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patho 300 exam 2 > alterations of cardiovascular function > Flashcards

alterations of cardiovascular function Flashcards

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1
Q

resistance to flow is determined by

A

length of tube

viscosity (thickness) (low rbc volume= thin so moves quick)

radius: 1 unit change in radius results in a fourfold change

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2
Q

laminar flow vs turbulent flow

A

usually due to radius or anemia

laminar:
smooth and streamlined

turbulent:
irregular and choatic

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3
Q

factors regulating cardiovascular function

A

preload

afterload

contractility

heart rate : recall CO=HR x SV

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4
Q

preload

A

provided by the degree of ventricular filling (End-Diastolic Volume (EDV)

preload reflects myocardial muscle length before contraction
*(degree of muscle stretch and relationship between actin and myosin fibers)

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5
Q

why is it left venticular EDV?

how do we assess ventrular EDV?

A

left side of the heart has a greater workload

ventricular EDV can be assessed thru:

echocardiography

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6
Q

afterload

A

resistance to outflow from the heart
(typically the left ventricular afterload is greater concern unless pt has pulmonary vascular problem with high V/Q ratio)

determined by the degree of systemic vascular resistance (SVR)

SVR is assessed by the mean arterial pressure (MAP)

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7
Q

what is MAP more influenced by?

A

diastolic pressure more than systolic

*bc more time is spent in diastolic filling phase
*due to this MAP is not a mean average of Systolic over diastolic BPS

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8
Q

contractility

A

strength of contraction at any given end diastolic volume (EDV)

a more forcefull contraction can cause a increase SV by causing greater ejection of blood (better emptying of ventricules)

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9
Q

how is contractility assessed

A

by ejection fraction (EF) of the left ventricle

EF = SV/EDV
normal 60-75%

EF can be assessed with an echocardiogram

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10
Q

heart rate

A

measure by pulse, apical HR or HR by monitor

CO=HR x SV which means increased HR will increase CO

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11
Q

capillaries

A

the presence of multiple parallel capillary channels reduces the effect of the small radius of each individual capillary

therefore the overall resistance to flow thru the capillary bed is low

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12
Q

arterial disorders:

atherosclerosis

A

formation of an atheroma (atherosclerotic plaque) within artery

AKA: arteriosclerosis
(hardening of arteries)

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13
Q

patho if atherosclerosis

A

atheroma formation is related to:
*blood vessel injury
*inflammation
*blood lipid levels

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14
Q

Hyperlipidemia

A

Increased lipids in blood

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15
Q

Dyslipidemia

A

Abnormal lipid levels but also reflects that levels of some lipid components can also be too low:

Triglycerides
Total cholesterol
HDL cholesterol
LDL cholesterol

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16
Q

Lipid panel

A

Triglycerides

Total cholesterol:
*uses protein transporter bc it can not dissolve into the plasma

HDL cholesterol: good (return lipids to liver)
LDL cholesterol: bad (for plaque)

Both are either high or low density lipoproteins so they carry proteins

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17
Q

Patho how atherosclerosis occurs

A

Platelets and monocytes try to fix injury

If LDL is increased then they will be engulfed by macrophages

Macrophages die and inflammation increased

Macrophage accumultion and we get plaques

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18
Q

Common sites for atherosclerotic vascular disease

A

Carotid artery
Cerebral artery
Coronary arter
Abdominal aorta
Iliac artery
Thoracic aorta
Femoral
Popiteal artery

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19
Q

Aneurysm

A

Weaking of aterial wall
Usually due to atherosclerosis

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20
Q

Common locations of aneurysms

A

Same locations as atheroscleotic plaque due to them being the main cause of aneuysms

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21
Q

Aneurysms with increased risk for mortality

A

Brain (cerebral aneurysm)
*increased incidence in arterial branching locations (circle of willis)

Aorta (aortic aneurysm)
*In the arch
*Increased risk to become a dissecting aneurysm due to highest presures
*high risk for people with marfan syndrome
*abdominal aortic aneurism (AAA)

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22
Q

Other Arterial disorders

A

Arterial vasculitis Aka: arteritis (or angitis)

Acute arterial occlusion

Peripheral artery disease (chronic)

Raynaud phenomenon (raynaud syndrome)

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23
Q

Peripheral artery disease (chronic)

A

Primary cause is atherosclerosis of peripheral arteries

Primary symptom is intermittent claudication

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24
Q

Raynaud phenomenon (raynaud syndrome)

A

Arterial vasospactic disorder (caused by the vasospastic)

Characterized bu intermittent arterial spasms

Triggers include cold exposure, strong emotions

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25
Venous disorders Venous thrombosis And Venous inflammation
Thrombosis: Deep venous thrombosis (DVT) Inflammation: Phlebitis Thrombophlebitis
26
Systemic hypertension
Increased BP in the systemic CV circulation Primary (essential) hypertension And Secondary hypertension
27
Primary (essential) hypertension
No specifically identifies physiologic cause
28
Secondary hypertension
Most causes originate outside the CV system Causes include: Renal disease (high blood volume due to decreased UO) Adrenocortical hormone excess (aldosterone excess causes NA and water retention) Pheochromocytoma (Adrenal medulla catecholamine excess) Coarctation of the aorta (Congential narrowing of aortic arch)
29
Complications of systemic HTN
Bc of End-Organ damage HTN retinopathy HTN cardiovascular disease HTN cerebrovascular disease Renal insufficiency & chronic kidney disease (chronic renal failure)
30
Orthostatic Hypotension
Rapid decrease in BP that occurs with change in position Fall risk
31
Action potential of myocardial cells
A: cells of electrical conducting system (SA node) *with “automaticity” (self gen of action potential thru slow leak of Ca into cell) B: atrial muscle cells C: ventricular muscle cells *have a plateau phase during depolarization (So ventricles can contract the blood out
32
EKG
Is a summated view of the movement of action potentials (electrical wave) thru heart
33
Diastole and systole
Diastole 1. Refractory period 2.atrial depolarization (P wave) 3. Atrial contraction and ejection (between P-Q segment) 4. Ventricular depolarization (QRS) Systole 5. S-T segment (venticular start to contract) 6.ventricular repolarization (T wave)
34
4 limb leads
Green is the electrical ground In 3 lead ecg monitoring the leg lead needs to be placed on the left leg
35
Case models: cardiac dysrhythmias
Artial dysrhythmias: *premature atrial contraction *supraventricular tachycardia *atrial fibrillation Ventricular dysrhythmias: *premature ventricular contration *ventricular tachycardia *ventricular fibrillation *long QT interval *Torsades de pointe
36
Premature atrial contration (PAC)
Early atrial contraction (stress) Pwave too early
37
Premature ventricular contraction (PVC)
Early ventricle contraction Abnormal QRS (Stress)
38
Supraventricular tachycardia (SVT)
Causes decreased CO Fast HR triggered from atrium (abnormal Rythm)
39
Ventricular tachycardia
Vtach Looks like shark teeth
40
Atrial fibrillation a-fib
Muscle of atrium are quivering and not contracting Fast irregular HR Tx: meds to decrease HR and anticoagulats due to blood stasis in atrium
41
Ventricular fibrillation
V-fib No QRS (no perfusion/CO)
42
Long QT interval
QT is the time from beginning of the QRS to the end of the T wave Associated with increase risk of a special life threatening type of ventricular tachycardia called (torsades de pointes)
43
Torsades de pointes
No cardiac output
44
Other causes of cardiac dysrhythmias
Acute coronary syndromes Electrolyte imbalances: Potassium Calcium
45
Coronary artery disease (CAD) Aka: coronary heart disease (CHD) atherosclerotic heart disease (ASHD)
Due to imbalance between myocardial oxygen supply vs demand Ischemia: Decreased tissue perfusion Inadequate perfusion to meet cell need for o2 and waste product removal leads to cell damage Infarction: Death of tissue caused bu ischemia
46
Myocardial ischemia
2 patterns of presentation *Chronic ischemic heart disease (partial blockage) *Acute coronary syndromes (sudden blockage or chronic becomes too much) Angina pectoris: Myocardial pain caused by ischemica Severe crushing pain Women often under diagnosed due to having different symptoms
47
Chronic ischemic heart disease
Main cause: atherosclerosis and vasospasm Presentations: Stable angia = *predictable pattern (trigger is increased activity, stress) Variant (vasopastic) angina = *associated with vasospasm and is unpredictable Silent myocardial ischemia = *myocardial tissue is ischemic but pt not experiencing symptoms
48
Actue coroncary syndromes Signs of ventricular ischemia (ekg)
Due to progressive (chronic) or sudden obstruction of cornoary blood flow, producing myocardial ischemia Signs of ischemia of ventricular muscle in ECG are changes to: ST segment T wave *these tell us ventricular cells are experiencing hypoxic-ischmic cell injury
49
What is happening in the cardiac cycle during ST segment and T wave ?
ST: venticular depolarization T: ventrical repolarization
50
Substances released from injured myocardial cells
*Potassium ion (alter resting membran potention) *Hydrogen ion (from lactic acid production by injured myocardial cells due to anaerobic metabolism) *intracellular enzymes and molecules These can lead to: *Injury of cells in the surrounding tissue *Distrubances of electrical membran potentail and electrical conduction problems *Systemic chemcial and electrolyte imbalances
51
Serum biomarkers for acute coroncary syndrome (cardiac panel)
Cardiac-specific troponin *troponin I *troponin T Increase in these we know are from heart bc their specific to cardiac muscle Creatinine kinase MK (CK-MB) *MB isoenzyme form is specific to cardiac muscle Myoglobin *not specific to cardiac muscle (in skeletal muscle too)
52
What cardiac bio markers are specific and not
Specific: Troponin I Troponin T Creatinine kinase MB Not specific: Myoglobin
53
Types of acute coronary syndrome
Unstable angina (UA) Non-ST segment elevation myocarial infarction (NSTEMI) ST segment elevation myocardial infarction (STEMI)
54
Unstable angina (UA)
ECG: Non-ST segment elevation Changes: *ST depression *T wave changes Location of damage: Subendocardial Serum biomarkers not present Effect on cell: ischemia (functional changes from reduced perfusion)
55
Non-ST segment elevation myocarial infarction (NSTEMI)
ECG: Non-ST segment elevation Changes: *ST depression *T wave changes Location of damage: Subendocardial Serum biomarkers are present Effect on cell: ischemic injury (Both structural (biomarkers) and functional changes)
56
ST segment elevation myocardial infarction (STEMI)
ECG: ST segment elevation Changes: *may have T wave changes *may progress to prolonged Q wave Location of damage: transmural Serum biomarkers are present Effect on cells: infarction (Necrotic death caused by ischemia)
57
Typical pattern of myocardial damage
Ischemia: *inversion of the T wave Injury: ST segment depression (subendocardial injury) ST segment elevation (transmural injury) Necrosis: Prolonged Q wave Permanent EKG change: indicating large are of myocardial cell death
58
Risks of myocardial ischemia
Risk for actual ischemic death of myocardial cell (Myocardial cells cannot regenerate) Therefore when they die cells are replaced with scar tissue with permanent impairements of myocardial function Fibrous scar tissue: Cannot conduct electrical impulses or contract
59
Clincial manifestation of MI
Pain and autonomic (SNS) responses related to ischemia Symtoms R/T impaired myocardial fucntion Symptoms R/T changes in electrical conduction Symtpoms R/T inflammation
60
Potential complications of MI
Sudden death Cardiogenic shock (circulatory failure/ can deliver) Congestive heart failure (due to scar tissue) Thromboembolism Strole Pericarditis Myocardial rupture Ventricular aneurysm Dysrhythmia
61
Myocardial disorders
Myocarditis (inflammation of heart) Cardiomyopathies: Dilated: stretches/cant contract Hypertrophic: growth of muscle *cant full bc muscle is too big (not due to afterload) Constrictive (restrictive) *becomes rigid on the outside

patho 300 exam 2 (6 decks)

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