Exam 3 - Diagnoses and ischemia, stenosis, regurgitation

What is included in a patient’s history and physical exam

• Present illness, chief complaint

• Previous illness → risk factors

  • Organ systems/diseases that may affect drug interactions

  • Bypass can make organ systems worse

• Surgical Risk Scoring

  • Method to predict short-term outcomes after cardiac surgery

    • Patient characteristics

    • Risk profiles

    • Surgical practice

    • Outcomes

CBC

hemoglobin/hematocrit assess oxygen carrying capacity, platelet count informs bleeding assessment

Chemistry lab assessment

creatinine assesses renal function; potassium, magnesium, and calcium influence cardiac rhythm and function

Cardiac troponin

Biomarker of myocardial injury

• Interpret changes with symptoms and ECG findings

BNP/NT-proBNP

supports assessment of suspected heart failure; interpret with clinical findings and ECG

PT/INR

coagulation test

• assesses extrinsic/common pathways; INR monitors warfarin (blood thinning)

aPTT

coagulation test

• assesses intrinsic/common pathways; used to monitor unfractionated heparin in appropriate settings

ACT

coagulation test

• monitors high-dose heparin anticoagulation during CPB; intrinsic and common pathways

CT - Computerized Tomography

• Uses radiation to take X-rays of bones and soft tissues from multiple angles

• Coronary CTA requires IV contrast; cardiac CT scoring

MRI – Magnetic Resonance Imaging

• No radiation, magnetic fields + radio waves; can use contrast dye

  • Can’t be used with metal implants - VADs

• Used for deeper soft tissues, cardiomyopathies, chamber size, and volume

• 15min – 2 hours

Stress perfusion imaging: SPECT/PET

Myocardial blood flow and patterns suggesting inducible ischemia or scar

Echocardiography: TTE/TEE

Ventricular function, regional wall motion, valve disease, and pericardial effusion

Cardiac MRI

Ventricular volumes/function and tissue characterization, including scar

What is evaluated in a cardiac assessment

• Heart rate, blood pressure, quality of pulses

• skin coloration (pink vs cyanosis), oxygenation, saturation

• Level of consciousness, urine output

What is evaluated in a respiratory assessment

• System of pulmonary diseases: cough, dyspnea, hemoptysis, cyanosis, COPD, asthma, and tobacco use

• Auscultation of breath sounds

Post-operative management

• Left ventricular performance – function may be temporarily decreased after the heart wakes up

• CO/CI, preload, afterload/SVR/PVR

• MAP, CVP, PAP, PCWP

• Atrial blood gas analysis, CBC, electrolytes, temperature, fluid balance

• EKG, ECHO

Factors that compromise Preload

• Decrease in vascular tone = vasodilation  less blood getting back to the RA

• Excessive diuresis → less blood volume

• Hemorrhage

Contractility, Oxygenation, and Cardiac Function

• Cardiac function is dependent on adequate oxygenation and supply

• Contractility is directly dependent on adequate oxygenation of the myocardium

  • Hypokinesis = weakly contractile

    • Global – weak contraction everywhere, poor myocardial protection

  • Akinetic = non-contractile

  • Dyskinetic = abnormal movement, bulging out in systole

Systolic heart failure

Ventricle can’t contract effectively

• Heart failure with reduced ejection fraction → LV ejection fraction less than 40%

• Impaired contractility → reduced stroke volume and cardiac output and increased LV end-diastolic pressure and volume (preload)

• Clinical: fatigue, hypoperfusion, pulmonary/systemic congestion

• S3 gallop

• Causes: ischemic heart disease, dilated cardiomyopathy, severe regurgitant valvular disease

• Eccentric Hypertrophy – baggy heart

Diastolic heart failure

Ventricle can’t relax properly

• Heart failure with preserved ejection fraction; LVEF greater than 50%

• Impaired relaxation and compliance  abnormal filling despite normal contractility

  • Normal EF + increased LV filling pressures due to reduced compliance

  • Concentric Hypertrophy

• Clinical: dyspnea, pulmonary congestion, exercise intolerance

• S4 gallop

• Causes: hypertension with LV hypertrophy, aging, restrictive/infiltrative cardiomyopathies, pericardial disease, aortic valve stenosis

Preload

Stretch of the myocardial muscle fibers at end-diastole

• As the radius of the ventricles increases the myocardial oxygen requirement also increases

• Starling law: increased myofibril stretch causes more forceful contraction and greater stroke volume

• We can't measure myocardial fiber length, but we can measure ventricular filling pressure via CVP and PCWP

  • Use ECHO to visualize chamber size

• Normal hearts have preload reserve to meet demands of the body from exercise or increased needs

• Heart failure: large increase in preload produces small increase in stroke volume because there is an optimal amount of stretch (x=preload; y=SV)

Compliance

Decreased compliance causes increased wall stiffness → higher pressure despite having the same amount of filling volume

• Increased myocardial oxygen demand due to having to work harder against elevated pressures

• Factors that decrease compliance

  • Ventricular hypertrophy

  • Myocardial fibrosis – may be due to previous MI

  • Pericardial Tamponade

  • Advanced Age

  • Hypoxia and Acidosis – ischemia event

Afterload

Sum of all forces against which the myocardial fibers shorten during systole

• Resistance the LV must overcome to provide outflow for aortic pressure

• Increased afterload increases myocardial stress and myocardial oxygen consumption

  • Has to work hard to generate greater pressure and stronger contraction to eject blood

  • Higher afterload = less stroke volume

• Diseased ventricles are sensitive to changes in afterload  greater dysfunction = more sensitive to changes

Cardiac Cath

• Minimally invasive procedure; thin, flexible catheter is inserted through a blood vessel in groin or wrist and guided up into your heart

• Fluoroscopy = live x-ray

Right heart cath

Right-sided filling pressures, tricuspid and pulmonic valve function, RV function, and mixed venous oxygenation.

• Venous entry; measures the pulmonary system

• Often performed using a Swan-Ganz catheter → measures how much pressure is building up in the lungs and how well the heart is pumping blood to them

• Diagnoses

  • Pulmonary hypertension

  • Evaluate patients for heart failure, heart transplant, or mechanical heart pump

  • Check tricuspid and pulmonary valve pressures

Left heart cath

Left heart provides diagnostic data on coronary anatomy (both right and left coronary arteries), LV function and contractility, and mitral and aortic valve function.

• Most common; enters through the arterial system; measures systemic system

• Identifies blockages in coronary arteries, LV function, and contractility

• Evaluate mitral and aortic valve stenosis or regurgitation

• Measures ejection fraction of the LV

• If severe blockage is found, a stent can be placed

Echocardiography

• Non-invasive ultrasound that uses sound waves to create moving pictures of the heart’s structure, chambers, valves, and blood flow

• Shows wall motion

  • Hypokinesis – reduced movement or contraction of a segment of heart muscle

  • Akinesis – lack of movement or contraction

  • Dyskinesis – abnormal movements

    • Instead of contraction in systole, segment of muscle bulges out

  • Hyperkinesis – increased contraction of heart muscle

    • May be associated with compensatory mechanisms for areas of hypokinesis

Transthoracic ECHO

most common, non-invasive test where a sonographer moves an ultrasound wand over your chest wall

Transesophageal ECHO

specialized probe is gently guided down your throat into the esophagus

ECHO Assessment

• Normal valves open widely to let blood flow forward and close tightly → smooth, thin valve leaflets that move freely

• Stenosis → valve is stiff, thick, or narrowed; cannot open fully

  • Pressure gradient increases because the heart must push harder against the restriction

  • Higher velocity = higher degrees of narrowing

• Regurgitations/insufficiency → leaky valve; valve does not close fully and allows blood to flow backward into the chamber it just left

• Valve area → calculated physical area of the valves: tricuspid: 4-6cm^2, mitral 4-5cm^2, aorta/pulmonary 3-4cm^2

Electrocardiogram - EKG/ECG

• Evaluates heart rate, rhythm, and conduction

• EKG changes can be suggestive of ischemia

  • ST-segment depression or elevation can be indicative of myocardial ischemia

  • Ventricular ectopic beats may also accompany ischemic episodes

Chronotropy

heart rate

• Normal sinus = 80-100 bpm

• Bradycardia less than 60 bpm

• Tachycardia greater than 100 bpm

• Balance between adequate CO and oxygen delivery vs increased energy used and O2 consumption

  • If heart rate increases to compensate for low SV, it uses more energy and therefore increases myocardial O2 consumption

Inotropy

force/strength of myocardial contraction

• How hard the ventricle contracts

• Influenced by calcium available within cardiac muscle contraction

• Positive = increased contractility → increased SV and more O2 consumption

• Negative = decreased contractility → decreased SV

How much oxygen is extracted from coronary blood?

• Myocardium extracts 70-80% of oxygen from coronary blood

• Coronary blood flow must increase to meet demands of myocardium

  • O2 need increases with increased contractility, increased afterload, and increased preload

Resting blood flow through the coronary arteries

• Resting blood flow uses only a small fraction of the coronary artery’s capacity

• Healthy coronaries can dilate to meet increased demand during exercise states

• Coronary stenosis may limit blood flow during exertion before resting flow is reduced

• Blood flow at rest does not decrease until the coronary is narrowed/blocked/reduced by ~80%

   CAD, Atherosclerosis, coronary embolism

   Vasospasm or constriction

   Hypertrophic cardiomyopathy, aortic stenosis

  
  

What can impair coronary perfusion

• Coronary stenosis: if there is a 50% blockage of the coronary artery, there is still enough room to perfuse the myocardium at rest, but during exercise there is not enough room, and the coronary artery cannot dilate enough to make up for it → angina

• Reduced aortic diastolic pressure and elevated LV end-diastolic pressure can impair coronary perfusion

Systolic abnormalities due to ischemia

• Ischemia reduces myocardial contractility and may cause regional wall-motion abnormalities

  • The force of myocardial contraction is directly dependent on oxygen availability

• Myocardial stunning – reversible contractile dysfunction that persists after blood flow is restored

• Hibernating myocardium - chronically dysfunctional but visible myocardium that may improve after revascularization

Diastolic abnormalities due to ischemia

• Occurs before changes in systolic function

• Poorly compliant and resistant to filling → increased filling pressure

• Reduced ventricular compliance increases filling pressures and may contribute to pulmonary congestion

Describe points of LV Pressure Loop

• A = End Systolic volume → volume and pressure in LV during diastole→ LV pressure drops below LA pressure and mitral valve opens

• I = Ventricular filling

• B = End diastolic volume → pressure increases with filling of ventricle

• G = Isovolumetric contraction → pressure rises in LV + depolarization

• C= LV pressure above aortic pressure → aortic valve opens

• F = Ventricular ejection → peak LV systolic pressure

• D = LV begins to relax → pressure drops below aorta → aortic valve closes

• H = isovolumetric relaxation → LV relaxes during diastole, pressure falls → below LA = Mitral valve opens → filling

Width of loop = stroke volume

Area within loop = stroke work  how much work the LV is doing

End-systolic pressure-volume (blue) and End-diastolic pressure-volume (green) relationships

Afterload and LV loop

increase resistance/pressure = more work for LV

• Shift Right + Taller + Narrower = increased afterload

• More resistance and work for the LV means that it has to work harder → generating more pressure and decreasing stroke volume

Preload and LV pressure loop

increased wall tension = increased pressure

• Shift Right + Taller + Wider = increased preload

• More wall tension = more pressure  higher peak pressure

• Increased preload generally increases stroke volume = wider

Contractility and LV pressure loop

Measured using the End-Systolic Pressure line (blue)

• Positive inotropy = increased slope (upward)  loop becomes wider and taller

  • Higher peak pressure + increased Stroke Volume due to stronger contraction

• Negative inotropy = decreased slope (downward)  loop becomes narrower (decreased SV)

Angina

chest discomfort caused by transient myocardial ischemia

Stable angina

Predictable symptoms with exertion or emotional stress; improve with rest or nitroglycerin, causing vasodilation

• Chronic coronary disease

• Plaque is fibrotic/calcified → the opening in the coronary lumen is fixed; if more O2 is required, it can’t supply it and doesn’t have the ability to dilate

Treatment: aspirin, nitroglycerin, beta blockers, lipid-lowering therapy, and CV risk factor management

Unstable angina

New, worsening, or resting symptoms concerning for acute myocardial ischemia

• Acute Coronary Syndrome: Lipid core plaque is vulnerable and can rupture

• No acute troponin rise/fall

• Ruptured plaque requires urgent evaluation for acute coronary syndrome → Door-to-balloon time of 90 minutes decreases mortality rate

Treatment: ECG monitoring, nitroglycerin, aspirin, beta-blockers, cardioversion, amiodarone, diltiazem,

Symptoms of angina

• Mental status → dizziness, weakness, anxiety

• Fast, regular/irregular heartbeat

• Pain with respiration, acute vs chronic ischemia, crackles

• Lactic acidosis, may be low due to low CO

• SVR is usually increased

• Right-sided pressures

  • PVR unchanged

  • CVP usually normal if acute

  • PAP/PCWP – elevated with non-compliant LV

Sympathetic hyperactivity

• Occurs in patients with anterior wall ischemia (less freq with inferior wall)

• Release Epinephrine (adrenal glands) to compensate for low cardiac output and Norepinephrine (sympathetic nerves)

• Increases force and velocity of contraction

• Increased force, contraction, and heart rate will require more O2 but demand is not met due to ischemia → injury may increase

Parasympathetic Hyperactivity

• Decrease heart rate and SVR → less work for the heart, less O2, but systemic perfusion may not be enough

• sinus bradycardia

• acute inferior wall ischemia

Cardiac Biomarkers for heart disease

• Troponin

• BNP/NT-proBNP

• Creatine kinase and CK-MB

cardiac troponin

• High-sensitivity cardiac troponin

  • Detects myocardial injury

  • Myocardial infarction requires acute myocardial injury plus evidence of ischemia

BNP/NT-proBNP

• A hormone and protein produced by your heart ventricles

• Measures the amount of BNP hormone circulating in your blood; it increases when your heart muscle stretches or is under heavy pressure and fluid overload.

• Assessment of suspected heart failure

Old biomarkers for heart failure

• Creatine kinase and CK-MB

Acute Myocardial Infarction

• Myocardial necrosis that results from prolonged ischemia

• Death of cells first occurs in the innermost lining of the myocardium → coronary arteries run through the myocardium to supply O2

  • beings in the subendocardium

Coronary blood flow and ischemia

• Ischemia begins in the subendocardium first

• Systolic myocardial tension and O2 demands are greatest in this area → O2/perfusion is lowest to this region during systole because contraction compresses arteries

• Diastolic coronary blood flow is limited within the region

Transitional Zones of Ischemia Myocardial Dysfunction

1. Area of Necrosis: central core; little to no blood flow; unable to sustain life

2. Area of Injury: middle zone; surrounds the dead core
   - metabolic derangements: rapid drop in ATP, failure of the cellular sodium-potassium pumps, and localized lactic acidosis
   - ST elevation

3. Area of Ischemia: outermost zone; less disruption; can still be hypokinetic (T-wave inversion)

Time is muscle → during an MI the area of necrosis is fully dead and can’t be restored → door-to-balloon time tries to ensure that area of injury and ischemia does not get engulfed by necrosis

Treatment of acute MI

1. Restore coronary blood flow
   - primary PCI for STEM
   - fibrinolysis for STEMI patients when timely - break down clot, not used for NSTEMI or unstable angina
   - CABG may be appropriate

2. Limit ongoing ischemia
   - antiplatelet and anticoagulant therapy
   - oxygen for hypoxemia; anti-ischemic medications as hemodynamics permit

Complications of acute MI

• Heart failure, shock, and arrhythmias (treatment)

• may need mechanical circulatory support

Hemodynamic support AMI: preload and afterload

• Reduce preload

  • Nitroglycerin reduces venous return and LV filling pressures

• Reduce afterload

  • Selected vasodilators may improve forward flow; avoid worsening hypoperfusion

Myocardial oxygen-demand reduction

Beta-blockers reduce heart rate and contractility in appropriate patients

Cardiogenic shock

hemodynamic support

• vasoactive and inotropic support

• Revascularization and evaluation for mechanical complications are priorities

Mechanical complications of acute MI

1. Papillary Muscle Dysfunction
   - failure of normal mitral valve closure → regurgitation
   - posteromedial papillary muscle perfused by PDA → most affected by ischemia
   - anterolateral papillary muscle has dual coronary supply from LAD and circumflex

2. Complete Rupture
   - MI patient with shock and pulmonary edema, high-pitched murmur
   - referred for emergency surgery

Acute Ventricular Septal Defect

• Rupture of the ventricular septum, rare

• PA catheter can help diagnose VSD + echo-Doppler

  • Elevated pulmonary pressures

Cardiac Rupture

• Rupture of the left ventricular free wall

• Occurs 3-6 days after the initial infarct → necrotic tissue is friable

• slow leaks

  • tamponade in the pericardial sac

  • persistent hypertension

Right Ventricular Infarction

• Occurs in 30-50% of inferior STEMI

• Hypotension: elevated JVP, clear lungs, bradycardia

• treatment:

  • optimize RV preload

  • avoid nitrates/diuretics, give inotropes

  • early reperfusion, PCI

Aortic Stenosis Common Causes

• Progressive narrowing of the valve orifice

• Causes

  • Congenital: abnormal valve development → bicuspid instead of tricuspid

  • Degenerative: lesions form from cusp fibrosis and calcium deposition

  • Rheumatic aortic stenosis: progressive fibrosis of the commissures

    • Could be both stenotic and regurgitant

    • Presents in patients with rheumatic fever

    • Usually accompanies mitral involvement

Systolic abnormalities of aortic stenosis

• LV requires higher pressure to overcome the pressure of the aortic valve in order to eject LV volume

• Mean Gradient → average pressure difference between the left ventricle and the aorta during the systolic ejection period

  • High in aortic stenosis because the LV has to generate much higher pressure to eject blood through the narrowed opening at the same rate

  • causes

    • higher myocardial O2 demand

    • low SV

    • compensatory vasoconstriction - to generate higher pressure

Diastolic Abnormalities with Aortic stenosis

• Concentric hypertrophy → increased myocardial work → LV hypertrophy

  • resists filling

  • atrial contraction → enlargement of LA

• increased myocardial oxygen demand

Grading of Aortic Stenosis

Mild: 2.0-2.9 peak aortic velocity; less than 20 mmHg mean gradient; greater than 1.5 valve area

Moderate: 3.0-3.9 peak aortic velocity, 20-39 mmHg mean gradient; 1.0-1.5 valve area

Severe: greater than 4 peak velocity, greater than 40 mmHg mean gradient; less than 1.0 valve area

Critical Aortic Stenosis

• Less than 0.7 cm² valve area

• high dicrotic notch and narrow pulse pressure on waveform

Aortic Regurgitation (insufficiency)

• Reflux of blood back into LV from an incompetent aortic valve

• Acute = profound circulatory deficits and pulmonary edema

• Chronic = hyperdynamic circulation, adaptive dilation and hypertrophy

• Waveform changes = diastolic notch lower (or absent), and pulse pressure widens

  • because the valve never really closes all the way

Causes of aortic regurgitation

• Primary valve deformity
  - rheumatic fever, infectious endocarditis
  - collagen vascular diseases
  - congenital defects
  - trauma

• Secondary to dilation of the aortic root
  - hypertension
  - aortic dissection, medial necrosis of the aorta

Mitral Stenosis

• Narrowing of the mitral valve that causes blood to back up into the left atrium can cause LA enlargement → causes pulmonary congestion and pulmonary hypertension

  • Left ventricle will reduce in size due to less filling

• Rheumatic Fever is the most common cause → scarring and fusion of chordae tendineae, fibrotic thickening

Left atrial enlargement

• Accommodates increasing left atrial blood volume

• distorts atrial muscle contraction → prone to premature contraction → SVT, atrial fibrillation

• increased pulmonary lymph flow, diminished permeability of alveolar capillary membrane, hypertrophy of the pulmonary arterioles

Mitral Valve Regurgitation

• Inadequate closure of the mitral valve causes enlargement of LA, high pulmonary pressures, pulmonary edema, and systemic blood failure

• Caused by

  • mitral valve prolapse → leaflets flop into the atrium during ventricular systole

    • degeneration of the valve tissue

    • excessive length of the chordae tendinae

    • enlarged valve annulus

  • rheumatic heart disease

  • ischemic heart disease

  • left ventricular dilation