PCCN Cardiovascular Flashcards
Heart Sounds (high-pitch)
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!!!
Heart Sounds (low-pitch)
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
Auscultation site of Heart Sounds
tested most on regurgitation murmurs
APT M
Aortic: 2nd ICS»_space;R sternal border **hear S2, diastole
**if murmur heard, aortic stenosis (use bell)
Pulmonic: 2nd ICS»_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
What part of stethoscope is used to listen for murmurs?
the Bell, small side.
How does acute mitral regurgitation present?
pulmonary edema, dyspnea and tachypnea
d/t rupture of papillary muscle
murmur heard in mitral position at apex
Are aneurysms loud or quiet?
quiet, not alot of blood moving around
Where are Baroreceptors and what do they detect?
Internal carotid arteries and aortic arch
»detect chgs in BP
–drop in BP, then sympathetic response activated
–incr in BP, then parasympathetic response
Where are chemoreceptors and what do they detect?
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
How do beta blockers work?
decrease HR and contractillity, quiets the heart
What happens when ventricles are overstretched?
decreased contractility, the muscle fibers are stiff;
also BNP is released (can detect how bad HF is)
How should dopamine be administered?
always thru a central line d/t tissue necrosis if infiltration occurs
Metabolic syndrome
> > 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
Risk factors of CV dz
HTN smoking sedentary lifestyle Obesity DM hyperlipidemia family hx of prevmature CVD Metabolic syndrome
ST segment abnormalities in non-ACS syndromes
DEPRESSION:
digitalis effect
ELEVATION: acute pericarditis (stemi in all leads) LV aneurysm BBB ***Hyperkalemia
T wave abnormalities in non-ACS
inverted T wave: pericarditis
***Prominent T wave: hyperkalemia
Cardioversion vs Defibrillation vs Pacing
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
What is the effect of nitroglycerin?
VASODILATOR
decreases preload mostly, decrease afterload as well which results in decreased myocardial O2 demand
pt with acute inferior wall MI is at risk for what?
sinus bradycardia and Av heart block
what effects do beta blockers have?
- -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
When and How should ADENOSINE be given?
–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
Long QT
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
Brugada Syndrome
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
Signs of instability with A-fib
SOB, chest pain, decrease LOC, hypotension
> > pt unstable: cardiovert immediately
pt stable: diltiazen or BB, possible anticoagulation if more than 48hrs
Chronic Afib treatment
Long term warfarin (coumadin)- prevent blood clots
Ca Ch Blocker or Beta blocker- control HR
Pericarditis
–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
Cardiac tamponade
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
Persistent ST seg elevation for weeks after an AMI may indicate what?
ventricular aneurysm
|»_space;complication after a heart attack d/t a patch of weakened tissue in ventricular wall
What does Amiodarone treat?
life threatening arrythmias!
Vtach, persistent Vfib, Afib
Which leads help distinguish RBBB from LBBB?
V1 or V2 (b/c monitoring septal) [V1 best]
Which lead is best for ST segment monitoring for demand related ischemia in pt w/ no cardiac hx?
V5
Which lead(s) are best for ST segment monitoring in pt with ACS or suspected ACS?
III and V3
Complications of PCI
**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
what is stress testing looking for?
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)
What is seen with transesophageal echo (TEE)?
used to detect if there is a thrombus in atria before cardioversion!!!
best visualization of valves, look for thrombus or vegetation (mass)
What is seen with ECHOcardiography?
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
Why is troponin detection linked to adverse events?
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
How often does Afib occur after heart sx? How do you treat?
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)
What is the most frequently missed preventable cause of sudden cardiac death?
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
s/s of abdominal aortic aneurysm
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
s/s of thoracic aortic aneurysm
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
Which 2 arrhythmias are seen post op valve replacement?
A-fib and Heart blocks
What dysrhythmia is most commonly assoc. w/ mitral stenosis?
Afib
mitral stenosis causes LA enlargement, leading to Afib
Pathophysiology of HF
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 !!!!
RAAS
Renin-Angiotensin-Aldosterone System
- liver releases hormone angiotensinogen
- in response kidney releases enzyme RENIN
- ***angiotensinogen + renin = ANGIOTENSIN-1
- in response to angiotensin-1 in blood stream, the lungs release ACE (angiotensin converting enzyme)
- ***angiotensin-1 + ACE = ANGIOTENSIN-2
- 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
What causes BNP to be released and what is effect?
BNP is stimulated by excessive stretch in ventricles
> > causes vasodilation, promote homeostasis w/ diuresis and excreting Na++ in the urine
Left Heart Failure
● 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)
Right Heart Failure
• 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
Diagnosing HF
- -Plasma BNP (>100pg/ml)
- -CSR (cardiomegaly, pleural effusions, pulmonary vascular congestion)
- -ECG
- -Coronary angiogram (assess CAD, used in coronary revascularization, hemodynamic measurements)
Treatment/Management of HF
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
What is most common type of cardiomyopathy in USA?
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
Why should drugs that decrease preload be avoided with hypertrophic cardiomyopathy?
hypovolemia is detrimental, LV is dependent of adequate preload for CO;
the ventricles are stiff, result in diastolic dysfunction;
ventricles can’t fill
HYPERTENSIVE emergency vs urgency
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
What is Beck’s triad?
muffled heart sounds, increased JVD and hypotension
CARDIAC TAMPONADE
> > pt needs Echo followed by pericardiocentesis
s/s Acute arterial occlusion
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.
DVT s/s
- 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
Drug tx of dilated cardiomyopathy is used to?
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
Plavix
- onset of action is 6hrs
- requires several passes thru the liver to convert to is active metabolite
- should be given prior to PCI
