Sinus Tachycardia causes include stimulants, pain, fever, shock, hemorrhage AV node intrinsic HR 40- 60 Afterload resistance LV must overcome to circulate blood. ↑aortic stenosis, septal hypertrophy, vasoconstriction ↓sepsis, vasodilation Stroke Volume (SV) volume of blood ejected by the heart with each beat Preload volume of blood in LV at end of diastole. Affected by venous return to heart, total blood volume, atrial kick and stiffness and thickness of heart. Ventricular Tachycardia (VT) wide and bizarre complexes, treat with synchronized cardioversion and meds, pulseless requires ACLS and code Positive inotrope increases heart pumping/ contraction ie. Digoxin Ejection Fraction (EF) percent of blood ejected by left ventricle. SV/EDV > 50% is normal Baroreceptors increase or decrease HR in response to pressure changes, ie: hypotension Positive chronotrope increases HR ie. Atropine Troponin only in heart muscle, elevates 3-6 hrs after injury, peaks at 12-48 hrs, returns to baseline 1-2 weeks after End Diastolic Volume (EDV) amount of blood in ventricles at end of diastole before contraction Compliance ability of ventricles to distend or expand Chemoreceptors sense changes in PaO2 or PaCO2, triggers SNS Natriuretic peptides cause vasodilation, increase natriuresis and inhibit SNS and RAAS Supraventricular Tachycardia (SVT) dysrhythmias that start above AV node, treat with carotid massage, Valsalva, adenosine SA node the natural pacemaker of the heart HR 60-100 Contractility ability of heart to pump, inotropy Torsades de Pointes Ventricular Tachycardia in the setting of prolonged QT interval. Can cause VF. Causes include electrolytes and medications Complete Heart Block atria beat independently of ventricles. 20-40 BPM, Low CO, requires pacemaker Negative chronotrope decreases HR ie. BB Creatinine kinase (CK) found in heart, brain and skeletal muscle Sinus Bradycardia causes include vagal responses, ICP, MI, BB, digoxin Starling’s Law the more the LV is stretched the more forceful the contraction. Can only stretch so much and for so long. Negative inotrope decreases the heart pumping/contraction ie. BB CK- MB specific to heart, elevates 3-12 hrs after injury, peaks at 24 hr returns to baseline 2-3 days after Cardiac Output (CO) the volume of blood ejected by the heart in 1 min. 4-6L at rest, HR x SV Sinus Tachycardia causes include stimulants, pain, fever, shock, hemorrhage AV node intrinsic HR 40- 60 Afterload resistance LV must overcome to circulate blood. ↑aortic stenosis, septal hypertrophy, vasoconstriction ↓sepsis, vasodilation Stroke Volume (SV) volume of blood ejected by the heart with each beat Preload volume of blood in LV at end of diastole. Affected by venous return to heart, total blood volume, atrial kick and stiffness and thickness of heart. Ventricular Tachycardia (VT) wide and bizarre complexes, treat with synchronized cardioversion and meds, pulseless requires ACLS and code Positive inotrope increases heart pumping/ contraction ie. Digoxin Ejection Fraction (EF) percent of blood ejected by left ventricle. SV/EDV > 50% is normal Baroreceptors increase or decrease HR in response to pressure changes, ie: hypotension Positive chronotrope increases HR ie. Atropine Troponin only in heart muscle, elevates 3-6 hrs after injury, peaks at 12-48 hrs, returns to baseline 1-2 weeks after End Diastolic Volume (EDV) amount of blood in ventricles at end of diastole before contraction Compliance ability of ventricles to distend or expand Chemoreceptors sense changes in PaO2 or PaCO2, triggers SNS Natriuretic peptides cause vasodilation, increase natriuresis and inhibit SNS and RAAS Supraventricular Tachycardia (SVT) dysrhythmias that start above AV node, treat with carotid massage, Valsalva, adenosine SA node the natural pacemaker of the heart HR 60-100 Contractility ability of heart to pump, inotropy Torsades de Pointes Ventricular Tachycardia in the setting of prolonged QT interval. Can cause VF. Causes include electrolytes and medications Complete Heart Block atria beat independently of ventricles. 20-40 BPM, Low CO, requires pacemaker Negative chronotrope decreases HR ie. BB Creatinine kinase (CK) found in heart, brain and skeletal muscle Sinus Bradycardia causes include vagal responses, ICP, MI, BB, digoxin Starling’s Law the more the LV is stretched the more forceful the contraction. Can only stretch so much and for so long. Negative inotrope decreases the heart pumping/contraction ie. BB CK- MB specific to heart, elevates 3-12 hrs after injury, peaks at 24 hr returns to baseline 2-3 days after Cardiac Output (CO) the volume of blood ejected by the heart in 1 min. 4-6L at rest, HR x SV
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causes include stimulants, pain, fever, shock, hemorrhage
intrinsic HR 40-60
resistance LV must overcome to circulate blood. ↑aortic stenosis, septal hypertrophy, vasoconstriction ↓sepsis, vasodilation
volume of blood ejected by the heart with each beat
volume of blood in LV at end of diastole. Affected by venous return to heart, total blood volume, atrial kick and stiffness and thickness of heart.
wide and bizarre complexes, treat with synchronized cardioversion and meds, pulseless requires ACLS and code
increases heart pumping/ contraction ie. Digoxin
percent of blood ejected by left ventricle. SV/EDV > 50% is normal
increase or decrease HR in response to pressure changes, ie: hypotension
increases HR ie. Atropine
only in heart muscle, elevates 3-6 hrs after injury, peaks at 12-48 hrs, returns to baseline 1-2 weeks after
amount of blood in ventricles at end of diastole before contraction
ability of ventricles to distend or expand
sense changes in PaO2 or PaCO2, triggers SNS
cause vasodilation, increase natriuresis and inhibit SNS and RAAS
dysrhythmias that start above AV node, treat with carotid massage, Valsalva, adenosine
the natural pacemaker of the heart HR 60-100
ability of heart to pump, inotropy
Ventricular Tachycardia in the setting of prolonged QT interval. Can cause VF. Causes include electrolytes and medications
atria beat independently of ventricles. 20-40 BPM, Low CO, requires pacemaker
decreases HR ie. BB
found in heart, brain and skeletal muscle
causes include vagal responses, ICP, MI, BB, digoxin
the more the LV is stretched the more forceful the contraction. Can only stretch so much and for so long.
decreases the heart pumping/contraction ie. BB
specific to heart, elevates 3-12 hrs after injury, peaks at 24 hr returns to baseline 2-3 days after
the volume of blood ejected by the heart in 1 min. 4-6L at rest, HR x SV
