Cardiac Flashcards

Question

L sided HF forward effect

Answer 1

Decreased cardiac output causes decreased tissue perfusion, which will activate RAAS in the kidneys This causes increased BP, fluid retention, and vasoconstriction, which further increases the left ventricular preload and thus the backwards pooling of blood into the atria and pulmonary system. (the forward effect ends up contributing to the backward effect)

Answer 2

- Pulmonary congestion - Dyspnea on exertion - Orthopnea - Cough - Paroxysmal (sudden) nocturnal dyspnea - Cyanosis - Basilar crackles

Answer 3

- Decreased perfusion> - Fatigue - Oliguria - Increased HR - Faint pulses - Restlessness, Confusion, Anxiety (poor perfusion to brain)

Answer 4

- Most common cause of right sided HF is left sided HF: When there is congestion in the lungs, the right side of the heart has to work harder due to the increased pressure. This can cause hypertrophy, which causes right sided HF. - Cor pulmonale also can cause right sided HF - Can be caused by cardiac cause like MI but this is less common

Answer 5

○ Hepatomegaly ○ Ascites ○ Splenomegaly ○ Anorexia ○ Subcut edema ○ JVD - Renal congestion

Answer 6

Same as L sided forward effects

Answer 7

Fluid retention Respiratory compromise Renal insufficiency Decreased GI function Arrhythmias Thrombi and emboli Neuro impairment/fatigue/weakness Cyanosis Sudden cardiac death

Answer 8

Atrial depolarization

Answer 9

Ventricular depolarization

Answer 10

Ventricular repolarization

Answer 11

EKG finds conduction issues, echocardiogram finds structural issues

Answer 12

Tricuspid and pulmonary

Answer 13

Aortic and mitral

Answer 14

Aging Calcification Rheumatic heart disease Rheumatoid arthritis SLE (Lupus) Congenital issues Systemic inflammation Chordae injury (the chords that control the valves)

Answer 15

LV works harder to pump blood to the body as some of it doesn't go into the aorta Leads to LA and LV hypertrophy and L sided failure Slow/abrupt onset Systolic murmur Radial pulse may have a pronounced upstroke

Answer 16

Blood will start backing up into the pulmonary vein, causing an increase in pulmonary vascular resistance (PVR) This leads to RV hypertrophy and R sided heart failure as the RV is pumping against the increasing PVR R sided HF impacts the SA and AV nodes leading to dysrhythmias like A-fib The static blood may clot and create emboli Pulmonary congestion Fatigue, weakness Low pitched diastolic murmur with an opening snap

Answer 17

LV has to work harder and hypertrophies Leads to ischemic angina (pain in the heart from lack of O2 to heart) Syncope from lack of perfusion L sided HF This condition can lead to someone suddenly dying because the valve can suddenly cut off all blood flow, causing zero perfusion to tissues Systolic murmur Weak upstroke on radial pulse

Answer 18

Increases pressure in the LV and makes LV work harder LV hypertrophy & failure Dyspnea, pulmonary edema, arrhythmias Widening pulse pressure (difference b/w systolic and diastolic) Tachycardia, pounding heart, pulsing carotids, head bob on systole Diastolic murmur

Answer 19

Oxygenated blood from placenta through inferior vena cava to RA Deoxygenated blood from body through superior vena cava to RA From RA most blood goes through open foramen ovale to LA & some of it through tricuspid valve to RV From RV minimal blood goes through pulmonary arteries to lungs (lots of pressure in lungs d/t them not expanding), most goes through open ductus arteriosus to aorta Systemic vascular pressure (SVR) is pretty low because it is not a closed system--connected to umbilical arteries ○ At birth when the cord is clamped the SVR goes up dramatically In a fetus the right side of the heart has a higher pressure than the left After birth, the pressure on the left side overtakes the pressure on the right, which closes the foramen ovale and ductus arteriosus

Answer 20

Acyanotic: Oxygenated blood is getting over to the R side of the heart directly Cyanotic: Deoxygenated blood is leaving the R side and going over to the L side

Answer 21

The foramen ovale did not close Initially, L -> R sided shunt causing oxygenated blood to pour into RA - Acyanotic Leading to more blood in RA and RV, causing the RV to pump harder RV hypertrophy, pulmonary HTN Eventually, RV hypertrophy increases RA pressure, causing a R -> L shunt - Cyanotic

Answer 22

There is a septum between the ventricles that should close off early in fetal development If it doesn't, it will cause a L -> R shunt from LV to RV (Acyanotic) RV is getting too much blood and starts to hypertrophy, and eventually reverses the shunt from R -> L (Cyanotic)

Answer 23

Oxygenated blood spills out of the aorta and back into the pulmonary artery to the right side of the heart L -> R shunt Right side has to fight harder to get blood to the lungs against the flow spilling in from the aorta > RV hypertrophy Once it is hypertrophied enough the flow reverses and the deoxygenated blood is going into the aorta in a R -> L shunt. Increased cardiac workload can then lead to LV failure Harsh, grinding systolic murmur Systolic thrill can be felt

Answer 24

Preductal (before ductus arteriosus) (more severe) ○ Blood backs up, ○ more blood to upper body and less to lower body ○ Aortic regurgitation ○ Intracranial hemorrhage ○ Aortic rupture Postductal (less severe) ○ more blood to upper body and less to lower body - Ductus arteriosus may open back up

Answer 25

Four defects: pulmonary valve stenosis, RV hypertrophy, ventricular septal defect, overriding aorta Starts as R -> L shunt The strong RV pumps blood that ricochets off the stenosed pulmonary valve and the septal defect, into the aorta Severity depends on level of stenosis Leads to infective endocarditis and polycythemia

Answer 26

The great vessels switch place so the aorta is connected to the RV and the pulmonary artery to the LV Leads to deoxygenated blood that never gets oxygenated, and oxygenated blood that never reaches the body Can be lethal immediately upon birth If baby is to survive there must be a septal defect that allows the blood to mix until it can be fixed by surgery

Answer 27

○ Genetics (most common cause) ○ Alcohol use ○ Pregnancy ○ Post-viral infection in heart - Reaction to chemo or radiation

Answer 28

Ventricles dilate -> increased cardiac workload -> myocardium degenerates and is replaced by fibrous tissue -> contractile failure -> slowly progressive CHF ○ May lead to emboli d/t static blood

Answer 29

Same as CHF

Answer 30

○ Most likely genetic Most common cause of death in young athletes

Answer 31

Sudden death, dyspnea, angina, can be asymptomatic, can lead to CVA, HF, a-fib "You may go at any time, you may live until your 90"

Answer 32

○ Diseases that increase fibrosis ○ Genetics ○ Virus ○ Malnutrition ○ Autoimmune - Radiation

Answer 33

Exercise intolerance, dyspnea, paroxysmal noctural dyspnea, orthopnea, weakness, ascites, peripheral edema, hepatomegaly

Answer 34

○ Infection ○ Immune response ○ Uremia (nitrogen compounds build up in the blood) ○ Cardiac surgery ○ Neoplasm (cancer of the heart) ○ Trauma Radiation

Answer 35

○ Sharp, abrupt chest pain that radiates to back, neck abdomen or side. Worsens with deep breathing, cough, swallowing, position change. Relieved when sitting up and forward. Dysphagia, fever, incr WBC, malaise, incr HR, friction rub, anxiety

Answer 36

○ CHF, hypoproteinemia (serous fluid), ○ blunt chest trauma, CPR (serosanguinous fluid), ○ obstructed lymph drainage (chylous fluid), penetrating trauma to heart (blood)

Answer 37

○ Effusion ○ Infection ○ Cancer ○ Tension pneumothorax ○ Trauma MI

Answer 38

○ Reduced stroke volume, increased HR, venous congestion, distended neck veins, pulsus paradoxus, dull chest pain, EKC and chest Xray changes Gradual, or rapid and deadly

Answer 39

○ Pathogens clump onto surface, get enmeshed in fibrin, form vegetations and block valves, form thrombi and emboli. Vegetations become fibrosed and calcified, valves can erode

Answer 40

Rheumatic heart disease, IV drug use, CHD, prosthetic valves, implanted cardiac defibrillator (ICD), pacemakers, immunosuppressed

Answer 41

○ Abrupt onset, serious symptoms, virulent pathogen ○ Fever, chills, murmur, splinter hemorrhages in fingernails Quickly turns to myocardial abscess, renal disease, emboli

Answer 42

○ Insidious onset, vague symptoms, less virulent Weight loss, fatigue, "flu", low grade fever

Answer 43

- Group A throat Strep infection -> rheumatic fever -> rheumatic heart disease Some people react to Strep A by directing antibodies against their own tissues as well as against the strep. Cross reactivity occurs between strep antigens and body tissues.

Answer 44

- Acute phase: Infection, sore throat, inflammation of CT in heart, blood vessels, joints and subcut tissue. - Recurrent phase: Heart inflames, carditis, valves swell and erode, platelets and fibrin clump on valve Chronic phase: Permanent valve deformity (can show up after 10 years from initial infection)