Cardiovascular Flashcards
S1
Normal heart sound
“Lub”
Caused by closure of the AV (mitral, tricuspid) valves
Loudest at the apex of the heart
Marks the end of diastole, the beginning of systole
S2
Normal heart sound
“Dub”
Caused by the closure of the semi lunar valves (aortic, pulmonic) valves
Loudest at the base of the heart
Marks the end of systole, the beginning of diastole
S2 splits on inspiration: wide, fixed splitting of S2 is caused by RBBB
52 is louder with a pulmonary embolism
S3
Abnormal heart sound
Caused by a rapid rush of blood into a dilated ventricle
Occurs early in diastole, right after S2
Heard best at the apex of the heart with the bell
Associated with heart failure; may occur before crackles
Ventricular gallop: “Kentucky”
Is also caused by: pulmonary HTN and cor pulmonale, mitral, aortic, or tricuspid insufficiency
S4
Abnormal heart sound
Caused by atrial contraction of blood into a noncompliant ventricle
Occurs right before S1
Best heard at the apex with the bell
Associated with myocardial ischemia, infarction, hypertension, ventricular hypertrophy and aortic stenosis
Atrial gallop: “Tennessee”
Pericardial friction rub
Due to pericarditis, associated with pain on inspiration
May be positional
Murmurs
Valvular disease
Septal defects ( atrial or ventricular)
Murmurs of insufficiency (regurgitation) occur when the value is closed
- acute or chronic
Murmurs of stenosis occur when the valve is open
-Chronic problem develops over time
- not acute
Pulse pressure
Systolic - diastolic = pulse pressure
Normal is 40- 60 mmHg (120/80)
SBP
Indirect measurement of the cardiac output and stroke volume
A decrease in SBP with little change or an increase in DBP is narrowing of the pulse pressure; often seen with severe hypovolemia or a severe drop in cardiac output
DBP
An indirect measurement of the systemic vascular resistance
A decrease in DBP that widens pulse pressure may indicate vasodilation, a drop in SVR; often seen in sepsis, septic shock
Diastole is normally 1/3 longer than systole
Coronary arteries are perfused during diastole
Causes of valvular heart disease
Coronary artery disease, ischemia, and MI
Dilated cardiomyopathy
Degeneration
Bicuspid aortic valve; genetic
Rheumatic fever
Infection
Connective tissue disorders
Valves
Normal heart sounds, S1 and S2, are due to valve closure
Valves open and close based on the pressure changes in the chamber above the value and below the valve
When the pressure in the chamber above a valve is higher than that below the valve, the value opens
When the pressure drops in the chamber above the value and the pressure is greater below the value, the valve closes
Systole: ejection, high pressure
Diastole: filling, low pressure
Diastole is 1/3 longer than systole, needs time for filling
Coronary arteries are perfused during diastole
Systolic murmurs
Lub….shhb…dub
Semilunar valves are open during systole
-Aortic stenosis
- pulmonic stenosis
AV valves are closed during systole
-Mitral insufficiency: will cause large, giant v-waves in the PAOP tracing if the patient has a PA catheter
- Triicuspid insufficiency
Ventricular septal defect, which is the most common with an acute MI, which may result in a systolic murmur
Diastolic murmur
Lub…dub…shhb
Semilunar values are closed during diastole
- aortic insufficiency
- pulmonic insufficiency
AV valves are open during diastole
- mitral stenosis is associated with a fib due to atrial enlargement that occurs over time
-Tricuspid stenosis
Acute coronary syndrome
Due to platelet-mediated thrombosis
May result in sudden cardiac death
Types include:
-Unstable angina: cp at rest, unpredictable, may be relieved NGT, trops (-), st depression, or t-wave inversion
- non ST elevation myocardial infarction: trops (+), st depression, T ware inversion, unrelenting cp
- st elevation myocardial infarction: trops (+), st elevation in 2 or more contiguous leads, unrelenting cp
* variant or prinzmetal’s angina
- a type of unstable angina associated with transient ST segment elevation
- due to coronary artery spasm with or without atherosclerotic lesions
- occurs at rest, may be cyclic (same time each day)
- may be precipitated by nicotine, etoh, and cocaine ingestion
- trops (-)
- NTG administration results in relief of cp, STs return to normal
Management of acute chest pain
Stat EKG done and read in 10 min
- allows categorization of steals o nstenu STEMI or NSTEMI/ unstable angina
Allows risk stratification to high, medium, low
Aspirin: give ASAP; is chewed: improves morbidity/ mortality
Anticoagulant: heparin or enoxaparin
Antiplatelet agents: clopidogrel (plavix), abciximab (reopro), eptifibatide (integrilin), tirosban (aggrastat)
Beta blockers
-Unless acs is due to cocaine
-Use cardioselective such as metoprolol (lopressor): do not use non-cardioselective such as proprandol (inderal)
- contraindications include hypotension, bradycardia, use of phosphodiesterate inhibitor drugs such as sildenafil (Viagra)
Treat pain: NTG, morphine
History, risk factor assessment: cardiac biomerkers, lipid profile, CBC, electrolytes, bun, creatinine, mg, PT, PTT
EKG changes and location of cad
Changes in II, III, aVF → RCA, inferior LV
Charges in V1, v2, v3, V4 → LAD, anterior LV
Changes in v5, V6, I, aVL → circumflex, lateral LV
Changes in v5, V6 → low lateral LV
Changes in I, AVL → high lateral LV
Changes in v1, V2 → RCA, posterior LV
Changes in V3R, v4R → RCA, R ventricular (RV) infarct
Inferior MI
Associated with the RCA occlusion
ST elevation in II, III, and aVF
Reciprocal changes in lateral wall
Associated with AV conduction disturbances: 2nd degree type I AV block, 3RD degree AV block, SSS, and sinus bradycardia
Development of systolic murmur: mitral valve regurgitation secondary to papillary muscle rupture (posterior papillary muscle was only one source of blood supply - the RCA)
Tachycardia is associated with an inferior MI → higher mortality
Also associated with RV infarct and posterior MI
Use beta blockers and NTG with caution
RV infarct
The RCA, which supplies the inferior wall of the LV, also supplies the RV; therefore, about 30% of inferior wall MI patients also have a RV infarct
Size of the infarct will determine Sx
A r sided EKG may demonstrate the ST changes
Signs/ Sx: JVD at 45°, high CVP, hypotension, usually clear lungs, bradyarrhythmias, EKG with ST elevation in V3R,V4R
Tx: fluids, positive inotropes
Avoid: preload reducers → nitrates, diuretics; caution with beta blockers, often cannot give initially due to hypotension
Anterior MI
Associated with LAD occlusion
St elevation in v1-v4: precordial leads, v leads
Reciprocal changes (ST depression) in inferior wall (II, III, aVF)
May develop 2ND - degree type II AV block or RBBB (the lad supplies the common bundle of his) → ominous sign
Development of systolic murmur: possible ventricular septal defect
Higher mortality than an inferior MI: heart failure
Lateral MI
St elevation in v5, v6 (low lateral)
St elevation in I, aVL (high lateral)
Generally involves LCA
Treatment of STEMI
Determine onset of infarct, if Sx <12 hrs → reperfusion
- percutaneous coronary intervention - standard is door to drug within 90 min
- fibrinolytic drug therapy - standard is door to drug in 30 min
Eligibility criteria
- st elevation in 2 or more contiguous leads or new onset LBBB
- onset of cp <12hrs
- cp of 30 min in duration
- cp unresponsive to sublingual NTG
Patient care following reperfusion for STEMI: PCI
90 min door - to balloon inflation in coronary artery at point of lesion
Monitor for signs of reocclusion: cp, ST elevation → contact physician
Monitor for vasovagal reaction during sheath removal → give fluids, atropine
- hypotension <90 systolic with or without bradycardia, absence of compensatory tachycardia
-Associated Sx of pallor, nausea, yawning, diaphoresis
Monitor for bleeding: sheath site
- immediately apply manual pressure 2 finger breadths above the puncture site
Continue manual pressure for a minimum of 20 min (30 min if still on GP IIb/ Illa inhibitors) to achieve homeostasis
Monitor for bleeding: retroperitoneal → fluids, blood products
- sudden hypotension, severe low back pain
Monitor for vascular complications → pulse assessment
Patient care following reperfusion for STEMI: fibrinolytic therapy
Absolute contraindications
- any prior intracranial hemorrhage
- known structural cerebral vascular lesions (e.g. Arteriovenous malformation)
- known malignant intracranial neoplasm (primary or metastatic)
-Ischemic stroke within 3 months except acute ischemic stroke within 3 hrs
- suspected aortic dissection
- active bleeding or bleeding diathesis (excluding menses)
- significant closed-head or facial trauma within 3 months
Evidence of reperfusion
-Cp relief: due to fibrinolysis of clot
- resolution of ST segment deviations: due to return of blood flow
- marked elevation of trops / ck-mb: due to myocardial “stunning” when vessel opens
- reperfusion arrhythmia (vt, vf, accelerated idioventricular rhythm (aivr): due to myocardial “stunning” when vessel opens
Nursing management
- assess for major and minor bleeding (major bleed, change in loc, brain bleed)
- institute bleeding precautions
- assess for reperfusion
- assess for reocclusion as evidenced by reoccurring cp, St deviation
Treatment of NSTEMI
No emergent reperfusion
Same meds as STEMI
If high risk score or continued cp, signs of instability, start GP IIb/ IIIa inhibitors (integrilin, reopro) and prepare for dx cardiac cath within 24 hrs
Complications of an acute MI
Arrhythmias-most common
V tach or V fib
- defibrillate VF
- drug therapy for stable, sustained VT and to prevent recurrent VF
- synchronized cardioversion for unstable, sustained VT
Bradycardia, heart blocks, SSS
Atrial fibrillation
- increases risk of mortality 10 - 15% even when returned to NSR
Heart failure
Cardiogenic shock
Reinfarction
Thromboembolic events
Pericarditis
Ventricular aneurysm
Ventricular septal defect
Papillary muscle rupture
Cardiac wall rupture
Interventional cardiology
Diagnostic cardiac cath
Percutaneous coronary intervention
- intracoronary stenting: most common PCI procedure
-Balloon angioplasty without stent (ptca): seldom used, high reocclusion rates
Percutaneous balloon valvotomy
Pacemaker implantation
Electrophysiology studies
-Implantable cardioverter defibrillator (icd)
- cardiac ablation therapy
Goal of PCI with stent
Restoration of blood flow distal to a coronary artery lesion with partial or total occlusion
Complications of PCI
In hospital death is rare 1.8%
In-hospital MI 0.4%
Coronary artery perforation
Distal coronary artery embolization
Intramural hematoma
Failure of stent deployment
Stent thrombosis
- most incidents occur acutely (within 24 hours of stent placement) or subacutely (within the first 30 days)
Stroke or TIA: greater risk if with aortic stenosis
Arrhythmias
Renal failure
Retroperitoneal bleed
Patient care during sheath removal
Record baseline peripheral pulses and vitals
Provide comfort (i.e. Morphine 2-4 mg IV) before removal
Monitor BP q5-10 min during sheath removal
Monitor for vasovagal response (hypotension <90 systolic with or without bradycardia, absence of compensatory tachycardia and associated sx of pallor, nausea, yawning, diaphoresis)
Vasovagal management
- hold nitrates
- atropine 0.5 mg iv (even in absence of bradycardia if other signs occur)
-IV bolus of 250 mL 0.9 NS if patient is not immediately responsive to atropine
- assess for anxiety/ pain as contributing factors
Achieve homeostasis
- Manual pressure for 20 to 30 min
- mechanical clamp compression using FemoStop or c-clamp
Manage complications of cardiac cath procedures
Monitor for signs of coronary artery reocclusion (if PCI): cp, st-elevation → contact physician
Monitor for vasovagal reaction during sheath removal → give fluids, atropine
Monitor for bleeding: sheath site
-Immediately apply manual pressure 2 finger breadths above the puncture site
-Continue manual pressure for a minimum of 20 min (30 min if still on GP IIb/ IIIa inhibitors) to achieve homeostasis
Monitor for bleeding: retropertoneal→ fluids, blood products
- sudden hypotension
- severe low back pain
Monitor fur vascular complications: pulse assessments
Monitor for hematoma at sheath insertion site: assess sheath insertion site for swelling
Hypertensive crisis/emergency
Hypertensive emergency or crisis is elevated BP with evidence of end organ damage (brain, kidney, heart, retina) that can be related to acute hypertension → needs critical care admission
Hypertensive urgency is elevated BP without evidence of end organ damage → usually no need for critical care admission
Greatest risk is stroke
Treatment of hypertensive crisis or emergency
Emergent lowering of BP needed
Nitroprusside (nipride)
- preload and afterload reducer
- assess for cyanide toxicity secondary to drug metabolite (thiocycnate): mental status change restlessness, lethargy), tachycardia, seizure, a need for increase in dose, unexplained metabolic acidosis, especially in those with renal impairment or when a drug is used >24 hours
Labetalol (normodyne, trandate)
-Intermittent IV doses preferred to a continuous infusion, due to the possibility of continuing the drug beyond the maximum dose of 300 mg
- duration of effect persists 4-6 hrs after IV dose is d/c
Peripheral artery disease signs and symptoms
Pain (activity, rest)
Pallor
Pulse absent or diminished
Paresthesia
Paralysis
Poikilothermia: loss of hair on toes or lower legs: glossy, thin, cool, dry skin (chronic sign of pad)
Additionally, cool to touch, minimal edema
Peripheral artery disease testing
Ankle brachial index (Abi)
- test to assess for pad
-Used to assess the adequacy of lower extremity perfusion
- normal is > 0.90
— divide the ankle pressure by the brachial pressure on the same side
Additional diagnostic testing
- Doppler ultrasand
- arteriography
Peripheral artery disease management
Embolectomy, bypass graft, angioplasty
Bed in reverse trendelenburg
Do not elevate the affected extremity - will decrease perfusion
Medications
-Thrombolytics (tpa)
- anticoagulants (heparin)
- anti platelet agents (Asa, clopidogrel)
- vasodilators
Acute symptomatic carotid artery disease signs and sx
Transient ischemic attack (tia)
Mononuclear visual disturbances
Aphasia
Stroke
Acute symptomatic carotid artery disease Dx test
Angiography (gold standard): risk of stroke during exam
Carotid duplex ultrasound
CTA
Magnetic resonance angiography (mra)
Acute symptomatic carotid artery disease management
Carotid endarectomy (cea)
Carotid stenting
