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