TEST 3: Cardiovascular Flashcards

Question

Really interesting sh** on alpha receptors in the heart (P. 1033)

Answer 1

-Alpha receptors cause smooth muscle contractions, thus VASOCONSTRICTION -Subtype of alpha 2 receptors effect is to inhibit more release of NorEpi to prevent excessive elevated BP

Answer 2

-The volume and pressure inside the ventricle at the end of diastole (blood returning to the heart from systemic circulation) -Determined by 2 primary factors: 1. The amount of blood left in the ventricle after systole 2. The amount of venous blood returning total be ventricle during diastole -Is estimated by your right atrial pressure (CVP) and the pulmonary artery wedge pressure for the left side -Gives you a sense of someone’s volume status -In HF, elevated preload can cause decreased SV

Answer 3

-The pressure the heart must pump against to get the blood out of the ventricle; the load the muscle has to move during contraction. -Mean arterial pressure (MAP) is a good indicator -Increased pressure is usually the result of increased SVR *In those with HTN, the increased SVR means that the afterload is chronically elevated (which makes the ventricular work harder and causes hypertrophy of myocardium* -Changes in afterload can also be the result of aortic valvular disease

Answer 4

-Lattice of cells with myofibrils (contraction units), a nucleus, mitochondria, internal membrane (sarcoplasmic reticulum), cytoplasm (sarcoplasm), and a plasma membrane (sarcolemma) that encloses the cell. -Lattice is composed of: ACTIN: thin protein filament, light band, or I band (isotropic) MYOSIN: thick protein filament, dark bands or A bands (anisotropic), small projections from sides form cross bridges -Z discs connect myofibrils (connect actin and myosin together) -Sarcomeres: portion of the myofibril between 2 Z-disks

Answer 5

-Has 3 protein components with a helix backbone Two types: 1. F actin (when activated, causes contraction of the heart) 2. G actin (active site for cross bridges with myosin)

Answer 6

-Is a relaxing molecule -White bands that wrap around the actin -the reason that the heart isn’t continually contracting -Blocks F actin strands, causing cardiac muscle to relax

Answer 7

- TROPONIN (relaxing protein) -3 types that attach to tropomyosin 1. Troponin I : affinity for actin (inhibits ATPase of actomyosin— 2. Troponin T: affinity for tropomyosin (aids in binding of the Troponin complex to actin and tropomyosin) 3. Troponin C: affinity for calcium (contains binding sites for calcium ions involved in contraction) Summary: when it’s time to contract, the influx of calcium causes the affinity of tropomyosin to bind with actin and activate it, causing heart contraction. When it’s time to relax, the calcium has left the cell, Troponin T will cause the myosin to block the F actin strand, causing relaxation of the heart. GEM *Troponin I and T are released into the bloodstream during myocardial injury *

Answer 8

-Made of a tail (2 polypeptide chains wrapped in spiral forming double helix) and a head (globular polypeptide with associated light chain proteins) -Myosin filaments are individual myosin molecules bundled together to form the body where the cross bridge hangs (myosin heads moving is what helps move the cardiac muscle and is what drives the physical movement of cardiac muscle contraction) *think of a rowboat with oars* -Cross bridge: flexible hinge and arm connected to myosin heads -ATPase: enzyme in myosin head for energy production (ie what you need to be a en to move the cardiac cell)

Answer 9

-At rest, active sites on actin filaments are blocked by TROPONIN and tropomyosin complexes (preventing myosin attachment to actin) -During action potential, as calcium enters the cell, Troponin C binds with ten calcium moves the complexes off of the active actin site, so actin and myosin can interact (which allows for contraction)

Answer 10

Aka the “Walk Along Theory” -After the head of the myosin cross bridge can attach to the actin filaments at the active site—> intermolecular forces cause the myosin head to tilt forward on a flexible hinge and drag the actin filament with it (power stroke) —> myosin head breaks away and then interacts with the next active actin site-> the Z disc pulls filaments together at the sarcomeres —> this produces muscle contraction -ATP is needed for this process

Answer 11

-An electrical stimulation that causes a change in charge across a cell membrane

Answer 12

-Potassium is high inside the membrane and low outside the membrane, so when it diffuses out of the cell you get a NEGATIVE INTRACELLULAR CHARGE -Sodium is low inside the membrane and high outside the membrane, so when it diffuses into the cell you get a POSITIVE INTRACELLULAR CHARGE

Answer 13

-At rest, negative intracellular charge -Depolarization: sodium leaks into cell and decreases the intracellular negativity, this opens the voltage gated ion channel to generate more positive ions (NA/CA) entry -Inside of the cell becomes more positive and an action potential is triggered -Repolarization: when potassium rapidly diffuses out of the cell and the intracellular negativity increase to resting state

Answer 14

Phase 0: Depolarization (resting phase, K inside cell, NA outside cell) *electrical stimulus* Phase 1: Early repolarization (rapid Na entering the cell; triggers contraction) Phase 2: Plateau (aka repolarization; Ca and Na slowly enter the cell) Phase 3: K moves out of the cell trying to get back to depolarization Phase 4: Return to resting potential (K is intracellular again and Na is extracellular) *GEM* Refractory period= refractory to additional cardiac stimulation BUT strong excitatory signal may generate a depolarization during this period

Answer 15

-Network of excitatory/ conductive fibers that cause contraction in heart -SA node=site of automaticity (due to the slow leak of Na ions intracellularly that slowly increase intracellular charge until action potential is fired) -electrical current generated releases calcium from the muscle fibers to cause myosin/ actin to contract

Answer 16

-End-diastolic volume: amount of blood in a heart chamber AFTER filling, BEFORE systole -End-systolic volume: amount of blood that REMAINS in the chamber after systole (when it contracts) -Stroke volume: amount of blood ejected with each contraction of the heart (volume of blood ejected during systole) -Ejection fraction: percent of blood in chamber that is ejected with each systole (% of total and diastolic volume ejected per beat); is increased by factors that increase contractility -Cardiac output: the amount of blood pumped into the aorta each minute (HR x SV)

Answer 17

-Abnormal signaling from atria (usually not SA node) that causes atria to contract much quicker than normal -P rate > 300, no P-R interval, QRS variable, rhythm irregular -Effect: decreased cardiac filling time—> fatigue, dizziness, dyspnea, irregular pulse -Associated with things that remodel the atria: HF, ischemic heart disease, HTN, obesity, OSA, *rheumatic heart disease* -Untreated risk = pooling of blood that doesn’t get ejected—> risk for thrombosis/ stroke

Answer 18

-Early beats without P waves -Effects: decreased CO from loss of atrial contribution to preload —> feel fluttering, pounding palpitations -Associates with: abnormal potassium, HYPERcalcemia, hypoxia, aging, anesthesia induction, caffeine, tobacco, drug use, exercise GEM *changes refractory period*

Answer 19

-Made up of lipids, phospholipids, cholesterol, and triglycerides -Their role is to manufacture and repair plasma membranes and the cholesterol needed for bile salts and steroid hormones -We get them from dietary fat packaged in the small intestines, they are transported as chylomicrons into the liver where they are processed into: 1. Very low density lipoproteins (triglycerides) 2. Low density lipoproteins (LDL) BAD 3. High density lipoproteins (HDL) GOOD

Answer 20

-An abnormal concentration of serum lipoproteins (aka dyslipoproteinemia) -Categorized under cholesterol (total level of) : -Very low density lipoprotein (triglycerides): strong predictor of risk for coronary events -Low density lipoprotein (LDL): is responsible for the delivery of cholesterol to the tissues, but is a strong indicator of coronary risk (but in the context of other factors, ie age, DM, CKD) -High density lipoprotein (HDL): is responsible for “reverse cholesterol transport” which returns excess cholesterol from the tissues to the liver to be processed into bile, is “protective” against atherosclerosis— we want high levels of HDL so excess cholesterol can be removed from the walls of arteries

Answer 21

Primary (familial): -genetics results in abnormal lipid metabolism and/ or abnormal lipid receptors Secondary: -Lifestyle (smoking, obesity, diet, sedentary) -Comorbities: HTN, DM, renal nephrosis, inflammation, hypothyroidism, and pancreatitis -Meds: diuretics, beta-blockers, steroids, antiretrovirals -Other: air pollution, radiation, microbiome

Answer 22

-A chronic inflammatory condition that is characterized by the thickening and hardening of the vessel wall that results in damage to arterial walls and plaque formation -Is a form of of arteriosclerosis that is caused by the accumulation of lipid laden macrophages, which leads to the plaque formation -Plaque (atheroma) = a lesion in arteries filled with lipids and macrophages (can be stable to complicated) -Can affect the vascular system throughout the body results in ischemic syndromes that vary in severity and manifestations

Answer 23

Begins with injury to the endothelium-> The injured endothelial cells then become inflamed (which then they cannot make normal amounts of antithrombotic and vasodilating cytokines and express the adhesion molecules that bind macrophages and other inflammatory responses) and trigger the inflammatory response—> monocytes and platelets go to site of injury

Answer 24

2. LDL enters the initial layer of the vessel —> inflammation that results in oxidative stress/ free radicals and macrophage activation —> LDL gets engulfed = results in foam cells (cells that form when macrophages ingest and accumulate lipids, and play a large role in the development of plaques)—> when foam cells accumulate= fatty streak (that produce more oxygen free radicals and secrete more inflammatory mediators that further progress the vessel wall damage)

Answer 25

3. Further inflammatory process is triggered in response to fatty streak—> macrophages release growth factors that stimulate smooth muscles to produce collagen and migrate over the fatty streak—> this is what forms that plaque *GEM* This plaque may stay a soft collagen covering over the streak OR it may calcify = Monckebergs atherosclerosis (where plaque calcifies, protrudes into vessel lumen, and obstruct blood flow to tissues) -Usually becomes symptomatic when plaque obstructs 70-80% of the vessel

Answer 26

Complicated lesions (unstable plaque): -Caused by ongoing inflammation, apoptosis of cells in plaque, or plaque hemorrhage (Prone to rupture) -Once a plaque ruptures, the clotting cascade is activated and localized thrombus formation can cause occlusion —> causing ischemia and infarction -Uncomplicated lesion (stable plaque)

Answer 27

-Atherosclerosis of the arteries that perfuse the limbs (particularly lower extremities) -Risk factors: age > 60, African Americans -It doubles the risk for CAD -Typically a slow, gradual process of vessel occlusion -Thus, can have intermittent claudication (pain with ambulation due to arterial blood flow obstruction and exercise related ischemia) -Most have no symptoms until an ischemic event—> severe pain, loss of pulse, color change -Dx: s/s of atherosclerotic disease (ie bruits), seeing a difference in BP in the arm vs the leg, measuring blood flow on US, CT, MRI -Tx: risk factor reduction, vasodilators for symptomatic PAD, anticoagulants (extreme cases cath or surgery)

Answer 28

-Sustained BP > 130/80 -Results from sustained increase in PVR/SVR, an increasing in circulating blood volume and CO, or both. -Primary HTN (95% of cases) caused by the interactions between our genetics and the environment -Secondary: caused by some underlying process that increases PVR or CO: -Renal disease-> RAAS system effected and increases fluid status -Pheochromocytoma (adrenal tumor/non-cancerous)—> stimulates catecholamine release with stress -Pregnancy—> placenta weight, increased fluid volume

Answer 29

-Specific cause not identified -interplay between genetics and environment leads to changes in neurohormones, insulin resistance, dysfunction of natriuretic hormones, and inflammation (combination of all these factors is causing sodium and water to be retained and peripheral vasoconstriction and increased blood volume causing sustained HTN) -how your body deals with HTN: REMODELING (changes to the structure of the vessel walls that results in permanent increases in PVR/SVR -what does this all result in? : Contribute to the development of ischemic heart disease, myocardial hypertrophy, heart failure, CVA

Answer 30

SNS activity —> increased HR + SVR, increased insulin resistance (which caused endothelial dysfunction), vascular remodeling + procoagulant effects (causing narrowing of vessels and vasospasm)—> all lead to HTN

Answer 31

1. Vascular remodeling—> fibrosis of the vessels—> injury to the organs perfumed by those vessels (cardiac muscle, retina, kidneys, brain) 2. Left ventricle hypertrophy—> HF 3. Hypertensive crisis: rapid increase in SBP > 140 —> cerebral arteries can’t regulate blood flow to cerebral capillaries—> cerebral edema—> encephalopathy (associated with pregnancy, cocaine, meth, adrenal tumor, ETOH withdrawal) is a MEDICAL EMERGENCY

Answer 32

-Increased NA—> water retention—> increased blood volume = HTN (Adequate levels of K, mag, ca, can support NA excretion) -Ca is deposited in tunica media and assists with vasoconstriction (increased Ca will increase BP) -Magnesium is a direct vasodilator (increasing magnesium decreases BP)

Answer 33

CAD: -Atherosclerosis of coronary arteries -Diminished blood supply Myocardial Ischemia -Local, temporary oxygen deprivation -Cells live but can’t function normally Acute Coronary Syndromes -Persistent ischemia or complete occlusion of coronary artery -Commonly results in MI

Answer 34

-High prevalence in the US (3-7% of US population over 20 have it -MI: #1 cause of death in men and women (1 death every minute and 20 seconds) -Risk factors: same as atherosclerosis -NON modifiable risk factors: age, male sex, women after menopause, family Hx

Answer 35

1. Plaque partially obstructs—> stable plaque—> stable angina—> possible myocardial ischemia 2. Plaque partially obstructs—> unstable plaque (with rupture or thrombosis)—> acute coronary syndromes—> transient ischemia—> unstable angina 3. Plaque partially obstructs—> unstable plaque (with rupture or thrombosis)—> acute coronary syndromes—> sustained ischemia—> MI—> myocardial inflammation and necrosis (along with stunned and hibernating myocytes, and myocardial remodeling)

Answer 36

-Transient inability of coronary arteries to deliver enough oxygen to the myocardial cells to meet demand (supply and demand mismatch) You can have this when: -Times of increase 02 demand: exercise, tachycardia, HTN, or valve disease -Times of decreased 02 supply: coronary spasm, hypotension, dysrythmia, anemia, hypoxia *GEM* Ischemia begins after 10 SECONDS, cells can survive around 20 MINUTES

Answer 37

Angina: chest pain caused by ischemia -Stable: (something usually stimulates it ie activity) transient pain, caused by accumulation of lactic acid—> ischemic stretching of myocardium—> myocardial nerve fibers are irritated *note* the manifestation of pain here varies as a result of afferent sympathetic fibers that transmit pain and enter the spinal cord from C3-T4 -Unstable (PRINZMETAL): occurs unpredictably (although tends to be at rest) -Vasospasm related to decreased vagal activity, hyperactive SNS, decreased nitric oxide activity, alters calcium channel function —> benign or serious dysryhtmias -Unstable angina CAN be reversible, but does forecast impending MI -Silent ischemia: non chest pain ischemia -Presents with vague symptoms: fatigue, SOB, “feelings of unease” -Happens due to left ventricle sympathetic innervation, DM, post cardiac surgery, mental stress

Answer 38

1. Unstable angina: STILL reversible, related to a superficial plaque erosion—> transient thrombotic vessel occlusion—> vasoconstriction at site of plaque damage -S/S: new onset angina, angina at rest > 20 minutes, increasing severity of angina -EKG: often shows ST depression or T wave inversion that GOES AWAY WHEN PAIN STOPS -NORMAL CARDIAC MARKERS (trop, ck-mb) *GEM* unstable angina is now categorized under the Umbrella of acute coronary syndrome NSTEMI (because it signals that plaques have started to rupture and MI may be soon) 2. Myocardial infarction: prolonged ischemia with irreversible damage to the heart muscle that results from rupture of an unstable plaque in coronary arteries and vessel is thrombosed -Two types: Non-STEMI/ STEMI

Answer 39

-Mechanisms for these is that plaque has been disrupted, clot is formed and ischemia has resulted Non-STEMI: Thrombus breaks up before complete distal tissue necrosis -Presents with ST depression and T wave inversion -Presents with elevated cardiac biomarkers -Intervention promptly needed as dislodged plaque is likely to cause thrombosis elsewhere -STEMI: infarction extends through the myocardium creating severe cardiac dysfunction -ST elevation -Elevated cardiac biomarkers

Answer 40

-Cell injury —> anaerobic metabolism—> increase H ions and lactic acid —> acidosis—> heart failure -Electrolyte disturbances (decreased K, Ca, mag)—> decreased contractility—> release of Catecholamines—> NorEpi (increases serum glucose)—> angiotensin II (vasoconstriction/ fluid retention/ spasm) -Reperfusion injury —> release of toxic oxygen radicals, ca influx, Ph change (cell death)—>inflammatory response—> myocardial tissue injury—> cooling therapies (not much else to do except limit reperfusion injury)

Answer 41

-Myocardial stunning: temporary loss of contractile function, results from prolonged ischemia with loss of contractile function (lasts hours to days) -Myocardial remodeling: myocyte hypertrophy, scarring and loss of function to area distant to infarction (can be limited and reversed with quick restoration of coronary blood flow) -Myocardial repair: degradation of Injured cell—> scar tissue (get decrease contractility, altered LV compliance, decreased SV, decreased EF, increased end diastolic pressure and volume, SA node malfunction

Answer 42

-Cardiac Troponin I: most specific indicator of MI -Elevation detectable 2-4 hour after symptoms onset, repeat at 6-9 hours and 12-24 hours -Estimates infarct size and likelihood of complications -CK-MB and LDH may be elevated -Leukocytosis and elevated CRP—> inflammation -Hyperglycemia

Answer 43

-Dysrythmia -Cardiogenic shock -Pericarditis -Ventircular aneurysm/ rupture -Papillary muscle rupture -Thromboembolism

Answer 44

-Condition where the heart is unable to generate adequate CO either from inadequate perfusion to tissues and/or increased diastolic filling pressure. -Risks: ischemic heart disease, HTN, age, smoking, obesity, DM, renal failure, valve disease, cardiomyopathy, CHD

Answer 45

-Inability of heart to generate adequate CO to perfume tissues -Has reduced EF -EF < 40% Can result from: -Contractility decreased (ex after MI) -increased preload (when contractility decreases, less blood is pumped out, more end diastolic volume, which results in increased preload and dilation of heart) -Increased after load (HTN, which causes increase work on the heart and hypertrophy)

Answer 46

-There becomes a worsening cycle of decreasing contractility, increasing preload, and increasing afterload -Decreasing contractility causes low EF and high LVEDV which increase preload which in turn worsens contractility (Renal failure makes this worse) -Decreasing contractility also decreases renal perfusion and stimulates RAAS, which increases your after load that also worsens contractility (HTN makes this worse)

Answer 47

-Pulmonary congestion despite normal stroke volume and CO -Can occur WITH reduced EF as well -More common in women -Associated with HTN/ hypertrophy Diastolic dysfunction from: -Decreased LV compliance -Abnormal relaxation of LV (lusitropy), that’s associated with changes in calcium transport and autonomic/ endothelial dysfunction

Answer 48

-LV doesn’t relax but it empties (normal EDV) but there is increased LV end diastolic pressure—> increases the left atrial pressure—> pulmonary edema -symptoms: dyspnea on exertion, Crackles, fatigue, S4 gallop, EKG with LV hypertrophy, CXR shows congestion -Can progress to pulmonary hypertension (blood flow backs up)

Answer 49

-Defined as the insufficiency of the right ventricle to provide adequate blood flow to the lungs at a normal CVP. -Often results from LV HF -Isolated RV failure is typical due to pulmonary hypertension -Initially RV hypertrophy in an attempt to compensate for increased pulmonary pressure but ultimately causes diastolic and systolic dysfunction, causing failure -Symptoms: JVD, peripheral edema, hepatosplenomegaly

Answer 50

-BNP: assists in diagnosis and evaluation of therapies (very good at ruling out heart failure and helpful in reduced EF HF) Inflammatory cytokines: -Endothelial hormones: potent vasoconstrictors and associated with poor HF prognosis (ie NO, PGI2, angiotensin II) -TNF alpha and IL-6: are elevated in HF, contribute to myocardial hypertrophy and remodeling -Insulin resistance: related to the activation of SNS and RAAS

Answer 51

-Hypertrophy and dilation of ventricle -Results in disruption of the normal myocardial extracellular structure and causes progressive contractile dysfunction -When contractility is decreased, SV falls and LV EDV increases, which causes dilation of the heart and increased preload

Answer 52

-Can be congenital or acquired related to inflammation, ischemia, trauma, degenerative process, or infection -most common cause worldwide of acquired is damage to endocardium secondary to rheumatic heart disease) -Most common cause in the US is due to degenerative calcific disease

Answer 53

-Stenosis: Valve is narrow and blood flow forward is constricted—> increase workload of chamber before stenosis -Regurgitation: valve leaflets don’t close completely, and blood continues to flow when the valve is supposed to be closed—> increased blood flow in the chamber affected —> increased workload—> dilation—> hypertrophy

Answer 54

-MOST COMMON valve abnormality -Resistance in blood flow from left ventricle to aorta -Causes: calcification of valve, congenital bicuspid valve, inflammation from rheumatic heart disease -Decreased blood flow from LV—> body -Results in LV hypertrophy

Answer 55

-Results from an inability of the aortic valve leaflets to close properly during diastole -Causes: Congenital bicuspid valve, degeneration, HTN, rheumatic heat disease, marfans syndrome -Normal blood flow kit do the LV in systole but the blood flow leaks back into the LV During diastole (back flow) -Results in LA dilation and hypertrophy -Over time, ventricular dilation and hypertrophy cannot compensate for aortic incompetence and heart failure develops

Answer 56

-Impairs the blood flow from the left atrium to the left ventricle -MOST common form of rheumatic heart disease and scars leaflets -You get left atrial hypertrophy—> atrial dysrhythmias and pulmonary edema, and right ventricular failure

Answer 57

-Permits backflow of the blood from the left ventricle into the left atrium during systole -Primarily related to mitral valve prolapse -You get left hypertrophy—> LA dilation—> pulm HTN—> RV failure

Answer 58

-Is when one or both cusps of the mitral valve billow upward (prolapse) into the left atrium during systole -Is the most common valve disorder in the US (also most common cause of mitral regurgitation) -Is associated with inherited tissue disorders and hyperthyroidism (most common cause is degeneration of the leaflets) -Many times asymptomatic (can sometimes hear a click on auscultation) -Symptoms are often vague and there is an excellent prognosis

Answer 59

-Infection and inflammation of the endocardium (esp the cardiac valves) -Over 80% of cases are caused by bacteria—> strep, staph, enterococci, viruses -STAPH AUREUS is most common cause Those at risk: prosthetic valves, IV drug use, heart disease, long term indwelling central lines Endocardial damage (heart valve disease/ trauma)—> bacteremia (bacterial adherence to endocardium) —> formation of vegetations (emboli, fever, night sweats, maladies, murmur, regurg, heart failure) *GEM* can throw infectious emboli throughout body Treatment: Antibiotics for several weeks, valve replacement when infection is clear, abx prophylaxis (ex before dental procedures)

Answer 60

CVP: Right atrial pressure (2-6 mmhg) RVP: Pulmonary artery pressure (15-30/ 0-8 mmhg) These are used interchangeably here. PCWP: Left atrial pressure and LVEDP (4-12mmhg) CO: 4-8 L/ min CI: 2.5-4 L/ min SV02: 60-80% -High pressures: often indicate heart failure, volume overload, pulmonary hypertension, valve disease -Low pressures: often indicate hypovolemia or reduced CO -CO is essential in assessing hearts ability to meet body’s metabolic demands -SV02 provides insight into the balance between oxygen delivery and utilization

Answer 61

-Pressure difference between two ends of a vessel (blood flows from regions of higher pressure to lower) -Resistance (the opposition to blood flow within a vessel and is inversely to the radius of the vessel) -Viscosity of the blood (The internal friction within the fluid that resists flow) -Length of the vessel (contributes to overall resistance to blood flow) Summary: -Greater pressure differences increase blood flow -Resistance is determined by vessel diameter, smaller diameter = greater resistance -High viscosity decreases blood flow -Longer vessels decrease blood flow

Answer 62

Right atrium: -Receives deoxygenated blood from the body via superior and inferior vena cava Left atrium: -Receives oxygenated blood from the lungs

Answer 63

Right: -Pumps deoxygenated blood to the lungs for oxygenation Left: -Pumps oxygenated blood to the rest of the body.

Answer 64

Pulmonary arteries (semilunar) : -carry deoxygenated blood from the right ventricle to the lungs Pulmonary veins: -Four veins deliver oxygen rich blood to the left atrium

Answer 65

LAD supplies: -Anterior wall of left and right ventricle -Anterior inter ventricular septum -Apex of heart Clinical relevance: WIDOWMAKER blockage Left Circumflex supplies: -Lateral/ posterior left ventricle -Left atrium Clinical relevance: can impact CO and cause lateral wall infarctions Right Coronary Artery supplies: -Anterior wall right ventricle -Posterior wall of ventricles -Right atrium -Inferior wall left ventricle -Parts of conduction system Clinical relevance: can result in inferior wall infarctions, arrhythmias and blocks

Answer 66

-Classified into 2 categories: acyanotic (normal oxygen delivery to tissues) or cyanotic (decrease in oxygen to tissues) Acyanotic: defects that cause left to right shunting (blood continues to flow thru the lungs before passing into circulation so no decrease in 02) Cyanotic: defects that cause shunting from right to the left (decreases blood flow through the pulmonary system, causing less oxygen to be delivered and that bluish color)

Answer 67

-An opening of the septal wall between the ventricles -One of the most common types of CHD -Allows blood to shunt from the left to the right ventricle -Show symptoms of excessive pulmonary blood flow (at risk for developing pulm HTN) -Ex. Eisenmenger syndrome

Answer 68

-An opening in the septal wall between the two atria -Allows blood to shunt from the left atrium to the right atrium -Significant morbidity and mortality if not treated early -Another form is patent foramen ovale (PFO) -It should close spontaneously, if it doesn’t, if not symptoms of heart failure

Answer 69

-A persistent connection between the aorta and the Pulmonary artery -Due to the failure of the fetal ductus arteriosis to close within hours after birth -Risk factor= prematurity -Show failure to thrive type symptoms -Is a characteristic, continuous murmur in systole and diastole

Answer 70

-An abnormal localized narrowing of the aorta just proximal to the insertion of the ductus arteriosis. -Symptoms depend on location of this narrowing -Can present with Low CO, tissue perfusion, hypotension -Can have decreased or absent pulses in lower extremes -Measurement of upper and lower extremities will differ, this is usually how they’re diagnosed

Answer 71

-QP : QS = Ratio of pulmonary blood flow (QP) to ratio of systemic blood flow (QS) -Is an indicator of how effectively the heart is pumping to both the lungs and the rest of the body -A normal ratio is close to 1:1 -Defects that cause increased blood flow cause a higher QP (VSD) and things that restrict blood flow (pulmonary stenosis) to the lungs lower QP

Answer 72

-Ca: crucial for muscle contraction; increased levels enhance contractility while decreased levels reduce it -K: essential for maintaining the resting membrane potential of heart cells; increased levels decreases contractility, low levels increased excitability -Mag: important for membrane stabilization; high levels decrease contractility, low levels can reduce as well -Na: crucial for action potential depolarization; high levels ca increase contractility, low levels reduces contractility

Answer 73

-Over activation of the RAAS system can lead to left ventricular hypertrophy (causes that thickening of the vessel walls) -Overall, cause LVH By increasing BP, stimulating heart muscle growth, and promoting fibrosis (overactivity of RAAS leads to remodeling of the heart) -LVH is commonly seen in HTN and heart Failure

Answer 74

1. T wave inversion = myocardial ischemia 2. ST depression= hallmark sign of ischemia 3. ST elevation =hallmark of MI, cell death (suggests ongoing damage) 4. Pathological Q waves= irreversible tissue damage *GEM* unlike MI, pericarditis is noted to have diffuse ST segment elevation, not localized

Answer 75

-“Fight or flight” hormones -Are a group of neurotransmitters and hormones produced by the adrenal medulla (SNS) that affect heart rate, blood pressure, glucose metabolism Epi: (adrenaline) most potent catecholamine, acts primarily on B1 and B2 receptors (a1 receptors to lesser extent) Norepi: (noradrenaline) released by sympathetic nerve endings, acts mainly on A1 and B1 receptors (to a lesser extent B2) Dopamine: has a complex cardiovascular role, acts on dopamine receptors and B1 at high doses (to a lesser extend A receptors)

Answer 76

Right: Usually in response to increased pressure in the pulmonary circulation or increased resistance in the right heart Causes: Pulm HTN, chronic lung disease, congenital heart disease, left heart failure, PE Symptoms: SOB on exertion, lower extremity edema, JVD, cyanosis Leads to: Cor Pulmonale Left: -Typically due to increased pressure or volume overload on left ventricle (more common than right) -Causes: HTN (most common), aortic stenosis or regurg, hypertrophic cardiomyopathy, CKD, obesity -Symptoms: SOB, angina, syncope, advanced stage heart failure Leads to: HF, arrhythmias, MI

Answer 77

-Can be acute, recurrent, chronic -Is the acute inflammation of the pericardium (thin sac that surrounds the heart) Causes: infection, autoimmunity, post MI, uremia, trauma/ surgery, cancer, meds, Radiation Symptoms: chest pain, fever, dyspnea, palpitations, cough Manifestations: pericardial friction rub, tachycardia, muffler heart sounds Diagnosis: diffuse ST elevation, echo showing pericardial effusion (or tamponade), mild trip elevation -complication: TAMPONADE

TEST 3: Cardiovascular Flashcards

(101 cards)