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PCCN study > PCCN Cardiovascular > Flashcards

PCCN Cardiovascular Flashcards

1
Q

Heart Sounds (high-pitch)

A

Use diaphram (bigger side)

S1 (systole) - tricuspid and mitral valves closing
(loudest at apex)

S2 (diastole)- aortic and pulmonic valves closing
(best heard at upper sternal)

***pericardial friction rub (1 systolic, 2 diastolic)
»scratching sound on sys and dia!!!

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2
Q

Heart Sounds (low-pitch)

A

Use Bell (smaller side)

Murmurs- when blood flows backwards d/t dmg’d valves **(best heard laying left lateral position at apex)
»systolic murmur: REGURGITATION (valve s/b closed, but doesn’t so back flow into atria)
»diastolic murmur: STENOSIS (valve s/b open, but narrowed)

S3 sloshing sound, S1 S2 S3
»in HF

S4 a stiff wall, S4 S1 S2 (late stage of diastole marked by the atrial kick when last 20% delivered to ventricles)
»in CAD, HTN, early CHF, cardiomyopathy, aortic stenosis

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3
Q

Auscultation site of Heart Sounds

tested most on regurgitation murmurs

A

APT M

Aortic: 2nd ICS&raquo_space;R sternal border **hear S2, diastole
**if murmur heard, aortic stenosis (use bell)

Pulmonic: 2nd ICS&raquo_space;L sternal border **hear S2
**if murmur heard, pulmonic stenosis (use bell)

Tricuspid: 4th ICS» L Sternal border

  • *may hear systole regurgitation w/ bell
  • *may hear diastole stenosis w/ bell

Mitral: 5th ICS» L MCL hear S1, systole

  • *may hear systole regurgitation w/ bell
  • *may hear diastole stenosis w/ bell
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4
Q

What part of stethoscope is used to listen for murmurs?

A

the Bell, small side.

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5
Q

How does acute mitral regurgitation present?

A

pulmonary edema, dyspnea and tachypnea

d/t rupture of papillary muscle
murmur heard in mitral position at apex

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6
Q

Are aneurysms loud or quiet?

A

quiet, not alot of blood moving around

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7
Q

Where are Baroreceptors and what do they detect?

A

Internal carotid arteries and aortic arch
»detect chgs in BP
–drop in BP, then sympathetic response activated
–incr in BP, then parasympathetic response

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8
Q

Where are chemoreceptors and what do they detect?

A

Internal carotid arteries and aortic arch
»detect chgs in pH, O2, CO2
–↓pH, ↓O2, ↑CO2 sympathetic response (resp acid)
–↑pH or a ↓CO2 parasympathetic response

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9
Q

How do beta blockers work?

A

decrease HR and contractillity, quiets the heart

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10
Q

What happens when ventricles are overstretched?

A

decreased contractility, the muscle fibers are stiff;

also BNP is released (can detect how bad HF is)

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11
Q

How should dopamine be administered?

A

always thru a central line d/t tissue necrosis if infiltration occurs

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12
Q

Metabolic syndrome

A

> > Abdominal obesity (Waist >=40 in men, >= 35 in women)
HDL cholesterol < 40 mg/dL men or < 50 mg/dL women
SBP of 130 or greater,
DB of 85 or greater
Triglyceride level of >= 150 mg/dl
Fasting glucose of 100 mg/dL or greater

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13
Q

Risk factors of CV dz

A 
HTN
smoking
sedentary lifestyle
Obesity
DM
hyperlipidemia
family hx of prevmature CVD
Metabolic syndrome
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14
Q

ST segment abnormalities in non-ACS syndromes

A

DEPRESSION:
digitalis effect

ELEVATION:
acute pericarditis (stemi in all leads)
LV aneurysm
BBB
***Hyperkalemia
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15
Q

T wave abnormalities in non-ACS

A

inverted T wave: pericarditis

***Prominent T wave: hyperkalemia

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16
Q

Cardioversion vs Defibrillation vs Pacing

A

CARDIOVERSION: pt has pulse; synchronized

  • -aims to convert an unstable, fast arrhythmia back to sinus rhythm
  • -energy delivered to specific part of rhythm, R or QRS complex

PACING: pt has atrial activity to pace

  • -used when HR TOO LOW to maintain perfusion or when pt has heart BLOCK
  • -keep until pt able to have pacemaker placed

DEFIBRILLATION: unsynchronized

  • -tx for life threatening arrhythmias
  • -Vfib and pulseless Vtach
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17
Q

What is the effect of nitroglycerin?

A

VASODILATOR

decreases preload mostly, decrease afterload as well which results in decreased myocardial O2 demand

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18
Q

pt with acute inferior wall MI is at risk for what?

A

sinus bradycardia and Av heart block

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19
Q

what effects do beta blockers have?

A
  • -decrease fight/flight response- block beta receptors
  • -quiets myocardium, *slowing conduction thru AV node
  • -decrease mortality in recent MI and HF
  • -preventing tachyarrhythmias; slow HR and ↓BP
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20
Q

When and How should ADENOSINE be given?

A

–to convert SVT rhythms (atrial)
–tell pt may feel CP for a moment
»6mg IV fast + rapid NS flush; no response 12mg IV fast
–will see long pause on EKG; stops ventricular

***medication effective if conversion to NSR

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21
Q

Long QT

A

QT interval = depolarization and repolarization of myocarium

QT interval dependent on HR, inverse

  • -↑HR, ↓QT interval
  • -↓HR, ↑QT interval

Long QT: risk of sudden cardiac death
>440 msec = 2-3x more likely
>0.50 is dangerously prolonged
**torsades de pointes

Short term tx for torsades:
—>cardioversion, replace Mg, K, Ca
»give Mg no matter serum level, give 2g over 2-3min

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22
Q

Brugada Syndrome

A

high risk for sudden cardiac death in young, healthy adults (nocturnal VT, Vfib, SVT common)
–genetic, drug induced or unmasked w/ Na+ channel blockers, Ca++ channel blockers, cocaine and alcohol
»distinct ↑ST seg in V2
»ST seg and Twave chgs in V1-V2-V3

Tx: ICD placement, genetic testing

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23
Q

Signs of instability with A-fib

A

SOB, chest pain, decrease LOC, hypotension

> > pt unstable: cardiovert immediately
pt stable: diltiazen or BB, possible anticoagulation if more than 48hrs

24
Q

Chronic Afib treatment

A

Long term warfarin (coumadin)- prevent blood clots

Ca Ch Blocker or Beta blocker- control HR

25
Q

Pericarditis

A

–is inflammation of pericardium
>friction rub at apex

  • -fever, CP (sharp/stabbing from rub),
  • *pulsus paradoxus (↓BP on inspiration)

> > **diffuse ST elevation in most leads
troponin ↑ (dmg from squeezed ♥)

INTERVENTION: have pt sit up and lean fwd, pain relief with NSAIDS or morphine

26
Q

Cardiac tamponade

A

EMERGENCY!!!
–is rapid fluid accumulation, so much the ♥ can’t pump

**narrowing pulse pressure (↓SBP ↑DBP) = hypotension + compensatory tachycardia
»leads to dramatic fall in CO b/c of impaired diastolic filling

INTERVENTION: elevate legs, O2, IVF to ↑preload, pericardiocentesis

27
Q

Persistent ST seg elevation for weeks after an AMI may indicate what?

A

ventricular aneurysm

|&raquo_space;complication after a heart attack d/t a patch of weakened tissue in ventricular wall

28
Q

What does Amiodarone treat?

A

life threatening arrythmias!

Vtach, persistent Vfib, Afib

29
Q

Which leads help distinguish RBBB from LBBB?

A

V1 or V2 (b/c monitoring septal) [V1 best]

30
Q

Which lead is best for ST segment monitoring for demand related ischemia in pt w/ no cardiac hx?

A

V5

31
Q

Which lead(s) are best for ST segment monitoring in pt with ACS or suspected ACS?

A

III and V3

32
Q

Complications of PCI

A

**Pseudoaneurysm–is a collection of blood that forms between the two outer layers of an artery (true includes all 3 layers)
»s/s: pain or burning at groin or back area, swelling at site, PULSATING MASS, ecchymosis

**AV fitstua: swelling, pain in groin or leg; tachycardia or ↓BP (b/c blood goes from high arterial to low venous pressure and cause swelling)

**Retroperitoneal hematoma: mod to severe BACK PAIN; tachycardia and ↓BP

**Arterial occlusion: loss of pulse; pain/pallor/paresthesia

**femoral neuropathy: pain, tingling at groin site, numbness at insertion site or down the leg, difficulty moving leg, decreased patellar tendon reflex

**stroke

33
Q

what is stress testing looking for?

A

dyspnea (difficult/labored breathing), dizziness, CP; chg in HR and BP and ST segment depression

  • -done with exercise or
  • -Rx: persantine, dobutamine or adenosine

(if pt taking digoxin, CCB and BB; hold 24-48hrs before if safe)–not for pt with abnormal resting EKG

**increased specificity and sensitivity increases with ECHO before/after stress test or use of nuclear imaging (less uptake of radioisotope means perfusion defect)

34
Q

What is seen with transesophageal echo (TEE)?

A

used to detect if there is a thrombus in atria before cardioversion!!!

best visualization of valves, look for thrombus or vegetation (mass)

35
Q

What is seen with ECHOcardiography?

A

see wall motion and valve activity and estimate EF

–can assess LV hypertrophy in adults w/o s/s of heart dz but are Hypertensive

36
Q

Why is troponin detection linked to adverse events?

A

I and T are VERY specific for myocardial injury b/c only in heart, not influenced by skeletal muscle

onset increase 3h after ischemia occurs
peak 14-18 hr
fall/rtn to normal 5-7d in ACS

  • -elevated w/ STEMI (+) and NSTEMI (may initially be -)
  • -elevated even w/o thrombus ischemia (ACS) b/c with problems like sepsis, bleeding and HF oxygen is not meeting the heart demand

*troponin does not go up with unstable angina

37
Q

How often does Afib occur after heart sx? How do you treat?

A

25-30% of pts, usually in 48-72 hours post-op

–less likely to occur with mag sulfate, preop statin, ASA, BB 12-24hrs post-op

If stable, rate cntrl, anticoagulate; convert to SR
–80% convert back to SR w/in 24h, especially if they were on BB
==Diltiazem (if pt had slow sinus prior), amiodarone for SVT afib; Mag sulfate converts 60% to NSR in 4hrs

> > if meds are unsuccessful in 24-36hrs, need to cardiovert (thrombus found by TEE in 14% of pt w/in 3d of developing AF)

38
Q

What is the most frequently missed preventable cause of sudden cardiac death?

A

aortic aneuryms
»can assess peripheral pulses and blood pressure on both sides; if BP difference >20mmHg in upper extremities, indicates dissection

–monitor UOP (flow to kidney), mentation (flow to brain), hemodynamic monitoring

39
Q

s/s of abdominal aortic aneurysm

A

INSTANT, SEVERE ONSET

> > absence of pulses, pulsation in abdomen, sharp severe abdominal pain that is continuous and ***radiates to back, hips, scrotum, pelvis (rupture)
–losing vascular blood!!! —>syncope, hypovolemic shock

40
Q

s/s of thoracic aortic aneurysm

A

INSTANT, SEVERE ONSET, TEARING OR RIPPING (pt feels like they will die)

> > sudden, treating CP radiating to the shoulders, neck and back, cough, weak voice, hoarseness

41
Q

Which 2 arrhythmias are seen post op valve replacement?

A

A-fib and Heart blocks

42
Q

What dysrhythmia is most commonly assoc. w/ mitral stenosis?

A

Afib

mitral stenosis causes LA enlargement, leading to Afib

43
Q

Pathophysiology of HF

A

HF leads to ↓CO, so less ↓kidney perfusion… less blood flow so the RAA system activated which causes Na+ and H2O retention, SNS stimulated to ↑HR and arterial vasoconstriction in periphery….

> > > myocardial remodeling»> chg in shape and fxn of the heart–change in each cell !!!!

44
Q

RAAS

Renin-Angiotensin-Aldosterone System

A
  1. liver releases hormone angiotensinogen
  2. in response kidney releases enzyme RENIN
  3. ***angiotensinogen + renin = ANGIOTENSIN-1
  4. in response to angiotensin-1 in blood stream, the lungs release ACE (angiotensin converting enzyme)
  5. ***angiotensin-1 + ACE = ANGIOTENSIN-2
  6. Angiotensin-2 (most potent vasoconstrictor) acts on…
    a) adrenal glands, which then releases tell pituitary to release ALDOSTERONE causing ↑ renal reabsorption of Na, increasing fluid retention = ↑BP
    b) Angiotensin-2 acts on kidneys causing vasoconstriction in arterioles = ↑BP
45
Q

What causes BNP to be released and what is effect?

A

BNP is stimulated by excessive stretch in ventricles

> > causes vasodilation, promote homeostasis w/ diuresis and excreting Na++ in the urine

46
Q

Left Heart Failure

A

● Pulmonary congestion/ edema
● Dyspnea/Shortness of breath/Tachypnea
● Cough (with/without pink-frothy sputum)
● Paroxysmal nocturnal dyspnea
● Adventitious lung sounds (crackles, expiratory wheezes)
● S3 and or S4
● Decreased cardiac output
● Fatigue, dizziness, syncope, confusion, restlessness
● Cool, pale skin
● Tachycardia/palpitations/angina
● Weak peripheral pulses
● Oliguria
● Displaced PMI
(An apical impulse that is laterally displaced past the midclavicular line)

47
Q

Right Heart Failure

A 
• Intravascular and interstitial
congestion
• Jugular Venous Distention (JVD)
• Peripheral/dependent edema
• Weight gain
• Hepatomegaly
• Ascites, distended abdomen
• Decreased appetite, nausea/vomiting
• Positive abdominojugular reflex
• Enlarged/tender liver
48
Q

Diagnosing HF

A
  • -Plasma BNP (>100pg/ml)
  • -CSR (cardiomegaly, pleural effusions, pulmonary vascular congestion)
  • -ECG
  • -Coronary angiogram (assess CAD, used in coronary revascularization, hemodynamic measurements)
49
Q

Treatment/Management of HF

A

Treat cause
»revascularization, manage BP, valve repair/repace, PCI stent

Manage fluid volume
»Diuretics (loop strongest- furosemide, bumetanide)
»2g/day sodium
»1500ml/day free water restriction
–evaluate electrolyte and renal function

improve ventricular fxn: vasodilation, ↓Na/H2O retention, preserve renal fxn, ↓ventricular remodeling

> > beta blocker- blunt sympathetic/stress response
–can cause hypotension, chg positions slowly; caution with asthma/COPD (bronchospasm)
>ACE inhibitor (-pril)- improve structure and fxn of heart
–ARB (-sartan) if ACEI not tolerated d/t cough

50
Q

What is most common type of cardiomyopathy in USA?

A

Dilated–both ventricles dilate
–systolic and diastolic dysfunction
»lower Stroke volume, EF, & CO –> incr HR
–when LV enlarged it pulls the mitral valve out and regurgitation occurs
–blood stasis precludes DVT; high risk of pulm embolism

51
Q

Why should drugs that decrease preload be avoided with hypertrophic cardiomyopathy?

A

hypovolemia is detrimental, LV is dependent of adequate preload for CO;

the ventricles are stiff, result in diastolic dysfunction;
ventricles can’t fill

52
Q

HYPERTENSIVE emergency vs urgency

A

EMERGENCY: immediate reduction
»SBP=>180
»DBP=>110

tx—initial goal: reduce MAP by no more than 25% to get to 160/100 in 2-6hr or a DBP of 100-110 in 30-60min
»>Clevidipine (specific for HTN crisis)–CaChBlker

URGENCY: need to reduce in few hours
»SBP=>160
»DBP=>100

53
Q

What is Beck’s triad?

A

muffled heart sounds, increased JVD and hypotension

CARDIAC TAMPONADE

> > pt needs Echo followed by pericardiocentesis

54
Q

s/s Acute arterial occlusion

A

Blood not getting to tissue

  • pain on elevation of extremity
  • pale, mottled if elevated; rubor (blush) if dependent
  • hair loss, shiny skin
  • weak or absent pulses
  • cool skin
  • sluggish capillary refill
  • bruit

When the blood clots go to your legs and block the artery, the legs tend to become very painful and then develop numbness, tend to be pale in color, tend to be cool and have no pulses, and you have just a few hours to get these diagnosed and treated as well before there is loss of tissue or parts of your limb distal to this.

55
Q

DVT s/s

A
  • Red areas on the leg
  • Swelling in one area or on one leg
  • Pain or tenderness in one leg
  • Temperature differences between the two legs (a leg with a clot may be warmer to the touch)

*no loss of pulse

56
Q

Drug tx of dilated cardiomyopathy is used to?

A

decrease preload and afterload

> > if too much fluid coming back to the heart, want to decrease b/c you don’t want the heart to work too hard to pump out

57
Q

Plavix

A
  • onset of action is 6hrs
  • requires several passes thru the liver to convert to is active metabolite
  • should be given prior to PCI

PCCN study (7 decks)

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