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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
Wall tension formula
RadiusXIVP/Thickness
26
Positive feedback loops which exacerbate HF
A1 and B@ RAAS Increased myocardial contractility (inotropy) Cardiac remodeling
27
Clinical manifestations of HF
``` SOB Orthopnea Paroxysmal nocturnal dyspnea Cardiac asthma Cheyne-strokes resps Pulmonary edema Fatigue, weakness, altered LOC JVD Ascites Oliguria ```
28
What is Acute Arterial Occlusion and where does it happen
From the heart, atherosclerotic plaques within an artery, fat from a fracture or amniotic fluid create an embolic occlusion
29
Seven P's of acute arterial occlusion
``` Pain Pallor Pulselessness Paresthesia Paralysis Pistol shot Polar (line of demarcation?) ```
30
Atherosclerotic occlusive disease
Narrowing of arterial lumen for atherosclerotic plaque resulting in ischemia, same risk/patho as coronary Most common in lower legs
31
S&S of atherosclerotic occlusive disease
Claudication Blanched legs when elevating Skin breakdown, ulceration, gangrene
32
Thromboangiitis obliterans
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
Thromboangiitis Obliterans most likely to effect
Smokers/ chewing tobacco users Tobacco causes immune response in susceptible pts Men 25-40 and most common in middle east/ far east
34
Raynauds
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
Aneurysm definition
Localized dilation of blood vessel (usually an artery)
36
True aneurysm
Bounded by complete vessel wall with at least 50% increase in diameter Blood is contained inside complete vessel (berry, saccular, fusiform)
37
False aneurysm
Rupture of part of the vascular wall causing formation of extravascular hematoma Blood is contained within segments of vascular wall or CT (dissecting)
38
Berry Aneurysm
Small, spherical dilation at bifurcation communicating with the main vessel by a small opening Involves all 3 layers
39
Saccular aneuysm
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
Fusiform
Tapering at both ends (aka circumferential) and involves all 3 layers
41
Dissecting aneurysm
Tear in intimal lining of vessel creating a blood filled cavity
42
Etiology of aneurysms
Atherosclerosis is most common (plaque erodes vessel wall) | Can also be caused by trauma, syphilis, infections, congenital defects
43
Patho of aneurysms
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
Aortic aneurysm
Is most common, linked to HTN and inheritance, atherosclerosis and has high mortality rates
45
Where can aortic aneursym hit
Ascending aorta, aortic arch, descending, thoracoabdiomainal or abdominal
46
Types of aneurysms associated with aortic aneurysms
Commonly fusiform but can be saccular Abdominal most commonly at bifurcation Bifurcation is normally 2cm, so 3cm means aneurysm
47
Merk aneurysms
Type A is confined to ascending aorta | Type B confined to descending aorta
48
Clinical manifestations of aneurysms
Palpable at 4cm Pulsating mass Mid-abdominal and lumbar pain Rupture will cause hypovolemic shock and profound hypotension
49
Aortic dissection patho
Usually ascending aorta, linked to HTN and degenerative smooth muscle disorders, intimal tear causes hemorrhage into vessel wall with resultant longitudinal tearing
50
Clinical manifestations of aortic dissection
Tearing pain in chest (ascending) back (descending) Unilateral BP Neuro symptoms from disruption of blood flow to CNS
51
Overview of varicose veins
Blood pooled creating tortous and dilated veins (varicosities) Most commonly involving saphenous veins Pain and edema
52
Primary varicose veins
Valve dysfunctions in superficial saphenous veins of legs from recurrent or prolonged increases in pressure (standing still, being preggo)
53
Secondary varicose veins
Dysfunction within deep venous channels of legs (DVT, fistula's, congenital malformations)
54
Causes of varicose veins
Genes, standing too long, preggos
55
Complications of varicose veins
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
EMS concerns of varicose veins
Blood flow in varicose veins is turbulent and slow, favors clotting and thrombi, thrombi can dislodge as emboli (PE)
57
Virchows Triad
Stasis of blood, increased coagulability, endothelial injury | immobility, oral contraceptives, trauma
58
High risk for venous thrombosis
``` Post partum Long hospital stays Orthopedic surg Leg casts Dehydration Varicose veins ```
59
Homan's sign
Passively dorsiflex foot with knee extended (squeeze calf)

Pathology (24 decks)

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