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Pathology > 5 Cardiac part 2 > Flashcards

5 Cardiac part 2 Flashcards

1
Q

Heart failure definition

A

Function/structural changes with decrease CO or pulmonary/systemic congestion

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2
Q

CHF

A

Left sided heart failure, which will cause right sided

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3
Q

Cor pulmonale

A

Right sided heart failure ONLY

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4
Q

Causes of CHF (left sided) in order

A 
HTN
CAD
LV MI
Aortic stenosis
Bicuspid stenosis
Cor pulmonale
Cardiomyopathy
Congenital defects
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5
Q

Right sided heart failure causes in order

A 
Left sided failure
CAD
RV MI
Pulmonary/tricuspid stenosis
Pulmonary disease
Cardiomyopathy
Congenital defects
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6
Q

CO = HR X SV

A

HR is regulated by SNS and PNS

SV is regualted by pre/after load and contractility

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7
Q

Preload determinants

A

Venous return and length of diastole

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8
Q

Two types of increased afterload

A

Systemic and pulmonary

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9
Q

Myocardial contractility

A

Inotropy = contractility
Myocardial cells have less SR (less Ca2+ stores)
Myocardial cells need calcium from two sources for depol
Release from SR AND
Influx of extracellular across sarcolemma into sarcoplasm

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10
Q

cAMP

A

Myocardial cells have large number of calcium channels, opening mediated by cAMP and B1 innervation directly stimulates production of cAMP

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11
Q

How dig works

A

Increased intracellular Na+ disrupts Na+/Ca2+ pump resulting in increase in intracellular Ca2+

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12
Q

Two types of dysfunction

A

Systolic and diastolic

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13
Q

Systolic dysfunction

A

Decrease myocardial contractility decreases ejection fraction which retains blood in ventricles.
This increases EDV and blood begins to back up

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14
Q

Causes of systolic dysfunction

A

Decreased contractility from CAD and cardiomyopathy
Volume overload from valve insufficiency and anemia
Pressure overload from valve stenosis and HTN

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15
Q

Diastolic dysfunction

A

Normal heart contractions, but relaxation is abnormal.

Creates less blood in ventricles which decreases CO and lack of filling causes backwards congestion

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16
Q

Causes of diastolic dysfunction

A

Impedance of expansion from pericardial effusion, pericarditis
Increased thickness from hypertrophy
Delayed relaxation from aging or ischemic heart disease

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17
Q

Left ventricular dysfunction

A 
L failure leads to backup of oxygenated blood in pulmonary circulation which causes edema and decreased CO from RV
Pulmonary edema (especially at night) and general decreased perfusion are common manifestations
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18
Q

RV dysfunction

A

Backup of deoxygenated blood into systemic and decreases preload so decreased CO
Commonly presents as peripheral edema, portal vein HTN and ascites, JVD

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19
Q

Compensatory mechanisms for heart failure

A

SNS
RAAS
Frank starling
Cardiac remodelling

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20
Q

SNS activity

A

Increased catechols increase ino, dromo, and chrontropy as well as PVR which leads to increased CO but also increased MVO2
Preload and contractility drop from increased rate and PVE leads to increased afterload, furthering the condition

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21
Q

RAAS

A

Decreased renal perfusion releases renin
Renin increases angiotension I which is converted to II in the lungs by ACE
Angio II causes PVR increase and ADH from pituitary and aldosterone from adrenals
which cause fluid retention (ADH is vasopressin, solute free)

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22
Q

How does RAAS negatively effect HF

A

Fluid retention increases preload and afterload, further exacerbating the condition

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23
Q

Frank starling and HF

A

Increase preload cannot be utilized by failing heart, but the MVO2 is still increased from it

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24
Q

Cardiac remodeling HF

A

Myocytes respond to an increase in pressure and volume by undergoing hypertrophy (increased wall thickness should decrease MVO2) but is often replaced with connective tissue

25
Q

Wall tension formula

A

RadiusXIVP/Thickness

26
Q

Positive feedback loops which exacerbate HF

A

A1 and B@
RAAS
Increased myocardial contractility (inotropy)
Cardiac remodeling

27
Q

Clinical manifestations of HF

A 
SOB
Orthopnea
Paroxysmal nocturnal dyspnea
Cardiac asthma
Cheyne-strokes resps
Pulmonary edema 
Fatigue, weakness, altered LOC
JVD
Ascites
Oliguria
28
Q

What is Acute Arterial Occlusion and where does it happen

A

From the heart, atherosclerotic plaques within an artery, fat from a fracture or amniotic fluid create an embolic occlusion

29
Q

Seven P’s of acute arterial occlusion

A 
Pain
Pallor
Pulselessness
Paresthesia
Paralysis
Pistol shot
Polar
(line of demarcation?)
30
Q

Atherosclerotic occlusive disease

A

Narrowing of arterial lumen for atherosclerotic plaque resulting in ischemia, same risk/patho as coronary
Most common in lower legs

31
Q

S&S of atherosclerotic occlusive disease

A

Claudication
Blanched legs when elevating
Skin breakdown, ulceration, gangrene

32
Q

Thromboangiitis obliterans

A

Beurger disease
Inflammatory arterial disorder leading to thrombosis of medium sized arteries of foot/lower leg (arms/hands too)
Inflammation can extend to adjacent nerves and veins

33
Q

Thromboangiitis Obliterans most likely to effect

A

Smokers/ chewing tobacco users
Tobacco causes immune response in susceptible pts
Men 25-40 and most common in middle east/ far east

34
Q

Raynauds

A

Primary type from SNS hyperactivity (unknown reason) and can be set off by emotional stress/cooling
Secondary is due to frostbite, vibrating tools, collagen disease, neuro disorder, chronic artery occlusive disorders (anything known to cause vasospasm)
4 in 10,000, more common in females
Presents as discoloured/numb fingers

35
Q

Aneurysm definition

A

Localized dilation of blood vessel (usually an artery)

36
Q

True aneurysm

A

Bounded by complete vessel wall with at least 50% increase in diameter
Blood is contained inside complete vessel (berry, saccular, fusiform)

37
Q

False aneurysm

A

Rupture of part of the vascular wall causing formation of extravascular hematoma
Blood is contained within segments of vascular wall or CT
(dissecting)

38
Q

Berry Aneurysm

A

Small, spherical dilation at bifurcation communicating with the main vessel by a small opening
Involves all 3 layers

39
Q

Saccular aneuysm

A

Weakness on one side of vessel and attached to main vessel via a small stem which appears like a sac
Involves all 3 layers

40
Q

Fusiform

A

Tapering at both ends (aka circumferential) and involves all 3 layers

41
Q

Dissecting aneurysm

A

Tear in intimal lining of vessel creating a blood filled cavity

42
Q

Etiology of aneurysms

A

Atherosclerosis is most common (plaque erodes vessel wall)

Can also be caused by trauma, syphilis, infections, congenital defects

43
Q

Patho of aneurysms

A

Atheroma with central soft core (lipid and cell debris) covered by fibrous cap can be ruptured by pressure which can cause intimal ulceration
Irregular blood flow by aneurysm (whorls and eddies) predispose individual to thrombosis

44
Q

Aortic aneurysm

A

Is most common, linked to HTN and inheritance, atherosclerosis and has high mortality rates

45
Q

Where can aortic aneursym hit

A

Ascending aorta, aortic arch, descending, thoracoabdiomainal or abdominal

46
Q

Types of aneurysms associated with aortic aneurysms

A

Commonly fusiform but can be saccular
Abdominal most commonly at bifurcation
Bifurcation is normally 2cm, so 3cm means aneurysm

47
Q

Merk aneurysms

A

Type A is confined to ascending aorta

Type B confined to descending aorta

48
Q

Clinical manifestations of aneurysms

A

Palpable at 4cm
Pulsating mass
Mid-abdominal and lumbar pain
Rupture will cause hypovolemic shock and profound hypotension

49
Q

Aortic dissection patho

A

Usually ascending aorta, linked to HTN and degenerative smooth muscle disorders, intimal tear causes hemorrhage into vessel wall with resultant longitudinal tearing

50
Q

Clinical manifestations of aortic dissection

A

Tearing pain in chest (ascending) back (descending)
Unilateral BP
Neuro symptoms from disruption of blood flow to CNS

51
Q

Overview of varicose veins

A

Blood pooled creating tortous and dilated veins (varicosities)
Most commonly involving saphenous veins
Pain and edema

52
Q

Primary varicose veins

A

Valve dysfunctions in superficial saphenous veins of legs from recurrent or prolonged increases in pressure (standing still, being preggo)

53
Q

Secondary varicose veins

A

Dysfunction within deep venous channels of legs (DVT, fistula’s, congenital malformations)

54
Q

Causes of varicose veins

A

Genes, standing too long, preggos

55
Q

Complications of varicose veins

A

Chronic venous insufficiency (inadequate venous return over long period of time)
Chronic pooling causes edema, sluggish circulation, cellular exchange is impaired, venous stasis ulcers

56
Q

EMS concerns of varicose veins

A

Blood flow in varicose veins is turbulent and slow, favors clotting and thrombi, thrombi can dislodge as emboli (PE)

57
Q

Virchows Triad

A

Stasis of blood, increased coagulability, endothelial injury

immobility, oral contraceptives, trauma

58
Q

High risk for venous thrombosis

A 
Post partum
Long hospital stays
Orthopedic surg
Leg casts
Dehydration
Varicose veins
59
Q

Homan’s sign

A

Passively dorsiflex foot with knee extended (squeeze calf)

Pathology (24 decks)

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