Cardiovascular Flashcards
When does myocardial perfusion occur?
Diastole
Coronary perfusion pressure
CPP = DBP - PAOP
60-80 mmHg
Preload
-Stretch on the myofibrils at the end of diastole prior to ejection
-Affected by ventricular volume & pressure at the end of diastole
Right heart - CVP or Right atrial pressure (RAP) 2-6 mmHg
Left heart - PAOP 6-12 mmHg
PAOP
6-12 mmHg
closely correlate with LVEDP or PA diastolic pressure
PAOP should not be higher than PA diastolic - check position (should be in Zone 3)
Factors that increase PA systolic
“Lung problems”
pulmonary hypertension
COPD
ARDS
PE
Factors that increase PA diastolic
“Heart problems”
cardiac tamponade
LV failure
Mitral valve disease
Factors that increase PAOP
Left-side heart dysfunction
Mitral stenosis/insufficiency
Cardiac tamponade
Constrictive pericarditis
LV failure
Volume overload
High PEEP (if PEEP>10, PAOP will be inaccurate)
Increased preload
Causes: HF, hypervolemia, bradydysrhythmias
Tx: diuretics, vasodilators (nitro, morphine, nitroprusside, CCBs), ACE inhibitors, ARBS
Decreased preload
Causes: hypovolemia, vasodilation, increased intrathoracic pressure, high PEEP, cardiac tamponade, RV infarct, tachydysrhythmias, afib
Tx: volume - NS, LR, colloids, blood products
Increased/decreased contractility
Increase - SNS stimulation, sympathomimetics (epi, dopamine, dobutamine)
Decrease - Myocardia infarction/ischemia, cardiomyopathy, acidosis, hypoxemia, drugs (anesthesia, barbituates, beta blockers, CCB, antidysrhythmics)
Tx to increase - positive inotropes (digoxin, dobutamin, dopamin)
Afterload
-Pressure that the ventricle must pump against in order to open the semilunar valve
-Affected by vascular resistance, diameter of the ventricular vessels, and volume and viscosity of blood
-Left heart: SVR 900-1400
-Right heart: PVR 100-250
Increased afterload
Causes: SNS stimulation, vasopressors, HTN, aortic valve disease/stenosis, coagulopathy
Tx: systemic vasodilators (Nitroprusside, nitroglycerin, hydralazine, CCBs, ACE inhibitors, ARBs, PDE inhibitors - Milirone); IABP; pulmonary Vasodilators (Oxygen, aminophylline, CCBs, NO, sildenafil - PDE 5 inhibitor)
Decreased afterload
Causes: Hypotension, vasodilation (e.g., shock)
Tx: Vasopressors (norepinephrine, phenylephrine, dopamine, vasopressin)
I, aVL, V5, V6
Lateral wall
LCA (left circumflex artery)
II, III, aVF
- Inferior wall
- RCA (right coronary artery)
- AV node involvement –> dysrhythmia (bradycardia, AV blocks - 1st degree & 2nd degree type I - Wenckebach)
- Check for RV involvement by doing (Rt ECG): avoid nitrates and morphine if confirmed d/t hypotension and give volume
V1
Ventricular septum
V2, V3, V4
Anterior
V1-V4
- Anterior/septal
- Most dangerous MI b/c can lead to possible HF & cardiogenic shock
- LAD (left anterior ascending artery) - supplies bundle of his and bundle branches
- Heart blocks (2nd degree type II, 3rd degree, BBB) - prepare to emergently pace!
- New loud murmur, suspect ventricular septal rupture or papillary muscle rupture
CVP/RAP
right atrial pressure
2-8 mmHg
right ventricle preload
Elevated - fluid overload
Central venous oxygen saturation/ScvO2
>70%
Regional reflection of blood oxygenation from the head and upper torso
Slightly higher than SvO2 as it has not mixed with the venous blood from the coronary sinus
PA pressure (PAP)
Systolic: 15-30
Diastolic: 8-15
“Quater over dime” 25/10
Mean (MPAP): 9-18
>25 mmHg with normal PAOP –> pulmonary hypertension
PA occlusive pressure (PAOP)
6-12 mmHg
Lt arterial pressure
LV preload
Closely correlates with LVEDP or PA diastolic
Elevated PAOP –> left heart failure
Cardiac output/index
4-8 L/min
Cardiac index 2.5 - 4.3 L/min/m^2
CO may be normal when pt is tachycardic w/ low SV as a compensation
Stroke volume/index
50-100 mL/beat
SI 35-60 mL/beat/m^2
PA waveform
a - left atrial contraction
c- Closure of mitral valve
v- left ventricular systole; passive left atrial filling during atrial diastole
A large “V” wave indicates an increase in left ventricular pressure (e.g., mitral regurgitation)
Mixed venous oxygen saturation (SvO2)
60-75%
True mixed venous O2 saturation
Global balance btw DO2 & VO2
Only obtained from a PA catheter
Normal oxygen extraction ratio (O2ER) = 25-30%; 70-75% oxygen still bound to Hgb and returns to the right side of the heart
Increase in SvO2
- Increased O2 supply/delivery
- Decreased demand: anesthesia, sedation, paralysis, hypothermia
- Decreased extraction at tissue level: early sepsis, cyanide toxicity
Left shift on oxyhemoglobin dissociation curve
“sticky” hgb to O2, alkaLOsis (high pH), hypothermia, decreased 2,3 DPG
Decrease in SvO2
- Inefficient O2 supply/demand
- Increased metabolic needs: sz, restlessness, shivering, hyperthermia
Right shift
“less affinity” hgb for O2, acidosis (low pH), muscles, increased temperature, increased 2,3 DPG
Intra-aortic balloon pump
- Treats refractive cardiac failure and cardiogenic shock until surgery
- Increases/augments diastolic BP
- Improves coronary blood flow
- Improves CO up to 15%
- Requires arterial line and EKG signal for time of cardiac cycle
- Inserted via femoral artery and tip rests in the descending aorta.
- Avoid occluding subclavian, carotid, and renal arteries.
Inflates at the beginning of the diastole when the aortic valve closes at dicrotic notch to augment diastolic filling and coronary blood flow.
Deflates before the beginning of the systole R-wave of ECG or upstroke of arterial pressure wave
- Sudden loss of aortic pressure reduces afterload –> lowers heart work to push blood thus myocardial O2 demand.
Contraindications: aortic valve insufficiency/regurgitation, aortic aneurysms, suspected aortic dissection.
Variant (Prinzmetal) Angina
- Vasospastic angina - spasms in coronary arteries
- Usually during rest; at the same time every day
- Results from cold weather, stress, med, smoking, cocaine
-Relieved with CCBs, nitrates
-Dx with provocative testing & ECG
Fibrolytic goal time
30 min from door-to-needle
Cath lab goal time
90 min from door-to-open vessel
Q wave
- 1st negative deflection before QRS
- Pathologic: current of necrosis/infarction
- Result from the absence of electrical activity
- Several hours to develop and rarely goes away
- width >30 ms (0.04 sec) - 1 small square; depth >25% of the height of the R wave
- If contiguous leads, indicative of myocardial necrosis
Nitroglycerin
- Vasodilator that reduces preload
- Decreases myocardia O2 consumption
- 0.4 mg SL Q5min X3 (SL, IV titration, transdermal)
- Monitor hypotension
- HA is common
- Careful with Inferior MI or RV involvement
- Contraindicated w/ concurrent use of PDE5 inhibitor & RV infarct
Cardiogenic shock
Acute impairment of the heart to pump blood effectively d/t:
- decrease in contractility: acute MI, contusion, myocarditis, acute decompensated HF, drug OD; meds - BB, CCB, barbituates
- impaired filling: dysrhythmias - electrolyte imbalance, cardiac tamponade, noncompliant ventricles
- impaired emptying: valvular dysfunction (stenosis/regurg, papillary muscle rupture), ventricular/septal rupture, massive pulmonary embolus, tension pneumothorax, dissecting aortic aneurysm
S/S: tachycardia, dysrhythmias, cool/clammy, S3, crackles, JVD, peripheral edema, decreased perfusion - mottled skin, decreased UOP
Dx: lactate, ABG, hypoxemia, CXR (pulmonary congestion/edema), elevated troponin, ECG (ST changes + Qwave), Echo (decreased wall motion, valvular abnormality, cardiac tamponade)
Hemodynamic values:
- Hypotension; decreased MAP <60
- Decreased CO/CI <2L/min/m^2
- Increased preload (CVP/PAOP) (w/ associated pulmonary sx)
- Increased SVR >1600 (d/t vasoconstrictive compensatory mechanisms)
- Decreased SvO2 <65%
Tx: Oxygen, CV support (Vasopressor to increase MAP & SVR, Inotropes - dobutamine to increase contractility, diuretic and nitro to decrease preload, vasodilator - nitro and Nipride - to reduce afterload), mechanical support (IABP, LVAD, Impella), treat the cause
Cardiac tamponade
- Compression of the heart d/t fluid in the pericardium
- Beck’s Triad: elevated CVP/JVD, hypotension, muffled heart sounds
- Other s/s: tachycardia, wide mediastinum on CXR, sudden drop in chest tube output, narrowed pulse pressure (normal 40), pulsus paradoxes (>10 drop in BP during inspiration), PEA, electrical tremens
- Tx: pericardiocentesis for pericardial effusion, median re-sternotomy for myocardial compression
S3
- Ventricular gallop
Rapid rush of blood into the dilated ventricle - Early in diastole, right after S2
- Normal in young, high cardiac output, and 3rd trimester of pregnancy
- Associated w/ HF; may occur before crackles
- Caused by: fluid overload/elevated preload (pulmonary HTN, cor pulmonale; mitral, aortic, tricuspid insufficiency; VSD; cardiomyopathy)
S4
- Atrial gallop
Atrial contraction of blood into the noncompliant ventricle - Right before S1
- Associated with myocardial ischemia, infarction, HTN, ventricular hypertrophy, and aortic stenosis
Dilated cardiac myopathy
- Damage to myofibrils resulting in decreased contractility and systolic dysfunction –> global dilation of the heart chambers
- Cardiac remodeling (ACE inhibitor reduces severity)
- Tako-tsubo-stress cardiomyopathy
- Dx: CXR (cardiomegaly, pulmonary congestion), ECG (afib), echo (decreased ventricular motion, decreased EF, enlarged chambers)
Hypertrophic cardiac myopathy (HOCM)
- Hypertrophy of heart muscle, ventricular septum, and walls –> rigid & non-compliant ventricles (diastolic dysfunction) –> sudden cardiac death
- Mitral regurgitation d/t stretching of papillary muscles and mitral valve; V4, mumur
- Decreased CO
- Inotropes contraindicated
- Tx: BB, CCB, ICD for sudden cardiac death and ventricular arrhythmias, surgical interventions
Systolic heart failure
- HFrEF <40%
- AKA “congested heart failure”; acute decompensated HF
- Dilated, thin walls; damage to myofibrils; elevated BNP d/t the stretch of ventricles
- Increase preload & afterload (CVP/RAP, PAOP, SVR, PVR)
- Tx: ACEI/ARBS; Angiotensin receptor blocker/Neprilysin inhibitor (Entreso); Beta blocker; Aldosterone antagonist (spironolactone); hydralazine (afterload reducer) + Isosorbide dinitrate (preload reducer); vasodilator (nitrates)l diuretics; cardiac glycosides (digoxin)
- Long-term Tx: biventricular pacing if BBB, cardiac transplant, LVAD/RVAD/BiVAD, (+) inotropes
Diastolic heart failure
- HFpEF>40%
- Stiff, thickened walls; LV hypertrophy
- Tx focus on treating HTN
Pericarditis
- Inflammation of pericardial sac
- Causes: post-MI, Dressler’s syndrome (2-12 weeks after MI, caused by an autoimmune response or viral infection), uremic, viral, neoplastic
- S/S: sharp stabbing CP; pain better sitting up, worse with coughing; pericardial friction rub; diffuse ST changes on ECG (ST elevation in ALL leads including I & II); pericardial effusion; fever
- Tx: pain improved by leaning forward; NSAIDs, Abx, pericardiocentesis, pericardial window
Aneurysm dissection
- separation of the layers of the arterial wall –> blood enters btw layers –> expands the tear and creates false lumen
- high BP & HR
Aneurysm rupture
- Complete perforation of the arterial wall; Medical emergency!
- Causes: HTN, pregnancy-induced HTN, atherosclerosis, smoking, COPD, male >65, connective tissue disorders (i.e., Marfan’s syndrome), congenital
- S/S: sudden, severe, central CP; acute hypotension; tachycardia; syncope; shock
- Tx: surgery; if high BP - Nipride (watch for thiocyanate toxicity), Beta blocker, CCBs; if low - IV bolus, blood tx
Pulmonic valve auscultation point
left sternal border, 2nd intercostal space
Aortic valve auscultation point
right sternal border, 2nd intercostal space
Mitral valve auscultation point
Apex
Left mid-clavicular, 5th intercostal space
Tricuspid valve auscultation point
Left sternal border, 4th intercostal space
Post-PCI therapy nursing care
- Retroperitoneal bleeding - “soft BP” responsive to fluid: tachycardia; late sign - flank ecchymosis (Grey-Turner’s sign); assess coags; control bleeding
- Monitor renal fxn 2/2 IV dye
Beta-blockers
- cardioprotective (i.e., metoprolol tartate); reduce arrhythmias
- reduce HR & contractility
- decrease myocardial O2 consumption
ACE inhibitors
- Used if <40%, new heart failure
- decrease intra-cardiac pressures
- prevents cardiac remodeling
- decrease preload & afterload
Posterior wall MI
- ST elevation in the posterior leads V7-V9
- Reciprocal changes in V1-V2 (ST depression & tall, broad R wave)
- RCA or left circumflex occlusion
Papillary muscle rupture
- associated w/ anterior or inferior wall MI
- hemodynamic instability; acute mitral regurgitation
–> new LOUD systolic murmur heard loudest at the APEX (left midclavicular line, 5th intercostal) - Dx by Echo
- Large “v” waves on PAOP
Ventricular septal rupture
- Associated with anterior/septal wall MI
- O2-rich blood shunts from left to right
- S/S: acute SOB, S3, crackles, holosystolic murmur - loudest at the sternal border, 5th intercostal
- Falsely elevated CO on PA d/t left to right shunt; increased SvO2
- Large “v” waves in CVP
Dopamine
- Catecholamine that acts on SNS; positive inotropic effect; stimulates B1 and some B2 & alpha
- Increase HR, BP, SVR
- Monitor for tachyarrhythmias & ventricular ectopy
Norepinephrine/Levophed
- Act on alpha and beta 1
- Increase BP
- Adverse effects: bradycardia, dysrhythmias, HTN, renal artery vasoconstriction
- 1st line for sepsis
Epinephrine (Adrenalin)
- Alpha, Beta 1 & 2
- Increase BP & HR
- Adverse effects: tachycardia, arrhythmia, CP, hyperglycemia
Phenylepinephrine (Neo-Synephrine)
- Pure alpha
- Increase BP
- Adverse effects: reflexive bradycardia, dysrhythmias, HTN, CP
Dobutamine (Dobutrex)
- Positive inotrope; stimulate B1 (some alpha)
- Increase CO & HR
- Side effects: tachycardia, hypo- or hypertension, ectomy, hypokalemia
Milrinone (Primacor)
- PDE inhibitor
- Increase CO, decrease preload; no effect on HR
- Vasodilator
- Long half-life
Nitroprusside (Nipride)
- Vasodilator; decrease SVR
- antihypertensive
- Monitor: hypotension, A-line to titrate, hypoxia d/t intrapulmonary shunt, increased HR from stimulation of baroreceptor, thiocyanate poisoning if given >72hr, methemoglobinemia
Left-side heart failure
“WET LUNGS” - blood backs up to the lungs
- Decreased CO/CI
- Tachypnea, tachycardia
- S3, MVR
- Displaced PMI (point of maximum impulse) - 5th ICS, MCL
- Crackles, cough, frothy sputum
- Increased PAP, PAOP, SVR
Right-side heart failure
“CLEAR LUNGS” - blood backs up to the venous periphery
- JVD, increased CVP/RAP
- Hepatojugular reflex, elevated LFT, hepatomegaly
- Peripheral edema, ascites
- Anorexia, N/V
- Tricuspid regurgitation
Aortic insufficiency/regurgitation
- Diastolic murmur; results in back flow of blood & reduces diastolic pressure –> over time, LV hypertrophy
- Causes: chronic HTN, rheumatic heart disease, endocarditis, Marfan’s syndrome, idiopathic
- S/S: DeMusset sign - head bobbin d/t brisk carotid upstroke, wide pulse pressure (high systolic, low diastolic); “water-hammer” pulse (rapid upstroke & down stroke w/ shorted peak)
Aortic stenosis
- Systolic murmur; pressure gradient between LV & aorta
- S/S: HF, SOB, activity intolerance
- Tx: surgical valve replacement, TAVR - monitor signs of stroke, femoral access site bleeding, bradycardia & heart block
Long QT syndrome (LQTS)
- Delayed repolarization can cause Torsade de Pointes (polymorphic VT)
- QTc >450 msec
- Causes: drugs - amiodarone, quinidine, haloperidol, procainamide; electrolytes - hypokalemia, hypocalcemia, hypomagnesemia
- Tx: Magnesium sulfate; antiarrhythmic based on the cause
Patient care following reperfusion for STEMI: PCI
- Monitor signs of re-occlusion: CP, ST elevation → Contact physician
- Vasovagal rxn during sheath removal → Atropine, fluids
- Retroperitoneal bleeding → fluid, blood products
Sudden hypotension, severe lower back pain - Vascular complications → pulse check
Complications:
- Stent thrombosis - most occurs acutely (w/in 24hrs of stent placement) or subacutely (within the first 30 days)
- Retroperitoneal bleed
Wolfe-Parkinson-White (WPW) Syndrome
- A genetic condition in an abnormal conduction pathway between atria & ventricles that allows re-entry of tachycardia to bypass normal AV node pathway resulting in SVT or pre-excited AFib.
- During SVT: palpitation, dizziness, CP, SOB, and syncope
- In SR, short PR interval & delta wave (slow rise of initial upstroke of QRS)
Tx:
- Radiofrequency ablation to eliminate the reentrant pathway
- Unstable SVT: Synchronize cardioversion or adenosine
- Pre-excited afib: beta-blockers, amiodarone, procainamide IV
- DO NOT give adenosine, digoxin, or CCBs → may enhance antegrade conduction through the abnormal pathway by increasing the refractory period in AV node → VF
Digoxin/Lanoxin
- Increase myocardial contractility
- Slows conduction of impulses through the AV node
- Control ventricular rate in afib or aflutter
- Know apical HR & K+ prior to administration b/c hypokalemia increase risk of Digoxin toxicity
- Digoxin toxicity: bradycardia, prolonged PR interval - 1st degree AV, prolonged QT, vision changes - yellow halos, N/V, dizziness
Pacemaker codes
- First letter: Chamber paced (A, V, or D)
- Second: Chamber sensed (A, V, or D)
- Third: Response to sensing (I - inhibits pacing if QRS is sensed, D - Inhibits & triggers, O - none)
Pacemaker malfunctions
- Failure to pace (no spike at all when expected)
- Failure to capture (spikes w/o QRS for ventricular packing)
- Failure to sense (pacing in native beats)
Hypertensive crisis/emergency
- Acute BP elevation with organ damage (kidney, retina, heart, brain)
- Biggest risk of HTN crisis: STROKE
- SBP>180, DBP >120
- BP both arms r/o aneurysm or steal syndrome
- 12 lead ECG
- Decrease BP by 25% in 1-2 hrs
- Beta-blockers (Esmolol, Labetalol - max 300mg total, Metoprolol)
-Nitrates (Nitroprusside - reduce preload & afterload, assess for Thiocyanate toxicity, mental status change, tachycardia, sz, metabolic acidosis - renal impairment) - CCBs ( Nicardipine, Clevidipine)
- Hydralazine
Peripheral artery disease
- S/S (6 P’s): Pain, Pallor, Pulse - diminished/absent, Paresthesia, Paralysis, Poikilothermia (Chronic)
-Dx: Doppler, arteriography
-
Ankle-brachial index: Normal >0.9
Ankle pressure/brachial pressure on the same side - Tx: Do not elevate extremity, Reverse Trendelenburg, Med - vasodilators, antiplatelet, thrombolytic, embolectomy, bypass graft, angioplasty
Aneurysm
- Causes: Atherosclerosis, HTN, smoking, obesity, bacterial infxn, congenital abnormalities, trauma, Marfan Syndrome: inherited d/o affective connective tissue
- Abdominal Aortic Aneurysms (75%): pulsation in the abdominal area; abdominal or low back pain; N/V; shock
- Thoracic Aortic Aneurysms (25%): sudden tearing/ripping in the chest that radiates to the shoulders, neck, and back; cough; hoarseness, dysphagia, dyspnea, dizziness; difficulty walking, and speaking; Widening mediastinum on CXR
- less than 5cm in diameter & no sx: monitor regularly (US or CT); tx HTN - Beta blocker may slow growth
- Marfan Syndrome often tx sooner
- Thoracic aortic aneurysm causing symptoms >6 cm: surgical repair; aggressive BP & HR control - labetalol gtt
- Dissection: SURGERY
Myocardial contusion
- damaged blood vessels bleed into the heart. Worse outcome than pericarditis
- S/S similar to MI: CP, dyspnea, low-grade fever, ST elevation in the area of injury, death can occur w/in the first 48 hrs
- Aortic valve most risk for trauma - most anterior in the chest
Pulmonary artery catheter (PAC)
- aka Swan-Ganz
- Contraindications: tricuspid/pulmonic prosthetic valve, right heart mass, tricuspid or pulmonic valve endocarditis, LBBB
- Waveforms: a - upstroke of atrial systole (after PR interval), c - often not visible (closure of tricuspid valve for CVP, mitral valve for PAOP), v - atrial diastole (after atrial diastole/tricuspid closure, QRS complex)
