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patho 300 exam 2 > heart part 2 > Flashcards

heart part 2 Flashcards

1
Q

disorders of pericardium

A

pericarditis

pericardial effusion (fluid accumulation in pericardial space)

cardiac tamponade (special form of pericardial effusion)

*fluid applys pressure on heart preventing effective contraction and ejection (causing OBSTRUCTIVE SHOCK)

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2
Q

endocardial disorders

A

endocarditis: inflammation of endocardium

subacute bacterial endocarditis (SBE) (bacterial infection)
*valvular vegetations form and damage valve function

prevention: pre-procedural antibiotic prophylaxis

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3
Q

Rheumatic heart disease

A

inflammation of the endocarial structure due to immune reaction to group A Beta hemolytic streptococcal pharyngeal infection (strep throat).

due to molecular mimicry (cells look similar and get destroyed)

valvular damage and valvular vegetative growth

prevention: antibiotics

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4
Q

valular disorders

A

valvular stenosis (narrowing)

valvular insufficiency (failure to close completely)
*aka regurgitation or incometent

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5
Q

aortic valve disorders

A

aortic stenosis

aortic insufficiency (regurgitation)

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6
Q

mitral valve disorder

A

mitral stenosis

mitral insufficiency (regurgitation)

mitral valve prolapse syndrome
*”ballons backward” into the atria

*if it is pure prolapse it will only muve backward but valve stays closed

*can also have incompetent mitral valve too with prolapse

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7
Q

heart disease in infants and children

A

congenital cardiac defects

kawasami syndrome

Covid-19 related “multisystem inflammatory disorder in children” (MIS-C)

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8
Q

congenital cardiac defects

A

higher to lower pressure and thru path of least resistance

1)defects with increased pulmonary blood flow

2)defects with decreased pulmonary blood flow

3)defecrs with miced effects on blood flow

4)defects with decreased systemic blood flow

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9
Q

3 fetal shunts

A

Ductus arteriosus:
*connects aorta and pulmonary artery

Foramen ovale:
*connects right and left atria

Ductus venosus:
*shunts blood across the liver

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10
Q

congenital cardiac defects

1)defects with increased pulmonary blood flow

intro

A

cause a left-to-right shunting of blood

oxygenated blood in left side of heart or aorta is redurected to right side or pulmonary artery then back to lungs again
*this increased pulmonary blood flow

remain acyanotic unless increased blood flow causes secondary pulmonary edema

if pulmonary edema develops patient becomes cyantic due to the pulmonary edma not the cardiac defect

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11
Q

congenital cardiac defects

1)defects with increased pulmonary blood flow

Patent ductus arteriosus (PDA)

A

left-to-right shunt from aorta to PA thru ductus arteriosus

(ex of oxygenated blood being pushed into right side increasing pulmonary blood flow)

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12
Q

congenital cardiac defects

1)defects with increased pulmonary blood flow

atrial septal defect (ASD)

ventricular septal defect (VSD)

A

left-to-right shunt thru the ASD

left-to-right shunt thru the VSD

(both examples of oxygentated blood going to right side of heart increasing pulmonary blood flow)

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13
Q

congenital cardiac defects

2)defects with decreased pulmonary blood flow

intro

A

blood flow from right side of heart to lungs is diminished or obstructed

the actual cardiac defect is what causes cuyanosis

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14
Q

congenital cardiac defects

2)defects with decreased pulmonary blood flow

examples

A

pulmonic stenosis (narrowing of pulmonary valve)

pulmonic atresia (the valve has no opening)

tetralogy of fallot (explained later)

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15
Q

congenital cardiac defects

2)defects with decreased pulmonary blood flow

Tetralogy of fallot (explained)

A

caused by comination of 4 defects:

*pulmonic stenosis (PS) (blockes PA)
*right ventricular hypertrophy (addes pressure)
*ventricular septal defect (VSD) (gives blood a place to go)
*overriding aorta
(opening of the aort overrides the VSD and taked its deoxygenated blood with the oxygenagted blood)

children have hypercyanotic “Tet Spells”

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16
Q

congenital cardiac defects

3) defects with mixed effects on blood flow

A

transposition of the greart vessels:

cyanotic:
*2 completely seperate circulatory systems

usually has PDA, ASD, VSD that allows some mixed of oxygenated and deoxygenated blood

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17
Q

congenital cardiac defects

4) defects with decreased systemic blood flow
intro

A

interference with outflow of blood from the left heart, which decreases systemic perfusion

will have cyanosis if the outflow is decreased enough

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18
Q

congenital cardiac defects

4) defects with decreased systemic blood flow

Coarctation of the Aorta

A

narrowing of the aorta-obstructs left ventricular outflow
*raisies pressure above level of obstruction but still reduces systemic perfusion below point of of aortic narrowing

above the obstruction is the branches of aorta so you have
increased pulses/BP in arms
decreased pulses /BP in legs (bc their below obstruction)

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19
Q

congenital cardiac defects

4) defects with decreased systemic blood flow

Aortic stenosis

A

narrowing at the aortic valve

due to congentially bicuspid aortic valve

no shunting of blood (obstructed outflow)

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20
Q

congenital cardiac defects

4) defects with decreased systemic blood flow
functionally single-ventricle anatomy
aka hypoplastic left heart

A

underdeveloped left ventricle with insuffiencient muscle mass to perfuse the systemic circuit

cyanotic after closure of Ductus Arteriosus

right ventricle must serve as pumping chamber for the heart

21
Q

heart disease in infants and children

Kawasaki syndrome

A

acute vasculitis (inflammation of BVs)

children under 5 y/o

caused by an immune response

begins with small vessels

22
Q

heart disease in infants and children

Kawasaki syndrome

inital stages
what vasculitis of coronary arteries can cause

A

inital phase: systemic inflammation

fever, rash, enlarged lymph nodes
bloodshot eyes
strawberry tongue
redness and swelling of hands and feet

vasculitis in CA can cause:

disrupted myocardial function (decrease contractility)
endocardial damage (vslve damage)
aneurysms of CA

23
Q

Heart failure

A

failure of pumping ability of the heart

unable to generate adequate cardiac output to meet metabolic demand of tissue

HF can be caused by any of the cardiac disorders that interferes with preload, afterload, contractility and HR

24
Q

compensatory response to HF

A

sympathetic reflexes:
*increase HR and contractility

Renal blood flow—renin-angiotensin-aldosterone mechanism—angiotensin II-vascular tone:
*vascular resistance (afterload)

Myocardial hypertrophy and remodeling

renal bloodflow—sodium and water retention—vascular volume—venous return (preload):
*frank-starling mechanism

25
Q

natriuretic factors released by heart

2 types

A

Atrial Natriuretic Factor (ANP): released from atria
Brain Natriuretic Factor (BNP): released from ventricles

used as lab markers for HF
increase in BNP indicated worsening HF

26
Q

BNP and ANP (natriuretic factors)

A

signals kidneys to increase GFR (glomrtulst filtration rate) and inhibit sodium and water reabsorption by renal tubules

inhibit SNS & RAAS, ADH secretion, salt appetite, and thirst

net effect is to decrease vascular volume to relieve cardiac wall stretch and ANP/BNP secretion decreases

27
Q

classifications of HF

A

Right vs left sided failure

systolic vs diastolic dysfunction

high output vs low output HF

28
Q

Right sided vs left sided HF

A

left-sided failure often causes right-sided (backs up)
(aka congestive HF, severe congestion of fluid in the heart and lungs)

isolated right-sided failure is often secondary to chronic pulmonary disease (ex: Cor Pulmonale)

29
Q

pulmonary edema in left HF

A

left HF causes backflow into pulmonary vasculature

leades to increased capillary hydrostatic pressure
*leads to pulmonary edema

30
Q

systolic vs diastolic dysfunction

systolic dysfunction (ejection)

A

decrease in:
* contractility and ejection fraction

this causes cardiac output to decrease and tissues dont get perfused

causes:
*ischemic heart disease
*cardiac dysrhythmias
*cardiomyopathies
*sustained hypertension

31
Q

Systolic vs diastolic dysfunction

diastolic dysfunction (filling)

A

diastolic filling is impaired but systolic ejection is fine

in LV diastolic dysfunction, blood backs up into pulmonary circulation:
causes pulmonary edema and pleural effusions

causes:
*Ventricular remodeling/hypertrophy
*Aortic or mitral valvular disease
*cardiomyopathies

32
Q

High output vs low output

High output HF

A

the metabolic needs of the tissue exceeds the hearts pumping ability
*demand of tissues due to comething like high fever outway the hearts ability

heart response by increasing CO in attempt to meet increased demand

33
Q

High output vs low output

Low output HF

A

any cardiac disorder in which impaired cardiac pumping ability leads to low cardiac output

34
Q

clinical manifestations of HF

A

fatigue, weakness

fluid retention (peripheral/ pulmonary edema)

dyspnea (paroxysmal nocturnal dyspnea)

changes in renal function (nocturia, oliguria(decrease)

mental confusion and/or cheyne-stoke breathing

cardiac dysrhythmias

35
Q

circulatory failure (shock)

A

failure of the cirulatory system to adequately deliver blood to the tissues

early compensatory resonse is SNS activation
(so try to recognize it so you can prevent)

36
Q

shock exists on a continuum

types of shock

A

compensated shock

hypotensive shock (decompensated)

irreverible

37
Q

compensated shock

A

SNS activation “compensates” and keeps the circulation working temporarily

blood pressure normal
urinary output normal
HR increased
SNS activation present

38
Q

Hypotensive shock (decompensated)

A

SNS compensatory mechanisms are failing

BP decrease
urine output decreases

39
Q

irreversible shock

A

circulatory failure cannot be reversed

pt will die

40
Q

what does shock lead to

A

total body hypoxic-ischemic cellular injury

41
Q

classifications of shock

A

cardiogenic shock
hypovolemic shock
obstructive shock
distributive shock
*neurogenic shock
*anaphylactic shock
*septic shock

42
Q

distributive shock

A

volume is still in body

but its not distributed properly to perfuse tissues

neurogenic shock: brain or spinal injury

anaphylactic shock: inflammatory response

septic shock: infection

43
Q

complications of shock

A

Lactic acidosis

DIC
acute lung injury, acute respiratory distress syndrome

acute kindey injury

decreased blood flow to GI tract

multiple organ dysfunction syndrome (MODS)

44
Q

complications of shock

lactic acidosis

A

type of metabolic acidosis

prolonged anaerobic metabolism using only glycolysis leads to lactic acidosis:
*greatly decreased ATP production

45
Q

complications of shock

DIC

A

unneeded clots and using up clot factor

46
Q

complications of shock

acute kidney injury

A

decreased renal blood flow in shock
*leads to renal isnchemia and injury

47
Q

complications of shock

gI

A

decreased GI perfusion = decreased mucus production and SNS response

cause:
*gastric stress ulcers

48
Q

complications of shock

multiple organ dysfunction syndrome (MODS)

A

circulatory failure (shock)—>
widespread hpoxic-ischemic cellular damage—>
multisystem organ failure

risk for death

patho 300 exam 2 (6 decks)

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