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Block 2 Week 2 Cardiovascular > DONE: Cardiac Lecture 2 > Flashcards

DONE: Cardiac Lecture 2 Flashcards

1
Q

Q. List the Cardiovascular Disorders:

A

A. ​
• Hypertension (HTN)- High BP
• Coronary Artery Disease (CAD)- Atherosclerosis
• Angina- Chest Pain R/T decreased perfusion to the heart
• Heart Failure (HF)- Heart cannot pump the amount of fluid
• Peripheral Vascular Disease (PVD)- Increased Systemic asular Resistance

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2
Q

Q. Name the types of Peripheral Vascular Disease (PVD)

A 
A. 
Venous:
Deep Vein Thrombosis (DVT)
Venous Insufficiency
Arterial:
Peripheral Artery Disease
Raynaud’s Disease & Buerger’s Disease
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3
Q

Q. What are the Classifications of HTN?

A 
A. Normal: less than 120/80
Prehypertension: 120-139/80-89+
Stage 1 hypertension: 140-159/90-99+
Stage 2 hypertension: over 160/over 100+
Severe Hypertension: over 180/ over 110+
Primary hypertension: idiopathic
Secondary hypertension: some kind of disease process and need to treat underlying cause
Ex. Pregnancy, Renal Arteries are narrow, Hyperaldosteronism
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4
Q

Q. If your 1 is high and diastolic is normal you are still considered 2

A
  1. Systolic 2 hypertensive
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5
Q

Q. What is the Direct relationship between HTN and CVD?

A

A. HTN increases risk of MI, Heart Failure, Cerebral Vascular Accident (stroke), Renal Failure & Dementia

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6
Q

Q. Name the Gender and ethnic differences regarding HTN

A

A. women more than men likely to suffer a stroke than a heart attack
men more than women likely to suffer a heart attack than a stroke
after 55 women are more likely to have HTN than men menopause and estrogen
before 55 men are more likely to have HTN than women
african americans have the highest prevalence of HTN in the world and develops in younger ages earlier. It can be more aggressive and end in more damage to organs that could be related to lack of access to care.
african american women have HTN more than african americanmen.
Hispancics are less likely to seek care for HTN than any other race.

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7
Q

Q. The 1 gets fed blood first during diastole/prefusion

A

heart

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8
Q

Q. What is the formula for Cardiac output?

A

Arterial BP = CO(cardiac output) x SVR(stroke volume)

– CO = SV X HR

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9
Q

Q. What is the first thing that changes w/person w/heart problems (normal hr 60-100 bpm)

A

A. heart rate fluctuates on a regular basis but when there is a significant change this is a sign that the heart is compensating in response to its needs or a change in demand.

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10
Q

Q. What are the 3 components of stroke volume?

A

preload, afterload and contractility

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11
Q

Q. Define: amount of blood incoming to the heart or venous return: TOO MUCH BLOOD TO THE HEART.

A

preload

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12
Q

Q. Define: amount of pressure the heart has to overcome to push blood through the body (bp)-heart is not strong enough to pump it out/can’t overcome the pressure

A

A. afterload

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13
Q

Q. Define: how much the muscle is stretched and the rebound of the muscle provides force ++want to maximize this to improve cardiac output++

A

contractility

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14
Q

Q. Describe the Pathophysiology of HTN:

A

To increase BP there Must be an increase in CO or Systemic Vascular Resistance

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15
Q

Q. What are the 4 causes of HTN?

A

A. Heredity (15-70% of HTN is contributed by genetics)

  • Water/Sodium Retention (limit salt intake)
  • Altered Renin-Angiotensin Mechanism (retains salt and water)
  • Stress/Increased SNS Activity (Stress causes vasoconstriction and release of renin to secrete aldosterone which causes body to retain salt and water)
  • Insulin Resistance and Hyperinsulinemia (glucose and insulin abnormalities are common in primary HTN. High insulin concentrations in the blood stimulates the SNS to vasoconstrict and impairs nitrous oxide which causes vasodilation and if inhibited causes vasoconstriction which will increase BP.
  • Endothelial Cell Dysfunction: Damaged endothelial cells lining the heart and vessels. In HTN they have a reduced vasodilator response to nitrous oxide (vasodilator) which leads to more vasoconstriction causing HTN
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16
Q

Q. What are the clinical manifestations of hypertension?

A 
“Silent Killer”
Fatigue
Reduced activity tolerance
Dizziness
Palpitations
Angina
Dyspnea
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17
Q

Q Hypertensive Heart Disease can cause these cardiovascular disorders:

A

A. Coronary Artery Disease /Artherosclerosis
Left Ventricular Hypertrophy - Enlarged Ventricle R/T Increased Workload
Heart Failure - More fluid than the heart is able to pump

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18
Q

Q. Hypertension can cause these Target Organ Diseases:

A

Cerebrovascular Disease - Stroke (Brain)
Peripheral Vascular Disease - Increased systemic Vascular Resistence (Extremities)
Nephrosclerosis-Damage to the kidneys due to increased pressure on the nephrons (Kidneys)
Retinal Damage - Ocular Damage due to increased pressure (Eyes)

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19
Q

Q. What are changes that occur with Hypertension?

A

Eye: visual changes
Brain: cerebrovascular accident (CVA)
Cardiovascular system: heart failure, hypertensive crisis
Kidneys: renal failure

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20
Q

Q. What are the Labs for HTN?

A
  • Monitor Blood Pressure
  • UA, BUN & Serum creatinine-shows kidney damage
  • Serum electrolytes- kidney issues
  • Sodium, Potassium, Chloride, Calcium
  • Checking the kidneys to make sure that excretion is not impaired or is there a secondary cause of HTN?
  • Blood Glucose-Hypertensive with diabetes. If yes then treat aggressively.
  • CBC - always check
  • Serum Lipid Profile – Won’t diagnose HTN but if they have high cholesterol you treat both.
  • Serum uric acid - HTN is treated by diuretics to decrease fluid volume and diuretics can increase uric acid levels
  • TSH Levels -Check for Hyperthyroidism because this can cause an increase in blood pressure.
  • 12-lead ECG & echocardiogram - To view overall cardiac status.
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21
Q

Q. What is the leading cause of death in the U.S. for men and women of all racial and ethnic groups?

A

CAD is the most common type of cardiovascular disease in adults

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22
Q

Q. What is the major cause of CAD?

A

Atherosclerosis is the major cause of CAD

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23
Q

Q. What is a detour that the blood vessels develop around a blocked vessel to create circulation to the myocardium?

A

Collateral Circulation- Death occurs more rapidly in the patient with no collateral circulation because of the inability to perfuse around a blockage

24
Q

Q. Name the types of vessel occlusions with collateral circulation:

A
  • Open, functioning coronary artery
  • Partial coronary artery closure with collateral circulation being established
  • Total coronary artery occlusion with collateral circulation bypassing the occlusion to supply blood to the myocardium
25
Q

Q. What are the non-modifiable Risk Factors for CAD?

A 
Age, Gender, Ethnicity
Modifiable
Elevated Serum Lipids
Hypertension
Tobacco Use
Physical Inactivity
Obesity
26
Q

Q. What are the Modifiable factors for CAD -Focus on these in your patient?

A 
Elevated Serum Lipids - Diet changes
Hypertension - Diet changes
Tobacco Use - Stop Smoking
Physical Inactivity - Promote Exercise
Obesity - Promote Exercise
27
Q

Q. What are the Clinical Manifestations of CAD?

A
  • Symptoms occur when the coronary artery is occluded to the point that inadequate blood supply to the heart muscle occurs, causing ischemia which equals angina.
  • Angina - Smoking, Diabetic have repeated injury to coronary arteries and cholesterol creates fatty streaks. When blood flow becomes diminished causing ischemia the heart begins to die and it begins to hurt which causes chest pain.
28
Q

Q. What are the clinical manifestations of Angina?

A

Need for oxygen to myocardium exceeds supply

Usually caused by atherosclerotic disease

29
Q

Q. Name the Types of Angina

A

– Stable- predictable and reversible/#1 nitroglycerin; know when it could happen/treatable associated with fats
– Unstable (Preinfarction angina)- had the stable angina but it now takes longer to recover; associated with fats/treatable but takes more than one nitroglycerin to get under control-will need to seek tx since the nitro is not working.
– Variant (Prinzmetal’s angina)- coronary spasms at night mostly in women; autoimmune; occurs during sleep (common in women going through menopause) pt’s treated with estrogen
– Silent- no symptoms but EKG shows signs/ caused by diabetics (have neuropathy) elderly
– Intractable/Refractory- unresponsive to intervention

30
Q

Q. predictable and reversible/#1 nitroglycerin; know when it could happen/treatable associated with fats

A

A Stable

31
Q

Q . had the stable angina but it now takes longer to recover; associated with fats/treatable but takes more than one nitroglycerin to get under control-will need to seek tx since the nitro is not working

A

A. Unstable (Preinfarction angina)

32
Q

Q. coronary spasms at night mostly in women; autoimmune; occurs during sleep (common in women going through menopause) pt’s treated with estrogen

A

A. Variant (Prinzmetal’s angina)

33
Q

Q. no symptoms but EKG shows signs/ caused by diabetics (have neuropathy) elderly

A

A. Silent

34
Q

Q. unresponsive to intervention

A

A. Intractable/Refractory

35
Q

Q. Name the clinical manifestations of angina:

A
  • Mild indigestion - patient will complain of heartburn
  • Choking
  • Heavy sensation in upper chest - patient will complain of feeling like an elephant is sitting on their chest
  • Discomfort to agonizing pain
  • Apprehension
  • Feeling on impending death
  • Weakness/numbness in arms, wrists, hands
  • Shortness of breath
  • Pallor
  • Diaphoresis
  • Dizziness
  • Nausea/Vomiting
  • Men- Have the most common signs and symptoms
  • Gerontologic manifestations - No typical pain symptomsdue to increased age may present with SOB, no symptoms, or tiredness and fatigue.
  • Female manifestations - May be SOB, tightness, Nausea/Vomiting, back pain, or jaw pain. Not the classic sign of midsternal chest pain radiating down an arm like men.
36
Q

Q. Name the clinical Female manifestations of angina:

A
  • upper chest
  • substernal radiating to neck and jaw
  • substernal radiating down left arm
  • epigastric
  • neck and jaw
  • intrascapular
  • left shoulder and down both arms
37
Q

Q. What are the clinical manifestations of HF?

A
  • Inability of the heart to maintain adequate cardiac output (CO) to meet the metabolic needs of the body because of impaired pumping ability
  • “The pump is broken”
38
Q

Q. What are the Causes of HF?

A
  • Advancing age
    -Valvular Disease – Decreases Cardiac Output
    -Coronary Artery Disease
    • Hypertension
    • Diabetes Mellitus
    • Cigarette smoking
    • Obesity
    • High cholesterol
    -Progressive renal failure causes fluid to back up into the body increasing fluid volume.
39
Q

Q. Describe the Pathology of HF

A
  • Systolic Failure
    • Problems with ineffective contraction and decreased ejection of blood. Pump is not able to push blood into the body.
  • Diastolic Failure
  • Problems with the heart relaxing and filling with blood. Pump is not able to dilate enough to fill with enough blood to supply the body with the amount of blood it needs. Patients can have both systolic and diastolic failure.
  • Preload is blood coming into the heart.
  • Afterload is the force the blood has to go against to get out into the body aka Blood Pressure
40
Q

Q. Describe the Compensatory Mechanisms to decrease Cardiac output in HF:

A

-HF = Low Cardiac Output and Decreased Stroke Volume. Body tries to restore blood flow to normal to compensate for the decreased cardiac output which causes decreased perfusion
• Compensatory mechanisms act to restore Cardiac Output to near normal levels.
• Initially this works => but over time can cause damaging effects to the pump (heart).
• DECOMPENSATION occurs after the compensatory mechanisms are exhausted. All compensatory mechanisms eventually fail.

41
Q

Q. Describe the Compensatory Mechanisms to increase Cardiac Output in HF

A

A. -SNS – Releases epinephrine and norepinephrine causes increased HR which increases Contractility which increases blood pressure by increasing vasoconstriction. It makes the heart work harder against increased afterload.

  • RAAS – Kidneys trigger this to retain fluid to increase blood flow to kidneys due to decreased cardiac output. Aldosterone retains salt and water also increasing blood pressure Canincrease afterload.
  • ADH – Triggers the body to hold onto water. The body does not need more water because it will increase preload.
  • Dilation – Causes the chambers of the heart to become thinner and enlarge. Increases preload. Frank Starling’s Law states as the heart dilates to stretch to have a stronger contraction. If the heart becomes overstretched then contractility will decrease.
  • Hypertrophy – Enlarges to create more cardiac wall causing thickening of the muscle to become stronger to increase cardiac output. With a bigger heart muscle you will need more blood flow to feed the heart.
42
Q

Q. Describe the Third heart sound (S3) and who it affects?

A

– Heard during diastole.
– “Ken-tuc-ky”
– Normal in children and young adults <30 years of age
– Associated with disease in older age groups.
• Congestive Heart Failure or mitral/tricuspid regurgitation
– Sound is created when increased volume enters a non-compliant ventricle.

43
Q

Q. Describe the Fourth Heart Sound (S4) and its symptoms.

A 
-too much preload
– Heard during atrial contraction immediately before S1.
– “Ten-nes-see”
– Occurs when ventricles are overloaded and diastolic pressure increased.
– Symptomology
• Myocardial infarction, CAD
• Congestive heart failure
• Pulmonary hypertension
44
Q

Q. Name the types of Peripheral Vascular Disease (PVD):

A 
– Venous Disorders
• Deep Vein Thrombosis (DVT)
• Venous Insufficiency
– Arterial Disorders
• Peripheral Arterial Occlusive Disease
• Raynaud’s Disease
• Thromboangiitis Obliterans (Buerger’s disease)
45
Q

Q. Describe the symptoms and tx of Deep vein thrombosis DVT: AKA PULMONARY EMBOLI

A

-thrombus formation-surgery, dehydration, bed rest
-inflammatory response
s/s – swelling, tenderness, redness, hot to touch
tx – elevate extremity, heparin

46
Q

Q. What is a high risk and common in the perioperative patient?

A

A. DVT is preventable by the RN.

47
Q

Q. What is commonly found in the iliac or femoral vein which can kill you or cause disability?

A

A. formation of thrombus or clot

48
Q

Q. What is the hospital trying to prevent?

A

A. Venous Thromboembolism and DVT + PE

49
Q

Q. What is the Etiology of DVT/VTE?

A

• Virchow’s Triad: These three things must occur in order for a DVT to occur? Muscle contractions push on the veins and push the blood back to the heart.
• Venous Stasis – leads to DVT/VTE because blood is not moving back to the heart it just sits there.
Ex. Of causes include Obesity, HF, Long plan trips, long surgeries, immobility, hip fractures, back fractures, Heart Attacks, pregnancy, chronic heart disease, HF
• Vessel Wall Damage – leads to DVT/VTE because vessel walls damaged by trauma, external pressure, lower extremity fractures, surgery, burns, trauma, childbirth, and infection can damage the walls and causes clots to form in the deep veins.
• Hypercoagulability of Blood leads to DVT/VTE because of genetic abnormality, breast cancer, GI tract cancer, brain cancer, pregnancy, hormone replacement therapy, corticosteroids, smoking, dehydration, and infection can lead to hypercoagulability of the blood.

50
Q

Q. What are the Clinical Manifestations of DVT?

A 
• Affected Extremity
– Edema
– Pain
– Warm skin
– Erythema
– Tenderness on palpation
– Elevated temperature
– + Homan’s sign (DO NOT DO THIS CAN CAUSE EMBOLI TO BREAK OFF AND BECOME A PULMONARY EMBOLISM)
– Can be asymptomatic or can only present with SOB
51
Q

Q. What causes Vascular Disorders: Venous Insufficiency?

A

A. Results from prolonged venous hypertension, which stretches the veins and damages the valves.
The resultant edema and venous stasis cause venous stasis ulcers, swelling, and cellulitis.

52
Q

Q. What causes Peripheral Arterial Occlusive Disease (PAOD)?

A

-PAOD strongly R/T other manifestations of cardiovascular disease.
All arteries are affected if the coronary artery is affected. Poor circulation caused by smoking, diabetes, and HTN, Pallor, Cool to the touch, and weak Dorsalis Pedis pulses. Strong indicator of Cardiovascular system diseases.
-PAOD = marker for advanced systemic atherosclerosis
-PAOD = 4-5 x the risk of dying from Myocardial Infarction & Cerebral Vascular Accidents.
-Atherosclerosis forming in arms, legs, and abdominal aorta supplies your brain and your heart with blood.
-The internal mammary is the only artery that does not form plaque.

53
Q

Q. Name 2 Arterial Disorders:

A

A. Raynaud’s disease and Buerger’s disease

54
Q

Q. What is Raynaud Disease along with tx and s/s:

A

A. vasospasm of small arteries in fingers and toes, then very red and swell as blood flow returns
s/s – pallor, numbness, sensation of cold in fingers and toes, may progress to gangrene
tx- remove stimulus, stop smoking, vasodilators, Ca-channel blockers, sympathectomy

55
Q

Q. What is Buerger’s disease (thromboangiitis obliterans), the s/s and treatments?

A
  • -young men, smokers
  • -s/s – pain and tenderness of hands and feet; may progress to gangrene
  • -TX- Stop smoking, vasodilators, sympathectomy (Deep inside your chest, a structure called the sympathetic nerve chain runs up and down along your spine. During a sympathectomy, a surgeon cuts or clamps this nerve chain. This keeps nerve signals from passing through it and used as a last resort)

Block 2 Week 2 Cardiovascular (2 decks)

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