heart part 2 Flashcards by Brendon Allen

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)

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endocardial disorders

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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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

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valular disorders

valvular stenosis (narrowing)

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

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aortic valve disorders

aortic stenosis

aortic insufficiency (regurgitation)

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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

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heart disease in infants and children

congenital cardiac defects

kawasami syndrome

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

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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

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3 fetal shunts

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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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

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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)

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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)

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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

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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)

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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”

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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

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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

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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)

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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)

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congenital cardiac defects

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

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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

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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

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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

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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

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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

heart part 2 Flashcards

(48 cards)