A

creates athero-plaques trans fat and saturated fat

65
Q

cholesterol

A

synthesized in body and from diet high levels are associteaed with premature atherosclerosis and increased CVD risk, transported by lipoproteins

66
Q

lipoproteins

A

two types LDL and HDL

67
Q

LDL

A

low density lipoprotein bad cholesterol carries cholesterol to the arteries

68
Q

HDL

A

high density lipoprotein good cholesterol protective increases with regular excessive stoping smoking and modest alcohol intake carries cholesterol to the liver for removal

69
Q

which medications cause drug included arrhythmias and infarcts

A

cocaine and methamphetamine intensifies effects of sympathetic nervous system

70
Q

effects of cocaine and meth on heart

A

increases heart rate (increased oxygen demand), muscle irritability (presdisposed to arrhythmia), peripheral vasoconstriction , and coronary artery spasm, fatal arrhythmias and MIs

71
Q

main risk factors for CAD

A

cigarette smoking diabetes CKD elevated blood lipids high BP

72
Q

secondary risk factors for CAD

A

obesity and type A personality

73
Q

complications of MI

A
  1. arrhythmia 2. heart failure 3. intracardial thrombi 4. pericarditis 5. cardiac rupture 6. papillary muscle dysfunction 7. ventricular aneurysm
74
Q

beta 1 adrenergic receptors

A

common in heart and mediate isotropy and chronotropy minimal vasoconstiction

75
Q

beta 2 adrenergic receptors

A

blood vessels induces vasodilation adronergic chronotrophy ionotrophy

76
Q

adronergic

A

sympathetic nervous system effect beta 2 receptors

77
Q

chronotropy

A

heart rate beta 2 receptors

78
Q

inotropy

A

strength of heart contraction beta 2 receptors

79
Q

dopamine receptors

A

present in renal splanchnic (mesenteric), coronary, and cerebral vascular beds

80
Q

Describe why a small pulmonary embolus is more likely to cause a pulmonary infarction

A

With a large emboli it is going to get caught in a main bronchus but it will have collateral blood flow so that is why they aren’t likely to cause infarction

With a small emboli, there is less likely to be collateral circulation to little alveoli in the depths of the lungs so its more likely to cause in infarction

KCSU17 Patho/Pharm Submodule 2 (14 decks)

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