Chap 19 Disorders of Cardiac Function Flashcards
Pericarditis
acute = ?
Causes:
Acute =
Pericarditis manifestations:
- Decreased CO
Pericardial friction rub- during auscultation from inflamed pericardial surfaces: tissue on tissue - Chest pain
Precordial- (space between parietal and visceral pericardium. Right by heart ). Start here and radiate to neck, back ,abd or side.
–Abrupt onset, sharp, radiates
–Scapula pain
–Increases with deep breath or cough
–Relief when leaning forward- takes the pressure of your chest off it. Feels much better - ECG changes
- Tx: depend on cause: antibiotics, antiinflams
What is Dressler Syndrome?
Post heart attack. Pericarditis a week or two after.
Pericardial Effusion:
- Accumulation of fluid in the pericardial cavity/space— compresses heart chambers.
- Higher fluid=higher compression.
- Small amount of fluid and may be symptomatic
Pericardial Effusion
Causes:
Causes:
- Inflammation of -pericardium
- Infection elsewhere, can end up in pericardium
- Neoplasms
- Cardiac surgery
- Trauma
- *Symptoms depend on how fast and amount of fluid build-up
cardiac tamponade:
- -Compression d/t fluid or blood in pericardial sac. EMERGEMCY.
- -Build up of blood of other fluid in pericardial sac puts pressure in the heart, which may prevent it from pumping effectively.
Cardiac Tamponade
Causes:
Causes: >Trauma >Myocardial rupture post MI >Cardiac surgery >Aortic dissection: inner wall of the aorta, the large blood vessel branching off the heart, tears. Blood surges through the tear, causing the inner and middle layers of the aorta to separate (dissect).
Cardiac Manifestations:
Dependent on amount and rapidity
- Limits stroke volume and CO = low SBP
>CNS: change in mentation
>Resp: dyspnea, tachypnea
>CVS: chest pain (from coronary arteries not filling), tachycardia - Elevated central venous pressure & jugular venous pressure
- Circulatory shock- not getting enough blood to organs
Tamponade Diagnosis:
- Muffled heart sounds
- Pulsus paradoxus- ***
- ->10 mmHg systolic fall with respiration
- -exaggeration of normal variation in systolic BP - ECG- see decreased voltage (electrocardiogram) reviles nonspecific T wave changes and low QRS voltage. Hearts electrical activity
- Echocardiogram- ultrasound of heart. Provides pictures of the structures.
- /6. CT, MRI
Tamponade Treatment:
depends on progression.
-In large: Pericardiocentesis (removal of fluid) tx of choice. With needle to draw fluid away from heart (release the pressure)
-in sml effusion- NSAIDS, colchicine or corticosteroids to min fluid accumulation.
Coronary Artery Disease =
Heart Disease.
Heart disease caused by impaired flow to coronary arteries
What assists coronary artery flow?
- -Endothelial cells lining arteries
- -Diastolic pressure in aorta
- -Time is diastole to fill coronary arteries
What impairs coronary artery flow?
Atherosclerosis
Non-Modifiable Risks for CAD
>Sex/Gender --Post-menopausal women >Age >Ethnicity >Genetics
Modifiable Risks for CAD
- -Diet
- -Exercise
- -Smoking
- -HTN
- -Hyperlipidemia
- -DM
- -obesity
- -Stress
Stable Angina
- Pain/pressure d/t transient ischemia
- Precordial/substernal
- -Possible radiation
- -Possible epigastric discomfort - Often a FIXED coronary narrowing
- Occurs with exercise/exertion/cold/emotions
Stable Angina relieved with?
rest & nitroglycerine**
- -relax (widen) bld vessels. Allows bld to flow more easily, reducing workload and amnt of O2 needed by heart. Dilate coronary arteries
- -You can have ASCD/CAD without angina!!!
Variant/Prinzmetal Angina
> d/t spasms of coronary artery
Cause is unclear
Often @ night when person is at rest. Midnight-early morn
Variable symptoms
Treatment is dependent on findings of investigative diagnostics
Silent MI:
atypical symptoms and more likely in the elderly.
Silent MI diagnosis:
causes:
Manifestations:
ECG -show the changes that happened to the heart during the silent MI
cause: often unsure.
>? Less myocardium involved
>? Neuropathy
Manifest:
Hypotension, low body temp, vague complications of discomfort, mild diaphoresis, stroke-like symp, dizzy, sensorium changes
Treatment is dependent on findings of investigative diagnostics
Acute Coronary Syndrome
two types:
-classified based on presence or absence of ST-segment.
> Risk is classified based on ECG changes
- Unstable Angina/Non ST-segment elevation Myocardial Infarction (non-STEMI)
- ST-segment elevation MI (STEMI)All caused by an imbalance in myocardial
oxygen supply and demand
Potential Causes of ACS
> Unstable plaque, rupturing to form a clot
Thin fibrous cap with fatty core is most unstable
> Coronary vasospasm
Atherosclerotic narrowing (progressive)
Inflammation/infection
> Secondary causes
- -Anemia
- -Fever
- -Hypoxemia
- -Surgery!!!!!
Unstable Angina/Non-ST MI
Typical pattern of Manifestations:
Typical Pattern of Manifestations
> With pre-diagnosis of “Stable Angina”
More severe or more often than usual
Unstable Angina/Non-ST M
Course of pain has 3 features:
- Occurs at rest (or minimal exertion) and Lasts more than 20 minutes
- Severe and described as flank pain and new onset
- More severe, prolonged and frequent than any prior experience
If biomarkers are elevated = non-STEMI
High risk of STEMI
Serum biomarkers for ACS are:
> Cardiac specific troponin I and troponin T, myoglobin and creatine kinase.
> As the myocardial cells become necrotic, their intracellular contents begin to diffuse into the surrounding interstitium and then into the blood
ST Elevation MI
Typical pattern of Manifestations:
Heart attack
Ischemic death of myocardial tissue
Typical Pattern of Manifestations: >Crushing/constricting pain; usually abrupt --Substernal with radiation to left arm, jaw, neck --Epigastric distress/nausea --Palpitations --Cool, clammy skin --SOB --Anxiety
Unrelieved by rest/nitro
ST Elevation MI
Cardiac muscle wall ischemia & necrosis
> Subendocardial
> Transmural (across entire wall or organ or vessel). Full thickness of the vent wall and common when there is obstruction of a single artery = Q wave
> “Stunned” myocardium- some myocardium can recover when blood flow is re-established but critical abnormalities in biochemical function may persist. Person might have areas of dysfunctional myocardium.
Cell death in 15-20 minutes
Early perfusion and revascularization can prevent necrosis!!!
Myocardial Ischemia/Necrosis result in
- Decreased contractile force
- -Decreased CO
- -Decreased coronary artery perfusion
- -Increased pulmonary vasculature pressure - Interruption of conduction
- -Dysrhythmia
Diagnosis also based on Serum Biomarkers
- Troponin-
- Rise within 2-3 hrs; remains 7-10 days
2.Myoglobin-
Rises within 1 hr, peaks at 4 hrs Also from skeletal muscle damage
- Creatine Kinase MB (CK-MB)-
- -Peaks at 4-6 hrs; gone in 2-3 days
- -Specific to cardiac muscle
Acute MI Treatment
- Oxygen
- Pain relief
- Reperfusion
>Fibrionolytics- clot busting drugs. If given in time, lessen the damage
>Percutaneous transluminal coronary angioplasty (PTCA)- through femoral/inguinal artery to open blocked artery d/t atherosclerosis. Blow up balloon and put a stent
>Stents - Coronary Artery Bypass Grafting (CABG)
Complication of an Acute MI
> Arrhythmias – most common cause of sudden death
Reinfarction- repeat infarction after initial infarct
Heart failure
Pericarditis
Embolic CVA or Pulmonary embolus
Valve deformities
Septal rupture
LV wall aneurysms/rupture
Cardiogenic shock- cell death from O2 and nutrient starvation
Dressler syndrome- post MI, consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion
Cardiomyopathies
Cardio = heart Myo = muscle Pathy = disorder/syndrome
“Idiopathic cardiomyopathy”- cause unknown
> Muscle disorders
- -Mechanical (HF)
- -Electrical (arrhythmias)
> Primary- genetic or acquired
> Secondary- presence of multisystem disorder. Other myocardial disorder. Drugs, DM, muscular dystrophy, autoimmune disorders.
Hypertrophic Cardiomyopathy (HCM)
*Leading cause of sudden cardiac death in young adults
> Unexplained genetic ventricular septal thickening
- -Poor diastolic filling
- -LV outflow obstruction
- -Left ventricular hypertrophy LVF
- -Disruption of normal conduction pathways
HCM Manifestations
> Variable- may progress to end stage heart failure
Decreased stroke volume d/t impaired diastolic filling
–Dyspnea,
–chest pain,
–syncope
Atrial fibrillation
Lethal ventricular arrhythmias
Endocarditis
Any infection of inner lining of heart
> Usually staphylococcus aureus
Vegetative (grows like a veg) leisions form on heart valves
Involvement of mitral & aortic valves most common
Acute: relatively healthy individual
Sub-acute/chronic: h/o valve abnormalities
Endocarditis Risk Factors:
- Infection elsewhere
- IV drug abuse, dental surgery
- family hx
- Valve prolapse (sudden or congenital)
Endocarditis
Manifestations:
Complications:
Manifestations – effects aortic and mitral valves
- -S&S of systemic infection, fever-chills
- -Heart sounds changes
- -Symptoms related to emboli
Complications
- -Emboli (lung, brain, renal)
- -Valve dysfunction
- -Arrhythmias
Rheumatic Heart Disease
- Caused by rheumatic fever
- -Which occurs after streptococcal pharyngitis
- -One or all layers
- -Aschoff bodies- inflam lesions within the connective tissue elements of the heart, bld vessels, joints and SC tissue - Immunological response but pathogenesis unclear
- Acute, chronic, or recurrent
Rheumatic Heart Disease
Acute phase:
Diagnosis:
Treatment:
Acute phase = pancarditis. Involves all 3 layers of heart (endo, myo, pericardium)
Diagnosis:
- -Evidence of GAS infection
- -Elevated WBC, ESR, CRP
- -Echocardiogram, Ultrasound
Treatment:
Antibiotics, prevention of complications
Valvular Disorders
causes:
- -Congenital
- -Trauma
- -Ischemic damage
- -Degenerative changes
- -Inflammation
Valvular Disorders
Diagnosis:
- -Auscultation
- -Doppler Echo
- -Ultrasound
Valvular Disorders
Treatment:
- -Preventative
- -APA
- -Symptoms
- -Percutaneous valvuloplasty
- -Surgery- repair or replacement
If an aortic valve is regurgitant, you will hear a murmur of blood leaking back through to left vent when
during diastole
this will cause a heart murmur
When Will You Hear Murmurs?
If a valve is stenotic, you will hear a murmur of blood shooting through the incomplete opening of the hardened valve
Mitral Valve Stenosis
> Fibrous, stiff tissue, often causing chordae tendinae to shorten
> Incomplete opening of mitral valve obstructs blood flow- left atrium distension and impaired filling of left vent
Mitral Valve Stenosis
Causes:
> RF- rheumatic fever (fever from inflam and pain in joints)
>Congenital
Mitral Valve Stenosis
Manifestations:
Depends on severity of obstruction and related to elevation in left atrial pressure and pulm congestinon, decreased CO, impaired L vent filling, L atrial enlargement, atrial arrhythmias and mural thrombi
Mitral Valve Stenosis
Complications:
Pulm congestion, paroxysmal dyspnea and orthopenea,
Palpations, chest pain, weakness, fatigue
Mitral Valve Regurgitation (MVR)
and causes:
> Incomplete closing
Some blood returns to LA during systole_
Causes:
- -RHD (rheumatic heart disease)
- -Chordae tendineae or papillary muscle rupture
- -LVH dilates orifice
- -Mitral valve prolapse (floppy mitral valve syndrome)
Mitral Valve Regurgitation
Manifestations:
> Slow process = compensation
Pulmonary congestion
Pansystolic heart murmur
L Atrial and LV hypertrophy
Mitral Valve Regurgitation
complications:
- -can be well tolerated, symptoms 6-10 yrs after diagnosis
- -left vent becomes impaired
- -forward stroke vol decresses
- -left atrial pressure increases
- -develop pulm congestion
Mitral Valve Prolapse
associated with:
Manifestations:
Complications:
> Leaflets enlarge, become floppy
Associated with:
Marfan’s sydrome & Osteogensis imperfecta
Manifestations:
Often asymptomatic
Minority have chest pain-mimic angina, dyspnea, fatigue, anxiety, palpations, and light-headedness
Complications:
- mainly asymptomatic
- some ppl have chest pain mimicking angina
- -dyspnea, fatigue, anxiety, palpitations, and light-headness
Aortic Valve Stenosis
Narrowing causing resistance to ejection from vent into aorta. L vent wall becomes thicker
Slow progression = compensation
Aortic Valve Stenosis
causes:
Congenital or acquired
Male, active inflammation
Aortic Valve Stenosis
Manifestations:
- -From auscultate- loud systolic ejection murmur or single paradoxically split second heart sound.
- -Then angina, syncope, HF develop
Aortic Valve Regurgitation
Causes:
Scarring of leaflet and/or enlarged orifice
Blood flow back into left ventricle during diastole
Causes:
RHD, ideopathic aortic dilation, congenital, endocarditis, Marfan’s, HTN, trauma
Chronic Aortic Regurgitation
Manifestations:
Slow progression = compensation
LV enlarges but works harder
Manifestations:
>high-pitched or blowing sound over valve
>Intra-aterial pulse pressure
>Korotkoff sounds persist to zero!
>Tachycardia or palpations, head pounding, premature vent contractions.
>Eventually orthopnea, dyspnea, paroxysmal nocturnal dyspnea
Acute Aortic Regurgitation
Causes:
Manifestations:
Causes:
>Acute endocarditis
>Trauma
>Aortic dissection
Manifestations:
>Too quick for compensation!
>Extreme rise in volume to left vent.
Dysrhythmias = lethal
Patent Ductus Arteriosus
Manifestations:
Persistent delay > 3 months
- -Normally closes @ 24-72hrs
- -Delay if premature
Manifestations:
Dependent on size
–continuous runoff from the of aortic blood to pulm artery.
– a large PD, runoff continuous resulting in increased pulm blood flow, pulm congestion and increased resistance against which the right side of the heart must pump
Atrial Septal Defects
> Non-closure of foramen ovale
Often asymptomatic until teenage
Manifestations:
Increased pulmonary pressures
Ventricular Septal Defects
Most common congenital heart defect
Cause:
Incomplete separation of ventricles during development invitro
1/3 close spontaneously
Manifestations dependent on size
Pulmonary Stenosis
Obstruction of blood flow from RV
Causes:
- -Pulmonary valve lesions
- -Pulmonary artery lesions
- -Combination
10% of all congenital cardiac disease
Often associated with other patho
Tetralogy of Fallot
Most common cyanotic congenital heart defect
- Pulmonic outflow channel narrowing (valve)
- RV hypertrophy
- Ventricular septal defect- opening between L and R septum
- Displacement of aorta over vent septal defect
Tetralogy of Falot
Manifestations:
Treatment:
Manifestations:
Cyanosis with increased oxygen demands
Treatment:
Knee-chest position
Surgery
Transposition of the Great Arteries
RV empties into aorta
LV empties into pulmonary arteries
Risk Factors:
Mothers with diabetes
Boys > girls
Manifestations:
–cyanosis most common
Coarctation of the Aorta
Associated with other congenital lesions
Manifestations:
–disparity in pulsations and BPs in arms and legs
