Unit 7: Cardiology STUDY GUIDE

Question 1

Differentiate between the terms “preload” and “afterload”.

Answer 1

Preload is volume and pressure in ventricle after filling with blood (diastole). Determined by how much blood is left at the end of contraction (ESV) and venous blood return during diastole. After load is the force of resistance that the heart has to overcome to pump blood. Preload is after diastole, after load is before systole.

Afterload is commonly caused by HTN and HF

Question 2

Explain what each segment of a normal electrocardiogram represents (P-wave, pr- interval, QRS interval, T-wave).

Answer 2

• P- wave is (R) atrial depolarization when the action begins after SA node starts it
• PR interval is the time between atrial activation to ventricle activation. Wildfire spreading from A to V.
• QRS interval captures the period of ventricular depolarization. Amp varies among ppl.
• T-wave is ventricular repolarization, when part is over.
• ST wave encompasses the depolarization and repolarization of the ventricles.

Question 3

Describe “orthostatic hypotension” and list the conditions that increase the risk of this happening.

Answer 3

AKA postural HTN is when systolic BP drops more than 20 mm/Hg or diastolic drops more than 10 mm/Hg. A drop in BP that occurs when the person stands up after sitting or lying. Pt will feel dizzy, and lightheaded, and may faint. Metabolic, endocrine, and CNS/PNS disorder may cause this.

Question 4

Differentiate between primary and secondary hypertension

Answer 4

Primary HTN is 140-159/90-99 it is when the systolic pressure is consistently high.
Involves genetics and environment. Influenced by neurohormonal effects and their effects on IV volume and peripheral vascular resistance. Increase risk of target organ disease, MI, kidney disease, and stroke. RAAS contributes to water and sodium retention and more vascular resistance, endothelial resistance, and platelet aggregation.

Secondary HTN is >160/>100
it is consistent elevation of diastolic BP. Also inr=creases risk for target organ disease, MI, kidney disease, and stroke. There is an underlying disease/med that causes increased peripheral vascular resistance or C.O. If you remove problem HTN will resolve. Ex: pheochromocytoma, meds, renal vascular or parenchymal disease, and adrenocorticol tumors.

Question 5

List the stages of hypertension and the resulting blood pressure readings that would indicate each stage.

Answer 5

Normal <120/<80
ELevated 120-139/80-89

Stage 1 HTN 140-159/90-99
Stage 2 HTN >160/>100

Question 6

Describe the stages of atherosclerosis in the order in which they occur.

Answer 6

Stage 1- Damage to the endothelium of a. Think smoking, HTN, toxins, viruses, and immune rxns.

Stage 2- Foam cells create a fatty streak when macrophages invade intima and engulf oxidized LDLs (foam cells).

STage 3- Fibrous plaque is formed as macrophages release growth factors which cause collagen to cover fatty streak.

Stage 4 Complicated plaques where they rupture. Leads to platelet adhesion, clotting cascade, and rapid thtombus formation.

Question 7

Describe how to calculate the Mean Arterial Pressure (MAP) and what it means to the health of the patient.

Answer 7

The average pressure against walls of the aa. in heart cycle. Normal range is 70-100mmHg and can tell us if blood is working well enough to supply vital organs. Less than 70 is concerning. SBP+(2xDBP)/ 3

Question 8

Describe the Ejection Fraction and indicate the normal levels for both genders.

Answer 8

Amount of blood ventricles eject with each heartbeat. EF= (SV/EDV)x100
SV- mL of blood per beat

Question 9

Describe how the sympathetic nervous system, Overactive RAAS and natriuretic hormones and electrolyte imbalances impact the development of primary hypertension.

Answer 9

the fight-or-flight system will cause HR to increase and vasoconstriction.

C.O. is increased and restricts peripheral vessels.

Narrows inner lumen which will increase intravascular pressure.

In primary HTN, RAAS is overactive which causes retention of salt and water and increases vascular resistance.

Natriuretic hormones keep Na excretion in balance, so changes in RAAS and SNS will decrease sodium excretion.

Question 10

Explain the impact of inflammation, obesity, insulin resistance, and chronic stress on primary hypertension.

Answer 10

Primary HTN is when systolic pressure is consistently elevated, an epigenetic disease. Inflammation is a natural response to a foreign substance that the body sees as a threat and it releases chemicals that will in turn damage to blood vessels. Can lead to high BP as macrophages raise blood flow. Obesity plays a role because extra fat will compress on organs, like kidneys which can activate RAAS system and that increases vascular resistance as well a decreased excretion of water and Na, causing heart to contract stronger and putting more pressure on walls.
Chronic stress will activate the SNS and the body will produce more hormones from adrenal glands which cause vessels to constrict in efforts to increase oxygen levels.

Question 11

Explain how increased vascular resistance impacts the development of primary hypertension (be sure to describe the role of the SNS system, arteriolar remodeling, and vessel dysfunction).

Answer 11

Increased vascular resistance can be due to a variety of reasons, but they all increase the pressure exerted against walls of blood vessels d/t a factor that increases the amount of work that must be done to get the blood to flow.

Question 12

Describe the cardiovascular complications associated with hypertension (heart, brain, blood vessels, kidneys, eyes, and encephalopathy)

Answer 12

HTN is consistently elevated BP d/t vasoconstriction, increased vascular resistance, and more fluid in blood.

The heart will work harder and less blood flow in aa. of heart. We can get LVF, MI, and even HF.

The brain will receive less blood, vessel walls will weaken and atherosclerosis will quicken. We can get TIAs, cerebral thrombosis, aneurysm, hemorrhage, acute brain infarction/

Blood vessels will constrict and weaken. We can get dissecting aneurysm

Kidneys will go on overdrive and the RAAS system will be overstimulated meaning more water and Na will be held onto. SNS will also be stimulated. We can get glomerulosclerosis, decreased GFR, and end-stage renal disease.

In the eyes, HTN will cause retinal vascular sclerosis, and increased retinal a. pressure and lead to HTN retinopathy, retinal exudates, and hemorrhages.

Encephalopathy: high arterial BP leads to cerebral arterioles being unable to regulate blood flow to cerebral capillary beds. Pushes fluid out of tissues. May lead to death.

Question 13

Describe the pathophysiology and signs and symptoms of Aortic aneurysms.

Answer 13

Patho: When blood vessels weaken, an aneurysm will form, which is like a balloon in the vessel. Most common cause of an arterial aneurysm is atherosclerosis, followed by HTN, smoking, infections, and collagen-vascular disorders.

After an MI, an aortic aneurysm is likely to occur because an MI weakens or kills the heart myocardium. Tension in the ventricles can cause the weakened mm. to stretch into a thin layer and a bulge will form.

S/S: generally, asymptomatic, once they rupture SEVERE pain and hypotension ensue in the area where it occurred.

True aneurysms affect the 3 layer of heart and are FUSIFORM

False aneurysms are from trauma and blood escapes the lumen of vessel, similar to fusiform shape .

Question 14

Describe the pathophysiology and signs and symptoms of Thoracic aortic aneurysms.

Answer 14

Patho: aortic aneurysm that has ruptured in the thoracic portion of the aorta d/t weakening of a. wall.
S/S: pain and hypotension. Dysphagia, dyspnea

Question 15

Describe the pathophysiology and signs and symptoms of Aneurysms in the extremities

Answer 15

patho: blood flow blocked, most commonly by HTN. Again, pressure in aa. increases and this causes the lining of vessels to extend and create fusiform or saccular aneurysms. Saccular is more common in the circle of Willis and fusiform outside of brain.
S/S: ischemia (localized pain, swelling, pallor, poikilothermia, and even paralysis.

Question 16

Describe the pathophysiology and signs and symptoms of Cerebral aneurysms in the circle of Willis

Answer 16

patho: Circle of Willis is the site where most aneurysms in brain occur. A result of increased IC pressure with a weak vessel that bulges out. Most are not found until after they rupture and hemorrhage.

S/S: depend on site and type. Often asymptomatic, but can cause severe headache or dizziness and CN compression.

Question 17

Describe the pathophysiology and signs and symptoms of aneurysms in the heart.

Answer 17

Patho is same as all other aneurysms, aa. weaken as a result of damage to vessel from HTN, atherosclerosis, etc.

S/S: abnormal heart rhythm or HF and may lead to blood clot in brain or other organs.

Question 18

Describe what happens when the heart muscle suffers myocardial ischemia (be sure to talk about the length of time until recovery of the tissue is no longer possible and what happens then).

Answer 18

MI happens when there is not enough O2 to meet demands. Cells are damaged from this lack of O2.

MI is most commonly caused by coronary blood flow decreasing from atherosclerosis in coronary circulation aka CAD.

Myocardial cells become ischemic within 10 secs of being deprived of O2. The heart starts to give out and pumps blood less effectively, lactic acid build-up because there is not enough glucose for aerobic respiration. The heart loses the ability to contract and CO decreases. If O2 isn’t replenished in cardiac cells within 20 min, MI will occur.

Question 19

Thoroughly describe the pathophysiology, signs and symptoms, and assessment associated with left- versus right-sided heart failure.

Answer 19

HF is when heart can no longer provide enough CO. Main culprit: MI.

Left-sided HF
Can be divided into LHF with preserved or reduced EF.
- LHF with reduced EF , aka systolic HF, is when EF is less than 40% (normal is 50-
- LHF with preserved EF aka diastolic HF. Can happen with systolic or on its own
Patho:

S/S: dyspnea, orthopnea, pulmonary edema, crackle and S3 gallop

Right-sided HF is the result of LHF. Patho: the increase in pulmonary circulation that caused the L-sided HF also increased vascular resistance. This causes peripheral edema and hepatosplenomegaly.

• Cor Pulmonale is RHF that happens without LHF. It is d/t pulmonary disease that causes hypoxia, such as COPD, CF, or ARDS which will cause increased R.V afterload

S/S:

Question 20

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with pericardial effusion

Answer 20

Pericardial effusion is when fluid accumulates in the pericardial cavity, as seen in pericarditis. In most cases, no known cause (20%) but can be caused by neoplasm or infection, acute pericarditis, surgery, chemo, or autoimmune disorders

Acute pericardial effusion is more dangerous because the heart does not have enough time to accommodate to the increased pressure from the influx of fluid.

This can lead to cardiac tamponade which will prevent the ventricles from expanding and functioning properly. If the pressure from the fluid is equal to the diastolic pressure, this can lead to increased venous pressure, systemic venous congestion, and s/s of RHF (JVD, edema, and hepatomegaly).

If there is not enough blood in atria, there won’t be enough in the ventricles, which causes decreased SV and reduced C.O.

Question 21

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with cardiomyopathy

COME BACK

Answer 21

Cardiomyopathy- a disorder of the myocardium.

patho: Primary or secondary. Primary occurs only in the myocardium, secondary affects other organs as well.

Primary can be idiopathic or arise from lack of O2, HTN, infections, toxins, inherited disorders autoimmunity, or myocarditis.

Secondary CM has similar causes, but can be further divided into three types
1. dilated- HF with reduced EF, dilated ventricles, and more fluid in heart. Causes include everything that puts strain on the heart.
s/s: dyspena, fatigue, and pedal edema, displaced apical pulse, JVD, and pulmonary congestion.

2. hypertrophic- myocardium has thickened
3. restrictive

s/s:

assessment findings:

Question 22

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with pericarditis (all types)

Answer 22

Acute or chronic inflammation of pericardium and can lead to pericardial effusion. Caused by MI, trauma, surgery, uremia, TB, connective tissue disease, or radiation therapy.
s/s: fever, sinus tachy. Friction rub at apex or left sternal border.

In constrictive pericarditis, fibrous scars may become calcified and cause pericardium and visceral layers to stick together. The heart is now in a rigid shell, so much so that the heart is compressed to the point where C.O. is reduced. It develops gradually and blood squeezing into the ventricles will be heard as a “pericardial knock”

Question 23

Differentiate between systolic and diastolic left-sided heart failure. Include a description of the signs and symptoms.

Answer 23

Left-sided heart failure (LSHF) is aka congestive heart failure because the lungs are congested as heart valves are weakened and dilated. Not enough blood is making it to the heart, so heart fails.

Systolic HF happens when the CO does not meet the needs for vital tissue perfusion. EF is less than 40%. If contraction falls, EDV (blood left after filling) will increase, and heart will dilate and preload (pressure in ventricles after filling) increases too.

s/s: dyspnea, orthopnea, cough, frothy sputum, fatigue, less urine output, and edema. S3 gallop also.

Diastolic left-sided HF happens with normal ejection fraction. So, while there is sufficient pumping happening and blood reaching the extremities, the ventricles do not relax properly during diastole and the LV won’t be as receptive to blood. This causes edema in the lungs as the fluid builds up. Poor prognosis.
s/s: dyspnea on exertion, fatigue, inspiratory crackles, pleural effusion.

Question 24

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with varicose veins

Answer 24

Patho: pooled blood from venous distention, caused by:
- trauma to saphenous vv. that damages valves
and/ or
- gradual distention by gravity after standing or sitting for a long period of time.
- both causes will increase volume and pressure in vv., leading to edema in tissues surrounding it, because of increased hydrostatic pressure.
s/s: edema in legs, hyperpigmentation, bulging, blue vv., aching, heavy feeling. RIsk factors are age, being a female, family Hx, obesity, pregnancy, DVT, leg injury.
findings associated with varicose vv.: venous distention will develop over time, decreasing vasospasm and making it difficult to maintain normal venous pressure.

Question 25

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Thromboangiitis Obliterans (Buerger’s disease)

Answer 25

Thromboangitis Obliterans or Buerger’s disease:

Autoimmune disease where clots are filled with immune and inflammatory cells. Peripheral aa. are also inflamed and will develop scars and thicken, this will block aa., so not enough bloodflow will lead to gangrene and the extremity will have to be amputated.

Clinical manifestations include pain and tenderness in affected areas. Rubor, cyanosis (ischemic phase), thick malformed nails, with chronic ischemia, we will have thin and shiny skin.

Most of the affected have a history of smoking, are over 45, and will have visible peripheral ischemia.

Question 26

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Raynaud Phenomenon/Disease

Answer 26

Raynaud phenomenon/disease is idiopathic, associated with primary vasospastic disorder.

patho: systemic collagen vascular diseases or long-term exposure to cold/vibrating machinery.

s/s: pain, tenderness, thick malformed nails, ischemia, cyanosis, numbness, cold sensation. Rubor upon blood flow return.

Tx includes removing stimulus, smoking cessation, vasodilators

Question 27

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with cardiac tamponade

Answer 27

Cardiac Tamponade: occurs when there is both fluid in the pericardium and when systemic BP drops by more than 10 mm Hg (i.e. pericardial effusion and pulsus paradoxus.

patho: When pressure in pericardial fluid is equal to or more than diastolic pressure.

s/s: fainting, dizziness, heart palpitations, tachy, dyspnea, jaundice

assessment findings: chest pains,

Question 28

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with prinzmetal angina

Answer 28

Prinzmetal angina is chest pain d/t transient ischemia of myocardium during REM sleep
s/s: increased heart rate, S3 gallop or murmur

caused by hyperactivity of SNS, decreased nitric oxide activity and increased Ca fxn in arterial tissue.

Question 29

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with silent angina

Answer 29

silent angina is when heart O2 supply has stopped bu t the person is unaware.

s/s: IF PRESENT, include fatigue, dyspnea, uneasy feeling.

Main cause: autnomic innervation abnormalities in heart after surgery. Also seen in those with chronic mental stress because chronic stress is linked to greater number of inflammatory cytokines and a state where coagulation is more likely to occur. Can cause serious CV events if left untreated.

Question 30

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with unstable angina

Answer 30

Unstable angina is when plaque erodes vessel and leads to blood clot which occludes vessel, in addition to vasoconstriction.

Sign that MI may happen soon

S/s” gallop, tacy, dyspnea, and diaphoresis. May cause anxiety.

B-blockers, ACE inhibitors, and anticoagulants can be used for Tx

Question 31

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with stable angina

Answer 31

Artery lumen narrows and hardens, along with inflammation and endothelial cell dysfxn, as well as less vasodilators. End-result: vessels can’t meet heart demands during exercise or emotional stress. Resting restores blood flow

Pain results from lactic acid buildup or abnormal streatchiing of ischemic heart m. that irritates nn.

pale, sweaty, dyspnea and pain

Question 32

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Cardiogenic shock

Answer 32

cardiogenic shock is when CO falls and tissue does not receive enough O2. a problem when the heart can’t compensate for lost O2. Usually seen after MI.

s/s: foggy thoughts, dyspnea, tachypnea, HTN, oliguria.

Tx: vasopressors to increase blood flow. Fluids should be controlled because kidney and G.I. are not working correctly, so the heart will be overloaded.

Question 33

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with hypovolemic shock

Answer 33

Hypovolemic shock is when too much fluid or blood is lost and the heart can’t supply blood to organs. D/t hemorrhage, plasma loss from burns, diaphoresis, DM, DI, diarrhea, diuresis.

• when IV volume has decreased by 15%
• s/s: high SVR., poor skin turgot, thirst, oliguria, low preloads, rapid HR, +1 pulse, declining mental status
• Tx: replace fluid loss ASAP with crystalloids and blood products.

Question 34

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Neurogenic/Vasogenic shock

Answer 34

Neurogenic/vasogenic shock is when someone has a cervical or thoracic (T6) injury. No fight or flight activity, only rest and digestion. HR and BP won’t be regulated well. Bradycardia, hypotension, vasodilation, and failed temp regulation are all common.

Question 35

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Anaphylactic shock

Answer 35

Anaphylactic shock is a hypersensitivity rxn to an allergen. Causes vasodilation with less volume in vessels among other things.

Once an allergen is detected, the humoral immune response begins. IgE antibodies are created. When allergens are bound to IgE, mast cells degranulate and cytokines are released which leads to inflammation and increased blood flow. This shock is sudden and can lead to death if not treated immediately.

Main s/s: dizziness, anxiety, dyspnea, stridor, wheezing, pruritus with hives, swollen lips and tongue, cramps in abdomen.

Dx by serum markers, Tx begins with removal of antigens. Epinephrine also given IM if allergen exposure is suspected, which will cause vessels to constrict and airways to open.

Question 36

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Septic shock.

Answer 36

Septic shock causes both inflammation and a dramatic drop in BP. Caused by bacteria in blood (bacteremia) which causes SIRS (systemic inflammation response syndrome), a systemic infection.

Septic shock can also make toxins that further damage blood vessels.

S/S: tachy, temp swings, jaundice, cognition issues, and kidney issues.

Tx: respiratory support, fluids, and antibiotics

If not treated,, MODS (multiple organ system failure) will result.

Question 37

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Tetralogy of Fallot

Answer 37

Tetralogy of Fallot is the most common cyanotic heart defect, where hypoxia and cyanosis are present. Tetra is 4, so there are 4 defects:
1. ventricular septal defect
2. pulmonary stenosis
3. overriding aorta
4. r. ventricular hypertrophy

How bad the pulmonary stenosis and septal defect are, determines severity because stenosis decreases blood flow to the lungs and O2 to left heart.

Occurs directly after birth OR in 12 mos infant.

Question 38

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Patent Ductus Arteriosus (PDA)

Answer 38

Patho: unclosed aorta is normal in the fetus, as blood does not have to stop by the lungs to get O2, however when born, blood must go to the lungs, so the hole in the aorta must close, if it doesn’t then it cannot receive O2. This hole, once connected to the aorta and pulmonary a. directly but must close after birth. Common in premature infants.

If PDA is small, the heart and lungs won’t have to work harder, so closing it is not necessary. If a large PDA, then surgically closing can fix the problem of increased blood flow to the lungs.

S/S: breathlessness (if large PDA)

Assessment findings: if PDA is small you may hear a murmur that sounds like a machine.

Question 39

Thoroughly describe the pathophysiology, signs, and symptoms, and assessment findings associated with Coarctation of the Aorta

Answer 39

Coarctation of the aorta means the aorta has narrowed near the ductus arteriosus ( a. connecting the aorta and pulmonary a. in the fetus). Blood flow to the lower extremities may slow by coarctation once the ductus closes after birth. If COA is severe, infants will have low C.O., poor tissue perfusion, acidosis, and hypotension. The infant will have weak or absent femoral pulses.

Children with undiagnosed COA will have unexplained upper extremity HTN when older.

Exercise may cause leg pain or cramping in children.

Question 40

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Ventricular septal defect

Answer 40

a ventricular septal defect is a congenital abnormality present at birth, where there is a hole in the septum of the heart between the ventricles.
It is harder to pump blood and often causes heart acromegaly in children.

Children are 10x more likely to develop hepatoblastoma.

Assessment findings: HF related, so tachypnea, crackles, enlarged liver, and murmurs

S/S: tachypnea, tachy, HTN, dyspnea, sweating, poor eating patterns, and easily tiring.

Question 41

Explain how myocardial hypertrophy occurs in patients with complicated hypertension.

Answer 41

Myocardial hypertrophy, or heart muscle growth, is d/t complicated HTN where the heart is working so hard to supply blood to the rest of the body. Micro-tears from the increased pressure in the heart heal but this causes the heart to thicken, leaving less space for blood to fill the heart in diastole. A bigger heart requires more O2, so contractions are impaired and MI is more likely, as is HF with reduced EF.

Question 42

Explain the Triad of Virchow and how this results in the formation of varicose veins or deep vein thrombosis.

Answer 42

Triad of Virchow, are three factors that increase risk of developing blood clots in the veins. #1 injury to endothelium #2 weird blood flow and #3 increased coagulability of blood

Question 43

Explain how arterial thrombi form and in which patient the nurse would use the PTT (partial Thromboblastin Time) versus the PT (protime)/INR (international ratio) tests.

Answer 43

Arterial thrombi, or a blood clot in the aa., forms when blood coagulates, inflammation after surgery, infection, or even obstruction of a. Inflammation will activate clotting cascade and platelets will stick to walls of aa. in heart valves that have been altered d/t endocarditis.

A nurse looking for a pt’s heparin levels, PTT test would be used to test how well the clotting factors work.

If warfarin levels were being monitored, then PT/INR test would be used. Tests how well prothrombin and coagulation work.

Question 44

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Superior Vena Cava Syndrome.

Answer 44

SVCS happens when the SVC is blocked for long periods and causes venous distention in upper extremities and head

Causes include bronchogenic cancer, lymphomas, metastasis, TB, mediastinal fibrosis, and CF, and invasive therapies.

S/S: edema and distended vv, in arms, face, and ocular beds.

C/O fullness in head, tight collar, rings

AN ONCOLOGIC EMERGENCY

Question 45

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Peripheral arterial disease. Explain the ankle-brachial index used to determine the presence of PAD and explain why aerobic exercise is important even though it is painful for these patients.

Answer 45

PAD, or peripheral arterial disease, is ischemia in the peripheral areas d/t atherosclerosis.
Intermittent claudication may occur, which is when blood flow in the a. is momentarily stopped which causes pain when walking.

Evaluated by careful H&P exam, bruits, ankle-brachial index to determine if there is a difference in blood pressure of ankle v. the arm.

Tx: reduce risk factors, Rx antiplatelets, aerobic exercise to get blood flow to area.

Question 46

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Coronary artery disease

Answer 46

Caused by atherosclerosis or arteriosclerosis. Athero more common.

Coronary aa. narrow or occluded. The primary cause of heart disease in the U.S.

CAD decreases heart m. blood supply until myocardial ischemia occurs.

Tissue ischemia can occur if the blood supply does not return to the heart, causing acute coronary syndrome.

S/S: MI, angina, pain, discomfort, dyspnea

Question 47

Thoroughly describe the pathophysiology, signs and symptoms, and assessment findings associated with Acute coronary syndrome

Answer 47

Acute coronary syndrome is when athersclerosis blocks blood flow to heart

Two plaques with two outcomes:
STable plaque leads to stable angina and unstable plaque leads to unstable angina.Unstable plaque can rupture leading to ACS, with less O2 to myocardium.

Risk factors are modifiable (lifestyle dependent) and unmodifiable (herdeity).

s/s: anigina, discomfort

Question 48

Explain what happens during a myocardial infarction. Be sure to discuss the flow of blood, accumulation of hydrogen ions and lactic acid, oxygen deprivation and electrolyte imbalance, release of catecholamines and angiotensin II. Explain Why these patients tend to have hyperglycemia 72 hours after the MI even if they do not have diabetes.

Answer 48

MI will happen when there is an interruption in blood flow for an extended period that leads to construction, which causes necrosis. Within 10 secs of infarction, blood clot causes ischemia. Lactic acid and H+ ions accumulate and suppress electrical impulse of heart, contraction, and leads to HF.

O2 deprivation will cause electrolyte imbalance

Question 49

Differentiate between mitral insufficiency (regurgitation) and stenosis and aortic insufficiency (regurgitation) and aortic stenosis (including signs and symptoms and assessment findings). Making a table would be very helpful.

Question 50

Thoroughly describe infective endocarditis.