heart part 2 Flashcards
disorders of pericardium
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)
endocardial disorders
endocarditis: inflammation of endocardium
subacute bacterial endocarditis (SBE) (bacterial infection)
*valvular vegetations form and damage valve function
prevention: pre-procedural antibiotic prophylaxis
Rheumatic heart disease
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
valular disorders
valvular stenosis (narrowing)
valvular insufficiency (failure to close completely)
*aka regurgitation or incometent
aortic valve disorders
aortic stenosis
aortic insufficiency (regurgitation)
mitral valve disorder
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
heart disease in infants and children
congenital cardiac defects
kawasami syndrome
Covid-19 related “multisystem inflammatory disorder in children” (MIS-C)
congenital cardiac defects
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
3 fetal shunts
Ductus arteriosus:
*connects aorta and pulmonary artery
Foramen ovale:
*connects right and left atria
Ductus venosus:
*shunts blood across the liver
congenital cardiac defects
1)defects with increased pulmonary blood flow
intro
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
congenital cardiac defects
1)defects with increased pulmonary blood flow
Patent ductus arteriosus (PDA)
left-to-right shunt from aorta to PA thru ductus arteriosus
(ex of oxygenated blood being pushed into right side increasing pulmonary blood flow)
congenital cardiac defects
1)defects with increased pulmonary blood flow
atrial septal defect (ASD)
ventricular septal defect (VSD)
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)
congenital cardiac defects
2)defects with decreased pulmonary blood flow
intro
blood flow from right side of heart to lungs is diminished or obstructed
the actual cardiac defect is what causes cuyanosis
congenital cardiac defects
2)defects with decreased pulmonary blood flow
examples
pulmonic stenosis (narrowing of pulmonary valve)
pulmonic atresia (the valve has no opening)
tetralogy of fallot (explained later)
congenital cardiac defects
2)defects with decreased pulmonary blood flow
Tetralogy of fallot (explained)
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”
congenital cardiac defects
3) defects with mixed effects on blood flow
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
congenital cardiac defects
4) defects with decreased systemic blood flow
intro
interference with outflow of blood from the left heart, which decreases systemic perfusion
will have cyanosis if the outflow is decreased enough
congenital cardiac defects
4) defects with decreased systemic blood flow
Coarctation of the Aorta
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)
congenital cardiac defects
4) defects with decreased systemic blood flow
Aortic stenosis
narrowing at the aortic valve
due to congentially bicuspid aortic valve
no shunting of blood (obstructed outflow)
congenital cardiac defects
4) defects with decreased systemic blood flow
functionally single-ventricle anatomy
aka hypoplastic left heart
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
heart disease in infants and children
Kawasaki syndrome
acute vasculitis (inflammation of BVs)
children under 5 y/o
caused by an immune response
begins with small vessels
heart disease in infants and children
Kawasaki syndrome
inital stages
what vasculitis of coronary arteries can cause
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
Heart failure
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
compensatory response to HF
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
natriuretic factors released by heart
2 types
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
BNP and ANP (natriuretic factors)
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
classifications of HF
Right vs left sided failure
systolic vs diastolic dysfunction
high output vs low output HF
Right sided vs left sided HF
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)
pulmonary edema in left HF
left HF causes backflow into pulmonary vasculature
leades to increased capillary hydrostatic pressure
*leads to pulmonary edema
systolic vs diastolic dysfunction
systolic dysfunction (ejection)
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
Systolic vs diastolic dysfunction
diastolic dysfunction (filling)
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
High output vs low output
High output HF
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
High output vs low output
Low output HF
any cardiac disorder in which impaired cardiac pumping ability leads to low cardiac output
clinical manifestations of HF
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
circulatory failure (shock)
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)
shock exists on a continuum
types of shock
compensated shock
hypotensive shock (decompensated)
irreverible
compensated shock
SNS activation “compensates” and keeps the circulation working temporarily
blood pressure normal
urinary output normal
HR increased
SNS activation present
Hypotensive shock (decompensated)
SNS compensatory mechanisms are failing
BP decrease
urine output decreases
irreversible shock
circulatory failure cannot be reversed
pt will die
what does shock lead to
total body hypoxic-ischemic cellular injury
classifications of shock
cardiogenic shock
hypovolemic shock
obstructive shock
distributive shock
*neurogenic shock
*anaphylactic shock
*septic shock
distributive shock
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
complications of shock
Lactic acidosis
DIC
acute lung injury, acute respiratory distress syndrome
acute kindey injury
decreased blood flow to GI tract
multiple organ dysfunction syndrome (MODS)
complications of shock
lactic acidosis
type of metabolic acidosis
prolonged anaerobic metabolism using only glycolysis leads to lactic acidosis:
*greatly decreased ATP production
complications of shock
DIC
unneeded clots and using up clot factor
complications of shock
acute kidney injury
decreased renal blood flow in shock
*leads to renal isnchemia and injury
complications of shock
gI
decreased GI perfusion = decreased mucus production and SNS response
cause:
*gastric stress ulcers
complications of shock
multiple organ dysfunction syndrome (MODS)
circulatory failure (shock)—>
widespread hpoxic-ischemic cellular damage—>
multisystem organ failure
risk for death
